Author: "Gillian Moore" - Searchworks@Jio Institute Digital Library Search Results

42 results on '"Gillian Moore"'

1. Development and characterisation of a panel of phosphatidylinositide 3-kinase – mammalian target of rapamycin inhibitor resistant lung cancer cell lines

Author: Susan Heavey, Paul Dowling, Gillian Moore, Martin P. Barr, Niamh Kelly, Stephen G. Maher, Sinead Cuffe, Stephen P. Finn, Kenneth J. O’Byrne, and Kathy Gately
Subjects: Medicine, Science
Abstract: Abstract The PI3K-mTOR pathway is involved in regulating all hallmarks of cancer, and is often dysregulated in NSCLC, making it an attractive therapeutic target in this setting. Acquired resistance to PI3K-mTOR inhibition is a major hurdle to overcome in the success of PI3K-mTOR targeted agents. H460, A549, and H1975 resistant cells were generated by prolonged treatment in culture with Apitolisib (GDC-0980), a dual PI3K-mTOR inhibitor over a period of several months, from age-matched parent cells. Resistance was deemed to have developed when a log fold difference in IC50 had been achieved. Resistant cell lines also exhibited resistance to another widely investigated PI3K-mTOR dual inhibitor; Dactolisib (BEZ235). Cell lines were characterised at the level of mRNA (expression array profiling expression of >150 genes), miRNA (expression array profiling of 2100 miRNAs), protein (bottoms-up label-free mass spectrometry) and phosphoprotein (expression array profiling of 84 phospho/total proteins). Key alterations were validated by qPCR and Western blot. H1975 cells were initially most sensitive to Apitolisib (GDC-0980), but developed resistance more quickly than the other cell lines, perhaps due to increased selective pressure from the impressive initial effect. In-depth molecular profiling suggested epithelial-mesenchymal transition (EMT) may play a role in resistance to PI3K-mTOR dual inhibition in NSCLC.
Published: 2018
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2. Top Notch Targeting Strategies in Cancer: A Detailed Overview of Recent Insights and Current Perspectives

Author: Gillian Moore, Stephanie Annett, Lana McClements, and Tracy Robson
Subjects: notch antibodies, gamma secretase inhibitors, cancer stem cells, drug resistance, clinical trial, breast tumours, Cytology, QH573-671
Abstract: Evolutionarily conserved Notch plays a critical role in embryonic development and cellular self-renewal. It has both tumour suppressor and oncogenic activity, the latter of which is widely described. Notch-activating mutations are associated with haematological malignancies and several solid tumours including breast, lung and adenoid cystic carcinoma. Moreover, upregulation of Notch receptors and ligands and aberrant Notch signalling is frequently observed in cancer. It is involved in cancer hallmarks including proliferation, survival, migration, angiogenesis, cancer stem cell renewal, metastasis and drug resistance. It is a key component of cell-to-cell interactions between cancer cells and cells of the tumour microenvironment, such as endothelial cells, immune cells and fibroblasts. Notch displays diverse crosstalk with many other oncogenic signalling pathways, and may drive acquired resistance to targeted therapies as well as resistance to standard chemo/radiation therapy. The past 10 years have seen the emergence of different classes of drugs therapeutically targeting Notch including receptor/ligand antibodies, gamma secretase inhibitors (GSI) and most recently, the development of Notch transcription complex inhibitors. It is an exciting time for Notch research with over 70 cancer clinical trials registered and the first-ever Phase III trial of a Notch GSI, nirogacestat, currently at the recruitment stage.
Published: 2020
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3. Preservation of the fecal microbiome is associated with reduced severity of graft-versus-host disease

Author: Marina Burgos da Silva, Doris M. Ponce, Anqi Dai, Sean M. Devlin, Antonio L. C. Gomes, Gillian Moore, John Slingerland, Roni Shouval, Gabriel K. Armijo, Susan DeWolf, Teng Fei, Annelie Clurman, Emily Fontana, Luigi A. Amoretti, Roberta J. Wright, Hana Andrlova, Oriana Miltiadous, Miguel-Angel Perales, Ying Taur, Jonathan U. Peled, and Marcel R. M. van den Brink
Subjects: Feces, Butyrates, Bacteria, Microbiota, Immunology, Hematopoietic Stem Cell Transplantation, Humans, Graft vs Host Disease, Dysbiosis, Cell Biology, Hematology, Biochemistry
Abstract: Following allogeneic hematopoietic cell transplantation (allo-HCT), the gastrointestinal (GI) tract is frequently affected by acute graft-versus-host disease (aGVHD), the pathophysiology of which is associated with a dysbiotic microbiome. Since microbial composition varies along the length of the GI tract, the authors hypothesized that microbiome features correlate with the pattern of organ involvement after allo-HCT. We evaluated 266 allo-HCT recipients from whom 1303 stool samples were profiled by 16S ribosomal gene sequencing. Patients were classified according to which organs were affected by aGVHD. In the 20 days prior to disease onset, GVHD patients had lower abundances of members of the class Clostridia, lower counts of butyrate producers, and lower ratios of strict-to-facultative (S/F) anaerobic bacteria compared with allograft recipients who were free of GVHD. GI GVHD patients showed significant reduction in microbial diversity preonset. Patients with lower GI aGVHD had lower S/F anaerobe ratios compared with those with isolated upper GI aGVHD. In the 20 days after disease onset, dysbiosis was observed only in GVHD patients with GI involvement, particularly those with lower-tract disease. Importantly, Clostridial and butyrate-producer abundance as well as S/F anaerobe ratio were predictors of longer overall survival; higher abundance of butyrate producers and higher S/F anaerobe ratio were associated with decreased risk of GVHD-related death. These findings suggest that the intestinal microbiome can serve as a biomarker for outcomes of allo-HCT patients with GVHD.
Published: 2022
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4. The Art of Advice

Author: Gillian Moore
Subjects: Medical education, Literature and Literary Theory, Psychology, Advice (programming)
Published: 2021
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5. Convalescent plasma in patients admitted to hospital with COVID-19 (RECOVERY): a randomised controlled, open-label, platform trial

Author: Obbina Abani, Ali Abbas, Fatima Abbas, Mustafa Abbas, Sadia Abbasi, Hakam Abbass, Alfie Abbott, Nabeel Abdallah, Ashraf Abdelaziz, Mohamed Abdelfattah, Bushra Abdelqader, David Abdo, Basir Abdul, Althaf Abdul Rasheed, Ajibode Abdulakeem, Rezan Abdul-Kadir, Amina Abdulle, Abdulfatahi Abdulmumeen, Rasheed Abdul-Raheem, Niyaz Abdulshukkoor, Kula Abdusamad, Yazeed Abed El Khaleq, Mai Abedalla, Abeer Ul Amna Abeer Ul Amna, Katrina Abernethy, Adebanke Aboaba, Hani Abo-Leyah, Ahmed Abou-Haggar, Mahmoud Abouibrahim, Miriam Abraham, Tizzy Abraham, Abraheem Abraheem, Judith Abrams, Hyacinth-John Abu, Ahmed Abu-Arafeh, Syed M Abubacker, Akata Abung, Yaa Aceampong, Amaka Achara, Devikumar Acharya, Sarah Acheampong, Janet Acheson, Andres Acosta, Catherine Acton, Jacqueline Adabie-Ankrah, Sara Adair, Fiona Adam, Matthew Adam, Huzaifa Adamali, Carol Adams, Charlotte Adams, Kate Adams, Lisa Adams, Richard Adams, Tim Adams, Kirsty Adcock, Jemaimah Addai, Ade Adebiyi, Ken Adegoke, Vicki Adell, Debo Ademokun, Sherna Adenwalla, Oluwasegun A Adesemoye, Emmanuel O Adewunmi, Joyce Adeyemi, Rina Adhikary, Gabrielle Adkins, Adnan Adnan, John Aeron-Thomas, Debbie Affleck, Dominic Affron, Carmel Afnan, Muhammad Afridi, Zainab A Aftab, Meenakshi Agarwal, Rachel Agbeko, Chris Agbo, Penny Agent, Sunil Aggarwal, Arameh Aghababaie, Shafana Ahamed Sadiq, Mohamed H Ahammed Nazeer, Humayun Ahmad, Mohammad Ahmad, Syed Ahmad, Asim Ahmed, Bilal Ahmed, Forizuddin Ahmed, Hamze Ahmed, Iram Ahmed, Irshad Ahmed, Khaled Ahmed, Liban Ahmed, Mahin Ahmed, Maria C Ahmed, Muhammad S Ahmed, Naseer Ahmed, Nausheen Ahmed, Osama Ahmed, Rajia A Ahmed, Rizwan Ahmed, Saif Ahmed, Sammiya Ahmed, Sara Ahmed, Sophia Ahmed, Syed Ahmed, Syed Haris Ahmed, Roa Ahmed Ali, Sana Ahmed, Sana Ahmer, Dhiraj Ail, Mark Ainsworth, Giulia Airoldi, Myriam Aissa, Lindianne Aitken, Bini Ajay, Francis Ajeneye, Abdulakeem Ajibode, Ayesha Ajmi, Tahir Akbar, Naim Akhtar, Nasim Akhtar, Nauman Akhtar, Suha Akili, Oludoyinsola Akindolie, Yinka Akinfenwa, Olugbenga Akinkugbe, Ibrahim Akinpelu, Olajide Akinwumiju, Olugbenro Aktinade, Ahmad Al Aaraj, Asma Al Balushi, Majd Al Dakhola, Aladdin Al Swaifi, Eslam Al-Abadi, Narendra Aladangady, Ayaz Alam, Sajid Alam, Abbas Al-Asadi, Karina Al-Asadi, Kyriaki Alatzoglou, Manaf Al-Bayati, Paul Albert, Lorraine Albon, Gemma Alcorn, Stephen Alcorn, Aggie Aldana, David Alderdice, Rayan Aldouri, Jonathan Aldridge, Nicolas Aldridge, Ana Alegria, Alison Alexander, John Alexander, Peter D G Alexander, Charlotte Alford, Julyan Al-Fori, Laith Alghazawi, Bahij Al-Hakim, Shams Al-Hity, Ali Ali, Asad Ali, Fawzia R Ali, Hoodo Ali, Jawad Ali, Mariam Ali, Mohammad Ali, Nayab Ali, Oudai Ali, Sabira Ali, Sakina Ali, Syed Ali, Abid Alina, Fine Aliyuda, Katrin Alizadeh, Maithem Al-Jibury, Saba Al-Juboori, Majid Al-Khalil, Moutaz Alkhusheh, Allameddine Allameddine, Fiona Allan, Rachel Allan, Alison Allanson, Robert Allcock, Beverley Allen, Eireann Allen, Jess Allen, Kerry Allen, Laura Allen, Louise Allen, Poppy Allen, Rebecca Allen, Sam Allen, Sharon Allen, Simon Allen, Kathryn Allison, Bethan Allman, Lynne Allsop, Hassan Al-Moasseb, Magda Al-Obaidi, Lina Alomari, Akram Al-Rabahi, Bahar Al-Ramadhani, Zayneb Al-Saadi, Inji Alshaer, Rustam Al-Shahi Salman, Warkaq Al-Shamkhani, Bashar Al-Sheklly, Sara Altaf, Mary Alvarez, Balaal Alyas, Maysaa Alzetani, Susan Amamou, Noor Amar, Sakkarai Ambalavanan, Sarah-Jayne Ambler, Robert Ambrogetti, Chris Ambrose, Amir Ameen, Kenneth Amenyah, Maria R Amezaga, Allison Amin, Amina Amin, Kanish Amin, Syed Amin, Tara Amin, Amjad Amjad, Neelma Amjad, Mariam Ammoun, Victoria Amosun, Khaled Amsha, Pugh Amy, Atul Anand, Rekha Anand, Samantha Anandappa, Julie Anderson, Kevin Anderson, Laura Anderson, Michelle Anderson, Nicola Anderson, Rachel Anderson, Rory Anderson, Wendy Anderson, Prematie Andreou, Angela Andrews, Antonette Andrews, Jill Andrews, Susan Andrews, Gregory Andrikopoulos, Kanayochukwu Aneke, Andrew Ang, Wan Wei Ang, Tammy Angel, Aramburo Angela, Paola Angelini, Lazarus Anguvaa, Oleg Anichtchik, Millicent Anim-Somuah, Krishnan Aniruddhan, Jessica Annett, Patrick J Anstey, Rebekah Anstey, Alpha Anthony, Aaron Anthony-Pillai, Philip Antill, Zhelyazkova Antonina, Varghese Anu, Muhammad Anwar, George Apostolides, Aristeidis Apostolopoulos, Sarah Appleby, Diane Appleyard, Maia Far Aquino, Bianca Araba, Samuel Aransiola, Mariana Araujo, Emily Arbon, Ann Archer, Denise Archer, Simon Archer, Christian Ardley, Ana-Maria Arias, Ryoki Arimoto, Charlotte Arkley, Charlotte Armah, Ilianna Armata, Adam Armitage, Ceri Armstrong, Maureen Armstrong, Sonia Armstrong, Sylvia Armstrong-Fisher, Philippa Armtrong, Heike Arndt, Clare Arnison-Newgass, David Arnold, Rachael Arnold, Sarah Arnott, Dhawal Arora, Kavan Arora, Pardeep Arora, Rishi Arora, Andrea Arroyo, Arslam Arter, Ayush Arya, Rita Arya, Denisa Asandei, Adeeba Asghar, Catherine Ashbrook-Raby, Glen Ashby, Helen Ashby, Jan Ashcroft, John Ashcroft, Samuel Ashcroft, Deborah Asher, Ayesha Ashfaq, Ben Ashford, Suhail Ashgar, Abdul Ashish, Sally Ashman-Flavell, Sundar Ashok, Abd-El-Aziz Ashour, Muhammad Z Ashraf, Saima Ashraf, Mohammad B Ashraq, Deborah Ashton, Susan Ashton, Andrew Ashworth, Rebecca Ashworth, Arshia Aslam, Harshini Asogan, Abigail Asquith, Atif Asrar, Omar Assaf, Raine Astin-Chamberlain, Richard Athay-Hunt, Deborah Athorne, Billie Atkins, Christopher Atkins, Stacey Atkins, John Atkinson, Vicki Atkinson, Brygitta Atraskiewicz, Claire Atterbury, Abdul Ahmad Attia, Rita Atugonza, Paula Aubrey, Avinash Aujayeb, Aye Chan Thar Aung, Hnin Aung, Kyaw Thu Aung, Ni Aung, Yin Aung, Zaw Myo Aung, Emily Austin, Karen Austin, Abdusshakur Auwal, Miriam Avery, Joanne Avis, Georgina Aviss, Cristina Avram, Paula Avram, Gabriel Awadzi, Atia Awan, Aszad Aya, Eman Ayaz, Amanda Ayers, Jawwad Azam, Mohammed Azharuddin, Ghazala Aziz, N Aziz, Ali Azkoul, Ashaari Azman Shah, Giada Azzopardi, Hocine Azzoug, Fiyinfoluwa Babatunde, Melvin Babi, Babiker Babiker, Gayna Babington, Matthew Babirecki, Marta Babores, Adetona O Babs-Osibodu, Sammy Bacciarelli, Roudi Bachar, Gina Bacon, Jenny Bacon, Bibi Badal, Gurpreet R Badhan, Shreya Badhrinarayanan, Joseph P Bae, Sibel Bafekr Mishamandani, Alice Baggaley, Amy Baggott, Graham Bagley, Dinesh Bagmane, Lynsey Bagshaw, Kasra Bahadori, James Bailey, Katie Bailey, Lindsey Bailey, Liz Bailey, Morgan Bailey, Pippa Bailey, Sarah Bailey, Stephen Bailey, Hamish Baillie, J Kenneth Baillie, Jennifer Bain, Sanchia Baines, Vikram Bains, Aimi Baird, David Baird, Susan Baird, Tracy Baird, Yolanda Baird, Aiysha Bajandouh, Charles Baker, Emma Baker, Evelyn Baker, Johanne Baker, Josephine Baker, Kenneth Baker, Rebecca Baker, Terri-Anne Baker, Victoria Baker, Hugh Bakere, Nawar Bakerly, Michelle Baker-Moffatt, Nauman Bakhtiar, Panos Bakoulas, Julie Balaam, Niranjan Balachandran, Andrea Balan, Theodosios Balaskas, Madhu Balasubramaniam, Alison Balcombe, Alexander Baldwin, Ashley Baldwin, Caron Baldwin, Danielle Baldwin, Rebekah Baldwin-Jones, James Balfour, Gagan Bali, Sonya Balkee, Ceri Ball, Kasia Ballard, Amy Ballinger, Ismael Balluz, Craig Balmforth, Emese Balogh, Amir Baluwala, Gabby Bambridge, Alasdair Bamford, Amy Bamford, Peter Bamford, Adefunke Bamgboye, Elizabeth Bancroft, Hollie Bancroft, Tanya Bancroft, Joyce Banda, Krishna Bandaru, Srini Bandi, Nageswar Bandla, Somaditya Bandyopadhyam, Amit Banerjee, Millie Banerjee, Ritwik Banerjee, Harrison Banks, Lauren Banks, Luke Banks, Paul Banks, Oliver Bannister, Bharat Bansal, Robert Banthorpe, Laura Banton, Mariamma Baptist, Tanya Baqai, Ananya Mouli Baral, Desislava Baramova, Alex Barber, Russel Barber, Emma Barbon, Miriam Barbosa, Monica Barbosa, Jamie Barbour, Alexander Barclay, Claire Barclay, George Bardsley, Stephanie Bareford, Shahedal Bari, Amy Barker, Debbie Barker, Helen Barker, Joseph Barker, Leon Barker, Oliver Barker, Kerry Barker-Williams, Sinha Barkha, Juliana Barla, Gavin Barlow, Richard Barlow, Valerie Barlow, James Barnacle, Alex Barnard, Debi Barnes, Nicky Barnes, Theresa Barnes, Calum Barnetson, Amy Barnett, Matthew Barnett, Ashton Barnett-Vanes, William Barnsley, Andrew Barr, David Barr, Shaney Barratt, Manuella Barrera, Amy Barrett, Fiona Barrett, Jessica Barrett, Joe Barry, Jazz Bartholomew, Claire Bartlett, Georgina Bartlett, Greg Barton, Jill Barton, Lorna Barton, Rachael Barton, Rosaleen Baruah, Sonia Baryschpolec, Archana Bashyal, Betsy Basker, Ayten Basoglu, Gilda Bass, John Bassett, G Bassett, Chris Bassford, Pavinder Bassi, Betsy Bassis, Bengisu Bassoy, Victoria Bastion, Anupam Basumatary, Tristan Bate, Harry J Bateman, Ian Bateman, Kathryn Bateman, Vhairi Bateman, Eleanor Bates, Hayley Bates, Michelle Bates, Simon Bates, Sally Batham, Ana Batista, Amit Batla, Dushyant Batra, Donna Batty, Harry Batty, Thomas Batty, Peter Baughan, Miranda Baum, Carina Bautista, Fareha Bawa, Fatima S Bawani, Simon Bax, Lydia Baxter, Matt Baxter, Nicola Baxter, Zachary Baxter, Hannah Bayes, Charlotte Baylem, Lee Bayliss, Eileen Bays, Farid Bazari, Rohit Bazaz, Ahmad Bazli, Laura Beacham, Wendy Beadles, Philip Beak, Andy Beale, Kirk Beard, Jack Bearpark, Karen Beaumont, Dawn Beaumont-Jewell, Theresa Beaver, Sarah Beavis, Christy Beazley, Sarah Beck, Virginia Beckett, Rosie Beckitt, Heidi Beddall, Seonaid Beddows, Deborah Beeby, Gail Beech, Michelle Beecroft, Sally Beer, Jane Beety, Gabriela Bega, Alison Begg, Susan Begg, Sara Beghini, Ayesha Begum, Salman Begum, Selina Begum, Teresa Behan, Jasmine Beharry, Roya Behrouzi, Jon Beishon, Claire Beith, James Belcher, Holly Belfield, Katherine Belfield, Ajay Belgaumkar, Dina Bell, Gareth Bell, Gill Bell, Gillian Bell, Joshua Bell, Lauren Bell, Louise Bell, Nicholas Bell, Pippa Bell, Stephanie Bell, Jennifer L Bell, Jennifer Bellamu, Mary Bellamy, Arianna Bellini, Amanda Bellis, Fionn Bellis, Lesley Bendall, Naveena Benesh, Nicola Benetti, Leonie Benham, Guy Benison-Horner, Alexander Bennett, Ann Bennett, Caroline Bennett, Christopher Bennett, Gillian Bennett, Ian Bennett, Kristopher Bennett, Lorraine Bennett, Sara Bennett, Karen Bennion, Vivienne Benson, Jane Benstead, Andrew Bentley, Dionne Bentley, James Bentley, Ian Benton, Eva Beranova, Matthew Beresford, Colin Bergin, Malin Bergstrom, Jolanta Bernatoniene, Thomas Berriman, Zoe Berry, Marnie Berwick, Kimberley Best, Ans-Mari Bester, Yvonne Beuvink, Emily Bevan, Sarah Bevins, Tom Bewick, Andrew Bexley, Sonay Beyatli, Fenella Beynon, Arjun Bhadi, Sanjay Bhagani, Shiv Bhakta, Rekha Bhalla, Khushpreet Bhandal, Kulbinder Bhandal, Ashwin Bhandari, Sangam Bhandari, Aashutosh Bhanot, Ravina Bhanot, Sruti Bhaskara, Prashanth Bhat, Nikhil Bhatia, Rahul Bhatnagar, Karan Bhatt, Janki Bhayani, Deepika Bhojwani, Salimuzzaman Bhuiyan, Anna Bibby, Fatima Bibi, Naheeda Bibi, Salma Bibi, Tihana Bicanic, Sarah Bidgood, Julie Bigg, Sarah Biggs, Alphonsa Biju, Andras Bikov, Sophie Billingham, Jessica Billings, Carron Bilton, Teodirico Binas, Martin Binney, Alice Binns, Muhammad BinRofaie, Oliver Bintcliffe, Catherine Birch, Jenny Birch, Louann Birch, Janet Birchall, Katherine Birchall, Sam Bird, Sumedha Bird, Charndip Biring, Mark Birt, Raquel Bisa, Kilanalei Bishop, Linda Bishop, Lisa Bishop, Karen Bisnauthsing, Nibedan Biswas, Sahar Biuk, Karen Blachford, Ethel Black, Helen Black, Karen Black, Mairead Black, Polly Black, Hayley Blackgrove, Bethan Blackledge, Joanne Blackler, Samantha Blackley, Helen Blackman, Stuart Blackmore, Caroline Blackstock, Loraine Blackwood, Francesca Blakemore, Helen Blamey, Alison Bland, Sujata Blane, Simon Blankley, Mary Blanton, Parry Blaxill, Jenny Blaxland, Katie Blaylock, Jane Blazeby, Carol Blears, Natalie Blencowe, Donna Blofield, Ben Bloom, Jack Bloomfield, Angela Bloss, Hannah Bloxham, Louise Blundell, Andrew Blunsum, Mark Blunt, Ian Blyth, Kevin Blyth, Andrew Blythe, Karen Blythe, Marilyn Boampoaa, Boniface Bobie, Karen Bobruk, Pritesh Bodalia, Neena Bodasing, Tanya Bodenham, Sherin Bodh, Gabriele Boehmer, Marta Boffito, Kristyna Bohmova, Sumit Bokhandi, Maria Bokhar, Saba Bokhari, Sakina Bokhari, Syed Owais Bokhari, Ambrose Boles, Sarah Bollington, Sam Bolton, Charlotte Bomken, Charlotte Bond, Hayley Bond, Helena Bond, Stuart Bond, Thomas Bond, Alice Bone, Georgia Boniface, Wendy Bonnert, Lizzy Bonney, Leigh Boorman, Catherine Booth, Joanne Borbone, Cameron Borhani, Naomi Borman, Rachel Borrell, Mamu Boshir, Fiona Bottrill, Laura Bough, Hayley Boughton, Zoe Boult, Miriam Bourke, Stephen Bourke, Michelle Bourne, Rachel Bousfield, Lucy Boustred, Darren Bowen, Kaye Bowen, Alexandra Bowes, Amy Bowes, Philip Bowker, Louise Bowman, Simon Bowman, Rachel Bowmer, Angie Bowring, Geoff Bowyer, Helen Bowyer, Carmel Boyd, Jenny Boyd, Laura Boyd, Maxine Boyd, Namoi Boyle, Pauline Boyle, Rosalind Boyle, Louise Boyles, Osman Bozdag, Leanna Brace, David Brack, Charlotte Brackstone, Rob Bradburn, Jodie Bradder, Barry Bradley, Clare Jane Bradley, Pamela Bradley, Patrick Bradley, Paul Bradley, Joanne Bradley-Potts, Lynne Bradshaw, Sarah Bradshaw, Zena Bradshaw, Rebecca Brady, Shirin Brady, Denise Braganza, Suhail Brailsford, Jill Braithwaite, Marie Branch, Thomas Brankin-Frisby, Jamie Brannigan, Louise Brassington, Sophie Brattan, Fiona Bray, Nancy Bray, Angela Brazier, Manny Brazil, Lucy Brear, Tracy Brear, Stephen Brearey, Laura Bremner, Morwenna Brend, Giovanna Bretland, Chris Brewer, Hannah Bridge, Gavin Bridgwood, Hayley Briggs, Mark Briggs, Sara Brigham, John Bright, Chris Brightling, Lutece Brimfield, Elaine Brinkworth, Robin Brittain-Long, Vianne Britten, Terri Brittin, Lauren Broad, Sarah Broad, Rosie Broadhurst, Andrew Broadley, Marie Broadway, Christopher Brockelsby, Megan Brocken, Tomos Brockley, Andrew Broderick, Mary Brodsky, Fiona Brogan, David Broggio, Liz Brohan, Felicity Brokke, Jacob Brolly, David Bromley, Hannah Brooke-Ball, Verity Brooker, Ceri Brookes, Matthew Brookes, Alison Brooks, Karen Brooks, Nicole Brooks, Philip Brooks, Rachel Brooks, Sophie Brooks, Natalie Broomhead, Chloe Broughton, Nathaniel Broughton, Matt Brouns, Marie Browett, Alison Brown, Ammani Brown, Carly Brown, Catrin Brown, Chloe Brown, Elizabeth Brown, Ellen Brown, Heather Brown, Janet Brown, Louise Brown, Niall Brown, Pauline Brown, Rachel Brown, Richard Brown, Robert Brown, Steven Brown, Tom Brown, Wayne Brown, Bria Browne, Charlotte Browne, Duncan Browne, Mitchell Browne, Stephen Brownlee, Alba Brraka, David Bruce, Johanna Bruce, Michelle Bruce, Wojciech Brudlo, Nigel Brunskill, Alan Brunton, Margaret Brunton, Mandy Bryan, Meera Bryant, April Buazon, Maya Buch, Julie Buchan, Ruaridh Buchan, Alexis Buchanan, Ruaridh Buchanan, Danielle Buche, Amanda Buck, Matthew Buckland, Laura Buckley, Philip Buckley, Sarah Buckley, Carol Buckman, Kathleen Buckmire, George Bugg, Ramadan Bujazia, Marwan Bukhari, Shanze Bukhari, Richard Bulbulia, Alex Bull, Damian Bull, Rhian Bull, Thomas Bull, Naomi Bulteel, Kasun Bumunarachchi, Roneleeh Bungue-Tuble, Caroline Burchett, Dorota Burda, Christy Burden, Thomas G Burden, Mika Burgess, Paula Burgess, Richard Burgess, Sophia Burgess, Paula Burgett, Adrian Burman, Sara Burnard, Caroline Burnett, John Burnett, Amanda Burns, Amy Burns, Collette Burns, James Burns, Karen Burns, Samuel Burns, Sarah Burns, Daniel Burrage, Sadie Burrage, Kate Burrows, Claire Burston, Ben Burton, Fiona Burton, Matthew Burton, Angela Busby, Deborah Butcher, Aaron Butler, Jessica Butler, Joanne Butler, Joshua Butler, Lesley Butler, Peter Butler, Susan Butler, Al-Tahoor Butt, Mohammad M Butt, Sophia Butt, Caryl Butterworth, Nicola Butterworth-Cowin, Robert Buttery, Tom Buttle, Heather Button, Daniel Buttress, Jane Byrne, Wendy Byrne, Victoria Byrne-Watts, Eleanor Byworth, Amanda Cabandugama, Ruth Cade, Anthony Cadwgan, Donna Cairney, James Calderwood, Darren Caldow, Moira Caldwell, Giorgio Calisti, Debbie Callaghan, Jennifer Callaghan, Claire Callens, Donaldson Callum, Caroline Calver, Melissa Cambell-Kelly, Tracey Camburn, David R Cameron, Eleanor Cameron, Fraser Cameron, Sarah Cameron, Sheena Cameron, Christian Camm, Renee F D Cammack, Alison Campbell, Amy Campbell, Barbara Campbell, Bridget Campbell, Debbie Campbell, Helen Campbell, Hilary Campbell, Jonathan Campbell, Mark Campbell, Robyn Campbell, Wynny Campbell, Quentin Campbell Hewson, Julie Camsooksai, Ana Canabarro, Lisa Canclini, Shaula Mae Candido, Janie Candlish, Cielito Caneja, Johnathon Cann, Ruby Cannan, Emma Cannon, Michael Cannon, Petra Cannon, Vivienne Cannons, Jane Cantliff, Ben Caplin, Santino Capocci, Noemi Caponi, Angelika Capp, Anne Capps-Jenner, Thomas Capstick, Ishmael Carboo, Nuria Cardenas, Mary Cardwell, Rachel Carey, Simon Carley, Tammy Carlin, Andrew Carlton, Samantha Carmichael, Mandy Carnahan, Rebecca Carnegie, Charlotte Caroline, Emily Carpenter, Jodi Carpenter, David Carr, Sharon Carr, Anna Carrasco, Samantha Carrington, Zoe Carrington, Paul Carroll, Caroline Carron, Anne Carstairs, Jonathan Carter, Michael Carter, Moira Carter, Paul Carter, Penny Carter, Steven Carter, Simon Carter-Graham, Douglas Cartwright, Jo-Anne Cartwright, Claire Carty, Sinead Carty, Jaime Carungcong, Carolyn Carveth-Marshall, Susan Casey, Annie Cassells, Barbara Cassimon, Teresa Castiello, Gail Castle, Bridget Castles, Melanie Caswell, Ana Maria Catana, Heidi Cate, Susanne Cathcart, Katrina Cathie, Christine Catley, Laura Catlow, Matthew Caudwell, Jill Caulfield, Anna Cavazza, Luke Cave, Simon Cavinato, Frianne Cawa, Kathryn Cawley, Chloe Caws, Hankins Cendl, Hannah Century, Jeva Cernova, Mansur Cesay, Ed Cetti, Stephanie Chabane, Manish Chablani, Cathleen Chabo, David Chadwick, Julie Chadwick, Robert Chadwick, Ela Chakkarapani, Arup Chakraborty, Mallinath Chakraborty, Mollika Chakravorty, James Chalmers, Richard Chalmers, Georgina Chamberlain, Sarah Chamberlain, Emma Chambers, Jonathan Chambers, Lucy Chambers, Naomi Chambers, Alex Chan, Carmen Chan, Cheuk Chan, Evelyn Chan, Kayen Chan, Kimberley Chan, Ping Chan, Rebekah (Pui-Ching) Chan, Xin Hui Chan, Chris Chandler, Heidi Chandler, Kim J Chandler, Stuart Chandler, Zoe Chandler, Vikki Chandler-Vizard, Sumit Chandra, Navin Chandran, Badrinathan Chandrasekaran, Cherry Chang, Yvonne Chang, Josephine Chaplin, Graeme Chapman, John Chapman, Katie Chapman, Laura Chapman, Lianne Chapman, Polly Chapman, Timothy Chapman, Lucy Chappell, Linda Chapple, Amanda Charalambou, Bethan Charles, Dianne Charlton, Sally Charlton, Kevin Chatar, Calvin Chatha, Ritesh Chaube, Muhammad YN Chaudhary, Iram Chaudhry, Nazia Chaudhuri, Muhammad Chaudhury, Anoop Chauhan, Ruchi S Chauhan, Vipul Chauhan, Nicola Chavasse, Iknam Chaven, Rosanna Chavez, Vipal Chawla, Maria Cheadle, Lindsay Cheater, James Cheaveau, Charlotte Cheeld, Michelle Cheeseman, Fang Chen, Hui Min Chen, Terence Chen, Lok Yin Cheng, Zhihang Cheng, Helen Chenoweth, Chun How Cheong, Shiney Cherian, Suzanne Cherif, Mary Cherrie, Helen Cheshire, Barry Chesterson, Betty Cheung, Chee Kay Cheung, Elaine Cheung, Michelle Cheung, Claire Cheyne, Swati Chhabra, Wei Ling Chia, Eric Chiang, Angela Chiapparino, Rosavic Chicano, Zviedzo A Chikwanha, Sam Chilcott, Phillipa Chimbo, KokWai Chin, Wen Jie Chin, Rumbidzai Chineka, Amol Chingale, Karen Chinn, Vashira Chiroma, Heather Chisem, Claire Chisenga, Ben Chisnall, Carolyn Chiswick, Sunder Chita, Nihil Chitalia, Matthew Chiu, Brenda Chivima, Catherine Chmiel, Soha Choi, Willy Choon Kon Yune, Vandana Choudhary, Sarah Choudhury, Bing-Lun Chow, Fateha Chowdhury, Mahibbur Chowdhury, Shahid Chowdhury, Victoria Christenssen, Peter Christian, Alexander Christides, Fiona Christie, Daniel Christmas, Thereza Christopherson, Mark Christy, Paris Chrysostomou, Yunli Chua, Shabs Chucha, Dip Chudgar, Richard Chudleigh, Srikanth Chukkambotla, Michael E Chukwu, Izu Chukwulobelu, Chi Y Chung, Ben Church, Elaine Church, Sara R Church, David Churchill, Nicole Cianci, Nick Ciccone, Paola Cicconi, Paola Cinardo, Zdenka Cipinova, Bessie Cipriano, Sarah Clamp, Melanie Clapham, Edel Clare, Sarbjit Clare, Andrew Clark, Charlotte Clark, Diane Clark, Felicity Clark, Gabrielle Clark, James Clark, Katherine Clark, Kaylea Clark, Louise Clark, Lucy Clark, Matthew Clark, Patricia Clark, Richard Clark, Thomas Clark, Wendy Clark, Zoe Clark, Andrea Clarke, Heather Clarke, Mark Clarke, Paul Clarke, Robert Clarke, Roseanne Clarke, Samantha Clarke, Sarah Clarke, Sheron Clarke, Tracy Clarke, Andrew Clarkson, Alleyna Claxton, Kate Clay, Elizabeth Clayton, Olivia Clayton, Jill Clayton-Smith, Chris Cleaver, Carlota Clemente de la Torre, Jayne Clements, Suzanne Clements, Francesca Clemons, Lee Clifford, Lynne Clifford, Rachael Clifford, Sarah Clifford, Amelia Clive, Jonathan Clouston, Samantha Clueit, Andrea Clyne, Michelle Coakley, Peter G L Coakley, Tony Coates, Kathryn Cobain, Alexandra Cochrane, Patricia Cochrane, Maeve Cockerell, Helen Cockerill, Shirley Cocks, Rachel Codling, Adam Coe, Samantha Coetzee, David Coey, Danielle Cohen, Jonathan Cohen, Oliver Cohen, Mike Cohn, Louise Coke, Olutoyin Coker, Nicholas Colbeck, Roghan Colbert, Carol Cole, Esther Cole, Jade Cole, Joby Cole, Julie Cole, Richard Cole, Sue Cole, Garry Coleman, Matt Coleman, Holly Coles, Rebecca Coles, Macleod Colin, Alicia Colino-Acevedo, Julie Colley, Dawn Collier, Heather Collier, Paul Collini, Emma Collins, Jaimie Collins, Joanne Collins, Nicola Collins, Sally Collins, Vicky Collins, Andrew Collinson, Bernadette Collinson, Jennifer Collinson, Matthew Collis, Madeleine Colmar, Hayley E Colton, James Colton, Katie Colville, Carolyn Colvin, Ryan Colwell, Edward Combes, David Comer, Alison Comerford, Mike Comery, Dónal Concannon, Robin Condliffe, Lynne Connell, Natalie Connell, Karen Connelly, Gavin Connolly, Mireille Connolly, Emma Connor, Samantha Conran, Antonia Conroy, Veronica Conteh, Rory Convery, Camilla Conway, Francesca Conway, Grainne Conway, Rhiannon Conway, Jo-Anna Conyngham, Colette Cook, Eloise Cook, Gemma Cook, Helen Cook, Julie Cook, Danielle Cooke, Graham Cooke, Katrina Cooke, Soo Cooke, Tim Cooke, Adele Cooper, Alison Cooper, Chris Cooper, David Cooper, Helen Cooper, Jamie Cooper, Joanne Cooper, Joshua Cooper, Laura Cooper, Lauren Cooper, Nick Cooper, Rowena Cooper, Emma Cooperwaite, Thomas Cope, Sinead Corbet, Carolyn Corbett, John Corcoran, Chris Cordell, Jessica Cordle, Alasdair Corfield, John Corless, Alison Corlett, Joe Cornwell, Michael Cornwell, Diana Corogeanu, Mirella Corredera, Ruth Corrigan, Catherine Corry, Rita Corser, Denise Cosgrove, Tracey Cosier, Patricia Costa, Charlie Coston, Susannah Cotgrove, Zoe Coton, Lisa-Jayne Cottam, Rhiannon Cotter, Donna Cotterill, Alice Cotton, Caroline Cotton, Katy Cotton, Andrew Coull, James Coulson, David Counsell, David Counter, Cherry Coupland, Ellie Courtney, Julia Courtney, Rebecca Cousins, Alexander Cowan, Elena Cowan, Ruth Cowburn, Richard Cowell, Louise Cowen, Steve Cowman, Amanda Cowton, Debra Anne Cox, Ellie Cox, Giles Cox, Karina Cox, Miriam Cox, Karen Coy, Beverly Craig, Victoria Craig, Felicity Craighead, Matthew Cramp, Beverley Crane, Jacolene Crause, Adrian Crawford, Angie Crawford, Emma Crawford, Isobel Crawford, Richard Crawforth, Sarah Crawshaw, Ben Creagh-Brown, Andrew Creamer, Ryan Creighton, Joanne Cremona, Saveria Cremona, Janet Cresswell, Mark Cribb, Charles Crichton, Declan Crilly, Lauren Crisp, Nikki Crisp, Dominic Crocombe, Maria Croft, Ian Cron, Derrick Crook, Jennifer Crooks, Helen Croot, Harriet Crosby, Sarah Cross, Tim Cross, Amy Crothers, Stephen Crotty, Susan Crouch, Madeleine Crow, Amanda Crowder, Kate Crowley, Teresa Crowley, Rebecca Croysdill, Callum Cruickshank, Conor Cruickshank, Irena Cruickshank, James Cruise, Helen Crumley, Carina Cruz, Trino Cruz Cervera, Dominic Cryans, Guanguo Cui, Helen Cui, Donna Cullen, Lorraine Cullen, Gillian Cummings-Fosong, Marie Cundall, Victoria Cunliffe, Lorraine Cunningham, Neil Cunningham, Nicola Cunningham, Jason Cupitt, Hollie Curgenven, Debra Curley, Gerens Curnow, David Curran, Simon Curran, Craig Currie, Jacqueline Currie, Scarlett Currie, Abi Curtis, Becca Curtis, Jonathan Curtis, Katrina Curtis, Olivia Curtis, Thomas Curtis, Rebecca Cuthbertson, Sean Cutler, Marta Czekaj, Patrycja Czylok, Joana da Rocha, Andrew Dagens, Helen Daggett, Phil Daggett, Jacqui Daglish, Sandeep Dahiya, Helen Dakers-Black, Anne Dale, Katie Dale, Michaela Dale, Sam Dale, Jolyon Dales, Helen Dalgleish, Nikki Dallas, Helen Dallow, Dermot Dalton, Zoe Daly, Akila Danga, Amelia Daniel, Priya Daniel, Allison Daniels, Adela Dann, Sandra Danso-Bamfo, Nimo Daoud, Alex Darbyshire, Janet Darbyshire, Paul Dargan, Paul Dark, Tace Darling, Kate Darlington, Tom Darton, Guledew Darylile, Manjusha Das, Sukamal Das, Martin Daschel, Joanne Dasgin, Dibyendu Datta, Anna Daunt, Emily Davenport, Mark Davey, Michelle Davey, Miriam Davey, Molly Davey, Arlene David, Mini David, Alexander Davidson, Laura Davidson, Neil Davidson, Richard Davidson, Albert Davies, Alison Davies, Amanda Davies, Amy Davies, Angela Davies, Carolyn Davies, Catrin Davies, Cheryl Davies, Drew Davies, Elaine Davies, Ffyon Davies, Helen Davies, James Davies, Jane Davies, Jeni Davies, Jim Davies, Karen Davies, Kelly Davies, Kim Davies, Louisa Davies, Mark Davies, Matthew Davies, Michelle Davies, Nina Davies, Owen Davies, Patrick Davies, Rachel Davies, Rhys Davies, Ruth Davies, Sarah Davies, Simon Davies, Alison Davis, Gwyneth Davis, Illinos Davis, Julie-Ann Davis, Katherine Davis, Peter Davis, Alexander Davison, Sophia Davison, Mark Davy, Christine Dawe, H Dawe, Mark Dawkins, Danielle Dawson, Elizabeth Dawson, Joy Dawson, Susan Dawson, Tom Dawson, Andrew Daxter, Andrew Day, Helena Day, Jacob Day, Jeremy Day, Lynn Day, Jamie D'Costa, Parijat De, Duneesha de Fonseka, Toni de Freitas, Frederico De Santana Miranda, Eleanor de Sausmarez, Shanika de Silva, Thushan de Silva, Jessica De Sousa, Paulo De Sousa, James de Souza, Anthony de Soyza, Natasha de Vere, Johannes de Vos, Bethan Deacon, Sharon Dealing, Anna Dean, Julie Dean, Katrina Dean, Stephen Dean, Tessa Dean, Jill Deane, James Dear, Effie Dearden, Alison Deary, Catherine Deas, Samuel Debbie, Gabor Debreceni, Vashist Deelchand, Matthew Deeley, Joanne Deery, Emmanuel Defever, Raji Dehulia, Max Deighton, Manuela Del Forno, Arnold Dela Rosa, Lisa Delaney, Amanda Dell, Carrie Demetriou, David DeMets, Jane Democratis, Jacqueline Denham, Emmanuelle Denis, Laura Denley, Craig Denmade, Kathy Dent, Martin Dent, Elise Denton, Tom Denwood, Nishigandh Deole, Darshita Depala, Maria Depante, Randle Derbyshire, Susan Dermody, Amisha Desai, Asmita Desai, Purav Desai, Sanjeev Deshpande, Vai Deshpande, Brendan Devine, Sirjana Devkota, Nicola Dewland, Prakash Dey, Vishal Dey, Rogin Deylami, Jazz Dhaliwal, Kevin Dhaliwal, Jas Dhalliwal, Mandeep Dhanda, Sundip Dhani, Amandeep Dhanoa, Mili Dhar, Devesh Dhasmana, Aman Dhesi, Ekanjali Dhillon, Reiss Dhillon, Pamela Diamond, Priya Dias, Stephanie Diaz, Kayleigh Diaz-Pratt, Debbie Dickerson, Pamela Dicks, Stuart Dickson, Julie Dijo, Sean Dillane, Sarah Diment, Paul Dimitri, Maria Dineen, ThaiHa Dinh, Tri Dinh, Alex Dipper, Laura Dirmantaite, Lisa Ditchfield, Sarah Diver, Lavanya Diwakar, Caroline Dixon, Giles Dixon, Stephen Dixon-Mould, Brice Djeugam, Petr Dlouhy, Laurence Dobbie, Marinela Dobranszky Oroian, Charlotte Dobson, Lee Dobson, Marie Docherty, David Dockrell, James Dodd, Jackie Dodds, Rebecca Dodds, Steve Dodds, Richi Dogra, Erin Doherty, Warren Doherty, Yumiko Doi, Iain Doig, Eleanor Doke, Daniel Dolan, Mark Dolman, Rozzie Dolman, Lisa Donald, Callum Donaldson, Christopher Donaldson, Denise Donaldson, Gillian Donaldson, Kate Donaldson, Joanne Donnachie, Christopher Donnelly, Eilish Donnelly, Ronan Donnelly, Aravindhan Donohoe, Gemma Donohoe, Bryan Donohue, Sinead Donton, Emma Dooks, Grainne Doran, Kane Dorey, Sharon Dorgan, Amanda Dornan, Moonira Dosani, Davinder Dosanjh, Paula Dospinescu, Katie Douglas, Jonathan Douse, Lucy Dowden, Michelle Dower, Kerry Dowling, Sud Dowling, Nicola Downer, Charlotte Downes, Rob Downes, Thomas Downes, Damian Downey, Philippa Downey, Robert Downey, Louise Downs, Simon Dowson, Cornel Dragan, Cristina Dragomir, Cristina Dragos, Maire Drain, Chelsea Drake, Victoria Drew, Olivia Drewett, Celine Driscoll, Helena Drogan, Nikki Drogman, Graham Drummond, Ronald Druyeh, Simon Drysdale, An Du Thinh, Hazel Dube, Judith Dube, Ophias Dube, Stephen Duberley, Hayley Duckles-Leech, Nicola Duff, Emma Duffield, Sam Duff-Miller, Helen Duffy, Lionel Dufour, Annette Duggan, Helen Duggan, Parveen Dugh, Janice Duignan, Mick Duley, Simon Dummer, Andrew Duncan, Christopher Duncan, Fullerton Duncan, Gregory Duncan, Stephanie Dundas, Alessia Dunn, Charlotte Dunn, Damian Dunn, Laura Dunn, Paul Dunn, Charlene Dunne, Karen Dunne, Fiona Dunning, Aidan Dunphy, Venkat Duraiswamy, Beatriz Duran, Ingrid DuRand, Steve Durgacharan, Natalie Duric, Alison Durie, Emily Durie, Hannah Durrington, Haris Duvnjak, Akshay Dwarakanath, Laasya Dwarakanath, Ellen Dwyer, Claudia Dyball, Lee Dyble, Kristyn Dyer, Harvey Dymond, Tom Dymond, Chris Eades, Laura 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Elliott, Toby Elliott, Annie Ellis, Ann-Marie Ellis, Christine Ellis, Kay Ellis, Kaytie Ellis, Tak-Yan Ellis, Yvette Ellis, Megan Ellison, Rahma Elmahdi, Einas Elmahi, Hannah-May Elmasry, Mohammed Elmi, Najla Elndari, Omer Elneima, Mohamed Elokl, Ahmed Elradi, Mohamed Elsaadany, Sally El-Sayeh, Hana El-Sbahi, Tarek Elsefi, Karim El-Shakankery, Robert Elshaw, Hosni El-Taweel, Sarah Elyoussfi, Jonathan Emberey, Jonathan R Emberson, John Emberton, Julian Emmanuel, Ingrid Emmerson, Michael Emms, Florence Emond, Marieke Emonts, Nicu Enachi, Angila Engden, Katy English, Emma Entwistle, Hene Enyi, Marios Erotocritou, Helen Escreet, Peter Eskander, Hanif Esmail, Lise Estcourt, Amy Evans, Brynach Evans, Chris Evans, Daren Evans, Debra Evans, Gail Evans, Gareth Evans, Jennifer Evans, Lisa Evans, Lynn Evans, Margaret Evans, Michelle Evans, Mim Evans, Morgan Evans, Ranoromanana Evans, Ryan Evans, Teriann Evans, Terry John Evans, Tony Eve, Caroline Everden, Serenydd Everden, Hayley Evison, Lynsey Evison, Penny Eyton-Jones, Jacqueline Faccenda, Leila Fahel, Youstina Fahmay, Sara Fairbairn, Terry Fairbairn, Andy Fairclough, Louise Fairlie, Mark Fairweather, Anne Fajardo, Naomi Falcone, Euan Falconer, Jonathan Falconer, John Fallon, Andrea Fallow, David Faluyi, Victoria Fancois, Qayyum Farah, Novin Fard, Amr Farg, Margaret Farinto, Adam Farmer, Katie Farmer, Toni Farmery, Samantha Farnworth, Faiyaz Farook, Hadia Farooq, Sidrah Farooq, Fiona Farquhar, Karen Farrar, Aaron Farrell, Barbara Farrell, James Farthing, Syeda Farzana, Rahmatu Fasina, Azam Fatemi, Mina Fatemi, Nibah Fatimah, Maria Faulkner, Saul N Faust, Joe Fawke, Sinmidele Fawohunre, Abul Fazal, Kelly Feane, Simon Fearby, Alex Feben, Federico Fedel, Daria Fedorova, James Feely-Henderson, Christopher Fegan, Mae Felongco, Lynsey Felton, Tim Felton, Kate Fenlon, Andrea Fenn, Isabelle Fenner, Ciara Fenton, Melisa Fenton, Cameron Ferguson, Jenny Ferguson, Kathryn Ferguson, Katie Ferguson, Stephanie Ferguson, Susan Ferguson, Susie Ferguson, Victoria Ferguson, Denzil Fernandes, Candida Fernandez, Eduardo Fernandez, Maria Fernandez, Sonia Fernandez Lopez, Callum Jeevan Fernando, Ahmed Feroz, Pietro Ferranti, Thais Ferrari Gersogamo, Eleanor Ferrelly, Alexandra Ferrera, Emma Ferriman, Nicholas Fethers, Ben Field, Janet Field, Rebecca Field, Karen Fielder, Lindsey Fieldhouse, Andra Fielding, Julie Fielding, Len Fielding, Sarah Fielding, Asma Fikree, Sarah Ann Filson, Sarah Finbow, Debbie Finch, Joanne Finch, Laurie Finch, Joanne Finden, Natalie Fineman, Lauren Finlayson, Adam Finn, Joanne Finn, Clare Finney, Sofia Fiouni, Jo Fiquet, Dani Fisher, Emily Fisher, James Fisher, Neil Fisher, Meadow Fisher Crisp, Daniel Fishman, Krystofer Fishwick, Lorraine Fitzgerald, Chloe Fitzpatrick-Creamer, Jan Flaherty, Michael Flanagan, Charles Flanders, Cathy Flatters, Julie Fleming, Lucy Fleming, Paul Fleming, William Flesher, Alison Fletcher, Jonathan Fletcher, Lucy Fletcher, Simon Fletcher, Sophie Fletcher, Karen Flewitt, Christopher Flood, Ian Floodgate, Vincent Florence, Sharon Floyd, Kelly Flynn, Rachel Flynn, Sara Flynn, Claire Foden, Adama Fofana, Georgina Fogarty, Claire Foley, Paul Foley, Linda Folkes, Daniela Mock Font, Evodian Fonyonga, Aiwyne Foo, Jane Foo, Andrew Foot, Jayne Foot, Jane Forbes, Jamie Ford, Kathy Ford, Jennifer Foreman, Caroline Fornolles, Adam Forrest, Ellie Forsey, Miranda Forsey, Thomas Forshall, Elliot Forster, Julian Forton, Emily Foster, Joseph Foster, Rachel A Foster, Tracy Foster, Theodora Foukanelli, Angela Foulds, Ian Foulds, Folakemi Fowe, Emily Fowler, Robert Fowler, Stephen Fowler, Caroline Fox, Claire Fox, Daniel Fox, Heather Fox, Jonathan Fox, Lauren Fox, Natalie Fox, Olivia Fox, Simon Fox, Sarah-Jane Foxton, Yasin Fozdar, Rebecca Frake, Alex Francioni, Olesya Francis, Rebecca Francis, Sarah Francis, Theodora Francis-Bacon, Jason Frankcam, Helen Frankland, Gayle Franklin, Jessica Franklin, Darron Franks, Catherine Fraser, Laura Fraser, Sharon Frayling, Martyn Fredlund, Matthew Free, Carol Freeman, Elaine Freeman, Hannah Freeman, Nicola Freeman, Clare Freer, Ian Freestone, Eleanor French, Matthew Frise, Renate Fromson, Claire Froneman, Adam Frosh, John Frost, Victoria Frost, Oliver Froud, Rachel Frowd, Arun Fryatt, Jake Fryer, Janet Fu, Bridget Fuller, Liz Fuller, Neil Fuller, Tracy Fuller, Duncan Fullerton, Jenny Fullthorpe, Carrie Fung, Gayle Fung, Sarah Funnell, John Furness, Charlene Furtado, Andrew Fyfe, Nytianandan G, Elizabeth Gabbitas, Claire Gabriel, Diana Gabriel, Hadiza Gachi, Rose Gad, Joshua Gahir, Sarveen Gajebasia, Katarzyna Gajewska-Knapik, Zacharoula Galani, Christopher Gale, Hugo Gale, Rebecca Gale, Swetha Gali, Karen Galilee, Bernadette Gallagher, Jude Gallagher, Rosie Gallagher, William Gallagher, Joanne Galliford, Catherine Galloway, Chris Galloway, Emma Galloway, Jacqui Galloway, James Galloway, Laura Gamble, Liz Gamble, Brian Gammon, Jaikumar Ganapathi, Ramesh Ganapathy, Kaminiben Gandhi, Sarah Gandhi, Usha Ganesh, Abrar Gani, Emma-James Garden, Antoni D Gardener, Emma Gardiner, Jill Gardiner, Michael Gardiner, Phil Gardiner, Siobhan Gardiner, Caroline Gardiner-Hill, Jonathan Gardner, Mark Garfield, Atul Garg, Nathan Garlick, Justin Garner, Lucie Garner, Zoe Garner, Kimberley Garnett, Robert Garney, Rosaline Garr, Michael Garstka, Peter Gartan, Florence Garty, Rachel Gascoyne, Hyeriju Gashau, Noha Gasmalseed, Michaela Gaspar, Aoife Gatenby, Erin Gaughan, Alok Gaurav, Mariana Gavrila, Jane Gaylard, Emma Gaywood, Catherine Geddie, Alison Geddis, Ian Gedge, Sarah Gee, Minerva Gellamucho, Karzan Gelly, Leila Gelmon, Sandra Gelves-Zapata, Gemma Genato, Susan Gent, Natalie Geoghegan, Chloe George, Sam George, Tina George, Simon Georges, Domonique Georgiou, Peter Gerard, Leigh Gerdes, Louise Germain, Helen Gerrish, Abel Getachew, Louise Gethin, Hisham Ghanayem, Amardeep Ghattaoraya, Anca Gherman, Alison Ghosh, Justin Ghosh, Sudhamay Ghosh, Sarra Giannopoulou, Malick Gibani, Andrew Gibb, Ben Gibbison, Kerry Gibbons, Alex Gibson, Bethan Gibson, Kimberley Gibson, Kirsty Gibson, Sian Gibson, Cat Gilbert, Jeanette Gilbert, Joanne Gilbert, Kayleigh Gilbert, Sean Gilchrist, Benjamin Giles, Mandy Gill, Rose Gill, Lynne Gill, Paul Gillen, Annelies Gillesen, Katherine Gillespie, Matt Gillespie, Elizabeth Gillham, Andrew Gillian, Deborah Gilliland, Robert Gillott, Danielle Gilmour, Kate Gilmour, Theodora Giokanini-Royal, Anna Gipson, Joanna Girling, Rhian Gisby, Angelena Gkioni, Aikaterini Gkoritsa, Effrossyni Gkrania-Klotsas, Amy Gladwell, James Glanville, Jessica Glasgow, Susannah Glasgow, Jon Glass, Lynn Glass, Sharon Glaysher, Lisa Gledhill, Ana Glennon, John Glover, Kyle Glover, Jan Glover Bengtsson, Chevanthy Gnanalingam, Julie Goddard, Wendy Goddard, Emily Godden, Jo Godden, Gillian Godding, Emma Godson, Gerry Gogarty, Sukanya Gogoi, Aiky Goh, Rebeca Goiriz, Sriya Gokaraju, Philip Gold, Raphael Goldacre, Arthur Goldsmith, Portia Goldsmith, Darren Gomersall, Lucia Gomez, Raquel Gomez-Marcos, Ali Gondal, Celia Gonzalez, Jack Goodall, Bob Goodenough, Laura Goodfellow, James Goodlife, Camelia Goodwin, Elizabeth Goodwin, Jayne Goodwin, Paula Goodyear, Rajiv Gooentilleke, Sharif Goolam-Hossen, Michelle Goonasekara, Sheila Gooseman, Shameer Gopal, Peter Gordon, Sally Gordon, Hugh Gorick, Caitlin Gorman, Claire Gorman, Stuart Gormely, Diana Gorog, Jan Gorry, Michelle Gorst, Thomas Gorsuch, Jayshreebahen Gosai, Rebecca Gosling, Sally Gosling, Georgina Gosney, Vanessa Goss, Dzintars Gotham, Naomi Gott, Elizabeth Goudie, Amanda Gould, Angela Gould, Susan Gould, Lysander Gourbault, Anna Gouveia, Abha Govind, Sharon Gowans, Girish Gowda, Rohit Gowda, Pauline Gowdy, Hannah Gower, Thomas Gower, Pankaj Goyal, Sunil Goyal, Sushant Goyal, Beverley Graham, Clive Graham, Jane Graham, Jonathan Graham, Justin Graham, Libby Graham, Sharon Graham, Matthew Graham-Brown, Julia Grahamslaw, Gianluca Grana, Tracyanne Grandison, Louis Grandjean, Alison Grant, Ann Grant, David Grant, Matthew Grant, Pauleen Grant, Rhys Gravell, Jenny Graves, Alasdair Gray, Catherine Gray, Georgina Gray, Harriet Gray, Ingrid Gray, Jackie Gray, Karen Gray, Nicola Gray, Sebastian Gray, Alan Grayson, Patricia Grealish, Fiona Greaves, Jack Greaves, Paul Greaves, Charlotte Green, Christopher Green, David Green, Frederick Green, Grace Green, Joel Green, Marie Green, Nicola Green, Stacey Green, Teresa Green, Diarra Greene, Philippa Greenfield, Alan Greenhalgh, Maraneka Greenslade, Daniel Greenwood, Sandra Greer, James Gregory, Jane Gregory, Katie Gregory, Tamsin Gregory, James Gregson, Jill Greig, Julia Greig, Rebecca Grenfell, Teena Grenier, Susan Grevatt, Glaxy Grey, Andrew Gribbin, Amy Gribble, Beverley Grice, Natasha Grieg, Douglas Grieve, Ben Griffin, Denise Griffin, Mel Griffin, Sian Griffith, Alexandra Griffiths, Andrew Griffiths, Daniel Griffiths, David Griffiths, Donna Griffiths, Isabel Griffiths, Mark Griffiths, Nicola Griffiths, Oliver Griffiths, Sarah Griffiths, Sharon Griffiths, Yvonne Griffiths, Sofia Grigoriadou, Steph Grigsby, Paul Grist, Stephen Grist, Evelina Grobovaite, Clarissa Grondin, Rachel Groome, Liliana Grosu, Jenny Grounds, Margaret Grout, Helen Grover, Jayne Groves, Neil Grubb, Julie Grundy, Francesca Guarino, Sharada Gudur, Sharazeq Guettari, Shivang Gulati, Vikas Gulia, Pumali Gunasekera, Malin Gunawardena, Kirun Gunganah, Jessica Gunn, Emma Gunter, Alok Gupta, Atul Gupta, Rajeev Gupta, Richa Gupta, Rishi Gupta, Tarun Gupta, Vineet Gupta, Ankur Gupta-Wright, Victoria Guratsky, Alvyda Gureviciute, Sambasivarao Gurram, Bhawana Gurung, Shraddha Gurung, Hazel Guth, Ruth Habibi, Berkin Hack, Pamela Hackney, Christian Hacon, Aiman Haddad, Denise Hadfield, Michalis Hadjiandreou, Nikolaos Hadjisavvas, Leah Hadzik, Anna Haestier, Nauman Hafiz, Rana Hafiz-Ur-Rehman, Javed Hafsa, Samantha Hagan, Jack W Hague, Rosemary Hague, Kate Haigh, Christina Haines, Scott Hainey, Morton Hair, Brigid Hairsine, Juraj Hajnik, Anne Haldeos, Writaja Halder, Jennie Hale, Carmel Halevy, Paul Halford, William Halford, Alistair Hall, Anthony Hall, Claire Hall, Elizabeth Hall, Emma Hall, Fiona Hall, Helen Hall, Jennifer Hall, Kathryn Hall, Bill Hall, Jan Hallas, Kyle Hallas, Charles Hallett, Becky-Lee Halls, Heather Halls, Maryam Hamdollah-Zadeh, Bilal Hameed, Imran Hamid, Mohamad Hamie, Bethany Hamilton, Fergus Hamilton, Leigh Hamilton, Nicola Hamilton, Ruth Hamlin, Eleanor Hamlyn, Beatrice Hammans, Shirley Hammersley, Kate Hammerton, Bev Hammond, Leah Hammond, Sara Hammond, Fiona Hammonds, Ibrahim Hamoodi, Karen Hampshire, Elizabeth Hampson, Jude Hampson, Lucy Hampson, Ozan Hanci, Ian Hancock, Sadiyah Hand, Jasmine Handford, Soran Handrean, Sarah Haney, Sheharyar Hanif, E Hanison, Alison Hanlon, Jennifer Hannah, Amy Hannington, Merhej Hannun, Aidan Hanrath, Anita Hanson, Jane Hanson, Kathryn Hanson, Steve Hanson, Helen Hanwell, Mazhar Ul Haq, Ala Haqiqi, Monjurul Haque, Lesley Harden, Zoe Harding, Simon Hardman, Joanna Hardy, Kumar Haresh, Rachel Harford, Beverley Hargadon, Carolyn Hargreaves, Emily Hargreaves, James Hargreaves, Alice Harin, Mohammed Haris, Edward Harlock, Sandra Harlow, Paula Harman, Tracy Harman, Mark Harmer, Muhammad A Haroon, Charlie Harper, Fiona Harper, Heather Harper, Melanie Harper, Peter Harper, Rosemary Harper, Sarah Harrhy, Sian Harrington, Yasmin Harrington-Davies, Jade Harris, Jess Harris, John Harris, Laura Harris, Marie-Clare Harris, Naomi Harris, Nichola Harris, Sophie Harris, Alex Harrison, David Harrison, Julie Harrison, Laura Harrison, Melanie Harrison, Rowan Harrison, Susie Harrison, Thomas Harrison, Wendy Harrison, Elizabeth Harrod, Ciaran Hart, Dominic Hart, Lisa Hartley, Rosemary Hartley, Ruth Hartley, Tom Hartley, William Hartrey, Phillipa Hartridge, Stuart Hartshorn, Heli Harvala, Alice Harvey, Angela Harvey, Max Harvey, Catherine Harwood, Helen Harwood, Brigitte Haselden, Kazi Hashem, Mohammed Hashimm, Tadaaki Hashimoto, Imranullah Hashmi, Sarah Haskins, Zena Haslam, Adil Hassan, Ali Hassan, Wagae UI Hassan, Waqar Ul Hassan, Sapna Hassasing, Jane Hassell, Philip Hassell, Alex Hastings, Bethany Hastings, Janice Hastings, Stephanie Hatch, Jonathan Hatton, Sheryl Haviland, May Havinden-Williams, Stefan Havlik, Daniel B Hawcutt, Kadean Hawes, Liz Hawes, Nicola Hawes, Annie Hawkins, Catherine Hawkins, Nancy Hawkins, Tanya Hawkins, Dan Hawley, Ed Hawley-Jones, Edward Haworth, Cathy Hay, Amna Hayat, Jamal Hayat, Mohamed-Riyal Hayathu, Tamsin Haydon, Anne Hayes, Jonas Hayes, Kate Hayes, Melony Hayes, Vanessa Hayes, Fiona Hayes, Patrick Hayle, Chloe Haylett, Antara Hayman, Melanie Hayman, Matthew Haynes, Richard Haynes, Rachel Hayre, Sarah Haysom, James Hayward, Patrick Haywood, Tracy Hazelton, Phoebe Hazenberg, Zhengmai He, Elizabeth Headon, Carrie Heal, Brendan Healy, Amy Hearn, Angela Heath, Rowan Heath, Diane Heaton, Kerry Hebbron, Gemma Hector, Andy Hedges, Katrine Hedges, Cheryl Heeley, Elaine Heeney, Rajdeep Heire, Ulla Hemmila, Cassie Hemmings, Scott Hemphill, Deborah Hemsley, Abigail Henderson, Jennifer Henderson, Steven Henderson, Lee Hennen, Kathryn Hennessy, Natalie Hennesy, Carol Ann Henry, Joanne Henry, Karol Henry, Lavinia Henry, Margo Henry, Natalie Henry, David Henshall, Mike Herbert, Gillian Herdman, Rosaleen Herdman-Grant, Morag Herkes, Emma Heron, Kay Heron, William Herrington, Emilia Heselden, Peta Heslop, Sharnie Beth Hesson, Simon Hester, Emily Hetherington, Joseph Hetherington, Chamila Hettiarachchi, Pramodh Hettiarachchi, Hayley Hewer, John Hewertson, Anna Hewetson, Sue Hewins, Jacqueline Hewitson, Claire Hewitt, Davina Hewitt, Richard Hewitt, Robert Heyderman, Nicolette Heydon, Mathis Heydtmann, Joseph Heys, Jonathan Heywood, Gareth Heywood-Beldon, Meg Hibbert, John Hickey, Naomi Hickey, Peter Hickey, Alex Hicks, Jenny Hicks, Rosie Hicks, Scott Rory Hicks, Daniel Higbee, Lucy Higgins, Andrew Higham, Martin Highcock, Judith Highgate, Mondy Hikmat, Alison Hill, Amanda Hill, Helen Hill, Joanne Hill, Lisa Hill, Martin Hill, Phoebe Hill, Uta Hill, Annette Hilldrith, Elizabeth Hillerby, Catherine Hillman-Cooper, Elisabeth Hilton, Zoe Hilton, Sarah Hinch, Marcus Hinde, Andrew Hindle, Alice Hindmarsh, Paul Hine, Kim Hinshaw, Clare Hird, Alison Hirst, Jemma Hives, Benson Ho, Michaela Hoare, David Hobden, Gill Hobden, Maria Hobrok, Simon Hobson, Renate Hodge, Simon Hodge, Lesley Hodgen, Holly Hodgkins, Louise Hodgkinson, Sally Hodgkinson, David Hodgson, Helen Hodgson, Luke Hodgson, Sheila Hodgson, Gemma Hodkinson, Kenneth Hodson, Matthew Hogben, Lucy Hogg, Lee Hoggett, Abigail Holborow, Catherine Holbrook, Catherine Holden, Melinda Holden, Thomas Holder, Niels Holdhof, Hannah Holdsworth, Lisa Holland, Maureen Holland, Nicky Holland, Marie Hollands, Elizabeth Holliday, Nina Holling, Gillian Hollis, Laszlo Hollos, Linda Holloway, Simon Holloway, Marcus Hollyer, Amy Holman, Ann Holmes, Benjamin Holmes, Megan Holmes, Raphael Holmes, Rebecca Holmes, Kelly Holroyd, Caroline Holt, Lyndsey Holt, Siobhan Holt, Susie Holt, Alexandra Holyome, Marie Home, Toni Home, Renate Homewood, Kate Hong, Laura Hontoria del Hoyo, Clare Hooper, Sarah Hoosdally, Samantha Hope, Susan Hope, Bridget Hopkins, Peter W Horby, Stephanie Horler, Anil Hormis, Daniel Hornan, Nicola Hornby, Zoey Horne, Latoya Horsford, Megan Horsford, Mark Horsford, Valana Horsham, Alexander Horsley, Ashley Horsley, Elizabeth Horsley, Sarah Horton, Nicola Horton-Turner, Jane Hosea, Toby Hoskins, Muhammad S Hossain, Rashed Hossain, Leanne Hostler, Maxine Hough, Sarah Hough, Brittany Houghton, Catherine Houghton, Iain Houghton, Kathryn Houghton, Rebecca Houlihan, Angela Houston, Hamish Houston, Tawedzegwa Hove, Roseanna Hovvels, Lee How, Laura Howaniec, Laura Howard, Linda Howard, Lucy Howard, Sarah Howard, Stuart Howard, Richard Howard-Griffin, Alison Howarth, Diane Howarth, Serena Howe, Mark Howells, Lyn Howie, Kerry Howlett, Sophie Howlett, Joanne Hoyle, Josh Hrycaiczuk, Naing Zaya Htoon, Su Htwe, Ying Hu, Chiang Ooi Huah Huah, Abby Huckle, Shahzya Huda, Alison Hudak, Lisa Hudig, Alex Hudson, Cara Hudson, Heather Hudson, Peter Hudson, Oli Hudson, Alison Hufton, Connor Huggins, Alistair Hughes, Eithne Hughes, Emma Hughes, Gareth Hughes, Heather Hughes, Luke Hughes, Rachel Hughes, Rebecca Hughes, Samantha Hughes, Stephen Hughes, Vikki Hughes, Wesley Hughes, Lukas Huhn, Ching Hui, Ruth Hulbert, Diana Hull, Grace Hull, Robert Hull, Amanda Hulme, Peter Hulme, Wendy Hulse, George Hulston, Ryan Hum, Laura Humber, Megan Hume, Charlotte Humphrey, Ismay Humphreys, Alasdair Humphries, Joanne Humphries, Lena Hunold, Fiona Hunt, Kristen Hunt, Luke Hunt, Sophie Hunt, Al Hunter, Alexandra Hunter, Isobel Hunter, Karl Hunter, Neil Hunter, George Huntington, Elizabeth Hurditch, Cian Hurley, Katrina Hurley, Mohammed A Husain, Syeda Yusra Husaini, Coralie Huson, Afreen Hussain, Ibraar Hussain, Ifza Hussain, Mohammad Hussain, Muhammad Hussain, Reda Hussain, Sajid Hussain, Samia Hussain, Sanniah Hussain, Wasim Hussain, Yasmin Hussain, Mohammed Hussam El-Din, Raheem Hussein, Rebecca Hussey, Camille Hutchinson, Dorothy Hutchinson, Elizabeth Hutchinson, John Hutchinson, Claire Hutsby, Paula Hutton, Daniella Hydes, Jamie Hyde-Wyatt, Niamh Hynes, Megan Hyslop, Mazen Ibraheim, Abdalla Ibrahim, Ahmed Ibrahim, Asil Ibrahim, Mohamed Ibrahim, Monzeer Ibrahim, Wadah Ibrahim, Adetokunbo I Idowu, Muhammad Idrees, Hina Iftikhar, Mawara Iftikhar, Chukwuemeka Igwe, Mohammad Ijaz, Amaju Ikomi, Clare Iles, Stamatina Iliodromiti, Mary Ilsley, Lorna Ilves, La'ali Imam-Gutierrez, Christopher Imray, Alison Imtiaz, Haider Imtiaz, Claire Ingall, Jack Ingham, Julie Ingham, Rory Ingham, Tejas Ingle, Jennifer Inglis, Anne Ingram, Luke Ingram, Peter Inns, Ken Inweregbu, Andreea A Ionescu, Ana Ionita, Ilian P Iordanov, Anil Ipe, Adil Iqbal, Madiha Iqbal, Mohammed Iqbal, Faisal Iqbal Sait, Jane Ireland, Robert Irons, Mohannad Irshad, Muhammad S Irshad, Janice Irvine, Val Irvine, Pamela Irving, Robert Irving, Mina Ishak, Erica Isherwood, Aminul Islam, Abdurrahman Islim, Ali Ismail, Omar Ismail, Caroline Ison, M'hamedi Israa, Sharon Isralls, Ali Issa, Monica Ivan, Catrina Ivel, Chineze Ivenso, Ashleigh Ivy, Sophie Iwanikiw, Karen Ixer, Menaka Iyer, Mia Iyer, Calum Jack, Amanda Jackson, Anthony Jackson, Ben Jackson, Beth Jackson, Douglas Jackson, Ella Jackson, Hayley Jackson, Helen Jackson, Jane Jackson, Julie Jackson, Karin Jackson, Lauren Jackson, Melanie Jackson, Nicola Jackson, Shane Jackson, Sharon Jackson, Nikita Jacob, Patricia Jacob, Reni Jacob, Nicola Jacques, Terri-Lisa Jacques-Brown, Anisa Jafar, Daniel Jafferji, Ali Jaffery, Chandrashekar Jagadish, Vijay Jagannathan, Sam Jaggard, Mandeep Jagpal, Fernandez R Jaime, Neemisha Jain, Seema Jain, Susan Jain, Sanjay Jaiswal, Danyal Jajbhay, Thomas Jaki, Bintou Jallow, Yusuf Jaly, Sabine Jamal, Zeba Jamal, Yasmin Jameel, Albie James, Christie James, Kate James, Lee James, Linda James, Mark James, Nicholas James, Olivia James, Rebecca James, Ruth James, Tracy James, Jack Jameson, Aaron Jamison, Phoebe Jane, Azara Janmohamed, Sabrina Jansz, Deepa Japp, Lorraine Jappy, Victor Jardim, Catherine Jardine, Emma Jarnell, Ellie Jarvie, Ann Jarvis, Claire Jarvis, Lisa Jarvis, Rosina Jarvis, Patrycja Jastrzebska, Hafsa Javed, Mays Jawad, Lona Jawaheer, Kauky Jawaid, Anu Jayachandran, Dinakaran Jayachandran, Angelina Jayakumar, Deepak Jayaram, Ravi Jayaram, Geeshath Jayasekera, Thilina Jayatilleke, Abi Jayebalan, Saman Jeddi, Vandana Jeebun, Mohammad S Jeelani, Zeynab Jeewa, Emma Jefferson, Katie Jeffery, Helen Jeffrey, Jenni Jeffrey, Rachel Jeffrey, Sue Jeffrey, Nathan Jeffreys, Benjamin Jeffs, Debbie Jegede, Taylor Jemima, Ifan Jenkin, Alison Jenkins, Christopher Jenkins, David Jenkins, Elinor Jenkins, Sarah Jenkins, Sian Jenkins, Stephen Jenkins, Jacqui Jennings, Louise Jennings, Rebecca Jennings, Virginia Jennings, Ellen Jerome, Douglas Jerry, Ellen Jessup-Dunton, Jorge Antonio Jesus Silva, Champa Jetha, Kishan Jethwa, Jeby Jeyachandran, Visuvanathan Jeyakumar, Dharshana Jeyapalan, Shaman Jhanji, Khoo Jian, Zhixin Jiao, Laura Jimenez, Ana Jimenez Gil, Jithin Jith, Teishel Joefield, Navraj Johal, Karine Johannessen, Aisyah Johari, Annie John, Anu John, Navin John, Sarah John, Emma Johns, Margaret Johns, Anne-Marie Johnson, Antoinette Johnson, David Johnson, Emma Johnson, Gillian Johnson, Kathryn Johnson, Katie Johnson, Luke Johnson, Mark Johnson, Nelsonseelan Johnson, Oliver Johnson, Rachel Johnson, Tracy Johnson, Zoe Johnson, Claire Johnston, Janet Johnston, Laura Johnston, Susan Johnston, Victoria Johnston, Dawn Johnstone, Ed Johnstone, Janet Johnstone, Manohar Joishy, Adam Jones, Alistair Jones, Annabel Jones, Ben Jones, Bryony Jones, Carys Jones, Ceri Jones, Charlotte Jones, Christine E Jones, Debra Jones, Emily Jones, Gareth Jones, Geraldine Jones, Hazel Jones, Jac Jones, James Jones, Jamie Jones, Jessica Jones, Jonathon Jones, Julie Jones, Karen Jones, Kate E Jones, Kevin Jones, Laura Jones, Laura M Jones, Lorna Jones, Louise Jones, Mathew Jones, Nicola Jones, Paul Jones, Rhianna Jones, Ruth E Jones, Samantha Jones, Sophie Jones, Stefanie Jones, Steve Jones, Taya Jones, Tim Jones, Tracey Jones, Ramya Jonnalagadda, Rebecca Jordache, Annette Jose, Sanal Jose, Anna Joseph, Joseph Joseph, Rosane Joseph, Sibet Joseph, Dhaara Joshi, Mehul Joshi, Pratichi Joshi, Revati Joshi, Benz Josiah, Tiffany Joyce, Adriel Ju Wen Kwek, Edward Jude, Parminder Judge, Jessica Juhl, Sirisha Jujjavarapu, Mark Juniper, Edmund Juszczak, Deepthi Jyothish, Kasamu Kabiru Dawa, Mark Kacar, Katarina Kacinova, Nikhil Kadam, Rebecca Kahari, Gail Kakoullis, Azad Kala Bhushan, Richard JK Kalayi, Roobala Kaliannan Periyasami, Efthymia Kallistrou, Seika Kalsoom, Elisa Kam, John Kamara, Mohamed Kamara, Ajay Kamath, Prakash Kamath, Ravindra Kamath, Siddharth Arun Kamerkar, Nick Kametas, Musaiwale Kamfose, Arul Kandaswamy, Leia Kane, Osei Kankam, Thogulava Kannan, Abhinav Kant, Vikas Kapil, Ritoo Kapoor, Sonal Kapoor, Sourjya Kar, Janaka Kara, Vasita Kara, Marina Karakantza, Rona Kark, Nicholas Karunaratne, Natashja Kasianczuk, Vidya Kasipandian, Rizwan Kassam, Janarth Kathirgamachelvam, Victoria Katsande, Kulbinder Kaul, Daljit Kaur, Dervinder Kaur, Jasmin Kaur, Jaspreet Kaur, Satvinder Kaur, Zunaira Kausar, Mohammad AA Kawser, Andrea Kay, Sarah Kay, Jossy N Kayappurathu, Callum Kaye, Ahemd Kazeem, Naved Kazi, Sharon Kaznica, Samantha Kearley, Rachel Kearns, Nichola Kearsley, Joanne Keating, John Keating, Liza Keating, Elizabeth Keddie-Gray, Katie Keen, Natalie Keenan, Jonathan Kefas, Stephen Kegg, Laura Keith, Uzoamaka Keke, Tosin Kelani, Joanne Kellett, Jeremy Kellington, Alison Kelly, Conor Kelly, David Kelly, Diane Kelly, Dominic Kelly, Emma Kelly, Laura Kelly, Martin Kelly, Michael Kelly, Rosalind Kelly, Sinead Kelly, Stephen Kelly, Thomas Kelly, Mary Kelly-Baxter, Marketa Keltos, Timothy Kemp, Kelly Kemsley, Alexandra Kendall-Smith, Sarah Kennard, Ann Kennedy, Caroline Kennedy, James Kennedy, Sophie Kennedy-Hay, Julia 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Korcierz, James Korolewicz, George Koshy, Chris Kosmidis, Jalpa Kotecha, Easwari Kothandaraman, Leonidas Koukouflis, Koushan Kouranloo, Rukhsana Kousar'c, Margarita Kousteni, Maja Kovac, Alex Kozak Eskenazia, Kestutis Krasauskas, Raghu Krishnamurthy, Vinodh Krishnamurthy, Manju Krishnan, Hari Krishnan, Suzanne Krizak, Sean Krupej, Agnieszka Kubisz-Pudelko, Soren Kudsk-Iversen, Aurimas Kudzinskas, Chirag Kukadiya, Nainesha Kulkarni, Aditi Kumar, Mayur Kumar, Ramesh Kumar, Ravi Kumar, Rita Kumar, Rupa Kumar, Satish Kumar, Vimal Kumar, Arun Kundu, Heinke Kunst, Amit Kurani, Mohammed Kurdy, Rincy Kurian, Vimal Kurmars, Cameron Kuronen-Stewart, Ranganai S Kusangaya, Vlad Kushakovsky, Mandy Kuunal, Apexa Kuverji, Amma Kyei-Mensah, Thyra Kyere-Diabour, Moe Kyi, Nyan M Kyi, Laura Kyle, Karali-Tsilimpari Kyriaki, Julius Labao, Louise Lacey, Nikki Lack, Emma Ladlow, Heather Lafferty, Shondipon Laha, Sushil Lahane, Clement Lai, James Lai, Emma Laing, Robert Laing, Inez Laing-Faiers, Emily Laity, Michelle Lake, Nicki Lakeman, David Lalloo, Fiona Lalloo, Alison Lam, Fiona Lamb, Lucy Lamb, Thomas Lamb, Nick Lambe, Pauline Lambert, Claudia Lameirinhas, Mohammed KG Lami, Abigail Lamikanra, Holly Lamont, Michal Lamparski, Djillali Lamrani, Christine Lanaghan, Rebecca Lanaway, Ivone Lancona-Malcolm, Julia Lancut, Geraldine Landers, Martin J Landray, Matthew Lane, Nicholas Lane, Alidih Lang, Stephen Lang, Daniel Langer, Margaret Langley, Charles Langoya, Emily Langthorne, Taiya Large, Wojciech Lason, Anna Last, Scott Latham, John Latham-Mollart, Afzal Latheef, Darren Latimer, Nang Latt, Carly-Jane Lattimore, Dawn Lau, Eva Lau, Myra Laurenson, Hou Law, Jennifer Law, Jessica Law, Penny Law, Richard Law, Colin Lawler, Mark Lawley, Emma Lawrence, Jo Lawrence, Neil Lawrence, Ryan Lawrie, Jemima Lawson, Joanne Lawson, Louise Lawson, Rebecca Lawton, Michael Lay, Christine Laycock, Reina Layug, Maria Lazo, Vietland Le, Amelia Lea, William Lea, Ian Leadbitter, Thomas Leahy, Richard Lean, Lorna 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Yates, David Yates, Edward Yates, Helen Yates, Julie Yates, Mark Yates, Charlotte Yearwood Martin, Andrew Yeatman, Khin Yein, Fiona Yelnoorkar, Peter Yew, Kawai Yip, Laura Ylquimiche, Laura Ylquimiche Melly, Inez Ynter, H Yong, Jemma Yorke, Jasmine Youens, Abdel Younes Ibrahim, Eoin Young, Gail Young, Louise Young, Richard Young, Asfand Yousafzar, Sajeda Youssouf, Ahmed Yousuf, Chrissie Yu, Bernard Yung, Daniel Yusef, Said Yusef, Intekhab Yusuf, Anna-Sophia Zafar, Silvia Zagalo, Su Zaher, Aqsa Zahoor, Kareem Zaki, Nabhan Zakir, Kasia Zalewska, Ane Zamalloa, Mohsin Zaman, Raisa Zaman, Shakir Zaman, Julie Zamikula, Louise Zammit, Marie Zammit-Mangion, Lynn Zarb, Esther Zebracki, Daniel Zehnder, Lisa Zeidan, Marian Zelman, Xiaobei Zhao, Dongling Zheng, Doreen Zhu, Madiha Zia, Omar Zibdeh, Rabia Zill-E-Huma, Ei Thankt Zin, Veronica Zindonda, Eleanor Zinkin, Vivian Zinyemba, Christos Zipitis, Arkadiusz Zmierczak, Azam Zubir, Roslin Zuha, Naz Zuhra, Rasha Zulaikha, Sabrina Zulfikar, Carol Zullo, Ana Zuriaga-Alvaro, Will Zuurbier, Sheba Zyengi, and University of St Andrews. School of Medicine
Subjects: Male, Convalescent plasma, medicine.medical_treatment, 030204 cardiovascular system & hematology, Antibodies, Viral, Rate ratio, 0302 clinical medicine, RA0421, RA0421 Public health. Hygiene. Preventive Medicine, Medicine, Hospital Mortality, 030212 general & internal medicine, 11 Medical and Health Sciences, Aged, 80 and over, Medicine(all), Mortality rate, Covid19, Articles, 3rd-DAS, General Medicine, Middle Aged, Hospitals, Treatment Outcome, Female, Open label, Coronavirus Infections, Life Sciences & Biomedicine, RM, medicine.medical_specialty, Coronavirus disease 2019 (COVID-19), 03 medical and health sciences, Medicine, General & Internal, SDG 3 - Good Health and Well-being, General & Internal Medicine, Internal medicine, Humans, In patient, Pandemics, COVID-19 Serotherapy, Aged, Mechanical ventilation, Science & Technology, SARS-CoV-2, business.industry, Significant difference, Immunization, Passive, COVID-19, Length of Stay, NIS, R1, Respiration, Artificial, United Kingdom, RM Therapeutics. Pharmacology, RECOVERY Collaborative Group, business
Abstract: Background: Many patients with COVID-19 have been treated with plasma containing anti-SARS-CoV-2 antibodies. We aimed to evaluate the safety and efficacy of convalescent plasma therapy in patients admitted to hospital with COVID-19. Methods: This randomised, controlled, open-label, platform trial (Randomised Evaluation of COVID-19 Therapy [RECOVERY]) is assessing several possible treatments in patients hospitalised with COVID-19 in the UK. The trial is underway at 177 NHS hospitals from across the UK. Eligible and consenting patients were randomly assigned (1:1) to receive either usual care alone (usual care group) or usual care plus high-titre convalescent plasma (convalescent plasma group). The primary outcome was 28-day mortality, analysed on an intention-to-treat basis. The trial is registered with ISRCTN, 50189673, and ClinicalTrials.gov, NCT04381936. Findings: Between May 28, 2020, and Jan 15, 2021, 11558 (71%) of 16287 patients enrolled in RECOVERY were eligible to receive convalescent plasma and were assigned to either the convalescent plasma group or the usual care group. There was no significant difference in 28-day mortality between the two groups: 1399 (24%) of 5795 patients in the convalescent plasma group and 1408 (24%) of 5763 patients in the usual care group died within 28 days (rate ratio 1·00, 95% CI 0·93–1·07; p=0·95). The 28-day mortality rate ratio was similar in all prespecified subgroups of patients, including in those patients without detectable SARS-CoV-2 antibodies at randomisation. Allocation to convalescent plasma had no significant effect on the proportion of patients discharged from hospital within 28 days (3832 [66%] patients in the convalescent plasma group vs 3822 [66%] patients in the usual care group; rate ratio 0·99, 95% CI 0·94–1·03; p=0·57). Among those not on invasive mechanical ventilation at randomisation, there was no significant difference in the proportion of patients meeting the composite endpoint of progression to invasive mechanical ventilation or death (1568 [29%] of 5493 patients in the convalescent plasma group vs 1568 [29%] of 5448 patients in the usual care group; rate ratio 0·99, 95% CI 0·93–1·05; p=0·79). Interpretation: In patients hospitalised with COVID-19, high-titre convalescent plasma did not improve survival or other prespecified clinical outcomes. Funding: UK Research and Innovation (Medical Research Council) and National Institute of Health Research.
Published: 2021
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6. Co-Targeting PIM Kinase and PI3K/mTOR in NSCLC

Author: Gillian Moore, Stephen P. Finn, Katie E. O’Sullivan, Carmen Blanco-Aparicio, Lauren Brady, Samira Elbai, Siobhan Nicholson, Michael O'Neill, Clara Lightner, Kenneth J. O'Byrne, Kathy Gately, Susan Heavey, Sinead Cuffe, and R. Ryan
Subjects: Cancer Research, PIM1, NSCLC, Article, PI3K-mTOR, hemic and lymphatic diseases, microRNA, STAT3, Protein kinase B, PI3K/AKT/mTOR pathway, RC254-282, PIM kinase, miRNA, drug resistance, biology, Kinase, Chemistry, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, tumor tissue explants, c-Myc, Oncology, Mitogen-activated protein kinase, biology.protein, Cancer research, biomarker, Signal transduction
Abstract: Simple Summary PIM kinases interact with major oncogenic players, including the PI3K/Akt pathway, and provide an escape mechanism leading to drug resistance. This study examined PIM kinase expression in NSCLC and the potential of PIM1 as a prognostic marker. The effect on cell signaling of novel preclinical PI3K/mTOR/PIM kinase inhibitor IBL-301 was compared to PI3K/mTOR inhibition in vitro and ex vivo. PI3K-mTOR inhibitor sensitive (H1975P) and resistant (H1975GR) cells were compared for altered IL6/STAT3 pathway expression and sensitivity to IBL-301. All three PIM kinases are expressed in NSCLC and PIM1 is a marker of poor prognosis. IBL-301 inhibited c-Myc, the PI3K-Akt and JAK/STAT pathways in vitro and in NSCLC tumor tissue explants. IBL-301 also inhibited secreted pro-inflammatory cytokine MCP-1. PIM kinases were activated in H1975GR cells which were more sensitive to IBL-301 than H1975P cells. A miRNA signature of PI3K-mTOR resistance was validated. Co-targeting PIM kinase and PI3K-mTOR warrants further clinical investigation. Abstract PIM kinases are constitutively active proto-oncogenic serine/threonine kinases that play a role in cell cycle progression, metabolism, inflammation and drug resistance. PIM kinases interact with and stabilize p53, c-Myc and parallel signaling pathway PI3K/Akt. This study evaluated PIM kinase expression in NSCLC and in response to PI3K/mTOR inhibition. It investigated a novel preclinical PI3K/mTOR/PIM inhibitor (IBL-301) in vitro and in patient-derived NSCLC tumor tissues. Western blot analysis confirmed PIM1, PIM2 and PIM3 are expressed in NSCLC cell lines and PIM1 is a marker of poor prognosis in patients with NSCLC. IBL-301 decreased PIM1, c-Myc, pBAD and p4EBP1 (Thr37/46) and peIF4B (S406) protein levels in-vitro and MAP kinase, PI3K-Akt and JAK/STAT pathways in tumor tissue explants. IBL-301 significantly decreased secreted pro-inflammatory cytokine MCP-1. Altered mRNA expression, including activated PIM kinase and c-Myc, was identified in Apitolisib resistant cells (H1975GR) by an IL-6/STAT3 pathway array and validated by Western blot. H1975GR cells were more sensitive to IBL-301 than parent cells. A miRNA array identified a dysregulated miRNA signature of PI3K/mTOR drug resistance consisting of regulators of PIM kinase and c-Myc (miR17-5p, miR19b-3p, miR20a-5p, miR15b-5p, miR203a, miR-206). Our data provides a rationale for co-targeting PIM kinase and PI3K-mTOR to improve therapeutic response in NSCLC.
Published: 2021
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7. Prognostic Significance of Glucocorticoid Receptor Expression in Cancer: A Systematic Review and Meta-Analysis

Author: Noor Bakour, Stephanie Annett, Gillian Moore, Frank Moriarty, and Tracy Robson
Subjects: 0301 basic medicine, Oncology, Cancer Research, medicine.medical_specialty, medicine.medical_treatment, Subgroup analysis, lcsh:RC254-282, 03 medical and health sciences, 0302 clinical medicine, Internal medicine, medicine, glucocorticoid receptor, cancer, Progression-free survival, Stage (cooking), Chemotherapy, business.industry, Cancer, Publication bias, lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens, medicine.disease, 030104 developmental biology, 030220 oncology & carcinogenesis, Meta-analysis, Biomarker (medicine), biomarker, Systematic Review, prognosis, business
Abstract: Simple Summary In solid tumours, emerging evidence indicates that signalling through the glucocorticoid receptor (GR) can encourage the growth and spread of tumours and so drugs targeting this receptor are in development for use in cancer treatment. For these reasons, GR may be useful in anticipating a patient’s outcome upon their cancer diagnosis or to predict their tumours response to drugs targeting this receptor. In this review we aim to ascertain whether GR expression in tumours affects cancer patient survival. Overall, GR expression did not affect patient survival when assessing all cancer types. However, we found that in certain cancer subtypes such as gynaecological cancers (endometrial and ovarian) and early stage, untreated triple negative breast cancers, high GR expression is linked with cancer progression and therefore a poorer patient prognosis. Further studies are needed to uncover the exact role of GR in specific tumour (sub)types in order to provide the correct patients with GR targeting therapies. Abstract In solid malignancies, the glucocorticoid receptor (GR) signalling axis is associated with tumour progression and GR antagonists are in clinical development. Therefore, GR expression may be a useful potential prognostic or predictive biomarker for GR antagonist therapy in cancer. The aim of this review is to investigate if GR expression in tumours is predictive of overall survival or progression free survival. Twenty-five studies were identified through systematic searches of three databases and a meta-analysis conducted using a random effects model, quantifying statistical heterogeneity. Subgroup analysis was conducted for cancer types and publication bias was assessed via funnel plots. There was high heterogeneity in meta-analysis of the studies in all cancer types, which found no association between high GR expression with overall survival (pooled unadjusted HR 1.16, 95% CI (0.89–1.50), n = 2814; pooled adjusted HR 1.02, 95% CI (0.77–1.37), n = 2355) or progression-free survival (pooled unadjusted HR 1.12, 95% CI (0.88–1.42), n = 3365; pooled adjusted HR 1.04, 95% CI (0.6–1.81), n = 582) across all cancer types. However, subgroup meta-analyses showed that high GR expression in gynaecological cancers (endometrial and ovarian) (unadjusted HR 1.83, 95% CI (1.31–2.56), n = 664) and early stage, untreated triple negative breast cancers (TNBCs) (unadjusted HR 1.73, 95% CI (1.35–2.23), n = 687) is associated with disease progression. GR expression in late stage, chemotherapy treated TNBC was not prognostic (unadjusted HR 0.76, 95% CI (0.44, 1.32), n = 287). In conclusion, high GR expression is associated with an increased risk of disease progression in gynaecological and early stage, untreated TNBC. Additional studies are required to elucidate the tumour specific function of the GR receptor in order to ensure GR antagonists target the correct patient groups.
Published: 2021

8. The Immunophilin Protein FKBPL and its Peptide Derivatives are Novel Regulators of Vascular Integrity and Inflammation via Nf-κB Signaling

Author: Adrien Kissenpfennig, Irina G. Tikhonova, Shaun Spence, Clive Drakeford, Amy Short, Stephanie Annett, Pauline Johnson, Ciaran Campbell, Carolina Denis Garciarena, Danny Sharpe, Jennifer Dowling, Margaret Dennehy, Anita Yakkundi, Steve Kerrigan, Gianpiero L. Cavalleri, Fiona Furlong, Jacqueline C.Y. Lai, Tracy Robson, James O'Donnell, and Gillian Moore
Subjects: Gene knockdown, business.industry, Angiogenesis, medicine.medical_treatment, Inflammation, NF-κB, Proinflammatory cytokine, chemistry.chemical_compound, Cytokine, FKBPL, chemistry, Cancer research, Phosphorylation, Medicine, Tumor necrosis factor alpha, medicine.symptom, business
Abstract: A breakdown in vascular integrity and excessive inflammation are hallmarks of serious pathological conditions including sepsis, acute respiratory distress syndrome (ARDs) and most recently, severe COVID-19. FK506 – binding protein like (FKBPL) is a member of the immunophilin protein superfamily with potent anti-tumor activity through inhibition of angiogenesis and cancer stemness. An FKBPL-based 23mer peptide, ALM201, displayed a good safety and pharmacokinetic profile in a Phase 1a oncology clinical trial and was subsequently designated orphan drug status by the FDA in ovarian cancer. Here we describe a novel role for FKBPL and its peptides in regulating vascular integrity and cytokine production though modulating NF-κB signaling. FKBPL knockdown promoted endothelial cell barrier permeability, which was further exacerbated upon stimulation with lipopolysaccharide (LPS) and accompanied by increased expression of TNF mRNA and phosphorylation of p65(RelA). Whilst treatment with the FKBPL based pre-clinical peptide, AD-01, increased VE-cadherin endothelial tight junctions following LPS stimulation. Bone marrow derived macrophages (BMDM) from FKBPL haploinsufficient mice (Fkbpl+/−) also demonstrated increased phosphorylation of p65(RelA) in response to LPS stimulation compared to wild-type mice. Furthermore, treatment with AD-01 inhibited p65(RelA) phosphorylation following LPS stimulation resulting in reduced NF-κB target gene expression and proinflammatory cytokine production. In an in vivo LPS survival model, Fkbpl+/− mice have reduced survival compared to wild-type mice. Moreover, treatment of wild-type mice with the clinical FKBPL-based peptide, ALM201, following LPS injection resulted in a 100% survival rate in mice at experimental endpoint, as well as an abrogation of production of pro-inflammatory cytokines, TNF and IL-6, in peritoneal lavage washings. Analysis of human genetic biobanks found an association between common genetic variants associated with FKBPL and traits associated with inflammatory disorders such as psoriasis, rheumatoid arthritis and high lymphocyte count. In summary, for the first time, we describe a novel role for FKBPL as a regulator of inflammation and vascular integrity through modulating NF-κB signaling and FKBPL based therapies demonstrate potent anti-inflammatory activity.
Published: 2021
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9. Obesity and Cancer Metastasis: Molecular and Translational Perspectives

Author: Stephanie Annett, Gillian Moore, and Tracy Robson
Subjects: 0301 basic medicine, Cancer Research, obesity, extracellular matrix, cancer metabolism, Adipokine, Adipose tissue, tumor progression, Review, medicine.disease_cause, lcsh:RC254-282, Metastasis, Extracellular matrix, 03 medical and health sciences, 0302 clinical medicine, Breast cancer, Medicine, metastasis, cancer relapse, extra cellular vesicles, adipokines, Tumor microenvironment, business.industry, medicine.disease, lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens, cytokines, adipose tissue, 030104 developmental biology, Oncology, Tumor progression, 030220 oncology & carcinogenesis, Cancer research, business, Carcinogenesis
Abstract: Simple Summary A major challenge in treating cancer is when the cancer spreads from its original site to other parts of the body, a process also known as metastasis. In order to survive, the cancer cells must communicate with their environment for survival. It is increasingly recognized that fat tissue supports the survival of metastatic cancer cells allowing tumors to form at distant sites. Obese patients therefore have a worse prognosis due to accelerated tumor spread. Preventing cancer cells from communicating with fat tissue could therefore lead to new treatments aimed at stopping this spread. In this review we discuss how dysfunctional fat tissue supports the metastatic process and evaluate new therapies and lifestyle interventions that aim to prevent the communication between cancer cells and fat tissue. Abstract Obesity is a modern health problem that has reached pandemic proportions. It is an established risk factor for carcinogenesis, however, evidence for the contribution of adipose tissue to the metastatic behavior of tumors is also mounting. Over 90% of cancer mortality is attributed to metastasis and metastatic tumor cells must communicate with their microenvironment for survival. Many of the characteristics observed in obese adipose tissue strongly mirror the tumor microenvironment. Thus in the case of prostate, pancreatic and breast cancer and esophageal adenocarcinoma, which are all located in close anatomical proximity to an adipose tissue depot, the adjacent fat provides an ideal microenvironment to enhance tumor growth, progression and metastasis. Adipocytes provide adipokines, fatty acids and other soluble factors to tumor cells whilst immune cells infiltrate the tumor microenvironment. In addition, there are emerging studies on the role of the extracellular vesicles secreted from adipose tissue, and the extracellular matrix itself, as drivers of obesity-induced metastasis. In the present review, we discuss the major mechanisms responsible for the obesity–metastatic link. Furthermore, understanding these complex mechanisms will provide novel therapies to halt the tumor–adipose tissue crosstalk with the ultimate aim of inhibiting tumor progression and metastatic growth.
Published: 2020

10. Foreword

Author: Gillian Moore
Published: 2020
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11. FK506 binding proteins and inflammation related signalling pathways; basic biology, current status and future prospects for pharmacological intervention

Author: Tracy Robson, Stephanie Annett, and Gillian Moore
Subjects: 0301 basic medicine, Cell signaling, medicine.medical_treatment, Biology, Tacrolimus, Tacrolimus Binding Proteins, 03 medical and health sciences, 0302 clinical medicine, Cancer immunotherapy, FKBPL, Drug Development, Neoplasms, medicine, Animals, Humans, Pharmacology (medical), PI3K/AKT/mTOR pathway, Pharmacology, Inflammation, Sirolimus, FKBP52, Cell biology, Tetratricopeptide, 030104 developmental biology, FKBP, 030220 oncology & carcinogenesis, Function (biology), Immunosuppressive Agents, Signal Transduction
Abstract: FK506 binding (FKBP) proteins are part of the highly conserved immunophilin family and its members have fundamental roles in the regulation of signalling pathways involved in inflammation, adaptive immune responses, cancer and developmental biology. The original member of this family, FKBP12, is a well-known binding partner for the immunosuppressive drugs tacrolimus (FK506) and sirolimus (rapamycin). FKBP12 and its analog, FKBP12.6, function as cis/trans peptidyl prolyl isomerases (PPIase) and they catalyse the interconversion of cis/trans prolyl conformations. Members of this family uniquely contain a PPIase domain, which may not be functional. The larger FKBPs, such as FKBP51, FKBP52 and FKBPL, contain extra regions, including tetratricopeptide repeat (TPR) domains, which are important for their versatile protein-protein interactions with inflammation-related signalling pathways. In this review we focus on the pivotal role of FKBP proteins in regulating glucocorticoid signalling, canonical and non-canonical NF-κB signalling, mTOR/AKT signalling and TGF-β signalling. We examine the mechanism of action of FKBP based immunosuppressive drugs on these cell signalling pathways and how off target interactions lead to the development of side effects often seen in the clinic. Finally, we discuss the latest advances in the role of FKBPs as therapeutic targets and the development of novel agents for a range of indications of unmet clinical need, including glucocorticoid resistance, obesity, stress-induced inflammation and novel cancer immunotherapy.
Published: 2020

12. A Phase 2 Study of F-652, a Novel Tissue-Targeted Recombinant Human Interleukin-22 (IL-22) Dimer, for Treatment of Newly Diagnosed Acute Gvhd of the Lower GI Tract

Author: Samira Fatmi, Cristina Soto, Doris M. Ponce, Gillian Moore, Paul A Giardina, Juliet N. Barker, William L. Daley, Amin M. Alousi, Jonathan U. Peled, John B. Slingerland, Jinru Shia, Marcel R.M. van den Brink, Karamjeet S. Sandhu, Antonio L.C. Gomes, Alan M. Hanash, Ryotaro Nakamura, and Xiaoqiang Yan
Subjects: Enterocolitis, Transplantation, medicine.medical_specialty, medicine.diagnostic_test, business.industry, medicine.medical_treatment, Phases of clinical research, Immunosuppression, Hematology, medicine.disease, Gastroenterology, Sepsis, Pneumonia, Intestinal mucosa, Internal medicine, Biopsy, medicine, medicine.symptom, business, Sinusitis
Abstract: Background IL-22 has been shown to support intestinal mucosa after damage through multiple mechanisms, including promotion of epithelial survival and regeneration as well as induction of innate antimicrobial molecules such as REG3. In experimental murine models, aGVHD resulted in elimination of host-derived IL-22-producing cells, IL-22 deficiency increased GVHD mortality and GI pathology, and early initiation of treatment with exogenous IL-22 reduced GI pathology and improved survival. We thus tested if the addition of IL-22 to corticosteroids could promote healing of GI tract injury and improve treatment response in patients with lower GI aGVHD. Methods We conducted a 27-patient open-label, single-cohort, multicenter prospective phase 2 study between 05/16 and 05/19. Eligible pts were ≥ 18 yrs old and had new onset biopsy-proven grade II-IV lower GI aGVHD following an allo-HCT. Pts received F-652 once weekly at a dose of 45 μg/kg x 4 weeks in combination with standard corticosteroid treatment. Primary endpoints included PK, safety, and day 28 lower GI aGVHD response. Additional endpoints included day 56 treatment response, evaluation of changes in gut microbiota by 16S sequencing, and plasma GVHD biomarkers. The study was powered to distinguish between an unpromising response rate of 35% and a promising response rate of 60%. Results The 27 pts (median age 55 yrs, mostly PBSC recipients) had predominantly stage 2-4 lower GI GVHD (17/27, 63%), with 6/27 (22%) pts having stage 3 and 6/27 (22%) pts having stage 4 disease. All pts had detectable F-652 levels. Overall, 19/27 achieved a day 28 response (70%, 90%CI: 56-79, Fig 1A). Response to treatment based on Ann Arbor Risk, evaluable in 20 pts, was 7/12 (58%) with high, 3/4 (75%) with intermediate, and 4/4 (100%) with low risk biomarkers (Fig 1B). At day 56, 16 pts (59%) remained treatment responders. 3 pts had repeat GI biopsy after treatment and demonstrated improvement in GI epithelial injury (Fig 2). Additionally, in a subset of 17 pts with stool samples collected, microbial diversity and relative abundance of protective commensal Blautia appeared increased in pts with a clinical response to F-652 (p = 0.082 and 0.048, respectively, Fig 3A-B). Serious TEAEs were observed in 11 pts (40%) including enterocolitis (n = 1), pyrexia (n = 1), infection (2 sepsis, 1 device-related, 1 pneumonia, 1 sinusitis), musculoskeletal (n = 2), and respiratory (n = 1). One patient was diagnosed with squamous cell carcinoma 8 months after F-652 treatment. Conclusion IL-22 in combination with corticosteroids was well tolerated and the 70% lower GI aGVHD response rate met the primary efficacy endpoint. These findings support further development of this approach and provide a proof-of-concept for combining standard immunosuppression with tissue-supportive strategies to enhance recovery of damaged mucosa, promote microbial health, and improve GVHD treatment response.
Published: 2020
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13. FKBPL-based peptide, ALM201, targets angiogenesis and cancer stem cells in ovarian cancer

Author: Catherine J. Kennedy, Amy Short, Ian Harley, Tracy Robson, W. Glenn McCluggage, Mark Bates, Anna deFazio, Fiona Furlong, Anita Yakkundi, Helen O. McCarthy, Cian M. McCrudden, John J. O'Leary, Donal J. Brennan, Gillian Moore, Nermeen Moustafa, Laura Nelson, Sharon O'Toole, Sudipto Das, Lana McClements, Stephanie Annett, Alison Brand, Darran P. O'Connor, Adrien Kissenpfennig, Raghwa Sharma, Andrea Marshall, and Ciaran O'Riain
Subjects: Cancer Research, Angiogenesis, Mice, SCID, Carcinoma, Ovarian Epithelial, Neovascularization, Mice, 0302 clinical medicine, Ovarian Neoplasms, 0303 health sciences, education.field_of_study, Neovascularization, Pathologic, biology, Cancer stem cells, Cell Differentiation, Hyaluronan Receptors, Oncology, 030220 oncology & carcinogenesis, Neoplastic Stem Cells, Female, medicine.symptom, Signal Transduction, STAT3 Transcription Factor, Population, In Vitro Techniques, Article, Tacrolimus Binding Proteins, 03 medical and health sciences, FKBPL, SDG 3 - Good Health and Well-being, Ovarian cancer, Cancer stem cell, Cell Line, Tumor, medicine, Animals, Humans, Vasculogenic mimicry, Oncology & Carcinogenesis, education, 030304 developmental biology, Interleukin-6, business.industry, QH, CD44, medicine.disease, Xenograft Model Antitumor Assays, QP, biology.protein, Cancer research, Peptides, business, Tumour angiogenesis, RC
Abstract: Background ALM201 is a therapeutic peptide derived from FKBPL that has previously undergone preclinical and clinical development for oncology indications and has completed a Phase 1a clinical trial in ovarian cancer patients and other advanced solid tumours. Methods In vitro, cancer stem cell (CSC) assays in a range of HGSOC cell lines and patient samples, and in vivo tumour initiation, growth delay and limiting dilution assays, were utilised. Mechanisms were determined by using immunohistochemistry, ELISA, qRT-PCR, RNAseq and western blotting. Endogenous FKBPL protein levels were evaluated using tissue microarrays (TMA). Results ALM201 reduced CSCs in cell lines and primary samples by inducing differentiation. ALM201 treatment of highly vascularised Kuramochi xenografts resulted in tumour growth delay by disruption of angiogenesis and a ten-fold decrease in the CSC population. In contrast, ALM201 failed to elicit a strong antitumour response in non-vascularised OVCAR3 xenografts, due to high levels of IL-6 and vasculogenic mimicry. High endogenous tumour expression of FKBPL was associated with an increased progression-free interval, supporting the protective role of FKBPL in HGSOC. Conclusion FKBPL-based therapy can (i) dually target angiogenesis and CSCs, (ii) target the CD44/STAT3 pathway in tumours and (iii) is effective in highly vascularised HGSOC tumours with low levels of IL-6.
Published: 2020
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14. Current perspectives on targeting PIM kinases to overcome mechanisms of drug resistance and immune evasion in cancer

Author: Lea Schäfer, Susan Heavey, Nathalie Simon, Tom Malone, Gillian Moore, Stephen P. Finn, Kathy Gately, and Sinead Cuffe
Subjects: 0301 basic medicine, Combination therapy, Antineoplastic Agents, 03 medical and health sciences, 0302 clinical medicine, Immune system, Proto-Oncogene Proteins c-pim-1, hemic and lymphatic diseases, Neoplasms, Medicine, Animals, Humans, Pharmacology (medical), Kinase activity, Protein kinase B, PI3K/AKT/mTOR pathway, Immune Evasion, Pharmacology, business.industry, Mechanism (biology), Kinase, Cancer, medicine.disease, 030104 developmental biology, Drug Resistance, Neoplasm, 030220 oncology & carcinogenesis, Cancer research, Drug Therapy, Combination, business
Abstract: PIM kinases are a class of serine/threonine kinases that play a role in several of the hallmarks of cancer including cell cycle progression, metabolism, inflammation and immune evasion. Their constitutively active nature and unique catalytic structure has led them to be an attractive anticancer target through the use of small molecule inhibitors. This review highlights the enhanced activity of PIM kinases in cancer that can be driven by hypoxia in the tumour microenvironment and the important role that aberrant PIM kinase activity plays in resistance mechanisms to chemotherapy, radiotherapy, anti-angiogenic therapies and targeted therapies. We highlight an interaction of PIM kinases with numerous major oncogenic players, including but not limited to, stabilisation of p53, synergism with c-Myc, and notable parallel signalling with PI3K/Akt. We provide a comprehensive overview of PIM kinase's role as an escape mechanism to targeted therapies including PI3K/mTOR inhibitors, MET inhibitors, anti-HER2/EGFR treatments and the immunosuppressant rapamycin, providing a rationale for co-targeting treatment strategies for a more durable patient response. The current status of PIM kinase inhibitors and their use as a combination therapy with other targeted agents, in addition to the development of novel multi-molecularly targeted single therapeutic agents containing a PIM kinase targeting moiety are discussed.
Published: 2019

15. The Rite of Spring

Author: Gillian Moore and Gillian Moore
Subjects: Ballet--Production and direction--History
Abstract: The story behind the scandalous first performance of one of the most influential works in the history of music, as part of the stunning Landmark Library series. On 29 May 1913, at the Théâtre des Champs-Elysées in Paris, a new ballet by Diaghilev's Ballets Russes, choreographed by Vaslav Nijinsky, received its premiere. Many of the cultural big names of Paris were there, or were rumoured to have been there: Debussy, Ravel, Proust, Gertrude Stein, Picasso. When the curtain rose on a cast of frenziedly stamping dancers, a near-riot ensued, ensuring the evening would enter the folklore of modernism. While it was the dancing that triggered the mayhem, Stravinsky's score contained shocks enough, with its innovations in form, rhythm, dissonance and its sheer sonic power. The Rite of Spring would achieve recognition in its own right as a concert piece, and is now seen as one of the most influential works of the 20th century. Gillian Moore explores the cultural climate that created The Rite, tells the story of the creation of the music and the ballet and provides a guide to the music itself, showing how a scandalous novelty of 1913 became a 21st-century concert staple. As well as considering its influence on 20th-century classical composers, she probes The Rite's impact on film music (including scores for Star Wars and Jaws); its extensive influence on jazz musicians (including Charlie Parker) and by artists as diverse as Weather Report, Joni Mitchell, Frank Zappa and The Pet Shop Boys.
Published: 2019

16. Abstract B14: Activation of the MACC1/PIM/cMyc axis confers resistance to PI3K/mTOR inhibition in PIK3CA mutant NSCLC

Author: Samira Elbai, Gillian Moore, Stephen P. Finn, Michael O'Neill, Kathy Gately, and Susan Heavey
Subjects: Cancer Research, Small interfering RNA, biology, medicine.diagnostic_test, Kinase, Chemistry, medicine.medical_treatment, PIM1, Stat3 Signaling Pathway, Targeted therapy, Oncology, Western blot, biology.protein, Cancer research, medicine, STAT3, Molecular Biology, PI3K/AKT/mTOR pathway
Abstract: Introduction: The PI3K pathway is often dysregulated in lung cancer, making it an ideal therapeutic target. Pan- and isoform-specific inhibitors of the PI3K pathway are currently being evaluated in clinical trials. However, all patients treated thus far develop progressive disease due to the emergence of bypass signaling mechanisms. We developed a panel of lung cancer preclinical models to elucidate potential mechanisms of resistance to PI3K-mTOR inhibitor GDC-0980 (apitolisib). In-depth characterization of the PIK3CA mutant positive H1975 sensitive cells (H1975P) versus apitolisib-resistant cells (H1975GR) identified activation of MACC1 as an early marker of drug resistance and the subsequent activation of all three PIM kinases. Inhibition of MACC1 and PIM kinase by siRNAs and the effect of IBL-301 (a novel PIM/PI3K/mTOR inhibitor) were examined for effects on cell viability/proliferation and downstream signaling pathways in vitro. Methods: Profiling of H1975P versus H1975GR cells was undertaken using a mRNA/lncRNA array (Arraystar Inc) to quantify the expression of 20,730 mRNAs and 40,173 lncRNAs. Concomitant changes were assessed in the IL6/STAT3 signaling pathway by a QPCR array, immunofluorescence, Western blot and miRNA arrays. The effect of MACC1 and PIM kinase inhibition by siRNAs and targeted agents were examined by Western blot and cell viability assays. Results: MACC1 mRNA was upregulated 77 fold in H1975GR cells after 1-month exposure to apitolisib, and its regulated proteins HGF and MET were upregulated (10.06 and 1.65 fold, respectively). At 4 months MACC1 mRNA was increased by 44 fold, HGF 2 fold and MET 6.6 fold while several members of the IL-6/STAT3 pathway including c-Myc and PIM1, PIM2 and PIM3 kinases were also significantly activated (25.5, 19.8, 3.3 and 31.9 fold respectively). Results were also validated by Western blot. A miRNA signature of PI3K/mTOR inhibitor resistance was validated that can be used to monitor patients on treatment. Inhibition of PIM kinases by siRNA and targeted therapy restored sensitivity to PI3K-mTOR inhibitors. Novel triple-targeted therapy IBL-301 decreased PIM kinase, c-Myc and MACC1 expression. IC50 values of IBL-301 were significantly less for H1975GR cells (0.02μM) compared to H1975P cells (0.75μM), highlighting activated PIM kinase as a mechanism of resistance to PI3K-mTOR inhibition. Conclusion: Activated MACC1, PIM kinases and their interacting partners play a role in resistance to PI3K-mTOR inhibitors in PIK3CA mutant NSCLC. Our data provide a rationale for combined or sequential targeting of PI3K-mTOR and PIM kinases to significantly delay resistance and provide durable treatment responses in patients with PIK3CA mutant lung tumors. Citation Format: Gillian Moore, Samira Elbai, Susan Heavey, Stephen Finn, Michael O'Neill, Kathy Gately. Activation of the MACC1/PIM/cMyc axis confers resistance to PI3K/mTOR inhibition in PIK3CA mutant NSCLC [abstract]. In: Proceedings of the AACR Special Conference on Targeting PI3K/mTOR Signaling; 2018 Nov 30-Dec 8; Boston, MA. Philadelphia (PA): AACR; Mol Cancer Res 2020;18(10_Suppl):Abstract nr B14.
Published: 2020
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17. Intestinal dysbiosis predicts lower gastrointestinal tract acute graft-versus-host (aGVHD) disease development

Author: Marina Burgos da Silva, Doris M. Ponce, Antonio L.C. Gomes, Gillian Moore, John B. Slingerland, Eric Pamer, Ying Taur, Jonathan U. Peled, and Marcel R.M. Van Den Brink
Subjects: Immunology, Immunology and Allergy
Abstract: Introduction aGVHD is a major complication after hematopoietic cell transplantation (HCT) and is driven by alloimmune targeting of intestine, liver, and skin. As aGVHD has been linked to intestinal dysbiosis and the majority of the intestinal microbiota biomass resides within the colon, we hypothesized that certain microbiota features confer protection to the lower GI tract. Methods We evaluated 16S stool profiles of 849 samples from 215 recipients of unmodified allo-HCT. Patients were classified in four groups according to aGVHD organ involvement: upper GI only (UGI, n =53), lower GI with/without upper GI (LGI, n=56), no GI involvement (non-GI, n=30) and no GVHD (n=76). Samples were grouped into pre-onset (day −20 to 0) and post-onset (day 1 to 20) aGVHD. Results Pre-onset, LGI patients showed a decreased strict anaerobes to facultative anaerobes (A/F) ratio vs. non-GI (p=0.036) and a low A/F ratio was associated with reduced overall survival (p=0.004) from aGVHD onset. After aGVHD onset, LGI patients had reduced microbial alpha diversity, abundance of predicted butyrate-producing (BP) bacteria and A/F ratio vs. non-GI patients (p=0.017, p=0.003 and p=0.020, respectively). LGI patients also had less BP bacteria, members of genus Blautia, and lower A/F ratio (p=0.0.017, p=0.008 and p=0.048 respectively) vs. UGI patients. Conclusions LGI patients had distinct microbial features consistent with dysbiosis, when compared to UGI and non-GI patients. Importantly, we observed microbiota disruption in the 20 days preceding aGVHD onset, suggesting a predictive marker of LGI aGVHD and an association with overall survival, which have potential practical implications for GVHD risk stratification and therapeutic interventions.
Published: 2020
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18. pSTAT3 Levels Have Divergent Expression Patterns and Associations with Survival in Squamous Cell Carcinoma and Adenocarcinoma of the Oesophagus

Author: Joanne Lysaght, John V. Reynolds, Gillian Moore, Eamon P. Breen, Adriana J. Michielsen, Katie E O' Sullivan, Ricardo Segurado, Jacintha O' Sullivan, Mary Clare Cathcart, and Esther O' Regan
Subjects: 0301 basic medicine, squamous cell carcinoma, Esophageal Neoplasms, Angiogenesis, Apoptosis, lcsh:Chemistry, STAT3, 0302 clinical medicine, Cell Movement, Medicine, Phosphorylation, lcsh:QH301-705.5, Spectroscopy, Tissue microarray, biology, General Medicine, Computer Science Applications, medicine.anatomical_structure, 030220 oncology & carcinogenesis, Carcinoma, Squamous Cell, Immunohistochemistry, Adenocarcinoma, STAT3 Transcription Factor, Cell Survival, Catalysis, Article, Inorganic Chemistry, 03 medical and health sciences, cancer, Humans, Physical and Theoretical Chemistry, Molecular Biology, Cell Proliferation, Proportional Hazards Models, adenocarcinoma, oesophagus, business.industry, Organic Chemistry, medicine.disease, Receptors, Interleukin-6, Survival Analysis, Epithelium, stomatognathic diseases, 030104 developmental biology, lcsh:Biology (General), lcsh:QD1-999, Cell culture, Tissue Array Analysis, Cancer research, biology.protein, business
Abstract: Signal transducers and activator of transcription (STAT)-3 is activated in cancers, where it promotes growth, inflammation, angiogenesis, and inhibits apoptosis. Tissue microarrays were generated using tissues from 154 patients, with oesophageal adenocarcinoma (OAC) (n = 116) or squamous cell carcinoma (SCC) (n = 38) tumours. The tissues were stained for pSTAT3 and IL-6R using immunohistochemistry. The OE33 (OAC) and OE21 (SCC) cell lines were treated with the STAT3 inhibitor, STATTIC. The Univariate cox regression analysis revealed that a positive pSTAT3 in SCC was adversely associated with survival (Hazard ratio (HR) 6.382, 95% CI 1.266&ndash, 32.184), while a protective effect was demonstrated with the higher pSTAT3 levels in OAC epithelium (HR 0.74, 95% CI 0.574&ndash, 0.953). The IL-6R intensity levels were higher in the SCC tumours compared with the OAC tumours for the core and leading edge tumour tissue. The pSTAT3 levels correlated positively with the IL-6R levels in both the OAC and SCC. The treatment of OE21 and OE33 cells with the STAT3 inhibitor STATTIC in vitro resulted in decreased survival, proliferation, migration, and increased apoptosis. The pSTAT3 expression was associated with adverse survival in SCC, but not in the OAC patients. The inhibition of STAT3 in both of the tumour subtypes resulted in alterations in the survival, proliferation, migration, and apoptosis, suggesting a potential role for therapeutically targeting STAT3.
Published: 2018

19. Photobiomodulation (PBM) Provides a Prompt and Near-Resolution Response to Advanced Oral Chronic Graft-Versus-Host Disease (cGVHD) after Allogeneic Hematopoietic Stem Cell Transplantation (allo-HSCT)

Author: Alina Markova, Esperanza B. Papadopoulos, Gillian Moore, Roni Tamari, Doris M. Ponce, Parastoo B. Dahi, Andrei Barash, Susan E. Prockop, and Sergio Giralt
Subjects: Transplantation, medicine.medical_specialty, Triamcinolone acetonide, Erythema, business.industry, Visual analogue scale, medicine.medical_treatment, Hematology, Hematopoietic stem cell transplantation, Pain scale, medicine.disease, Gastroenterology, Graft-versus-host disease, Internal medicine, Mucositis, Medicine, medicine.symptom, business, Adverse effect, medicine.drug
Abstract: Background cGVHD is a major complication after allo-HSCT. The oral cavity is frequently affected and may present with painful ulcerations, intraoral discomfort, and limitation to oral intake. While systemic corticosteroids remain first line therapy for moderate/ severe cGVHD, topical and intralesional immunosuppressant (IS)-based therapies have been used with modest effect. PBM, a non-invasive light therapy, appears to promote tissue recovery via direct absorption of cytochrome C oxidase and activation of TGF-β1, and has been used for the prevention and treatment of radiation-induced mucositis in head & neck cancer. However, the effect of PBM therapy in oral cGVHD is currently unknown. Methods We evaluated 7 patients (median age 47) who underwent allo-HSCT (7 PBSC grafts) after myeloablative (n = 3) and reduced (n = 4) conditioning between 09/2015-05/2017. Patients developed moderate (n = 2) or severe (n = 5) oral cGVHD and received PBM (2x/week for 3 weeks) after failure to improve with topical corticosteroid and/or topical tacrolimus therapy +/- intralesional triamcinolone injections and systemic IS. Thor® laser LX2 with wavelengths of 660 nm (visible-red) and 810 nm (near-infrared) was applied extra-orally. The psychometric questionnaire for pain rating (Visual Analogue Scale [VAS], scale 0-10), and oral GVHD (OGVHD) score (severity of erythema, lichenoid changes, ulcers and mucoceles, scale 0-15) were used weekly for the assessment of therapeutic response. Results The baseline oral cGVHD evaluation revealed high VAS (median 7, range 3-8) and OGVHD (median 9, range 6-9) scores. Patients had affected oral cavity that included lichen planus-like changes, ulcers, mucositis, gingivitis, and/or erythema (Fig. 1A-B). The first therapeutic response assessment was obtained 1 week after initiation of therapy and showed improvement in pain by VAS score (median 3). Subsequent assessments were obtained for the duration of PBM therapy and showed overall improvement in the pain scale and healing of the oral cavity (Fig. 1C-D, 2A-B). At the end of treatment, the median VAS score was 2 (range 1-2) and OGVHD was 3 (range 1-4). Treatment was well tolerated, and all patients received the intended number of PBM treatments in the planned period of 3 weeks. No adverse events were reported as related to PBM. Conclusions Advanced oral cGVHD achieved near-complete resolution of pain and oral cavity lesions after PBM therapy. Notable, patients who previously failed to respond to upfront topical and systemic IS treatment achieved high therapeutic response with PBM. Improvement in pain scale was observed 1 week after starting therapy and healing of the oral cavity was observed at 2 weeks. This non-IS treatment appears feasible, safe and promising in oral cGVHD. A prospective study is needed to confirm these preliminary findings.
Published: 2019
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20. Pre-Transplant and Peri-d100 Gastrointestinal Dysbiosis Is Associated with the Subsequent Development of Chronic Graft-Versus-Host Disease

Author: Kate A. Markey, Antonio L.C. Gomes, Jonathan U. Peled, Miguel-Angel Perales, Molly Maloy, Sean M. Devlin, Sergio Giralt, Ann E. Slingerland, Samira Fatmi, Annelie Clurman, Marcel R.M. van den Brink, Doris M. Ponce, Eric R. Littmann, Eric G. Pamer, John B. Slingerland, Gillian Moore, and Ying Taur
Subjects: Transplantation, medicine.medical_specialty, biology, business.industry, Peri, Patient characteristics, Hematology, biology.organism_classification, medicine.disease, Gastroenterology, Pathogenesis, Graft-versus-host disease, immune system diseases, hemic and lymphatic diseases, Internal medicine, Cohort, medicine, Prevotella, Biomarker (medicine), business, Dysbiosis
Abstract: Chronic GVHD affects ∼50% of long-term survivors of allo-HCT, and is the leading cause of mortality in patients who survive to two years. Unlike aGVHD, cGVHD pathology is fibrotic and shares features with the autoimmune conditions Sjogrens syndrome and systemic sclerosis. Gastrointestinal microbiota signatures have been associated with these conditions, and we thus hypothesized that the configuration of microbial communities would also be associated with cGVHD, and may serve as predictive biomarkers or offer mechanistic insights into cGVHD pathogenesis. We identified a cohort of 55 cGVHD patients, confirmed by formal clinical consensus (NIH criteria), transplanted at MSKCC from 2013-2017. The majority received unmodified PBSC (60%) with the remainder receiving CD34-selected (20%), and marrow or cord-blood grafts (20%). 532 stool samples from 55 cGVHD cases were compared with 1462 samples from 165 controls (matched for graft source). Median cGVHD onset was d194. Patient characteristics in the cases and controls were equivalent, including rate of aGVHD prior to day 100 (55% vs 46%; p = 0.27). In addition, we compared the cGVHD cases with an independent cohort of patients with Gr3-4 aGVHD (n = 71 patients, contributing 835 samples), and an additional control group (matched for graft-source, n = 213 patients, 1786 samples) who remained GVHD-free. All stool samples underwent 16S-targeted sequencing on the Illumina platform. In addition, available peri-d100 samples underwent shotgun metagenomic sequencing (cGVHD, n = 9; controls, n = 25). There were no differences in a-diversity as a function of time peri-HCT, nor did we observe clustering of community characteristics in tSNE-space, or differences using the linear discriminant effect size (LEfSE) pipeline when we specifically examined samples collected pre-transplant, peri-engraftment, or peri-d100. In contrast, a set of genera reported to be enriched in intestinal communities of patients with autoimmune diseases were selected for targeted analysis and revealed higher relative abundance in Prevotella prior to HCT in cGVHD cases (case vs source-matched control p Here, we report for the first time, intestinal microbial signatures that are associated with cGVHD and are identifiable pre-HCT and peri-d100. The cGVHD-associated dysbiosis we have identified may have value as both a biomarker for cGVHD risk and mechanistic relevance.
Published: 2019
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21. A comparison of psychological and medical indices pre– and post–bariatric surgery: A pilot study

Author: Gillian Moore-Groarke, Colm O’Boyle, and Amy-Rose Hayes
Abstract: BackgroundBariatric surgery is an effective intervention in the morbidly obese to achieve marked weight loss and improve physical comorbidities, yet its impact on psych logical health has yet to be determined and requires ongoing longitudinal research. This study aims to examine the differences in nine psychological indices pre– and post–bariatric surgery.MethodsAll patients undergoing bariatric surgical intervention consented to a detailed psychological assessment immediately prior to surgery and at six months following the procedure. Measures assessed included Quality of Life, Self–esteem, Beck Depression, General Health, Hospital Anxiety and Depression, Coping Measures, Physical Complaints, Eating Attitudes and Profile of Moods.FindingsOf the psychological measures assessed, scales pertaining to quality of life, self-esteem, depression, general health and anxiety were all significantly improved post–operatively. There was no significant improvement in scales pertaining to coping, physical complaints, eating attitudes, or mood volatility after surgery.DiscussionThe results of this study suggest that psychosocial outcomes of bariatric surgery are largely positive, though this must be interpreted cautiously. This study also suggests the importance of follow–up psychological evaluation and education post–operatively.
Published: 2016
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22. PO-505 Targeting PIM kinase to overcome resistance to PI3K-mTOR inhibition in NSCLC

Author: Michael O'Neill, Kenneth J. O'Byrne, Kathy Gately, Sinead Cuffe, Susan Heavey, Gillian Moore, and Stephen P. Finn
Subjects: Cancer Research, biology, Angiogenesis, Kinase, Cell, PIM1, Receptor tyrosine kinase, medicine.anatomical_structure, Oncology, biology.protein, Cancer research, medicine, Viability assay, PI3K/AKT/mTOR pathway, Insulin-like growth factor 1 receptor
Abstract: Introduction Non-small cell lung cancer (NSCLC) is the leading cause of cancer mortality globally, having a 5 year survival rate of less than 15%. PI3K-mTOR signalling has been implicated in various hallmarks of cancer and is frequently dysregulated in NSCLC. Efforts to therapeutically target the PI3K-mTOR pathway have been hampered by the inevitable emergence of drug resistance inhibiting a durable response to treatment. Our group developed NSCLC cell line models of acquired resistance to PI3K-mTOR inhibitor GDC-0980. Resistant cells (H1975GR) were also less sensitive to PI3K-mTOR dual targeting inhibitor, BEZ235 compared to matched parent cells (H1975P) making them an ideal model to identify and interrogate drug resistance mechanisims. Material and methods The sensitivity of GDC-0980 resistant cells (H1975GR) versus age-matched parent cells (H1975P) to BEZ235 following a 72 hour treatment was compared using a Cell Titre Blue cell viability assay (n=3). Alterations to the mRNA expression profile of H1975GR versus H1975P were examined using an IL-6/STAT3 signalling-specific RT2 gene profiler array (n=1). Selected genes from the array were validated by SYBR-based qPCR, immunofluorescence (IF) and western blot analysis (n=3–4). 11 miRNAs (regulated by or regulators of c-Myc/PIM) plus housekeeping control miRNAs were quantified in the H1975P/GR model by QPCR. IC50 values of pan-PIM kinase inhibitors AZD1208, IBL101 and novel PI3K/mTOR/PIM inhibitor IBL301 inhibiting growth in H1975P versus H1975GR were compared using the BrdU assay. The effect of these drugs on RTK and c-Myc expression were examined in H1975GR by IF and western blot analysis. Results and discussions In-depth characterisation of the H1975GR cells identified activation of several receptor tyrosine kinases (RTKs) including EGFR, IGF1R, EPHA2 and members of the IL-6/STAT3 pathway including c-Myc and PIM1, PIM2 and PIM3 kinases. IL-6/STAT3 overexpression in cancer stimulates angiogenesis, migration, invasiveness, cytokine signalling and notably drug resistance. A miRNA signature of PI3K/mTOR inhibitor resistance was validated which can be used to monitor patients on treatment. IC50 values of IBL301 were significantly less for H1975GR cells (0.02 uM) compared to H1975P cells (0.75 uM) highlighting activated PIM kinase as a mechanism of resistance to PI3K-mTOR inhibition. Targeting PIM kinase in H1975GR cells inhibits activated c-Myc and RTKs. Conclusion Dual targeting of both PIM and PI3K-mTOR may provide a more durable response to treatment for patients with NSCLC.
Published: 2018
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23. Sparing of the Lower Gastrointestinal Tract Microbiota Is Associated with Reduced Acute Graft-Versus-Host Disease

Author: Doris M. Ponce, Gillian Moore, Ying Taur, Eric G. Pamer, Marcel R.M. van den Brink, Jonathan U. Peled, John B. Slingerland, Antonio L.C. Gomes, and Marina Burgos da Silva
Subjects: medicine.medical_specialty, Gastrointestinal tract, business.industry, Immunology, Allopurinol, Cell Biology, Hematology, medicine.disease, Biochemistry, Gastroenterology, Graft-versus-host disease, Internal medicine, Acute graft versus host disease, medicine, Anaerobic bacteria, Microbiome, business, Dysbiosis, Feces, medicine.drug
Abstract: Introduction. Clinical graft-versus-host disease (GVHD) phenotypes can selectively involve the upper or lower tract and extraintestinal tissues and organs. High gut microbiota diversity and the abundance of certain bacterial commensals within the Clostridiales order are associated with decreased risk of GVHD-related mortality after allogeneic stem cell transplantation (allo-HCT). The microbiota-derived short-chain fatty acid butyrate has been found beneficial in reducing murine GI aGVHD. Conversely, microbiota disruption is associated with expansions of potentially pathogenic bacteria, including facultative anaerobes, and can worsen allo-HCT outcomes. Since the vast majority of the intestinal microbiota biomass resides within the colon, we hypothesized that certain features of the colonic microbiota confer local protection to the lower GI tract. Methods. We evaluated 216 patients (median age 55 years) who underwent unmodified allo-HCT and had stool samples collected under our institutional fecal microbiome biobank between 01/2011 and 02/2017. Patients were classified in three groups according to the organ involved in aGVHD: Upper GI only (UGI, n = 56), lower GI with or without upper GI involvement (LGI, n =61 ), no GI tract involvement (non-GI, n = 29). A fourth group of 70 control patients with no GVHD whatsoever were selected on the basis of the study inclusion and exclusion criteria and having evaluable samples in our biobank in a temporal distribution that matched onset of GVHD. Microbial diversity was computed using Simpson's reciprocal index. Results. A total of 902 stool specimens were analyzed with an average of 4.2 samples/patient. Samples were grouped into pre-onset (day -20 to day 0) and post-onset (day 1 to day 20) aGVHD. Trends in intestinal microbiota features relative to the day of aGVHD onset showed distinct dynamics among the groups. Prior to aGVHD onset, all groups showed similar microbial diversity, and similar abundance of anaerobic commensals, including members of genus Blautia (Fig 1A-C). After aGVHD onset, microbial diversity and commensal anaerobe abundance in LGI cases were significantly lower than non-GI (p = 0.01 and 0.008, respectively) and UGI (p = 0.03 and 0.03, respectively) groups (Fig. 1A, 1B). The LGI group also had significantly lower abundance of the genus Blautia (p = 0.02, Fig 1C). Conversely, the LGI group had increased prevalence of facultative anaerobes (LGI vs. non-GI, p = 0.03, Fig. 1D). Prior to aGVHD onset, the LGI cases had lower abundance of predicted butyrate-producing bacteria (LGI vs. no-GVHD, p = 0.03), which was maintained in all three GVHD groups post-onset aGVHD (Fig 1E). Conclusions. Patients without GVHD, non-GI and UGI aGVHD phenotypes had higher microbial diversity, abundance of anaerobe commensals including genus Blautia, and predicted butyrate-producing bacteria after aGVHD onset than patients with lower GI tract involvement by aGVHD. In contrast, the LGI cases had features consistent with microbiota dysbiosis including prevalence of facultative anaerobes, and lower abundance of butyrate-producing bacteria before and after aGVHD. These findings are consistent with a model in which a diverse microbiota abundant in potential beneficial commensals exerts a local protective effect in the lower GI tract and have potential practical implications in future prophylactic and therapeutic interventions in aGVHD. Figure 1 Disclosures Gomes: Seres Therapeutics: Other: Part of Salary. Slingerland:Seres Therapeutics: Other: Salary supported by Seres funding. Pamer:Bristol Myers Squibb: Honoraria; Celgene: Honoraria; Seres Therapeutics: Honoraria, Patents & Royalties; MedImmune: Honoraria; Novartis: Honoraria; Ferring Pharmaceuticals: Honoraria. Peled:Seres therapeutics: Consultancy, Honoraria. van den Brink:Acute Leukemia Forum (ALF): Consultancy, Honoraria; Merck & Co, Inc.: Consultancy, Honoraria; Magenta and DKMS Medical Council: Membership on an entity's Board of Directors or advisory committees; Juno Therapeutics: Other: Licensing; Seres Therapeutics: Consultancy, Honoraria, Membership on an entity's Board of Directors or advisory committees, Research Funding; Amgen: Consultancy, Honoraria; Jazz Pharmaceuticals: Consultancy, Honoraria; Therakos: Consultancy, Honoraria; Flagship Ventures: Consultancy, Honoraria; Novartis: Consultancy, Honoraria; Evelo: Consultancy, Honoraria.
Published: 2019
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24. P2.03-19 Co-Targeting PIM Kinase to Overcome MET Amplified Resistance to EGFR TKIs in NSCLC

Author: N. Simon, S.P. Finn, A. Mahon, Michael O'Neill, Sinead Cuffe, Gillian Moore, Kathy Gately, Boe Sandahl Sorensen, and A. Tranberg Madsen
Subjects: Pulmonary and Respiratory Medicine, Egfr tki, Oncology, Kinase, business.industry, Cancer research, Medicine, business
Published: 2019
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25. Parallel Profiles of Inflammatory and Effector Memory T Cells in Visceral Fat and Liver of Obesity-Associated Cancer Patients

Author: Gillian Moore, Melissa J. Conroy, John V. Reynolds, Ann Marie Mongan, Joanne Lysaght, Suzanne L. Doyle, Karen C. Galvin, Maria E. Kavanagh, Aoife Cannon, Health Research Board, Ireland, and Health Research Award
Subjects: 0301 basic medicine, obesity, Pathology, medicine.medical_specialty, Chemokine, Esophageal Neoplasms, medicine.medical_treatment, T cell, Immunology, T cells, Inflammation, Adenocarcinoma, Intra-Abdominal Fat, liver, Proinflammatory cytokine, 03 medical and health sciences, Liver disease, 0302 clinical medicine, T-Lymphocyte Subsets, omentum, Neoplasms, Medicine and Health Sciences, medicine, cancer, Immunology and Allergy, Humans, Obesity, biology, business.industry, Cancer, medicine.disease, body regions, 030104 developmental biology, Cytokine, medicine.anatomical_structure, Oncology, Liver, 030220 oncology & carcinogenesis, biology.protein, Cytokines, medicine.symptom, business, Immunologic Memory, Omentum, Dietetics and Clinical Nutrition
Abstract: In the midst of a worsening obesity epidemic, the incidence of obesity-associated morbidities, including cancer, diabetes, cardiac and liver disease is increasing. Insights into mechanisms underlying pathological obesity-associated inflammation are lacking. Both the omentum, the principal component of visceral fat, and liver of obese individuals are sites of excessive inflammation, but to date the T cell profiles of both compartments have not been assessed or compared in a patient cohort with obesity-associated disease. We have previously identified that omentum is enriched with inflammatory cytokines, chemokines and T cells. Here, we compared the inflammatory profile of T cells in the omentum and liver of patients with the obesity-associated malignancy oesophageal adenocarcinoma (OAC). Furthermore, we assessed the secreted cytokine profile in OAC patient serum, omentum and liver to assess systemic and local inflammation. We observed parallel T cell cytokine profiles and phenotypes in the omentum and liver of OAC patients, in particular CD69(+) and inflammatory effector memory T cells. This study reflects similar processes of inflammation and T cell activation in the omentum and liver, and may suggest common targets to modulate pathological inflammation at these sites.
Published: 2016

26. Abstract LB-054: FKBPL as a novel therapeutic target and prognostic biomarker in high grade serous ovarian cancer

Author: Ian Harley, Adrien Kissenpfenning, Ken Arthur, Laura Nelson, Neermeen Moustafa, Stephanie Annett, Andrea Marshall, Darran P. O'Connor, Gillian Moore, Fiona Furlong, Lana McClements, Tim Harrison, Amy Short, Graham Cotton, Cian M. McCrudden, Helen O. McCarthy, Sudipto Das, Glen McCluggage, Tracy Robson, and Anita Yakkundi
Subjects: Cancer Research, education.field_of_study, biology, Angiogenesis, business.industry, CD44, Population, Tumor initiation, medicine.disease, Oncology, FKBPL, Cancer stem cell, medicine, biology.protein, Cancer research, Ovarian cancer, business, education, Clonogenic assay
Abstract: FKBPL is a secreted protein with well-established anti-angiogenic and anti-cancer stem cell activity. A novel therapeutic peptide, ALM201, derived from this protein has successfully completed a phase I clinical trial and was granted orphan drug status, by the FDA, for the treatment of ovarian cancer. Ovarian cancer is the most lethal gynecological cancer and there are no prognostic biomarkers currently used in the clinic. It is associated with a high incidence of recurrent chemo-resistant disease and this has been attributed to a treatment-resistant subpopulation of CD44+ cancer stem cells (CSCs). Previously, we presented evidence that CD44 is a potential target of ALM201 and here, for the first time, we investigate its ability to target both angiogenesis and CSCs in HGSOC. Tumorsphere and flow cytometry assays demonstrated that ALM201 is effective at reducing CSCs in a range of HGSOC cell lines and primary patient samples in vitro. Clonogenic assays demonstrated that ALM201 is not cytotoxic, but rather mediates ovarian CSC differentiation. In vitro, ALM201 displayed potent anti-CSC activity in the HGSOC cell line, OVCAR3. However, OVCAR3 tumor xenografts are not dependent on angiogenesis for their growth and therefore ALM201 did not elicit a strong response in this model. Furthermore, OVCAR3 xenografts dramatically upregulated the inflammatory cytokines IL-6 and IL-8, which is consistent with the lack of anti-CSC activity of ALM201 in vivo compared to in vitro. In contrast, treatment of highly angiogenic Kuramochi tumor xenografts, another HGSOC cell line, resulted in a statistically significant delay in both tumor growth and tumor initiation. This was associated with disruption of the CD31+ vascular network and a 10 fold decrease in the CSC population. Finally, using HGSOC tissue microarrays we demonstrated that high endogenous expression of FKBPL correlated with increased progression free interval; indicating the potential for FKBPL to be used as a prognostic biomarker in HGSOC. HGSOC cell lines display marked differences in tumor vascularisation in vivo. ALM201, a peptide fragment of FKBPL, has potent anti-CSC and anti-angiogenic activity in an HGSOC xenograft which is dependent on angiogenesis for growth; an important finding for the clinical development of ALM201. Our data also strongly suggest that FKBPL is a potential novel prognostic biomarker in HGSOC, supporting its endogenous anti-tumor activity. Citation Format: Stephanie Annett, Gillian Moore, Amy Short, Neermeen Moustafa, Sudipto Das, Darran O'Connor, Cian McCrudden, Adrien Kissenpfenning, Laura Nelson, Ian Harley, Ken Arthur, Anita Yakkundi, Glen McCluggage, Andrea Marshall, Fiona Furlong, Helen O. McCarthy, Graham Cotton, Timothy Harrison, Lana McClements, Tracy Robson. FKBPL as a novel therapeutic target and prognostic biomarker in high grade serous ovarian cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr LB-054.
Published: 2018
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27. ‘A vigorous unbroken tradition’

Author: Gillian Moore
Published: 2015
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28. P3.02c-010 Resistance Mechanisms to PI3K-mTOR Inhibition in NSCLC

Author: Gillian Moore, Stephen P. Finn, Michael O'Neill, Susan Heavey, Sinead Cuffe, Kathy Gately, and Kenneth J. O'Byrne
Subjects: Pulmonary and Respiratory Medicine, Oncology, business.industry, medicine.medical_treatment, Cancer research, Medicine, business, PI3K/AKT/mTOR pathway, Targeted therapy
Published: 2017
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29. P1.02-065 Elucidating the Role of PIM Kinase and Its Therapeutic Potential in NSCLC

Author: Michael O'Neill, Gillian Moore, Stephen P. Finn, Clara Lightner, Sinead Cuffe, Kathy Gately, Lauren Brady, Susan Heavey, and Kenneth J. O'Byrne
Subjects: 0301 basic medicine, Pulmonary and Respiratory Medicine, 03 medical and health sciences, 030104 developmental biology, Oncology, Kinase, business.industry, Cancer research, Medicine, business
Published: 2017
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30. Activated cMyc/PIM kinase promotes resistance to PI3K/mTOR inhibition in NSCLC

Author: S.P. Finn, Gillian Moore, Kathy Gately, S. Cuffe, Michael O'Neill, Susan Heavey, and Kenneth J. O'Byrne
Subjects: 0301 basic medicine, Pulmonary and Respiratory Medicine, Cancer Research, biology, Kinase, business.industry, Drug resistance, medicine.disease, Blockade, 03 medical and health sciences, 030104 developmental biology, 0302 clinical medicine, Oncology, Cell culture, 030220 oncology & carcinogenesis, biology.protein, Cancer research, medicine, STAT3, Lung cancer, business, IC50, PI3K/AKT/mTOR pathway
Abstract: Therapeutically targeting the PI3K-mTOR pathway has shown promising clinical efficacy, however the inevitable emergence of drug resistance inhibits a durable response to treatment. We developed cell line models of acquired resistance to a PI3K-mTOR inhibitor Apitolisib following treatments with IC50 drug doses. Here we investigate the role the IL-6/STAT3 pathway contributes to PI3K-mTOR blockade resistance.
Published: 2018
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31. Weight Loss Surgery : A New Medical Approach

Author: Dr. Gillian Moore Groarke, Dr. Colm O'Boyle, Dr. Gillian Moore Groarke, and Dr. Colm O'Boyle
Subjects: Obesity--Surgery, Weight loss, Liposuction
Abstract: Weightloss Surgery: A comprehensive medical team approach - Edited by Dr. Gillian Moore Groarke and Consultant Bariatric Surgeon Colm O'Boyle. Weight Loss Surgery – A comprehensive medical team approach is a unique book written by members of a multi-disciplinary bariatric team. This book, is a practical guide for patients considering bariatric surgery. It details the most widely utilized and most effective weight-loss surgical procedures. There is a detailed explanation of the perioperative psychological and dietary implications. There are chapters discussing the more common obesity-related conditions such as sleep apnoea, diabetes and cardiovascular disease. The pre and post-operative nursing care plan and follow-up physiotherapy programme are also detailed. Throughout the book there are examples of patient experiences, written by the patients themselves, and detailing the positive impact that bariatric surgery has had on their lives. •Multidisciplinary team with breadth and depth of knowledge and experience. •Easy to read explanations with diagrams •Answers to questions you may be afraid to ask •Detailed perioperative advice •Real life patient experiences •Extensive dietary & exercise advice •List of useful information, websites and resources About the authors: Gillian Moore Groarke: Dr. Gillian Moore-Groarke is a consultant registered health psychologist. She is a member of the Division of health psychology, PSI and BPS. She has a specialist interest in eating disorders and is author of a number of books and publications in this area. As well as being attached to the Bon Secours hospital she also runs a private practise in Harley Court, Wilton, cork. She is a regular contributor to the media on all aspects of psychology and also was a columnist for the Irish Examiner. She has lectured in UCC for a number of years. She has also been involved in various research programmes in the school of medicine, school of psychology and school of speech and language therapy and has acted as health advisor to various organisations, and has provided a number of employment assistant programmes. Mr. Colm O'Boyle: Mr O'Boyle qualified at Trinity College Dublin in 1990. He completed his higher surgical training in Yorkshire, UK. He worked as Senior Surgical Registrar at Leeds General Infirmary and Hull Royal Infirmary. In 2000 he was the International Travelling Fellow and Senior Surgical Registrar at the Royal Adelaide Hospital, Australia. He was appointed as Consultant General Surgeon and Lead Clinician for Upper Gastrointestinal surgery at Hull Royal Infirmary in 2002. He was appointed as Consultant in General, Laparoscopic and Bariatric surgery to the Bon Secours Hospital, Cork in January 2008. He is a member of the British Obesity and Metabolic Surgical Society (BOMSS) and the International Federation for the Surgery of Obesity (IFSO). Mr O'Boyle has been performing laparoscopic surgery for patients with obesity since 1998. He is one of the most experienced bariatric surgeons in the UK and Ireland. Weightloss Surgery – A comprehensive medical team approach is published by Currach Press.
Published: 2012

32. Cross-Talk between Cancer Cells and the Tumour Microenvironment: The Role of the 5-Lipoxygenase Pathway

Author: Gillian Moore and Graham P. Pidgeon
Subjects: Vascular Endothelial Growth Factor A, 0301 basic medicine, Cell, Review, Cell Communication, medicine.disease_cause, lcsh:Chemistry, angiogenesis, Neoplasms, leukotrienes, Tumor Microenvironment, Myeloid Cells, Lymphocytes, lcsh:QH301-705.5, Spectroscopy, Neovascularization, Pathologic, biology, General Medicine, adipose tissue, Computer Science Applications, medicine.anatomical_structure, Biochemistry, Arachidonate 5-lipoxygenase, 5-lipoxygenase, medicine.symptom, tumour microenvironment, Signal Transduction, Cell type, Inflammation, Catalysis, Immunomodulation, Inorganic Chemistry, 03 medical and health sciences, immune cells, Immune system, medicine, Animals, Humans, Physical and Theoretical Chemistry, Molecular Biology, Arachidonate 5-Lipoxygenase, Organic Chemistry, Cancer, Fibroblasts, Lipid Metabolism, medicine.disease, Biosynthetic Pathways, 030104 developmental biology, lcsh:Biology (General), lcsh:QD1-999, Cyclooxygenase 2, Cancer cell, biology.protein, Cancer research, Carcinogenesis
Abstract: 5-lipoxygenase is an enzyme responsible for the synthesis of a range of bioactive lipids signalling molecules known collectively as eicosanoids. 5-lipoxygenase metabolites such as 5-hydroxyeicosatetraenoic acid (5-HETE) and a number of leukotrienes are mostly derived from arachidonic acid and have been shown to be lipid mediators of inflammation in different pathological states including cancer. Upregulated 5-lipoxygenase expression and metabolite production is found in a number of cancer types and has been shown to be associated with increased tumorigenesis. 5-lipoxygenase activity is present in a number of diverse cell types of the immune system and connective tissue. In this review, we discuss potential routes through which cancer cells may utilise the 5-lipoxygenase pathway to interact with the tumour microenvironment during the development and progression of a tumour. Furthermore, immune-derived 5-lipoxygenase signalling can drive both pro- and anti-tumour effects depending on the immune cell subtype and an overview of evidence for these opposing effects is presented.
Published: 2017
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33. An Introduction to Journalism

Author: Carole Fleming, Emma Hemmingway, Gillian Moore, and Dave Welford
Published: 2006
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34. Bacterial detection of platelets : current problems and possible resolutions

Author: Erik A.M. Beckers, Gillian Moore, Ebbe Dickmeiss, Morris A. Blajchman, Lilly Lin, and Ludo Muylle
Subjects: Blood Platelets, Quality Control, medicine.medical_specialty, Blood transfusion, Drug Contamination, medicine.medical_treatment, Clinical Biochemistry, Platelet Transfusion, Sepsis, medicine, Humans, Platelet, Intensive care medicine, Societies, Medical, Bacteria, business.industry, Biochemistry (medical), Transfusion medicine, Bacterial Infections, Hematology, Congresses as Topic, medicine.disease, Disinfection, Bacterial sepsis, Platelet transfusion, Blood Preservation, Immunology, Disease risk, Human medicine, business
Abstract: The greatest transfusion-transmitted disease risk facing a transfusion recipient is that of bacterial sepsis. The prevalence of bacterial contamination in platelets and red blood cells is approximately 1 in 3000 units transfused. The available data indicate that transfusion-associated sepsis develops after 1 in 25 000 platelet transfusions and 1 in 250 000 red blood cell transfusions. One of the most widely used strategies for decreasing bacterial sepsis risk is bacterial detection. A roundtable meeting of experts was convened during the XXVIII Annual Congress of the International Society of Blood Transfusion (Edinburgh, UK, July 2004) to provide a forum for experts to share their experiences in the routine bacterial detection of platelet products. This article summarizes the presentations, discussions, and recommendations of the panel. The data presented indicate that some of the current bacterial screening technology is useful for blocking the issuance of platelet units that contain relatively high levels of contaminating bacteria. Platelet units are usually released based on a test-negative status, which often become test-positive only upon longer storage. These data thus suggest that bacterial screening may not prevent all transfusion-transmitted bacterial infections. Two transfusion-transmitted case reports further highlighted the limitation of the routine bacterial screening of platelet products. It was felt that newer technologies, such as pathogen inactivation, may represent a more reliable process, with a higher level of safety. The panel thus recommended that the Transfusion Medicine community may need to change its thinking (paradigm) about bacterial detection, toward the possibility of the pathogen inactivation of blood products, to deal with the bacterial contamination issue. It was suggested, where permitted by regulatory agencies, that blood centers should consider adopting first-generation pathogen inactivation systems as a more effective approach to reducing the risk of transfusion-associated sepsis than some of the approaches currently available. AN EXPERT PANEL roundtable meeting on bacterial detection convened was during the XXVIII Annual Congress of the International Society of Blood Transfusion in Edinburgh, UK, on July 13, 2004, under the chairmanship of Dr MA Blajchman. Appendix A provides a list of participants who attended. This roundtable meeting provided a forum for the panelists to discuss the current transfusion risks due to the bacterial contamination of platelet concentrates, the impact of the implementation of routine bacterial screening, the testing methods available, the necessary actions to be taken when a positive test is obtained, and the benefits and limitations of routine bacterial testing. The panelists presented the protocols they have in place in their institutions for bacterial detection and their experiences since first application of bacterial detection. Clinical cases were presented to highlight the problems associated with transfusion-associated sepsis. The panel recognized that the bacterial contamination of blood products is the most common microbiologic risk of transfusion. The prevalence of contamination of cellular blood products is reported to be approximately 1 in 3000 blood product units. The prevalence of significant clinical events is reported to be approximately 1 in 25 000 for platelet transfusions and 1 in 250 000 for red blood cell (RBC) transfusions.1 Underreporting and underrecognition are acknowledged as being considerable problems. The panel discussed such subjects as screening technology, when to sample, the sample volume, the clinical significance of anaerobic organisms, whether RBCs should be screened, the clinical significance of low levels of bacterial contamination, and which universally effective measures might be taken to reduce this readily preventable transfusion risk. The ultimate purpose of this roundtable meeting was to provide guidance on issues related to the bacterial detection in blood products. This report summarizes the presentations, discussions, and recommendations of the panel.
Published: 2005

35. To examine the effectiveness of a hospital-based nurse-led secondary prevention clinic

Author: Paula M. Mainie, A.A.Jennifer Adgey, Gillian Moore, and John W. Riddell
Subjects: Male, medicine.medical_specialty, Outpatient Clinics, Hospital, Cardiovascular risk factors, Adrenergic beta-Antagonists, Angiotensin-Converting Enzyme Inhibitors, Coronary Disease, Pilot Projects, Nursing Staff, Hospital, 030226 pharmacology & pharmacy, Body Mass Index, 03 medical and health sciences, Nurse led, 0302 clinical medicine, Risk Factors, medicine, Humans, Myocardial infarction, Aged, Specialties, Nursing, Advanced and Specialized Nursing, Secondary prevention, business.industry, Incidence (epidemiology), Hospital based, Middle Aged, medicine.disease, Medical–Surgical Nursing, Cholesterol, Nurse-led clinic, 030220 oncology & carcinogenesis, Emergency medicine, Hypertension, Female, Medical emergency, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Cardiology and Cardiovascular Medicine, business, Program Evaluation
Abstract: Modification of cardiovascular risk factors can reduce the incidence of myocardial infarction (MI), effectively extend survival, decrease the need for interventional procedures, and improve quality of life in persons with known cardiovascular disease. Pharmacological treatments and important lifestyle changes reduce people's risks substantially (by 1/3 to 2/3) and can slow and perhaps reverse progression of established coronary disease. When used appropriately, these interventions are more cost-effective than many other treatments, currently provided by the National Health Service [Department of Health National Service Frameworks: coronary heart disease. Preventing coronary heart disease in high risk patients. 2000. HMSO.] Secondary prevention clinics are effective means by which to ensure targets are achieved and assist primary care in long-term maintenance of lifestyle change and drug optimisation. A 2-year hospital-based pilot project was established at the Royal Hospitals, April 2001–April 2003. The aim of the project was to target patients with coronary heart disease, post-MI and/or coronary artery bypass grafting and/or percutaneous coronary intervention, 6 months following their cardiac event. The plan was to assess patient risk factors and medication a minimum of 6 months following their cardiac event to ascertain if government targets were being achieved; secondly, to examine the effectiveness of a hospital-based nurse-led secondary prevention clinic on modifying risk factors and optimising drug therapies.
Published: 2004

36. Introduction to Journalism

Author: Carole Fleming, Emma Hemmingway, Gillian Moore, Dave Welford, Carole Fleming, Emma Hemmingway, Gillian Moore, and Dave Welford
Subjects: Journalism, Reporters and reporting--Great Britain, Journalism--Great Britain, Journalism--Practice
Abstract: ′The book does what it says on the label. It is punctuated throughout with useful and relevant quotes from working journalists - their opinions, tips and warnings - a technique that drives home the message and adds life and colour′ -THES Textbook Guide The job of a journalist has changed dramatically over the past few decades with satellite links, 24 hour rolling news, and the Internet creating constant pressure for the latest updates. But for all that, the fundamentals of doing the job remain the same: it′s about identifying a story, getting the interviews, and delivering a balanced and interesting report. ′Introduction to Journalism′ examines the skills needed to work as a journalist in newspapers, television, radio and online:'Provides case studies as a guide to researching stories, interviewing, and writing for each medium, as well as recording material for both radio and television.'Offers a wide range of comment and tips on the best way to approach stories'Includes interviews with journalists working on a variety of news outlets from the BBC to weekly newspapers. This book provides a lively and authoritative introduction to journalism and readers will enjoy the insight from a range of journalists.
Published: 2006

37. Obsessions

Author: Gaye Warde, Gillian Moore-Groarke, Sylvia Thompson, and Yvonne Ward
Subjects: General Medicine
Published: 1996
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38. Petrol and polar bears

Author: Gillian Moore
Subjects: Jupiter, Multidisciplinary, Ecology (disciplines), media_common.quotation_subject, Art, media_common, Astrobiology
Abstract: Man, Nature and Ecology. By Keith Reid, J. A. Lauwerys, Joyce Joffe and Anthony Tucker. Pp. 418. (Aldus, Jupiter: London, March 1974.) £3.95.
Published: 1974
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39. Highly strung

Author: GILLIAN MOORE
Subjects: Multidisciplinary
Published: 1974
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40. Game of Chance

Author: Gillian Moore
Subjects: Game of chance, Non-cooperative game, Multidisciplinary, Strategy, Sequential game, Computer science, Repeated game, Mathematical economics
Published: 1973
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41. DEVONSHIRE FOLK-RHYME

Author: Gillian Moore
Subjects: Literature, Linguistics and Language, Literature and Literary Theory, business.industry, Rhyme, media_common.quotation_subject, Art, Library and Information Sciences, business, Language and Linguistics, media_common
Published: 1962
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42. Pharmacologic Approach to Management of Clostridium difficile Infection.

Author: Martin LT, Vincent S, Gillian S, Moore K, Ratermann D, and Droege CA
Subjects: Clostridioides difficile pathogenicity, Cross Infection prevention & control, Hospitals, Humans, Probiotics, Proton Pump Inhibitors, Anti-Bacterial Agents therapeutic use, Clostridioides difficile isolation & purification, Clostridium Infections diagnosis, Clostridium Infections drug therapy
Abstract: Clostridium difficile is a gram-positive, anaerobic, spore-forming bacterium that is the leading cause of nosocomial infections in hospitals in the United States. Critically ill patients are at high risk for C. difficile infection (CDI) and face potentially detrimental effects, including prolonged hospitalization, risk of recurrent disease, complicated surgery, and death. CDI requires a multidisciplinary approach to decrease hospital transmission and improve treatment outcomes. This article briefly reviews the current literature and guideline recommendations for treatment and prevention of CDI, with a focus on antibiotic treatment considerations including dosing, routes of administration, efficacy data, adverse effects, and monitoring parameters.
Published: 2019
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