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1,870 results on '"Bailey, Peter"'

4. Axon guidance cue SEMA3A promotes the aggressive phenotype of basal-like PDAC.

Author

Lupo, Francesca, Pezzini, Francesco, Pasini, Davide, Fiorini, Elena, Adamo, Annalisa, Veghini, Lisa, Bevere, Michele, Frusteri, Cristina, Delfino, Pietro, Dagosto, Sabrina, Andreani, Silvia, Piro, Geny, Malinova, Antonia, Wang, Tian, De Sanctis, Francesco, Lawlor, Rita, Hwang, Changil, Carbone, Carmine, Amelio, Ivano, Bailey, Peter, Bronte, Vincenzo, Tuveson, David, Scarpa, Aldo, Ugel, Stefano, and Corbo, Vincenzo

Subjects
PANCREATIC CANCER, Animals, Humans, Mice, Axon Guidance, Carcinoma, Pancreatic Ductal, Cell Line, Tumor, Cell Movement, Neuropilin-1, Pancreatic Neoplasms, Phenotype, Semaphorin-3A, Signal Transduction
Abstract

OBJECTIVE: The dysregulation of the axon guidance pathway is common in pancreatic ductal adenocarcinoma (PDAC), yet our understanding of its biological relevance is limited. Here, we investigated the functional role of the axon guidance cue SEMA3A in supporting PDAC progression. DESIGN: We integrated bulk and single-cell transcriptomic datasets of human PDAC with in situ hybridisation analyses of patients tissues to evaluate SEMA3A expression in molecular subtypes of PDAC. Gain and loss of function experiments in PDAC cell lines and organoids were performed to dissect how SEMA3A contributes to define a biologically aggressive phenotype. RESULTS: In PDAC tissues, SEMA3A is expressed by stromal elements and selectively enriched in basal-like/squamous epithelial cells. Accordingly, expression of SEMA3A in PDAC cells is induced by both cell-intrinsic and cell-extrinsic determinants of the basal-like phenotype. In vitro, SEMA3A promotes cell migration as well as anoikis resistance. At the molecular level, these phenotypes are associated with increased focal adhesion kinase signalling through canonical SEMA3A-NRP1 axis. SEMA3A provides mouse PDAC cells with greater metastatic competence and favours intratumoural infiltration of tumour-associated macrophages and reduced density of T cells. Mechanistically, SEMA3A functions as chemoattractant for macrophages and skews their polarisation towards an M2-like phenotype. In SEMA3Ahigh tumours, depletion of macrophages results in greater intratumour infiltration by CD8+T cells and better control of the disease from antitumour treatment. CONCLUSIONS: Here, we show that SEMA3A is a stress-sensitive locus that promotes the malignant phenotype of basal-like PDAC through both cell-intrinsic and cell-extrinsic mechanisms.

Published
2024

9. The pluripotency factor NANOG contributes to mesenchymal plasticity and is predictive for outcome in esophageal adenocarcinoma

Author

van der Zalm, Amber P., Dings, Mark P. G., Manoukian, Paul, Boersma, Hannah, Janssen, Reimer, Bailey, Peter, Koster, Jan, Zwijnenburg, Danny, Volckmann, Richard, Bootsma, Sanne, Waasdorp, Cynthia, van Mourik, Monique, Blangé, Dionne, van den Ende, Tom, Oyarce, César I., Derks, Sarah, Creemers, Aafke, Ebbing, Eva A., Hooijer, Gerrit K., Meijer, Sybren L., van Berge Henegouwen, Mark I., Medema, Jan Paul, van Laarhoven, Hanneke W. M., and Bijlsma, Maarten F.

Published
2024
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16. Imagining Future Digital Assistants at Work: A Study of Task Management Needs

Author

Khaokaew, Yonchanok, Holcombe-James, Indigo, Rahaman, Mohammad Saiedur, Liono, Jonathan, Trippas, Johanne R., Spina, Damiano, Belkin, Nicholas, Bailey, Peter, Bennett, Paul N., Ren, Yongli, Sanderson, Mark, Scholer, Falk, White, Ryen W., and Salim, Flora D.

Subjects
Computer Science - Human-Computer Interaction
Abstract

Digital Assistants (DAs) can support workers in the workplace and beyond. However, target user needs are not fully understood, and the functions that workers would ideally want a DA to support require further study. A richer understanding of worker needs could help inform the design of future DAs. We investigate user needs of future workplace DAs using data from a user study of 40 workers over a four-week period. Our qualitative analysis confirms existing research and generates new insight on the role of DAs in managing people's time, tasks, and information. Placing these insights in relation to quantitative analysis of self-reported task data, we highlight how different occupation roles require DAs to take varied approaches to these domains and the effect of task characteristics on the imagined features. Our findings have implications for the design of future DAs in work settings, and we offer some recommendations for reduction to practice., Comment: 59 pages

Published
2022

20. Metavert synergises with standard cytotoxics in human PDAC organoids and is associated with transcriptomic signatures of therapeutic response

Author

An, Jingyu, Kurilov, Roma, Peccerella, Teresa, Bergmann, Frank, Edderkaoui, Mouad, Lim, Adrian, Zhou, Xu, Pfütze, Katrin, Schulz, Angela, Wolf, Stephan, Hu, Kai, Springfeld, Christoph, Mughal, Sadaf S., Zezlina, Lenart, Fortunato, Franco, Beyer, Georg, Mayerle, Julia, Roth, Susanne, Hulkkonen, Johannes, Merz, Daniela, Ei, Shigenori, Mehrabi, Arianeb, Loos, Martin, Al-Saeedi, Mohammed, Michalski, Christoph W., Büchler, Markus W., Hackert, Thilo, Brors, Benedikt, Pandol, Stephen J., Bailey, Peter, and Neoptolemos, John P.

Published
2024
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21. Persister cell phenotypes contribute to poor patient outcomes after neoadjuvant chemotherapy in PDAC

Author

Zhou, Xu, An, Jingyu, Kurilov, Roma, Brors, Benedikt, Hu, Kai, Peccerella, Teresa, Roessler, Stephanie, Pfütze, Katrin, Schulz, Angela, Wolf, Stephan, Hohmann, Nicolas, Theile, Dirk, Sauter, Max, Burhenne, Jürgen, Ei, Shigenori, Heger, Ulrike, Strobel, Oliver, Barry, Simon T., Springfeld, Christoph, Tjaden, Christine, Bergmann, Frank, Büchler, Markus, Hackert, Thilo, Fortunato, Franco, Neoptolemos, John P., and Bailey, Peter

Published
2023
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23. Tenecteplase versus alteplase for thrombolysis in patients selected by use of perfusion imaging within 4·5 h of onset of ischaemic stroke (TASTE): a multicentre, randomised, controlled, phase 3 non-inferiority trial

Author

Phan, Timmy, Selmes, Christine, Lees, Kennedy, Kaste, Markku, MacIsaac, Rachael, Wellings, Tom, Loiselle, Andre, Pepper, Elizabeth, Miteff, Ferdi, Krishnamurthy, Venkatesh, Ang, Timothy, Alanati, Khaled, Gangadharan, Shyam, Zareie, Hossein, Starling, Rita, Dunkerton, Sophie, He, Jiacheng, Datta, Raka, Royan, Angela, Kerr, Erin, Kaauwai, Lara, Belevski, Linda, Ormond, Sally, Johnson, Annalese, Evans, Malcolm, Lachapelle, Nicole, Ombelet, Fouke, Bladin, Chris, Dewey, Helen, Wong, Joseph, Park, Peter, Cody, Ross, Tan, Peter, Callaly, Edward, Senanayake, Channa, Thomas, Grace, Liu, Jennifer, Busch, Tessa, Stuart, Narelle, Chung, Malcohm, Yassi, Nawaf, Valente, Michael, Sharobeam, Angelos, Cooley, Regan, Zhao, Henry, Alemseged, Fana, Williams, Cameron, Ng, Jo Lyn, Balabanski, Anna, dos Santos, Angela, Williamson, John, Pavlin-Premrl, Davor, Beharry, James, Ma, Margaret, Park, Ashley, Yan, Bernard, Hand, Peter, Jackson, David, McDonald, Amy, Fisicchia, Laura, Parsons, Nicola, Olenko, Liudmyla, Johns, Hannah, Guha, Prodipta, Rokaha, Birendra, Dhimal, Niruta, Harvey, Jackson, Cagi, Lavenia, Chia, Nicholas, Goh, Rudy, Palanikumar, Log, El-Masri, Shaddy, Mahadevan, Joshua, Kuranawai, Craig, Waters, Michael, Vallat, Wilson, Cheong, Eddie, Drew, Roy, Cordato, Dennis, McDougall, Alan, Cappelen-Smith, Cecilia, Venkat, Abhay, Edwards, Leon, Blair, Christopher, Thomas, James, Helou, Jacob, Green, Daniel, Nguyen, Tram, Pham, Timmy, Khan, Jasmeen, Miller, Megan, Loubiere, Laurence, Buck, Brian, Butcher, Ken, Fairall, Paige, Butt, Asif, Kalashyan, Hayrapet, Nomani, Ali, Lloret, Mar, Mishra, Sachin, Thirunavukkarasu, Sibi, Sivakumar, Leka, D'Souza, Atlantic, Tsai, Chon-Haw, Tseng, Billy, Tai, Iris, Chiang, I-Husan, Kuan, Angela, Tsai, Vivian, Hsu, Alice, Hsu, Sammi, Alchin, Deborah, Sanjuan, Estela, Fink, John, Wilson, Duncan, Mason, Deborah, Berry-Norohna, Alexander, Winders, Joel, Eagle, Jane, Green, Rosemary, Bremner, Kathleen, Celestino, Sherisse, Lee, Jiunn-Tay, Chou, Chung-Hsing, Tsai, Chia-Kuang, Sung, Yueh-Feng, Tsai, Chia-Lin, Lin, Yu-Kai, Kao, Hung-Wen, Vuong, Jason, Thirugnanachandran, Tharani, Hervet, Marie Veronic, Simmons, Karen, Sabet, Arman, Bailey, Peter, Urbi, Berzenn, Kurakose, Sumole, Martinez-Majander, Nicolas, Räty, Silja, Tiainen, Marjaana, Sibolt, Gerli, Ivanoff, Terhi, Sanz, Ana Calleja, García, Elisa Cortijo, De Lera Alfonso, Mercedes C., Araque, Maria Ester Ramos, Gómez, Alicia Sierra, Peñacoba, Gonzalo Valle, Vicente, Beatriz Gómez, Muñoz, Javier Reyes, Muñoz Rubio, Pedro Luis, Shah, Darshan, Harrison, Emma, Bendall, Carol, Subramanian, Ganesh, Jeng, Jiann-Shing, Tang, Sung-Chun, Tsai, Li-Kai, Yeh, Shin-Joe, Chen, Chih-Hao, Chung, Tai-Chun, Wong, Andrew, Muller, Claire, Skinner, Genevieve, Gunathilagan, Gunaratnam, Natarajan, Indira, Coutts, Shelagh, Menon, Bijoy, Kenney, Carol, Clarke, Brian, Ghatala, Rita, Mudd, Paul, Chen, Chih-Hung, Lemmens, Robin, Demeestere, Jelle, Mahant, Neil, Sun, Mu-Chien, Parsons, Mark W, Yogendrakumar, Vignan, Churilov, Leonid, Garcia-Esperon, Carlos, Campbell, Bruce C V, Russell, Michelle L, Sharma, Gagan, Chen, Chushuang, Lin, Longting, Chew, Beng Lim, Ng, Felix C, Deepak, Akshay, Choi, Philip M C, Kleinig, Timothy J, Cordato, Dennis J, Wu, Teddy Y, Fink, John N, Ma, Henry, Phan, Thanh G, Markus, Hugh S, Molina, Carlos A, Strbian, Daniel, Meretoja, Atte, Arenillas, Juan F, Buck, Brian H, Devlin, Michael J, Brown, Helen, Butcher, Ken S, O'Brien, Billy, Wijeratne, Tissa, Bivard, Andrew, Grimley, Rohan S, Agarwal, Smriti, Munshi, Sunil K, Donnan, Geoffrey A, Davis, Stephen M, Miteff, Ferdinand, Spratt, Neil J, and Levi, Christopher R

Published
2024
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24. Tenecteplase versus standard of care for minor ischaemic stroke with proven occlusion (TEMPO-2): a randomised, open label, phase 3 superiority trial

Author

Salluzzi, Marina, Blenkin, Nicole, Dueck, Ashley, Doram, Craig, Zhang, Qiao, Kenney, Carol, Ryckborst, Karla, Bohn, Shelly, Collier, Quentin, Taylor, Frances, Lethebe, B. Cord, Jambula, Anitha, Sage, Kayla, Toussaint, Lana, Save, Supryia, Lee, Jaclyn, Laham, N, Sultan, A.A., Deepak, A., Sitaram, A., Demchuk, Andrew M., Lockey, A., Micielli, A., Wadhwa, A., Arabambi, B., Graham, B., Bogiatzi, Chrysi, Doshi, Darshan, Chakraborty, D., Kim, Diana, Vasquez, D, Singh, D, Tse, Dominic, Harrison, E., Smith, E.E., Teleg, E., Klourfeld, E., Klein, G., Sebastian, I.A., Evans, J, Hegedus, J, Kromm, J, Lin, K, Ignacio, K, Ghavami, Kimia, Ismail, M., Moores, M., Panzini, M.A., Boyko, M., Almekhlafi, M.A., Newcommon, Nancy, Maraj, N., Imoukhuede, O., Volny, O., Stys, Peter, Couillard, Phillipe, Ojha, P., Eswaradass, P., Joundi, Raed, Singh, R., Asuncion, R.M., Muir, R.T., Dey, S., Mansoor, S., Wasyliw, S., Nagendra, S., Hu, Sherry, Althubait, S., Chen, S., Bal, S., Van Gaal, Stephen, Peters, Steven, Ray, Sucharita, Chaturvedi, S., Subramaniam, Suresh, Fu, Vivian, Villaluna, K., Maclean, G., King-Azote, P., Ma, C., Plecash, A., Murphy, C., Gorman, J., Wilson, L., Zhou, L., Benevente, O., Teal, P., Yip, S., Mann, S., Dewar, B., Demetroff, M., Shamloul, R., Beardshaw, R., Roberts, S., Blaquiere, D., Stotts, G., Shamy, M., Bereznyakova, O., Fahed, R., Alesefir, W., Lavoie, Suzy, Hache, A., Collard, K, Mackey, A., Gosselin-Lefebvre, S., Verreault, S., Beauchamp, B., Lambourn, L., Khaw, A., Mai, L., Sposato, L., Bres Bullrich, M., Azarpazhooh, R., Fridman, S., Kapoor, A., Southwell, A., Bardi, E., Fatakdawala, I., Kamra, M, Lopes, K., Popel, N., Norouzi, V., Liu, A., Liddy, A.M., Ghoari, B., Hawkes, C., Enriquez, C.A., Gladstone, D.J., Manosalva Alzate, H.A., Khosravani, H., Hopyan, J.J., Sivakumar, K., Son, M., Boulos, M.I., Hamind, M.A., Swartz, R.H., Murphy, R., Reiter, S., Fitzpatrick, T., Bhandari, V., Good, J., Penn, M., Naylor, M., Frost, S., Cayley, A., Akthar, F., Williams, J., Kalman, L., Crellin, L., Wiegner, R., Singh, R.S., Stewart, T., To, W., Singh, S., Pikula, A., Jaigobin, C., Carpani, F., Silver, F., Janssen, H., Schaafsma, J., del Campo, M., Alskaini, M., Rajendram, P., Fairall, P., Granfield, B., Crawford, D., Jabs, J., White, L., Sivakumar, L., Piquette, L., Nguyen, T., Nomani, A., Wagner, A., Alrohimi, A., Butt, A., D'Souza, A., Gajurel, B., Vekhande, C., Kamble, H., Kalashyan, H., Lloret, M., Benguzzi, M., Arsalan, N., Ishaque, N., Ashayeriahmadabad, R., Samiento, R., Hosseini, S., Kazi, S., Das, S., Sugumar, T., Selchen, D., Kostyrko, P., Muccilli, A., Saposnik, A.G., Vandervelde, C., Ratnayake, K., McMillan, S., Katsanos, A., Shoamanesh, A., Sahlas, D.J., Naidoo, V., Todorov, V., Toma, H., Brar, J., Lee, J., Horton, M., Shand, E., Weatherby, S., Jin, A., Durafourt, B., Jalini, S., Gardner, A., Tyson, C., Junk, E., Foster, K., Bolt, K., Sylvain, N., Maley, S., Urroz, L., Peeling, L., Kelly, M., Whelan, R., Cooley, R., Teitelbaum, J., Boutayeb, A., Moore, A., Cole, E., Waxman, L., Ben-Amor, N., Sanchez, R., Khalil, S., Nehme, A., Legault, C., Tampieri, D., Ehrensperger, E., Vieira, L., Cortes, M., Angle, M., Hannouche, M., Badawy, M., Werner, K., Wieszmuellner, S., Langer, A., Gisold, A., Zach, H., Rommer, P., Macher, S., Blechinger, S., Marik, W., Series, W., Baumgartinger, M., Krebs, S., Koski, J., Eirola, S., Ivanoff, T., Erakanto, A., Kupari, L., Sibolt, G., Panula, J., Tomppo, L., Tiainen, M., Ahlstrom, M., Martinez Majander, N., Suomalainen, O., Raty, S., Levi, C., Kerr, E., Allen, J., Kaauwai, L.P., Belevski, L., Russell, M., Ormond, S., Chew, A., Loiselle, A., Royan, A., Hughes, B., Garcia Esperon, C., Pepper, E., Miteff, F., He, J., Lycett, M., Min, M., Murray, N., Pavey, N., Starling de Barros, R., Gangadharan, S., Dunkerton, S., Waller, S., Canento Sanchez, T., Wellings, T., Edmonds, G., Whittaker, K.A., Ewing, M., Lee, P., Singkang, R., McDonald, A., Dos Santos, A., Shin, C., Jackson, D., Tsoleridis, J., Fisicchia, L., Parsons, N., Shenoy, N., Smith, S., Sharobeam, A., Balabanski, A., Park, A., Williams, C., Pavlin-Premri, D., Rodrigues, E., Alemseged, F., Ng, F., Zhao, H., Beharry, J., Ng, J.L., Williamson, J., Wong, J.Z.W., Li, K., Kwan, M.K., Valente, M., Yassi, N., Yogendrakumar, V., McNamara, B., Buchanan, C., McCarthy, C., Thomas, G., Stephens, K., Chung, M., Chung, M.F., Tang, M., Busch, T., Frost, T., Lee, R., Stuart, N., Pachani, N., Menon, A., Borojevic, B., Linton, C.M., Garcia, G., Callaly, E.P., Dewey, H., Liu, J., Chen, J., Wong, J., Nowak, K., To, K., Lizak, N.S., Bhalala, O., Park, P., Tan, P., Martins, R., Cody, R., Forbes, R., Chen, S.K., Ooi, S., Tu, S., Dang, Y.L., Ling, Z., Cranefield, J., Drew, R., Tan, A., Kurunawai, C., Harvey, J., Mahadevan, J.J., Cagi, L., Palanikumar, L., Chia, L.N., Goh, R., El-Masri, S., Urbi, B., Rapier, C., Berrill, H., McEvoy, H., Dunning, R., Kuriakose, S., Chad, T., Sapaen, V., Sabet, A., Shah, D., Yeow, D., Lilley, K., Ward, K., Mozhy Mahizhnan, M., Tan, M., Lynch, C., Coveney, S., Tobin, K., McCabe, J., Marnane, M., Murphy, S., Large, M., Moynihan, B., Boyle, K., Sanjuan, E., Sanchis, M., Boned, S., Pancorbo, O., Sala, V., Garcia, L., Garcia-Tornel, A., Juega, J., Pagola, J., Santana, K., Requena, M., Muchada, M., Olive, M., Lozano, P.J., Rubiera, M., Deck, M., Rodriguez, N., Gomez, B., Reyes Munoz, F.J., Gomez, A.S., Sanz, A.C., Garcia, E.C., Penacoba, G., Ramos, M.E., de Lera Alfonso, M., Feliu, A, Pardo, L., Ramirez, P., Murillo, A., Lopez Dominguez, D., Rodriguez, J., Terceno Izaga, M., Reina, M., Viturro, S.B., Bojaryn, U., Vera Monge, V.A., Silva Blas, Y., R Siew, R., Agustin, S J, Seet, C., Tianming, T., d'Emden, A., Murray, A., Welch, A., Hatherley, K., Day, N., Smith, W., MacRae, E., Mitchell, E.S., Mahmood, A., Elliot, J., Neilson, S., Biswas, V., Brown, C., Lewis, A., Ashton, A., Werring, D., Perry, R., Muhammad, R., Lee, Y.C., Black, A., Robinson, A., Williams, A., Banaras, A., Cahoy, C., Raingold, G., Marinescu, M., Atang, N., Bason, N., Francia, N., Obarey, S., Feerick, S., Joseph, J., Schulz, U., Irons, R., Benjamin, J., Quinn, L., Jhoots, M., Teal, R., Ford, G., Harston, G., Bains, H., Gbinigie, I., Mathieson, P., Sim, C.H., Hayter, E., Kennedy, K., Binnie, L., Priestley, N., Williams, R., Ghatala, R., Stratton, S., Blight, A., Zhang, L., Davies, A., Duffy, H., Roberts, J., Homer, J., Roberts, K., Dodd, K., Cawley, K., Martin, M., Leason, S., Cotgreave, S., Taylor, T., Nallasivan, A., Haider, S., Chakraborty, T., Webster, T., Gil, A., Martin, B., Joseph, B., Cabrera, C., Jose, D., Man, J., Aquino, J., Sebastian, S., Osterdahl, M., Kwan, M., Matthew, M., Ike, N., Bello, P., Wilding, P., Fuentes, R., Shah, R., Mashate, S., Patel, T., Nwanguma, U., Dave, V., Haber, A., Lee, A., O'Sullivan, A., Drumm, B., Dawson, A.C., Matar, T., Roberts, D., Taylor, E., Rounis, E., El-Masry, A., O'Hare, C., Kalladka, D., Jamil, S., Auger, S., Raha, O., Evans, M., Vonberg, F., Kalam, S., Ali Sheikh, A., Jenkins, I.H., George, J., Kwan, J., Blagojevic, J., Saeed, M., Haji-Coll, M., Tsuda, M., Sayed, M., Winterkron, N., Thanbirajah, N., Vittay, O., Karim, R., Smail, R.C., Gauhar, S., Elmamoun, S., Malani, S., Pralhad Kelavkar, S., Hiden, J., Ferdinand, P., Sanyal, R., Varquez, R., Smith, B., Okechukwu, C., Fox, E., Collins, E., Courtney, K., Tauro, S., Patterson, C., McShane, D., Roberts, G., McIImoyle, J., McGuire, K., Fearon, P., Gordon, P., Isaacs, K., Lucas, K., Smith, L., Dews, L., Bates, M., Lawrence, S., Heeley, S., Patel, V., Chin, Y.M., Sims, D., Littleton, E., Khaira, J., Nadar, K., Kieliszkowska, A., Sari, B., Domingos Belo, C., Smith, E., Manolo, E.Y., Aeron-Thomas, J., Doheny, M., Garcia Pardo, M., Recaman, M., Tibajia, M.C., Aissa, M., Mah, Y., Yu, T., Meenakshisundaram, S., Heller, S., Alsukhni, R., Williams, O., Farag, M., Benger, M., Engineer, A., Bayhonan, S., Conway, S., Bhalla, A., Nouvakis, D., Theochari, E., Boyle, F., Teo, J., King-Robson, J., Law, K.Y., Sztriha, L., McGovern, A., Day, D., Mitchell-Douglas, J., Francis, J., Iqbal, A., Punjabivaryani, P., Anonuevo Reyes, J., Anonuevo Reyes, M., Pauls, M., Buch, A., Hedstrom, A., Hutchinson, C., Kirkland, C., Newham, J., Wilkes, G., Fleming, L., Fleck, N., Franca, A., Chwal, B., Oldoni, C., Mantovani, G., Noll, G., Zanella, L., Soma, M., Secchi, T., Borelli, W., Rimoli, B.P., da Cunha Silva, G.H., Machado Galvao Mondin, L.A., Barbosa Cerantola, R., Imthon, A.K., Esaki, A.S., Camilo, M., Vincenzi, O.C., ds Cruz, R.R., Morillos, M.B., Riccioppa Rodrigues, G.G., Santos Ferreira, K., Pazini, A.M., Pena Pereira, M.A., de Albuquerque, A.L.A., Massote Fontanini, C.E., Matinez Rubio, C.F., dos Santos, D.T., Dias, F.A., Alves, F.F.A., Milani, C., Pegorer Santos, B., Winckler, F., De Souza, J.T., Bonome, L.A.M., Cury Silva, V.A., Teodoro, R.S., Modolo, G.P., Ferreira, N.C., Barbosa dos Santos, D.F., dos Santos Moreira, J.C., Cruz Guedes de Morais, A.B., Vieira, J., Mendes, G., de Queiroz, J.P., Coutts, Shelagh B, Ankolekar, Sandeep, Appireddy, Ramana, Arenillas, Juan F, Assis, Zarina, Bailey, Peter, Barber, Philip A, Bazan, Rodrigo, Buck, Brian H, Butcher, Ken S, Camden, Marie-Christine, Campbell, Bruce C V, Casaubon, Leanne K, Catanese, Luciana, Chatterjee, Kausik, Choi, Philip M C, Clarke, Brian, Dowlatshahi, Dar, Ferrari, Julia, Field, Thalia S, Ganesh, Aravind, Ghia, Darshan, Goyal, Mayank, Greisenegger, Stefan, Halse, Omid, Horn, Mackenzie, Hunter, Gary, Imoukhuede, Oje, Kelly, Peter J, Kennedy, James, Kleinig, Timothy J, Krishnan, Kailash, Lima, Fabricio, Mandzia, Jennifer L, Marko, Martha, Martins, Sheila O, Medvedev, George, Menon, Bijoy K, Mishra, Sachin M, Molina, Carlos, Moussaddy, Aimen, Muir, Keith W, Parsons, Mark W, Penn, Andrew M W, Pille, Arthur, Pontes-Neto, Octávio M, Roffe, Christine, Serena, Joaquin, Simister, Robert, Singh, Nishita, Spratt, Neil, Strbian, Daniel, Tham, Carol H, Wiggam, M Ivan, Williams, David J, Willmot, Mark R, Wu, Teddy, Yu, Amy Y X, Zachariah, George, Zafar, Atif, Zerna, Charlotte, and Hill, Michael D

Published
2024
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25. Expression of the membrane tetraspanin claudin 18 on cancer cells promotes T lymphocyte infiltration and antitumor immunity in pancreatic cancer

Author

De Sanctis, Francesco, Dusi, Silvia, Caligola, Simone, Anselmi, Cristina, Petrova, Varvara, Rossi, Barbara, Angelini, Gabriele, Erdeljan, Michael, Wöll, Stefan, Schlitter, Anna Melissa, Metzler, Thomas, Steiger, Katja, Borok, Zea, Bailey, Peter, Bauer, Aline, Halin, Cornelia, Boschi, Federico, Giugno, Rosalba, Canè, Stefania, Lawlor, Rita, Corbo, Vincenzo, Scarpa, Aldo, Constantin, Gabriela, Ugel, Stefano, Vascotto, Fulvia, Sahin, Ugur, Türeci, Özlem, and Bronte, Vincenzo

Published
2024
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26. Driver gene combinations dictate cutaneous squamous cell carcinoma disease continuum progression

Author

Bailey, Peter, Ridgway, Rachel A., Cammareri, Patrizia, Treanor-Taylor, Mairi, Bailey, Ulla-Maja, Schoenherr, Christina, Bone, Max, Schreyer, Daniel, Purdie, Karin, Thomson, Jason, Rickaby, William, Jackstadt, Rene, Campbell, Andrew D., Dimonitsas, Emmanouil, Stratigos, Alexander J., Arron, Sarah T., Wang, Jun, Blyth, Karen, Proby, Charlotte M., Harwood, Catherine A., Sansom, Owen J., Leigh, Irene M., and Inman, Gareth J.

Published
2023
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28. Diversifying Reply Suggestions using a Matching-Conditional Variational Autoencoder

Author

Deb, Budhaditya, Bailey, Peter, and Shokouhi, Milad

Subjects
Computer Science - Computation and Language, Computer Science - Artificial Intelligence, Computer Science - Machine Learning, Statistics - Machine Learning
Abstract

We consider the problem of diversifying automated reply suggestions for a commercial instant-messaging (IM) system (Skype). Our conversation model is a standard matching based information retrieval architecture, which consists of two parallel encoders to project messages and replies into a common feature representation. During inference, we select replies from a fixed response set using nearest neighbors in the feature space. To diversify responses, we formulate the model as a generative latent variable model with Conditional Variational Auto-Encoder (M-CVAE). We propose a constrained-sampling approach to make the variational inference in M-CVAE efficient for our production system. In offline experiments, M-CVAE consistently increased diversity by ~30-40% without significant impact on relevance. This translated to a 5% gain in click-rate in our online production system.

Published
2019

29. Genomic basis for RNA alterations in cancer.

Author

PCAWG Transcriptome Core Group, Calabrese, Claudia, Davidson, Natalie R, Demircioğlu, Deniz, Fonseca, Nuno A, He, Yao, Kahles, André, Lehmann, Kjong-Van, Liu, Fenglin, Shiraishi, Yuichi, Soulette, Cameron M, Urban, Lara, Greger, Liliana, Li, Siliang, Liu, Dongbing, Perry, Marc D, Xiang, Qian, Zhang, Fan, Zhang, Junjun, Bailey, Peter, Erkek, Serap, Hoadley, Katherine A, Hou, Yong, Huska, Matthew R, Kilpinen, Helena, Korbel, Jan O, Marin, Maximillian G, Markowski, Julia, Nandi, Tannistha, Pan-Hammarström, Qiang, Pedamallu, Chandra Sekhar, Siebert, Reiner, Stark, Stefan G, Su, Hong, Tan, Patrick, Waszak, Sebastian M, Yung, Christina, Zhu, Shida, Awadalla, Philip, Creighton, Chad J, Meyerson, Matthew, Ouellette, BF Francis, Wu, Kui, Yang, Huanming, PCAWG Transcriptome Working Group, Brazma, Alvis, Brooks, Angela N, Göke, Jonathan, Rätsch, Gunnar, Schwarz, Roland F, Stegle, Oliver, Zhang, Zemin, and PCAWG Consortium

Subjects
PCAWG Transcriptome Core Group, PCAWG Transcriptome Working Group, PCAWG Consortium, Humans, Neoplasms, DNA, Neoplasm, RNA, Genomics, Gene Expression Regulation, Neoplastic, Genome, Human, DNA Copy Number Variations, Transcriptome, DNA, Neoplasm, Gene Expression Regulation, Neoplastic, Genome, Human, General Science & Technology
Abstract

Transcript alterations often result from somatic changes in cancer genomes1. Various forms of RNA alterations have been described in cancer, including overexpression2, altered splicing3 and gene fusions4; however, it is difficult to attribute these to underlying genomic changes owing to heterogeneity among patients and tumour types, and the relatively small cohorts of patients for whom samples have been analysed by both transcriptome and whole-genome sequencing. Here we present, to our knowledge, the most comprehensive catalogue of cancer-associated gene alterations to date, obtained by characterizing tumour transcriptomes from 1,188 donors of the Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium of the International Cancer Genome Consortium (ICGC) and The Cancer Genome Atlas (TCGA)5. Using matched whole-genome sequencing data, we associated several categories of RNA alterations with germline and somatic DNA alterations, and identified probable genetic mechanisms. Somatic copy-number alterations were the major drivers of variations in total gene and allele-specific expression. We identified 649 associations of somatic single-nucleotide variants with gene expression in cis, of which 68.4% involved associations with flanking non-coding regions of the gene. We found 1,900 splicing alterations associated with somatic mutations, including the formation of exons within introns in proximity to Alu elements. In addition, 82% of gene fusions were associated with structural variants, including 75 of a new class, termed 'bridged' fusions, in which a third genomic location bridges two genes. We observed transcriptomic alteration signatures that differ between cancer types and have associations with variations in DNA mutational signatures. This compendium of RNA alterations in the genomic context provides a rich resource for identifying genes and mechanisms that are functionally implicated in cancer.

Published
2020

31. N-glycosylation Regulates Intrinsic IFN-γ Resistance in Colorectal Cancer: Implications for Immunotherapy

Author

Krug, Julia, Rodrian, Gabriele, Petter, Katja, Yang, Hai, Khoziainova, Svetlana, Guo, Wei, Bénard, Alan, Merkel, Susanne, Gellert, Susan, Maschauer, Simone, Spermann, Monika, Waldner, Maximilian, Bailey, Peter, Pilarsky, Christian, Liebl, Andrea, Tripal, Philipp, Christoph, Jan, Naschberger, Elisabeth, Croner, Roland, Schellerer, Vera S., Becker, Christoph, Hartmann, Arndt, Tüting, Thomas, Prante, Olaf, Grützmann, Robert, Grivennikov, Sergei I., Stürzl, Michael, and Britzen-Laurent, Nathalie

Published
2023
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32. Loss of FGFR4 promotes the malignant phenotype of PDAC

Author

D’Agosto, Sabrina, Pezzini, Francesco, Veghini, Lisa, Delfino, Pietro, Fiorini, Claudia, Temgue Tane, Gael D., Del Curatolo, Anais, Vicentini, Caterina, Ferrari, Giorgia, Pasini, Davide, Andreani, Silvia, Lupo, Francesca, Fiorini, Elena, Lorenzon, Giulia, Lawlor, Rita T., Rusev, Borislav, Malinova, Antonia, Luchini, Claudio, Milella, Michele, Sereni, Elisabetta, Pea, Antonio, Bassi, Claudio, Bailey, Peter, Scarpa, Aldo, Bria, Emilio, and Corbo, Vincenzo

Published
2022
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34. The role of ABHD11 in the regulation of the hypoxia inducible transcription factors

Author

Bailey, Peter Stephen John and Nathan, James

Subjects
616.07, hypoxia, oxygen sensing, HIF, HIF1a, TCA cycle, 2-oxoglutarate, 2-OG, OGDH complex, L-2-hydroxyglutarate, lipoate, lipoylation, ABHD11, lipid peroxidation
Abstract

Hypoxia inducible transcription factors (HIFs) mediate a highly conserved cellular oxygen sensing system, driving a diverse set of transcriptional changes that allow adaptation to hypoxic conditions. However, HIFs can also be activated independently of oxygen by changes in levels of mitochondrial metabolites, a mechanism which is important in the development of certain HIF-driven cancers. Critical to understanding this metabolic axis is the recognition that the prolyl hydroxylase enzymes (PHDs), the oxygen sensors within the HIF pathway, are members of a diverse group of enzymes termed 2-oxoglutarate-dependent dioxygenases. These enzymes all require oxygen, iron and the Tricarboxylic Acid (TCA) cycle metabolite, 2-oxoglutarate (2-OG/a-ketoglutarate) for catalytic activity. Therefore, understanding how 2-OG levels are regulated is essential to dissect the relative contribution of metabolism to activation of HIFs. A key determinant of 2-OG metabolism is the 2-oxoglutarate dehydrogenase complex (OGDHc) – a rate limiting step for conversion of 2-OG to succinyl-CoA within the TCA cycle. Genetic disruption of the OGDHc leads to HIF stabilisation through the accumulation of 2-OG and formation of L-2-hydroxyglutarate, an inhibitor of PHDs. Patients with hereditary mutations in the OGDHc develop tumour syndromes, typical of HIF activation. However, how the OGDHc is regulated is not known. In this thesis, I optimise CRISPR/Cas9 forward genetic screens in oxygen replete conditions to identify genes involved in HIF metabolic activation, focusing on the OGDHc. These screens successfully identify known determinants of 2-OG metabolism, including core components of the OGDHc. In addition, they identified ABHD11 as an uncharacterised mitochondrial protein that, on depletion, leads to metabolic stabilisation of HIF-1⍺. Using a combination of cell biology, LC-MS metabolomics and in vitro enzymatic assays, I demonstrate that ABHD11 localises to the mitochondrial matrix and is required for normal TCA cycle function. ABHD11 depletion decreases the activity of the OGDHc, leading to 2-OG accumulation and L-2-hydroxyglutarate formation, consistent with a central role for OGDHc function in HIF metabolic activation. ABHD11 associates with the OGDHc, but ABHD11 depletion does not alter protein levels of the subunits. Instead, ABHD11 is required to maintain an essential post-translational fatty acid modification on the OGDHc E2 subunit (DLST), lipoylation, which is sensitive to damage from reactive oxygen species and lipid peroxidation products. Together, these studies identify ABHD11 as a new component maintaining TCA cycle function through regulating the lipoylation of the OGDHc.

Published
2019
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35. Targeting DNA Damage Response and Replication Stress in Pancreatic Cancer

Author

Allison, Sarah, Bailey, Peter J., Bailey, Ulla-Maja, Biankin, Andrew V., Beraldi, Dario, Brunton, Holly, Caligiuri, Giuseppina, Cameron, Euan, Chang, David K., Cooke, Susanna L., Cunningham, Richard, Dreyer, Stephan, Grimwood, Paul, Kelly, Shane, Lampraki, Eirini-Maria, Marshall, John, Martin, Sancha, McDade, Brian, McElroy, Daniel, Musgrove, Elizabeth A., Nourse, Craig, Paulus-Hock, Viola, Ramsay, Donna, Upstill-Goddard, Rosie, Wright, Derek, Jones, Marc D., Evers, Lisa, Rebus, Selma, Rahib, Lola, Serrels, Bryan, Hair, Jane, Jamieson, Nigel B., McKay, Colin J., Westwood, Paul, Williams, Nicola, Duthie, Fraser, Johns, Amber L., Mawson, Amanda, Scarlett, Christopher J., Brancato, Mary-Anne L., Rowe, Sarah J., Simpson, Skye H., Martyn-Smith, Mona, Thomas, Michelle T., Chantrill, Lorraine A., Chin, Venessa T., Chou, Angela, Cowley, Mark J., Humphris, Jeremy L., Mead, R. Scott, Nagrial, Adnan M., Pajic, Marina, Pettit, Jessica, Pinese, Mark, Rooman, Ilse, Wu, Jianmin, Tao, Jiang, DiPietro, Renee, Watson, Clare, Steinmann, Angela, Lee, Hong Ching, Wong, Rachel, Pinho, Andreia V., Giry-Laterriere, Marc, Daly, Roger J., Sutherland, Robert L., Grimmond, Sean M., Waddell, Nicola, Kassahn, Karin S., Miller, David K., Wilson, Peter J., Patch, Ann-Marie, Song, Sarah, Harliwong, Ivon, Idrisoglu, Senel, Nourbakhsh, Ehsan, Manning, Suzanne, Wani, Shivangi, Gongora, Milena, Anderson, Matthew, Holmes, Oliver, Leonard, Conrad, Taylor, Darrin, Wood, Scott, Xu, Christina, Nones, Katia, Fink, J. Lynn, Christ, Angelika, Bruxner, Tim, Cloonan, Nicole, Newell, Felicity, Pearson, John V., Bailey, Peter, Quinn, Michael, Nagaraj, Shivashankar, Kazakoff, Stephen, Waddell, Nick, Krisnan, Keerthana, Quek, Kelly, Wood, David, Samra, Jaswinder S., Gill, Anthony J., Pavlakis, Nick, Guminski, Alex, Toon, Christopher, Asghari, Ray, Merrett, Neil D., Pavey, Darren, Das, Amitabha, Cosman, Peter H., Ismail, Kasim, O’Connnor, Chelsie, Lam, Vincent W., McLeod, Duncan, Pleass, Henry C., Richardson, Arthur, James, Virginia, Kench, James G., Cooper, Caroline L., Joseph, David, Sandroussi, Charbel, Crawford, Michael, Gallagher, James, Texler, Michael, Forest, Cindy, Laycock, Andrew, Epari, Krishna P., Ballal, Mo, Fletcher, David R., Mukhedkar, Sanjay, Spry, Nigel A., DeBoer, Bastiaan, Chai, Ming, Zeps, Nikolajs, Beilin, Maria, Feeney, Kynan, Nguyen, Nan Q., Ruszkiewicz, Andrew R., Worthley, Chris, Tan, Chuan P., Debrencini, Tamara, Chen, John, Brooke-Smith, Mark E., Papangelis, Virginia, Tang, Henry, Barbour, Andrew P., Clouston, Andrew D., Martin, Patrick, O’Rourke, Thomas J., Chiang, Amy, Fawcett, Jonathan W., Slater, Kellee, Yeung, Shinn, Hatzifotis, Michael, Hodgkinson, Peter, Christophi, Christopher, Nikfarjam, Mehrdad, Mountain, Angela, Biobank, Victorian Cancer, Eshleman, James R., Hruban, Ralph H., Maitra, Anirban, Iacobuzio-Donahue, Christine A., Schulick, Richard D., Wolfgang, Christopher L., Morgan, Richard A., Hodgin, Mary, Scarpa, Aldo, Lawlor, Rita T., Beghelli, Stefania, Corbo, Vincenzo, Scardoni, Maria, Bassi, Claudio, Tempero, Margaret A., Graham, Janet S., Dreyer, Stephan B., Paris, Clara, Dray, Eloise, Plenker, Dennis, Galluzzo, Zachary, Tesson, Mathias, Jones, Marc, Moran-Jones, Kim, Wright, Derek W., Oien, Karin, McGregor, Grant A., Gulati, Aditi, Brough, Rachel, Bajrami, Ilirjana, Pettitt, Stephan, Dziubinski, Michele L., Candido, Juliana, Balkwill, Frances, Barry, Simon T., Grützmann, Robert, Johns, Amber, Froeling, Fieke E.M., Beer, Phillip, Petersen, Gloria M., Ashworth, Alan, Frame, Margaret C., Crawford, Howard C., Simeone, Diane M., Lord, Chris, Mukhopadhyay, Debabrata, Pilarsky, Christian, Tuveson, David A., Morton, Jennifer P., and Sansom, Owen J.

Published
2021
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36. Estrogen-related receptor alpha drives mitochondrial biogenesis and resistance to neoadjuvant chemoradiation in esophageal cancer

Author

Dings, Mark P.G., van der Zalm, Amber P., Bootsma, Sanne, van Maanen, Tatum F.J., Waasdorp, Cynthia, van den Ende, Tom, Liu, Dajia, Bailey, Peter, Koster, Jan, Zwijnenburg, Danny A., Spek, C. Arnold, Klomp, Jan P.G., Oubrie, Arthur, Hooijer, Gerrit K.J., Meijer, Sybren L., van Berge Henegouwen, Mark I., Hulshof, Maarten C., Bergman, Jacques, Oyarce, Cesar, Medema, Jan Paul, van Laarhoven, Hanneke W.M., and Bijlsma, Maarten F.

Published
2022
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37. Endovascular thrombectomy versus standard bridging thrombolytic with endovascular thrombectomy within 4·5 h of stroke onset: an open-label, blinded-endpoint, randomised non-inferiority trial

Author

Desmond, Patricia, Yassi, Nawaf, Zhao, Henry, Williams, Cameron, Alemseged, Fana, Ng, Felix C, Yogendrakumar, Vignan, Bailey, Peter, De Villiers, Laetitia, Phan, Thanh, Thirugnanachandran, Tharani, Chong, Winston, Asadi, Hamed, Slater, Lee Anne, Manning, Nathan, Wenderoth, Jason, McDougall, Alan, Cappelen-Smith, Cecilia, Whitley, Justin, Edwards, Leon, Esperon, Carlos Garcia, Spratt, Neil, Pepper, Elizabeth, Levi, Chris, Faulder, Ken, Harrington, Timothy, Krause, Martin, Waters, Michael, Fink, John, Ma, Gaoting, Shen, Xiangpeng, Song, Xiangkong, Gao, Yonglei, Guangxian, Nam, Guo, Zaiyu, Zhang, Heliang, Han, Hongxing, Wang, Hao, Liao, Geng, Zhang, Zhenyu, Li, Chaomao, Yang, Zhi, Cai, Chuwei, Huang, Chuming, Hong, Yifan, Mitchell, Peter J, Yan, Bernard, Churilov, Leonid, Dowling, Richard J, Bush, Steven J, Bivard, Andrew, Huo, Xiao Chuan, Wang, Guoqing, Zhang, Shi Yong, Ton, Mai Duy, Cordato, Dennis J, Kleinig, Timothy J, Ma, Henry, Chandra, Ronil V, Brown, Helen, Campbell, Bruce C V, Cheung, Andrew K, Steinfort, Brendan, Scroop, Rebecca, Redmond, Kendal, Miteff, Ferdinand, Liu, Yan, Duc, Dang Phuc, Rice, Hal, Parsons, Mark W, Wu, Teddy Y, Nguyen, Huy-Thang, Donnan, Geoffrey A, Miao, Zhong Rong, and Davis, Stephen M

Published
2022
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39. AmpliconSuite: an end-to-end workflow for analyzing focal amplifications in cancer genomes

Author

Luebeck, Jens, primary, Huang, Edwin, additional, Kim, Forrest, additional, Liefeld, Ted, additional, Dameracharla, Bhargavi, additional, Ahuja, Rohil, additional, Schreyer, Daniel, additional, Prasad, Gino, additional, Adamaszek, Michal, additional, Kenkre, Rishaan, additional, Agashe, Tushar, additional, Torvi, Devika, additional, Tabor, Thorin, additional, Giurgiu, Madalina, additional, Kim, Soyeon, additional, Kim, Hoon, additional, Bailey, Peter, additional, Verhaak, Roel G. W., additional, Deshpande, Viraj B, additional, Reich, Michael M, additional, Mischel, Paul S., additional, Mesirov, Jill, additional, and Bafna, Vineet, additional

Published
2024
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41. PDAC Subtypes/Stratification

Author

Brunton, Holly, Caligiuri, Giuseppina, Inman, Gareth J., Bailey, Peter, Coleman, William B., Series Editor, Tsongalis, Gregory J., Series Editor, Michalski, Christoph W., editor, Rosendahl, Jonas, editor, Michl, Patrick, editor, and Kleeff, Jörg, editor

Published
2020
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42. Safety and efficacy of pioglitazone for the delay of cognitive impairment in people at risk of Alzheimer's disease (TOMMORROW): a prognostic biomarker study and a phase 3, randomised, double-blind, placebo-controlled trial

Author

Aarsland, Dag, Ackermann, Oda, Agron-Figueroa, Joscelyn, Arnold, Thomas, Bailey, Peter, Ballard, Clive, Barton, Scott, Belden, Christine, Bergthold, James, Bond, Wendy, Bradley, Ronald, Braude, Walter, Brody, Mark, Brown, Richard, Burke, James, Butchart, Joseph, Campbell, Theresa, Carusa, Sandra, Clarnette, Roger, Cohen, Robert, Connelly, Peter, Copeland, Jacquelynn, Coulthard, Elizabeth, Crusey, Jill, Curtis, Craig, De Sanctis, Virginia, Demakis, George, Denburg, Natalie, Donikyan, Mardik, Doody, Rachelle, Ellenbogen, Aaron, Fleischman, Debra, Floel, Agnes, Forchetti, Concetta, Galvez-Jimenez, Nestor, Goldstein, Jerome, Goldstein, Felicia, Goozee, Kathryn, Gruener, Daniel, Halsten, Jerry, Hassman, Howard, Henderson, Elliot, Herbst, Heinz-Peter, Higham, Steve, Hofner, Ronald, Huang, DeRen, Inglis, Fraser, Johnson, Clark, Kass, Joseph, Kirk, Gregory, Klostermann, Arne, Knopman, Alex, Koplin, Anne, Krefetz, David, Kressig, Reto, Lai, Rosalyn, Lefebvre, Gigi, Leger, Gabriel, Leibowitz, Mark, Levey, Allan, Leyhe, Thomas, Losk, Scott, Lyons, Kara, Martin, Jane, Massman, Paul, McWilliam, Christopher, Micallef, Silvana, Middleton, Lefkos, Miller, Hugh, Mintzer, Jacobo, Mitchell, Robert, Mofsen, Ricky, Monsch, Andreas, Moore, Philip, Munic-Miller, Donna, Nash, Marshall, Neugroschl, Judith, Newson, Margaret, Noad, Rupert, Olivera, Esteban, Olley, Amanda, Omidvar, Omid, Parra, Mario, Pearson, Stephen, Perneczky, Robert, Peters, Oliver, Potter, Guy, Price, Geraint, Raymont, Vanessa, Rice, Linda, Ritchie, Craig, Ritter, Aaron, Robinson, Jennifer, Robinson, Sylvia, Ross, Jeffrey, Rujescu, Dan, Sabbagh, Marwan, Sabet, Ahad, Samson, Laura, Sass, John, Saxena, Manish, Schaerf, Frederick, Schlegel, Eugen, Shah, Raj, Shingleton, Richard, Sohrabi, Hamid, Stephenson, Robert, Stratmann, Liebhild, Tariot, Pierre, Thein, Stephen, Till, Haydn, Voight, Nancy, Votolato, Ralph, Wallace, Lorna, Watson, David, White, Alexander, Woodward, Michael, Zamrini, Edward, Zimmerman, Christina, Burns, Daniel K, Alexander, Robert C, Welsh-Bohmer, Kathleen A, Culp, Meredith, Chiang, Carl, O’Neil, Janet, Evans, Rebecca M, Harrigan, Patrick, Plassman, Brenda L, Burke, James R, Wu, Jingtao, Lutz, Michael W, Haneline, Stephen, Schwarz, Adam J, Schneider, Lon S, Yaffe, Kristine, Saunders, Ann M, and Ratti, Emiliangelo

Published
2021
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43. Recurrent noncoding regulatory mutations in pancreatic ductal adenocarcinoma

Author

Feigin, Michael E, Garvin, Tyler, Bailey, Peter, Waddell, Nicola, Chang, David K, Kelley, David R, Shuai, Shimin, Gallinger, Steven, McPherson, John D, Grimmond, Sean M, Khurana, Ekta, Stein, Lincoln D, Biankin, Andrew V, Schatz, Michael C, and Tuveson, David A

Subjects
Biological Sciences, Bioinformatics and Computational Biology, Pancreatic Cancer, Rare Diseases, Cancer, Digestive Diseases, Adenocarcinoma, Carcinoma, Pancreatic Ductal, Gene Expression Regulation, Neoplastic, Humans, Mutation, Pancreatic Neoplasms, Receptor-Like Protein Tyrosine Phosphatases, Class 8, Sodium-Potassium-Chloride Symporters, Medical and Health Sciences, Developmental Biology, Agricultural biotechnology, Bioinformatics and computational biology, Genetics
Abstract

The contributions of coding mutations to tumorigenesis are relatively well known; however, little is known about somatic alterations in noncoding DNA. Here we describe GECCO (Genomic Enrichment Computational Clustering Operation) to analyze somatic noncoding alterations in 308 pancreatic ductal adenocarcinomas (PDAs) and identify commonly mutated regulatory regions. We find recurrent noncoding mutations to be enriched in PDA pathways, including axon guidance and cell adhesion, and newly identified processes, including transcription and homeobox genes. We identified mutations in protein binding sites correlating with differential expression of proximal genes and experimentally validated effects of mutations on expression. We developed an expression modulation score that quantifies the strength of gene regulation imposed by each class of regulatory elements, and found the strongest elements were most frequently mutated, suggesting a selective advantage. Our detailed single-cancer analysis of noncoding alterations identifies regulatory mutations as candidates for diagnostic and prognostic markers, and suggests new mechanisms for tumor evolution.

Published
2017

44. An integrative approach unveils FOSL1 as an oncogene vulnerability in KRAS-driven lung and pancreatic cancer.

Author

Vallejo, Adrian, Perurena, Naiara, Guruceaga, Elisabet, Mazur, Pawel K, Martinez-Canarias, Susana, Zandueta, Carolina, Valencia, Karmele, Arricibita, Andrea, Gwinn, Dana, Sayles, Leanne C, Chuang, Chen-Hua, Guembe, Laura, Bailey, Peter, Chang, David K, Biankin, Andrew, Ponz-Sarvise, Mariano, Andersen, Jesper B, Khatri, Purvesh, Bozec, Aline, Sweet-Cordero, E Alejandro, Sage, Julien, Lecanda, Fernando, and Vicent, Silve

Subjects
Cell Line, Tumor, Animals, Mice, Inbred BALB C, Mice, Knockout, Humans, Mice, Nude, Pancreatic Neoplasms, Lung Neoplasms, Proto-Oncogene Proteins c-fos, Xenograft Model Antitumor Assays, Gene Expression Profiling, Cell Proliferation, Gene Expression Regulation, Neoplastic, RNA Interference, Mutation, Oncogenes, Proto-Oncogene Proteins p21(ras), Kaplan-Meier Estimate, HEK293 Cells, RNAi Therapeutics, Cell Line, Tumor, Gene Expression Regulation, Neoplastic, Mice, Inbred BALB C, Knockout, Nude
Abstract

KRAS mutated tumours represent a large fraction of human cancers, but the vast majority remains refractory to current clinical therapies. Thus, a deeper understanding of the molecular mechanisms triggered by KRAS oncogene may yield alternative therapeutic strategies. Here we report the identification of a common transcriptional signature across mutant KRAS cancers of distinct tissue origin that includes the transcription factor FOSL1. High FOSL1 expression identifies mutant KRAS lung and pancreatic cancer patients with the worst survival outcome. Furthermore, FOSL1 genetic inhibition is detrimental to both KRAS-driven tumour types. Mechanistically, FOSL1 links the KRAS oncogene to components of the mitotic machinery, a pathway previously postulated to function orthogonally to oncogenic KRAS. FOSL1 targets include AURKA, whose inhibition impairs viability of mutant KRAS cells. Lastly, combination of AURKA and MEK inhibitors induces a deleterious effect on mutant KRAS cells. Our findings unveil KRAS downstream effectors that provide opportunities to treat KRAS-driven cancers.

Published
2017

46. PDX1 dynamically regulates pancreatic ductal adenocarcinoma initiation and maintenance

Author

Roy, Nilotpal, Takeuchi, Kenneth K, Ruggeri, Jeanine M, Bailey, Peter, Chang, David, Li, Joey, Leonhardt, Laura, Puri, Sapna, Hoffman, Megan T, Gao, Shan, Halbrook, Christopher J, Song, Yan, Ljungman, Mats, Malik, Shivani, Wright, Christopher VE, Dawson, David W, Biankin, Andrew V, Hebrok, Matthias, and Crawford, Howard C

Subjects
Cancer, Rare Diseases, Digestive Diseases, Pancreatic Cancer, Aetiology, 2.1 Biological and endogenous factors, Acinar Cells, Animals, Carcinoma, Pancreatic Ductal, Cell Transformation, Neoplastic, Gene Deletion, Gene Expression Regulation, Neoplastic, Homeodomain Proteins, Humans, Mice, Pancreatic Neoplasms, Tissue Array Analysis, Trans-Activators, Tumor Cells, Cultured, pancreatic cancer, pancreatitis, EMT, dedifferentiation, Biological Sciences, Medical and Health Sciences, Psychology and Cognitive Sciences, Developmental Biology
Abstract

Aberrant activation of embryonic signaling pathways is frequent in pancreatic ductal adenocarcinoma (PDA), making developmental regulators therapeutically attractive. Here we demonstrate diverse functions for pancreatic and duodenal homeobox 1 (PDX1), a transcription factor indispensable for pancreas development, in the progression from normal exocrine cells to metastatic PDA. We identify a critical role for PDX1 in maintaining acinar cell identity, thus resisting the formation of pancreatic intraepithelial neoplasia (PanIN)-derived PDA. Upon neoplastic transformation, the role of PDX1 changes from tumor-suppressive to oncogenic. Interestingly, subsets of malignant cells lose PDX1 expression while undergoing epithelial-to-mesenchymal transition (EMT), and PDX1 loss is associated with poor outcome. This stage-specific functionality arises from profound shifts in PDX1 chromatin occupancy from acinar cells to PDA. In summary, we report distinct roles of PDX1 at different stages of PDA, suggesting that therapeutic approaches against this potential target need to account for its changing functions at different stages of carcinogenesis. These findings provide insight into the complexity of PDA pathogenesis and advocate a rigorous investigation of therapeutically tractable targets at distinct phases of PDA development and progression.

Published
2016

47. Author Correction: Genomic basis for RNA alterations in cancer

Author

Calabrese, Claudia, Davidson, Natalie R., Demircioğlu, Deniz, Fonseca, Nuno A., He, Yao, Kahles, André, Lehmann, Kjong-Van, Liu, Fenglin, Shiraishi, Yuichi, Soulette, Cameron M., Urban, Lara, Greger, Liliana, Li, Siliang, Liu, Dongbing, Perry, Marc D., Xiang, Qian, Zhang, Fan, Zhang, Junjun, Bailey, Peter, Erkek, Serap, Hoadley, Katherine A., Hou, Yong, Huska, Matthew R., Kilpinen, Helena, Korbel, Jan O., Marin, Maximillian G., Markowski, Julia, Nandi, Tannistha, Pan-Hammarström, Qiang, Pedamallu, Chandra Sekhar, Siebert, Reiner, Stark, Stefan G., Su, Hong, Tan, Patrick, Waszak, Sebastian M., Yung, Christina, Zhu, Shida, Awadalla, Philip, Creighton, Chad J., Meyerson, Matthew, Ouellette, B. F. Francis, Wu, Kui, Yang, Huanming, Brazma, Alvis, Brooks, Angela N., Göke, Jonathan, Rätsch, Gunnar, Schwarz, Roland F., Stegle, Oliver, and Zhang, Zemin

Published
2023
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48. Genomic basis for RNA alterations in cancer

Author

Calabrese, Claudia, Davidson, Natalie R., Demircioğlu, Deniz, Fonseca, Nuno A., He, Yao, Kahles, André, Lehmann, Kjong-Van, Liu, Fenglin, Shiraishi, Yuichi, Soulette, Cameron M., Urban, Lara, Greger, Liliana, Li, Siliang, Liu, Dongbing, Perry, Marc D., Xiang, Qian, Zhang, Fan, Zhang, Junjun, Bailey, Peter, Erkek, Serap, Hoadley, Katherine A., Hou, Yong, Huska, Matthew R., Kilpinen, Helena, Korbel, Jan O., Marin, Maximillian G., Markowski, Julia, Nandi, Tannistha, Pan-Hammarström, Qiang, Pedamallu, Chandra Sekhar, Siebert, Reiner, Stark, Stefan G., Su, Hong, Tan, Patrick, Waszak, Sebastian M., Yung, Christina, Zhu, Shida, Awadalla, Philip, Creighton, Chad J., Meyerson, Matthew, Ouellette, B. F. Francis, Wu, Kui, Yang, Huanming, Brazma, Alvis, Brooks, Angela N., Göke, Jonathan, Rätsch, Gunnar, Schwarz, Roland F., Stegle, Oliver, and Zhang, Zemin

Published
2020
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49. Palaces of Pleasure: From Music Halls to the Seaside to Football, How the Victorians Invented Mass Entertainment

Author

Bailey, Peter

Subjects
Palaces of Pleasure: From Music Halls to the Seaside to Football, How the Victorians Invented Mass Entertainment (Nonfiction work) -- Jackson, Lee, Books -- Book reviews, Humanities, Social sciences
Abstract

Palaces of Pleasure: From Music Halls to the Seaside to Football, How the Victorians Invented Mass Entertainment, by Lee Jackson; pp. xii + 304. New Haven and London: Yale University [...]

Published
2021

50. Whole genomes redefine the mutational landscape of pancreatic cancer

Author

Biankin, Andrew V, Johns, Amber L, Mawson, Amanda, Chang, David K, Scarlett, Christopher J, Brancato, Mary-Anne L, Rowe, Sarah J, Simpson, Skye H, Martyn-Smith, Mona, Thomas, Michelle T, Chantrill, Lorraine A, Chin, Venessa T, Chou, Angela, Cowley, Mark J, Humphris, Jeremy L, Jones, Marc D, Scott Mead, R, Nagrial, Adnan M, Pajic, Marina, Pettit, Jessica, Pinese, Mark, Rooman, Ilse, Wu, Jianmin, Tao, Jiang, DiPietro, Renee, Watson, Clare, Steinmann, Angela, Ching Lee, Hong, Wong, Rachel, Pinho, Andreia V, Giry-Laterriere, Marc, Daly, Roger J, Musgrove, Elizabeth A, Sutherland, Robert L, Grimmond, Sean M, Waddell, Nicola, Kassahn, Karin S, Miller, David K, Wilson, Peter J, Patch, Ann-Marie, Song, Sarah, Harliwong, Ivon, Idrisoglu, Senel, Nourse, Craig, Nourbakhsh, Ehsan, Manning, Suzanne, Wani, Shivangi, Gongora, Milena, Anderson, Matthew, Holmes, Oliver, Leonard, Conrad, Taylor, Darrin, Wood, Scott, Xu, Christina, Nones, Katia, Lynn Fink, J, Christ, Angelika, Bruxner, Tim, Cloonan, Nicole, Newell, Felicity, Pearson, John V, Bailey, Peter, Quinn, Michael, Nagaraj, Shivashankar, Kazakoff, Stephen, Waddell, Nick, Krisnan, Keerthana, Quek, Kelly, Wood, David, Fadlullah, Muhammad ZH, Samra, Jaswinder S, Gill, Anthony J, Pavlakis, Nick, Guminski, Alex, Toon, Christopher, Asghari, Ray, Merrett, Neil D, Pavey, Darren, Das, Amitabha, Cosman, Peter H, Ismail, Kasim, O’Connnor, Chelsie, Lam Duncan McLeod, Vincent W, Pleass, Henry C, Richardson, Arthur, James, Virginia, Kench, James G, Cooper, Caroline L, Joseph, David, Sandroussi, Charbel, Crawford, Michael, Gallagher, James, Texler, Michael, Forest, Cindy, Laycock, Andrew, Epari, Krishna P, Ballal, Mo, Fletcher, David R, Mukhedkar, Sanjay, and Spry, Nigel A

Subjects
Cancer, Human Genome, Pancreatic Cancer, Digestive Diseases, Genetics, Rare Diseases, 2.1 Biological and endogenous factors, Aetiology, Adenocarcinoma, Animals, Carcinoma, Pancreatic Ductal, DNA Mutational Analysis, DNA Repair, Female, Genes, BRCA1, Genes, BRCA2, Genetic Markers, Genome, Human, Genomic Instability, Genomics, Genotype, Humans, Mice, Mutation, Pancreatic Neoplasms, Platinum, Point Mutation, Poly(ADP-ribose) Polymerase Inhibitors, Xenograft Model Antitumor Assays, Australian Pancreatic Cancer Genome Initiative, General Science & Technology
Abstract

Pancreatic cancer remains one of the most lethal of malignancies and a major health burden. We performed whole-genome sequencing and copy number variation (CNV) analysis of 100 pancreatic ductal adenocarcinomas (PDACs). Chromosomal rearrangements leading to gene disruption were prevalent, affecting genes known to be important in pancreatic cancer (TP53, SMAD4, CDKN2A, ARID1A and ROBO2) and new candidate drivers of pancreatic carcinogenesis (KDM6A and PREX2). Patterns of structural variation (variation in chromosomal structure) classified PDACs into 4 subtypes with potential clinical utility: the subtypes were termed stable, locally rearranged, scattered and unstable. A significant proportion harboured focal amplifications, many of which contained druggable oncogenes (ERBB2, MET, FGFR1, CDK6, PIK3R3 and PIK3CA), but at low individual patient prevalence. Genomic instability co-segregated with inactivation of DNA maintenance genes (BRCA1, BRCA2 or PALB2) and a mutational signature of DNA damage repair deficiency. Of 8 patients who received platinum therapy, 4 of 5 individuals with these measures of defective DNA maintenance responded.

Published
2015

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