Author: "Matthew D Wilkerson" - Searchworks@Jio Institute Digital Library Search Results

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284 results on '"Matthew D Wilkerson"'

1. Correction: Molecular Subtypes in Head and Neck Cancer Exhibit Distinct Patterns of Chromosomal Gain and Loss of Canonical Cancer Genes.

Author: Vonn Walter, Xiaoying Yin, Matthew D Wilkerson, Christopher R Cabanski, Ni Zhao, Ying Du, Mei Kim Ang, Michele C Hayward, Ashley H Salazar, Katherine A Hoadley, Karen Fritchie, Charles J Sailey, Mark C Weissler, William W Shockley, Adam M Zanation, Trevor Hackman, Leigh B Thorne, William D Funkhouser, Kenneth L Muldrew, Andrew F Olshan, Scott H Randell, Fred A Wright, Carol G Shores, and D Neil Hayes
Subjects: Medicine, Science
Abstract: [This corrects the article DOI: 10.1371/journal.pone.0056823.].
Published: 2018
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2. Tsc2 disruption in mesenchymal progenitors results in tumors with vascular anomalies overexpressing Lgals3

Author: Peter J Klover, Rajesh L Thangapazham, Jiro Kato, Ji-an Wang, Stasia A Anderson, Victoria Hoffmann, Wendy K Steagall, Shaowei Li, Elizabeth McCart, Neera Nathan, Joshua D Bernstock, Matthew D Wilkerson, Clifton L Dalgard, Joel Moss, and Thomas N Darling
Subjects: galectin-3, tuberous sclerosis complex, mTORC1, Medicine, Science, Biology (General), QH301-705.5
Abstract: Increased mTORC1 signaling from TSC1/TSC2 inactivation is found in cancer and causes tuberous sclerosis complex (TSC). The role of mesenchymal-derived cells in TSC tumorigenesis was investigated through disruption of Tsc2 in craniofacial and limb bud mesenchymal progenitors. Tsc2cKOPrrx1-cre mice had shortened lifespans and extensive hamartomas containing abnormal tortuous, dilated vessels prominent in the forelimbs. Abnormalities were blocked by the mTORC1 inhibitor sirolimus. A Tsc2/mTORC1 expression signature identified in Tsc2-deficient fibroblasts was also increased in bladder cancers with TSC1/TSC2 mutations in the TCGA database. Signature component Lgals3 encoding galectin-3 was increased in Tsc2-deficient cells and serum of Tsc2cKOPrrx1-cre mice. Galectin-3 was increased in TSC-related skin tumors, angiomyolipomas, and lymphangioleiomyomatosis with serum levels in patients with lymphangioleiomyomatosis correlating with impaired lung function and angiomyolipoma presence. Our results demonstrate Tsc2-deficient mesenchymal progenitors cause aberrant morphogenic signals, and identify an expression signature including Lgals3 relevant for human disease of TSC1/TSC2 inactivation and mTORC1 hyperactivity.
Published: 2017
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3. Combined Targeted DNA Sequencing in Non-Small Cell Lung Cancer (NSCLC) Using UNCseq and NGScopy, and RNA Sequencing Using UNCqeR for the Detection of Genetic Aberrations in NSCLC.

Author: Xiaobei Zhao, Anyou Wang, Vonn Walter, Nirali M Patel, David A Eberhard, Michele C Hayward, Ashley H Salazar, Heejoon Jo, Matthew G Soloway, Matthew D Wilkerson, Joel S Parker, Xiaoying Yin, Guosheng Zhang, Marni B Siegel, Gary B Rosson, H Shelton Earp, Norman E Sharpless, Margaret L Gulley, Karen E Weck, D Neil Hayes, and Stergios J Moschos
Subjects: Medicine, Science
Abstract: The recent FDA approval of the MiSeqDx platform provides a unique opportunity to develop targeted next generation sequencing (NGS) panels for human disease, including cancer. We have developed a scalable, targeted panel-based assay termed UNCseq, which involves a NGS panel of over 200 cancer-associated genes and a standardized downstream bioinformatics pipeline for detection of single nucleotide variations (SNV) as well as small insertions and deletions (indel). In addition, we developed a novel algorithm, NGScopy, designed for samples with sparse sequencing coverage to detect large-scale copy number variations (CNV), similar to human SNP Array 6.0 as well as small-scale intragenic CNV. Overall, we applied this assay to 100 snap-frozen lung cancer specimens lacking same-patient germline DNA (07-0120 tissue cohort) and validated our results against Sanger sequencing, SNP Array, and our recently published integrated DNA-seq/RNA-seq assay, UNCqeR, where RNA-seq of same-patient tumor specimens confirmed SNV detected by DNA-seq, if RNA-seq coverage depth was adequate. In addition, we applied the UNCseq assay on an independent lung cancer tumor tissue collection with available same-patient germline DNA (11-1115 tissue cohort) and confirmed mutations using assays performed in a CLIA-certified laboratory. We conclude that UNCseq can identify SNV, indel, and CNV in tumor specimens lacking germline DNA in a cost-efficient fashion.
Published: 2015
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4. The influence of microbial colonization on inflammatory versus pro-healing trajectories in combat extremity wounds

Author: Seth A. Schobel, Eric R. Gann, Desiree Unselt, Scott F. Grey, Felipe A. Lisboa, Meenu M. Upadhyay, Michael Rouse, Simon Tallowin, Nicholas A. Be, Xijun Zhang, Clifton L. Dalgard, Matthew D. Wilkerson, Milos Hauskrecht, Stephen F. Badylak, Ruben Zamora, Yoram Vodovotz, Benjamin K. Potter, Thomas A. Davis, and Eric A. Elster
Subjects: Medicine, Science
Abstract: Abstract A combination of improved body armor, medical transportation, and treatment has led to the increased survival of warfighters from combat extremity injuries predominantly caused by blasts in modern conflicts. Despite advances, a high rate of complications such as wound infections, wound failure, amputations, and a decreased quality of life exist. To study the molecular underpinnings of wound failure, wound tissue biopsies from combat extremity injuries had RNA extracted and sequenced. Wounds were classified by colonization (colonized vs. non-colonized) and outcome (healed vs. failed) status. Differences in gene expression were investigated between timepoints at a gene level, and longitudinally by multi-gene networks, inferred proportions of immune cells, and expression of healing-related functions. Differences between wound outcomes in colonized wounds were more apparent than in non-colonized wounds. Colonized/healed wounds appeared able to mount an adaptive immune response to infection and progress beyond the inflammatory stage of healing, while colonized/failed wounds did not. Although, both colonized and non-colonized failed wounds showed increasing inferred immune and inflammatory programs, non-colonized/failed wounds progressed beyond the inflammatory stage, suggesting different mechanisms of failure dependent on colonization status. Overall, these data reveal gene expression profile differences in healing wounds that may be utilized to improve clinical treatment paradigms.
Published: 2024
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5. Proteogenomic analysis of enriched HGSOC tumor epithelium identifies prognostic signatures and therapeutic vulnerabilities

Author: Nicholas W. Bateman, Tamara Abulez, Anthony R. Soltis, Andrew McPherson, Seongmin Choi, Dale W. Garsed, Ahwan Pandey, Chunqiao Tian, Brian L. Hood, Kelly A. Conrads, Pang-ning Teng, Julie Oliver, Glenn Gist, Dave Mitchell, Tracy J. Litzi, Christopher M. Tarney, Barbara A. Crothers, Paulette Mhawech-Fauceglia, Clifton L. Dalgard, Matthew D. Wilkerson, Mariaelena Pierobon, Emanuel F. Petricoin, Chunhua Yan, Daoud Meerzaman, Clara Bodelon, Nicolas Wentzensen, Jerry S. H. Lee, The APOLLO Research Network, David G. Huntsman, Sohrab Shah, Craig D. Shriver, Neil T. Phippen, Kathleen M. Darcy, David D. L. Bowtell, Thomas P. Conrads, and G. Larry Maxwell
Subjects: Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract: Abstract We performed a deep proteogenomic analysis of bulk tumor and laser microdissection enriched tumor cell populations from high-grade serous ovarian cancer (HGSOC) tissue specimens spanning a broad spectrum of purity. We identified patients with longer progression-free survival had increased immune-related signatures and validated proteins correlating with tumor-infiltrating lymphocytes in 65 tumors from an independent cohort of HGSOC patients, as well as with overall survival in an additional 126 HGSOC patient cohort. We identified that homologous recombination deficient (HRD) tumors are enriched in pathways associated with metabolism and oxidative phosphorylation that we validated in independent patient cohorts. We further identified that polycomb complex protein BMI-1 is elevated in HR proficient (HRP) tumors, that elevated BMI-1 correlates with poor overall survival in HRP but not HRD HGSOC patients, and that HRP HGSOC cells are uniquely sensitive to BMI-1 inhibition.
Published: 2024
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6. Molecular subtypes in head and neck cancer exhibit distinct patterns of chromosomal gain and loss of canonical cancer genes.

Author: Vonn Walter, Xiaoying Yin, Matthew D Wilkerson, Christopher R Cabanski, Ni Zhao, Ying Du, Mei Kim Ang, Michele C Hayward, Ashley H Salazar, Katherine A Hoadley, Karen Fritchie, Charles J Sailey, Mark C Weissler, William W Shockley, Adam M Zanation, Trevor Hackman, Leigh B Thorne, William D Funkhouser, Kenneth L Muldrew, Andrew F Olshan, Scott H Randell, Fred A Wright, Carol G Shores, and D Neil Hayes
Subjects: Medicine, Science
Abstract: Head and neck squamous cell carcinoma (HNSCC) is a frequently fatal heterogeneous disease. Beyond the role of human papilloma virus (HPV), no validated molecular characterization of the disease has been established. Using an integrated genomic analysis and validation methodology we confirm four molecular classes of HNSCC (basal, mesenchymal, atypical, and classical) consistent with signatures established for squamous carcinoma of the lung, including deregulation of the KEAP1/NFE2L2 oxidative stress pathway, differential utilization of the lineage markers SOX2 and TP63, and preference for the oncogenes PIK3CA and EGFR. For potential clinical use the signatures are complimentary to classification by HPV infection status as well as the putative high risk marker CCND1 copy number gain. A molecular etiology for the subtypes is suggested by statistically significant chromosomal gains and losses and differential cell of origin expression patterns. Model systems representative of each of the four subtypes are also presented.
Published: 2013
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7. Differential pathogenesis of lung adenocarcinoma subtypes involving sequence mutations, copy number, chromosomal instability, and methylation.

Author: Matthew D Wilkerson, Xiaoying Yin, Vonn Walter, Ni Zhao, Christopher R Cabanski, Michele C Hayward, C Ryan Miller, Mark A Socinski, Alden M Parsons, Leigh B Thorne, Benjamin E Haithcock, Nirmal K Veeramachaneni, William K Funkhouser, Scott H Randell, Philip S Bernard, Charles M Perou, and D Neil Hayes
Subjects: Medicine, Science
Abstract: Lung adenocarcinoma (LAD) has extreme genetic variation among patients, which is currently not well understood, limiting progress in therapy development and research. LAD intrinsic molecular subtypes are a validated stratification of naturally-occurring gene expression patterns and encompass different functional pathways and patient outcomes. Patients may have incurred different mutations and alterations that led to the different subtypes. We hypothesized that the LAD molecular subtypes co-occur with distinct mutations and alterations in patient tumors.The LAD molecular subtypes (Bronchioid, Magnoid, and Squamoid) were tested for association with gene mutations and DNA copy number alterations using statistical methods and published cohorts (n = 504). A novel validation (n = 116) cohort was assayed and interrogated to confirm subtype-alteration associations. Gene mutation rates (EGFR, KRAS, STK11, TP53), chromosomal instability, regional copy number, and genomewide DNA methylation were significantly different among tumors of the molecular subtypes. Secondary analyses compared subtypes by integrated alterations and patient outcomes. Tumors having integrated alterations in the same gene associated with the subtypes, e.g. mutation, deletion and underexpression of STK11 with Magnoid, and mutation, amplification, and overexpression of EGFR with Bronchioid. The subtypes also associated with tumors having concurrent mutant genes, such as KRAS-STK11 with Magnoid. Patient overall survival, cisplatin plus vinorelbine therapy response and predicted gefitinib sensitivity were significantly different among the subtypes.The lung adenocarcinoma intrinsic molecular subtypes co-occur with grossly distinct genomic alterations and with patient therapy response. These results advance the understanding of lung adenocarcinoma etiology and nominate patient subgroups for future evaluation of treatment response.
Published: 2012
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8. SWISS MADE: Standardized WithIn Class Sum of Squares to evaluate methodologies and dataset elements.

Author: Christopher R Cabanski, Yuan Qi, Xiaoying Yin, Eric Bair, Michele C Hayward, Cheng Fan, Jianying Li, Matthew D Wilkerson, J S Marron, Charles M Perou, and D Neil Hayes
Subjects: Medicine, Science
Abstract: Contemporary high dimensional biological assays, such as mRNA expression microarrays, regularly involve multiple data processing steps, such as experimental processing, computational processing, sample selection, or feature selection (i.e. gene selection), prior to deriving any biological conclusions. These steps can dramatically change the interpretation of an experiment. Evaluation of processing steps has received limited attention in the literature. It is not straightforward to evaluate different processing methods and investigators are often unsure of the best method. We present a simple statistical tool, Standardized WithIn class Sum of Squares (SWISS), that allows investigators to compare alternate data processing methods, such as different experimental methods, normalizations, or technologies, on a dataset in terms of how well they cluster a priori biological classes. SWISS uses Euclidean distance to determine which method does a better job of clustering the data elements based on a priori classifications. We apply SWISS to three different gene expression applications. The first application uses four different datasets to compare different experimental methods, normalizations, and gene sets. The second application, using data from the MicroArray Quality Control (MAQC) project, compares different microarray platforms. The third application compares different technologies: a single Agilent two-color microarray versus one lane of RNA-Seq. These applications give an indication of the variety of problems that SWISS can be helpful in solving. The SWISS analysis of one-color versus two-color microarrays provides investigators who use two-color arrays the opportunity to review their results in light of a single-channel analysis, with all of the associated benefits offered by this design. Analysis of the MACQ data shows differential intersite reproducibility by array platform. SWISS also shows that one lane of RNA-Seq clusters data by biological phenotypes as well as a single Agilent two-color microarray.
Published: 2010
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9. Lack of association between classical HLA genes and asymptomatic SARS-CoV-2 infection

Author: Astrid Marchal, Elizabeth T. Cirulli, Iva Neveux, Evangelos Bellos, Ryan S. Thwaites, Kelly M. Schiabor Barrett, Yu Zhang, Ivana Nemes-Bokun, Mariya Kalinova, Andrew Catchpole, Stuart G. Tangye, András N. Spaan, Justin B. Lack, Jade Ghosn, Charles Burdet, Guy Gorochov, Florence Tubach, Pierre Hausfater, Clifton L. Dalgard, Shen-Ying Zhang, Qian Zhang, Christopher Chiu, Jacques Fellay, Joseph J. Grzymski, Vanessa Sancho-Shimizu, Laurent Abel, Jean-Laurent Casanova, Aurélie Cobat, Alexandre Bolze, Alessandro Aiuti, Saleh Al-Muhsen, Fahd Al-Mulla, Ali Amara, Mark S. Anderson, Evangelos Andreakos, Andrés A. Arias, Lisa M. Arkin, Hagit Baris Feldman, Paul Bastard, Alexandre Belot, Catherine M. Biggs, Dusan Bogunovic, Anastasiia Bondarenko, Alessandro Borghesi, Ahmed A. Bousfiha, Petter Brodin, Yenan Bryceson, Manish J. Butte, Giorgio Casari, John Christodoulou, Roger Colobran, Antonio Condino-Neto, Stefan N. Constantinescu, Megan A. Cooper, Murkesh Desai, Beth A. Drolet, Xavier Duval, Jamila El Baghdadi, Philippine Eloy, Sara Espinosa-Padilla, Carlos Flores, José Luis Franco, Antoine Froidure, Peter K. Gregersen, Bodo Grimbacher, Filomeen Haerynck, David Hagin, Rabih Halwani, Lennart Hammarström, James R. Heath, Elena W.Y. Hsieh, Eystein Husebye, Kohsuke Imai, Yuval Itan, Emmanuelle Jouanguy, Elżbieta Kaja, Timokratis Karamitros, Kai Kisand, Cheng-Lung Ku, Yu-Lung Lau, Yun Ling, Carrie L. Lucas, Tom Maniatis, Davood Mansouri, László Maródi, France Mentré, Isabelle Meyts, Joshua D. Milner, Kristina Mironska, Trine H. Mogensen, Tomohiro Morio, Lisa F.P. Ng, Luigi D. Notarangelo, Antonio Novelli, Giuseppe Novelli, Cliona O'Farrelly, Satoshi Okada, Keisuke Okamoto, Tayfun Ozcelik, Qiang Pan-Hammarström, Jean W. Pape, Rebeca Perez de Diego, Jordi Perez-Tur, David S. Perlin, Graziano Pesole, Anna M. Planas, Carolina Prando, Aurora Pujol, Anne Puel, Lluis Quintana-Murci, Sathishkumar Ramaswamy, Laurent Renia, Igor Resnick, Carlos Rodríguez-Gallego, Anna Sediva, Mikko R.J. Seppänen, Mohammad Shahrooei, Anna Shcherbina, Ondrej Slaby, Andrew L. Snow, Pere Soler-Palacín, Vassili Soumelis, Ivan Tancevski, Ahmad Abou Tayoun, Şehime Gülsün Temel, Christian Thorball, Pierre Tiberghien, Sophie Trouillet-Assant, Stuart E. Turvey, K. M. Furkan Uddin, Mohammed J. Uddin, Diederik van de Beek, Donald C. Vinh, Horst von Bernuth, Joost Wauters, Mayana Zatz, Pawel Zawadzki, Serge Bureau, Yannick Vacher, Anne Gysembergh-Houal, Lauren Demerville, Abla Benleulmi-Chaachoua, Sebastien Abad, Radhiya Abassi, Abdelrafie Abdellaoui, Abdelkrim Abdelmalek, Hendy Abdoul, Helene Abergel, Fariza Abeud, Sophie Abgrall, Noemie Abisror, Marylise Adechian, Nordine Aderdour, Hakeem Farid Admane, Frederic Adnet, Sara Afritt, Helene Agostini, Claire Aguilar, Sophie Agut, Tommaso Francesco Aiello, Marc Ait Kaci, Hafid Ait Oufella, Gokula Ajeenthiravasan, Virginie Alauzy, Fanny Alby-Laurent, Lucie Allard, Marie-Alexandra Alyanakian, Blanca Amador Borrero, Sabrina Amam, Lucile Amrouche, Marc Andronikof, Dany Anglicheau, Nadia Anguel, Djillali Annane, Mohammed Aounzou, Caroline Aparicio, Gladys Aratus, Jean-Benoit Arlet, Jeremy Arzoine, Elisabeth Aslangul, Mona Assefi, Adeline Aubry, Laetitia Audiffred, Etienne Audureau, Christelle Nathalie Auger, Jean-Charles Auregan, Celine Awotar, Sonia Ayllon Milla, Delphine Azan, Laurene Azemar, Billal Azzouguen, Marwa Bachir Elrufaai, Aïda Badsi, Prissile Bakouboula, Coline Balcerowiak, Fanta Balde, Elodie Baldivia, Eliane-Flore Bangamingo, Amandine Baptiste, Fanny Baran-Marszak, Caroline Barau, Nathalie Barget, Flore Baronnet, Romain Barthelemy, Jean-Luc Baudel, Camille Baudry, Elodie Baudry, Laurent Beaugerie, Adel Belamri, Nicolas Belaube, Rhida Belilita, Pierre Bellassen, Rawan Belmokhtar, Isabel Beltran, Ruben Benainous, Mourad Benallaoua, Robert Benamouzig, Amélie Benbara, Jaouad Benhida, Anis Benkhelouf, Jihene Benlagha, Chahinez Benmostafa, Skander Benothmane, Miassa Bentifraouine, Laurence Berard, Quentin Bernier, Enora Berti, Astrid Bertier, Laure Berton, Simon Bessis, Alexandra Beurton, Celine Bianco, Clara Bianquis, Frank Bidar, Philippe Blanche, Clarisse Blayau, Alexandre Bleibtreu, Emmanuelle Blin, Coralie Bloch-Queyrat, Marie-Christophe Boissier, Diane Bollens, Marion Bolzoni, Rudy pierre Bompard, Nicolas Bonnet, Justine Bonnouvrier, Shirmonecrystal Botha, Wissam Boucenna, Fatiha Bouchama, Olivier Bouchaud, Hanane Bouchghoul, Taoueslylia Boudjebla, Noel Boudjema, Catherine Bouffard, Adrien Bougle, Meriem Bouguerra, Leila Bouras, Agnes Bourcier, Anne Bourgarit Durand, Anne Bourrier, Fabrice Bouscarat, Diane Bouvry, Nesrine Bouziri, Ons Bouzrara, Sarah Bribier, Delphine Brugier, Melanie Brunel, Eida Bui, Anne Buisson, Iryna Bukreyeva, Côme Bureau, Jacques Cadranel, Johann Cailhol, Ruxandra Calin, Clara Campos Vega, Pauline Canavaggio, Marta Cancella, Delphine Cantin, Albert Cao, Lionel Carbillon, Nicolas Carlier, Clementine Cassard, Guylaine Castor, Marion Cauchy, Olivier Cha, Benjamin Chaigne, Salima Challal, Karine Champion, Patrick Chariot, Julie Chas, Simon Chauveau, Anthony Chauvin, Clement Chauvin, Nathalie Chavarot, Kamélia Chebbout, Mustapha Cherai, Ilaria Cherubini, Amelie Chevalier, Thibault Chiarabini, Thierry Chinet, Richard Chocron, Pascaline Choinier, Juliette Chommeloux, Christophe Choquet, Laure Choupeaux, Benjamin Chousterman, Dragosmarius Ciocan, Ada Clarke, Gaëlle Clavere, Florian Clavier, Karine Clement, Sebastien Clerc, Yves Cohen, Fleur Cohen, Adrien Cohen, Audrey Coilly, Hester Colboc, Pauline Colin, Magalie Collet, Chloé Comarmond, Emeline Combacon, Alain Combes, Celine Comparon, Jean-Michel Constantin, Hugues Cordel, Anne-Gael Cordier, Adrien Costantini, Nathalie Costedoat Chalumeau, Camille Couffignal, Doriane Coupeau, Alain Creange, Yannie Cuvillier Lamarre, Charlène Da Silveira, Sandrine Dautheville Guibal El Kayani, Nathalie De Castro, Yann De Rycke, Lucie Del Pozo, Quentin Delannoy, Mathieu Delay, Robin Deleris, Juliette Delforge, Laëtitia Delphine, Noemie Demare, Sophie Demeret, Alexandre Demoule, Aurore Deniau, François Depret, Sophie Derolez, Ouda Derradji, Nawal Derridj, Vincent Descamps, Lydia Deschamps, Celine Desconclois, Cyrielle Desnos, Karine Desongins, Robin Dhote, Benjamin Diallo, Morgane Didier, Myriam Diemer, Stephane Diez, Juliette Djadi-Prat, Fatima-Zohra Djamouri Monnory, Siham Djebara, Naoual Djebra, Minette Djietcheu, Hadjer Djillali, Nouara Djouadi, Severine Donneger, Catarina Dos Santos, Nathalie Dournon, Martin Dres, Laura Droctove, Marie Drogrey, Margot Dropy, Elodie Drouet, Valérie Dubosq, Evelyne Dubreucq, Estelle Dubus, Boris Duchemann, Thibault Duchenoy, Emmanuel Dudoignon, Romain Dufau, Florence Dumas, Clara Duran, Emmanuelle Duron, Antoine Durrbach, Claudine Duvivier, Nathan Ebstein, Jihane El Khalifa, Alexandre Elabbadi, Caroline Elie, Gabriel Ernotte, Anne Esling, Martin Etienne, Xavier Eyer, Muriel Sarah Fartoukh, Takoua Fayali, Marion Fermaut, Arianna Fiorentino, Souha Fliss, Marie-Céline Fournier, Benjamin Fournier, Hélène Francois, Olivia Freynet, Yvann Frigout, Isaure Fromont, Axelle Fuentes, Thomas Furet, Joris Galand, Marc Garnier, Agnes Gaubert, Stéphane Gaudry, Samuel Gaugain, Damien Gauthier, Maxime Gautier, Sophie Georgin-Lavialle, Daniela Geromin, Mohamed Ghalayini, Bijan Ghaleh, Myriam Ghezal, Aude Gibelin, Linda Gimeno, Benoit Girard, Bénédicte Giroux Leprieur, Doryan Gomes, Elisabete Gomes-Pires, Anne Gouge, Amel Gouja, Helene Goulet, Sylvain Goupil, Jeanne Goupil De Bouille, Julien Gras, Segolene Greffe, Lamiae Grimaldi, Paul Guedeney, Bertrand Guidet, Matthias Guillo, Mariechristelle Gulczynski, Tassadit Hadjam, Didier Haguenauer, Soumeya Hammal, Nadjib Hammoudi, Olivier Hanon, Anarole Harrois, Coraline Hautem, Guillaume Hekimian, Nicholas Heming, Olivier Hermine, Sylvie Ho, Marie Houllier, Benjamin Huot, Tessa Huscenot, Wafa Ibn Saied, Ghilas Ikherbane, Meriem Imarazene, Patrick Ingiliz, Lina Iratni, Stephane Jaureguiberry, Jean-Francois Jean-Marc, Deleena Jeyarajasingham, Pauline Jouany, Veronique Jouis, Clement Jourdaine, Ouifiya Kafif, Rim Kallala, Sandrine Katsahian, Lilit Kelesyan, Vixra Keo, Flora Ketz, Warda Khamis, Enfel Khelili, Mehdi Khellaf, Christy Gaëlla Kotokpo Youkou, Ilias Kounis, Gaelle Kpalma, Jessica Krause, Vincent Labbe, Karine Lacombe, Jean-Marc Lacorte, Anne Gaelle Lafont, Emmanuel Lafont, Lynda Lagha, Lionel Lamhaut, Aymeric Lancelot, Cecilia Landman, Fanny Lanternier, Cecile Larcheveque, Caroline Lascoux Combe, Ludovic Lassel, Benjamin Laverdant, Christophe Lavergne, Jean-Rémi Lavillegrand, Pompilia Lazureanu, Loïc Le Guennec, Lamia Leberre, Claire Leblanc, Marion Leboyer, Francois Lecomte, Marine Lecorre, Romain Leenhardt, Marylou Lefebvre, Bénédicte Lefebvre, Paul Legendre, Anne Leger, Laurence Legros, Justyna Legrosse, Sébastien Lehuunghia, Julien Lemarec, Jeremie Leporrier-Ext, Manon Lesein, Hubert Lesur, Vincent Levy, Albert Levy, Edwige Lopes, Amanda Lopes, Vanessa Lopez, Julien Lopinto, Olivier Lortholary, Badr Louadah, Bénédicte Loze, Marie-Laure Lucas, Axelle Lucasamichi, Liem Binh Luong, Arouna Magazimama-Ext, David Maingret, Lakhdar Mameri, Philippe Manivet, Cylia Mansouri, Estelle Marcault, Jonathan Marey, Nathalie Marin, Clémence Marois, Olivier Martin, Lou Martineau, Cannelle Martinez-Lopez, Pierre Martyniuck, Pauline Mary De Farcy, Nessrine Marzouk, Rafik Masmoudi, Alexandre Mebazaa, Frédéric Mechai, Fabio Mecozzi, Chamseddine Mediouni, Bruno Megarbane, Mohamed Meghadecha, Élodie Mejean, Arsene Mekinian, Nour Mekki Abdelhadi, Rania Mekni, Thinhinan Sabrina Meliti, Breno Melo Lima, Paris Meng, Soraya Merbah, Fadhila Messani, Yasmine Messaoudi, Baboo-Irwinsingh Mewasing, Lydia Meziane, Carole Michelot-Burger, Françoise Mignot, Fadi Hillary Minka, Makoto Miyara, Pierre Moine, Jean-Michel Molina, Anaïs Montegnies-Boulet, Alexandra Monti, Claire Montlahuc, Anne-Lise Montout, Alexandre Moores, Caroline Morbieu, Helene Mortelette, Stéphane Mouly, Rosita Muzaffar, Cherifa Iness Nacerddine, Marine Nadal, Hajer Nadif, Kladoum Nassarmadji, Pierre Natella, Sandrine Ndingamondze, Stefan Neraal, Caroline Nguyen, Bao N'Guyen, Isabelle Nion Larmurier, Luc Nlomenyengue, Nicolas Noel, Hilario Nunes, Edris Omar, Zineb Ouazene, Elise Ouedraogo, Wassila Ouelaa, Anissa Oukhedouma, Yasmina Ould Amara, Herve Oya, Johanna Oziel, Thomas Padilla, Elena Paillaud, Solenne Paiva, Beatrice Parfait, Perrine Parize, Christophe Parizot, Antoine Parrot, Arthur Pavot, Laetitia Peaudecerf, Frédéric Pene, Marion Pepin, Julie Pernet, Claire Pernin, Mylène Petit, Olivier Peyrony, Marie-Pierre Pietri, Olivia Pietri, Marc Pineton De Chambrun, Michelle Pinson, Claire Pintado, Valentine Piquard, Christine Pires, Benjamin Planquette, Sandrine Poirier, Anne-Laure Pomel, Stéphanie Pons, Diane Ponscarme, Annegaelle Pourcelot, Valérie Pourcher, Anne Pouvaret, Florian Prever, Miresta Previlon, Margot Prevost, Marie-Julie Provoost, Cyril Quemeneur, Cédric Rafat, Agathe Rami, Brigitte Ranque, Maurice Raphael, Jean Herle Raphalen, Anna Rastoin, Mathieu Raux, Amani Rebai, Michael Reby, Alexis Regent, Asma Regrag, Matthieu Resche-Rigon, Quentin Ressaire, Christian Richard, Mariecaroline Richard, Maxence Robert, Benjamin Rohaut, Camille Rolland-Debord, Jacques Ropers, Anne-Marie Roque-Afonso, Charlotte Rosso, Mélanie Rousseaux, Nabila Rousseaux, Swasti Roux, Lorène Roux, Claire Rouzaud, Antoine Rozes, Emma Rubenstein, Jean-Marc Sabate, Sheila Sabet, Sophie-Caroline Sacleux, Nathalie Saidenberg Kermanach, Faouzi Saliba, Dominique Salmon, Laurent Savale, Guillaume Savary, Rebecca Sberro, Anne Scemla, Frederic Schlemmer, Mathieu Schwartz, Saïd Sedfi, Samia Sefir-Kribel, Philippe Seksik, Pierre Sellier, Agathe Selves, Nicole Sembach, Luca Semerano, Marie-Victoire Senat, Damien Sene, Alexandra Serris, Lucile Sese, Naima Sghiouar, Johanna Sigaux, Martin Siguier, Johanne Silvain, Noémie Simon, Tabassome Simon, Lina Innes Skandri, Miassa Slimani, Aurélie Snauwaert, Harry Sokol, Heithem Soliman, Nisrine Soltani, Benjamin Soyer, Gabriel Steg, Lydia Suarez, Tali-Anne Szwebel, Kossi Taffame, Yacine Tandjaoui-Lambiotte, Claire Tantet, Mariagrazia Tateo, Igor Theodose, Pierre clement Thiebaud, Caroline Thomas, Kelly Tiercelet, Julie Tisserand, Carole Tomczak, Krystel Torelino, Fatima Touam-Ext, Lilia Toumi, Gustave Toury, Mireille Toy-Miou, Olivia Tran Dinh Thanh Lien, Alexy Trandinh, Jean-Marc Treluyer, Baptiste Trinque, Jennifer Truchot, Sarah Tubiana, Simone Tunesi, Matthieu Turpin, Agathe Turpin, Tomas Urbina, Rafael Usubillaga Narvaez, Yurdagul Uzunhan, Prabakar Vaittinadaayar, Arnaud Valent, Maelle Valentian, Nadia Valin, Hélène Vallet, Marina Vaz, Miguel-Alejandro Vazquezibarra, Benoit Vedie, Laetitia Velly, Celine Verstuyft, Cedric Viallette, Eric Vicaut, Dorothee Vignes, Damien Vimpere, Myriam Virlouvet, Guillaume Voiriot, Lena Voisot, Emmanuel Weiss, Nicolas Weiss, Anaïs Winchenne, Youri Yordanov, Lara Zafrani, Mohamad Zaidan, Wissem Zaidi, Cathia Zak, Aida Zarhrate-Ghoul, Ouassila Zatout, Suzanne Zeino, Michel Zeitouni, Naïma Zemirli, Lorene Zerah, Ounsa Zia, Marianne Ziol, Oceane Zolario, Julien Zuber, Claire Andrejak, François Angoulvant, Delphine Bachelet, Marie Bartoli, Romain Basmaci, Sylvie Behillil, Marine Beluze, Dehbia Benkerrou, Krishna Bhavsar, Lila Bouadma, Sabelline Bouchez, Maude Bouscambert, Minerva Cervantes-Gonzalez, Anissa Chair, Catherine Chirouze, Alexandra Coelho, Sandrine Couffin-Cadiergues, Eric d’Ortenzio, Marie-Pierre Debray, Laurene Deconinck, Dominique Deplanque, Diane Descamps, Mathilde Desvallée, Alpha Diallo, Alphonsine Diouf, Céline Dorival, François Dubos, Brigitte Elharrar, Vincent Enouf, Hélène Esperou, Marina Esposito-Farese, Manuel Etienne, Eglantine Ferrand Devouge, Nathalie Gault, Alexandre Gaymard, Tristan Gigante, Morgane Gilg, Jérémie Guedj, Alexandre Hoctin, Isabelle Hoffmann, Ikram Houas, Jean-Sébastien Hulot, Salma Jaafoura, Florentia Kaguelidou, Sabrina Kali, Antoine Khalil, Coralie Khan, Cédric Laouénan, Samira Laribi, Minh Le, Quentin Le Hingrat, Soizic Le Mestre, Hervé Le Nagard, François-Xavier Lescure, Sophie Letrou, Yves Levy, Bruno Lina, Guillaume Lingas, Jean-Christophe Lucet, Denis Malvy, Marina Mambert, Amina Meziane, Hugo Mouquet, Jimmy Mullaert, Nadège Neant, Duc Nguyen, Marion Noret, Saad Nseir, Aurélie Papadopoulos, Christelle Paul, Nathan Peiffer-Smadja, Thomas Perpoint, Ventzislava Petrov-Sanchez, Gilles Peytavin, Huong Pham, Olivier Picone, Oriane Puéchal, Christian Rabaud, Manuel Rosa-Calatrava, Bénédicte Rossignol, Patrick Rossignol, Carine Roy, Marion Schneider, Richa Su, Coralie Tardivon, Marie-Capucine Tellier, François Téoulé, Olivier Terrier, Jean-François Timsit, Christelle Tual, Sylvie Van Der Werf, Noémie Vanel, Aurélie Veislinger, Benoit Visseaux, Aurélie Wiedemann, Yazdan Yazdanpanah, Loubna Alavoine, Charlotte Charpentier, Aline Dechanet, Jean-Luc Ecobichon, Wahiba Frezouls, Nadhira Houhou, Jonathan Lehacaut, Pauline Manchon, Mariama Nouroudine, Caroline Quintin, Michael Thy, Sylvie van der Werf, Valérie Vignali, Abir Chahine, Nawal Waucquier, Maria-Claire Migaud, Félix Djossou, Mayka Mergeay-Fabre, Aude Lucarelli, Magalie Demar, Léa Bruneau, Patrick Gérardin, Adrien Maillot, Christine Payet, Bruno Laviolle, Fabrice Laine, Christophe Paris, Mireille Desille-Dugast, Julie Fouchard, Thierry Pistone, Pauline Perreau, Valérie Gissot, Carole L.E. Goas, Samatha Montagne, Lucie Richard, Kévin Bouiller, Maxime Desmarets, Alexandre Meunier, Marilou Bourgeon, Benjamin Lefévre, Hélène Jeulin, Karine Legrand, Sandra Lomazzi, Bernard Tardy, Amandine Gagneux-Brunon, Frédérique Bertholon, Elisabeth Botelho-Nevers, Christelle Kouakam, Leturque Nicolas, Layidé Roufai, Karine Amat, Hélène Espérou, Samia Hendou, Giuseppe Foti, Giuseppe Citerio, Ernesto Contro, Alberto Pesci, Maria Grazia Valsecchi, Marina Cazzaniga, Giacomo Bellani, Jorge Abad, Giulia Accordino, Micol Angelini, Sergio Aguilera-Albesa, Aina Aguiló-Cucurull, Esra Akyüz Özkan, Ilad Alavi Darazam, Jonathan Antonio Roblero Albisures, Juan C. Aldave, Miquel Alfonso Ramos, Taj Ali Khan, Anna Aliberti, Seyed Alireza Nadji, Gulsum Alkan, Suzan A. AlKhater, Jerome Allardet-Servent, Luis M. Allende, Rebeca Alonso-Arias, Mohammed S. Alshahrani, Laia Alsina, Zahir Amoura, Arnau Antolí, Romain Arrestier, Mélodie Aubart, Teresa Auguet, Iryna Avramenko, Gökhan Aytekin, Axelle Azot, Seiamak Bahram, Fanny Bajolle, Fausto Baldanti, Aurélie Baldolli, Maite Ballester, Benoit Barrou, Federica Barzaghi, Sabrina Basso, Gulsum Iclal Bayhan, Liliana Bezrodnik, Agurtzane Bilbao, Geraldine Blanchard-Rohner, Ignacio Blanco, Adeline Blandinières, Daniel Blázquez-Gamero, Marketa Bloomfield, Mireia Bolivar-Prados, Raphael Borie, Elisabeth Botdhlo-Nevers, Aurore Bousquet, David Boutolleau, Claire Bouvattier, Oksana Boyarchuk, Juliette Bravais, M. Luisa Briones, Marie-Eve Brunner, Raffaele Bruno, Maria Rita P. Bueno, Huda Bukhari, Jacinta Bustamante, Juan José Cáceres Agra, Ruggero Capra, Raphael Carapito, Maria Carrabba, Carlos Casasnovas, Marion Caseris, Irene Cassaniti, Martin Castelle, Francesco Castelli, Martín Castillo de Vera, Mateus V. Castro, Emilie Catherinot, Jale Bengi Celik, Alessandro Ceschi, Martin Chalumeau, Bruno Charbit, Cécile Boulanger, Père Clavé, Bonaventura Clotet, Anna Codina, Cloé Comarmond, Patrizia Comoli, Angelo G. Corsico, Taner Coşkuner, Aleksandar Cvetkovski, Cyril Cyrus, David Dalmau, François Danion, David Ross Darley, Vincent Das, Nicolas Dauby, Stéphane Dauger, Paul De Munte, Loic de Pontual, Amin Dehban, Geoffroy Delplancq, Isabelle Desguerre, Antonio Di Sabatino, Jean-Luc Diehl, Stephanie Dobbelaere, Elena Domínguez-Garrido, Clément Dubost, Olov Ekwall, Şefika Elmas Bozdemir, Marwa H. Elnagdy, Melike Emiroglu, Akifumi Endo, Emine Hafize Erdeniz, Selma Erol Aytekin, Maria Pilar Etxart Lasa, Romain Euvrard, Giovanna Fabio, Laurence Faivre, Antonin Falck, Muriel Fartoukh, Morgane Faure, Miguel Fernandez Arquero, Ricard Ferrer, Jose Ferreres, Bruno Francois, Victoria Fumadó, Kitty S.C. Fung, Francesca Fusco, Alenka Gagro, Blanca Garcia Solis, Pierre Garçon, Pascale Gaussem, Zeynep Gayretli, Juana Gil-Herrera, Laurent Gilardin, Audrey Giraud Gatineau, Mònica Girona-Alarcón, Karen Alejandra Cifuentes Godínez, Jean-Christophe Goffard, Nacho Gonzales, Luis I. Gonzalez-Granado, Rafaela González-Montelongo, Antoine Guerder, Belgin Gülhan, Victor Daniel Gumucio, Leif Gunnar Hanitsch, Jan Gunst, Marta Gut, Jérôme Hadjadj, Selda Hancerli, Tetyana Hariyan, Nevin Hatipoglu, Deniz Heppekcan, Elisa Hernandez-Brito, Po-ki Ho, María Soledad Holanda-Peña, Juan P. Horcajada, Sami Hraiech, Linda Humbert, Ivan F.N. Hung, Alejandro D. Iglesias, Antonio Íñigo-Campos, Matthieu Jamme, María Jesús Arranz, Marie-Thérèse Jimeno, Iolanda Jordan, Saliha Kanık-Yüksek, Yalcin Kara, Aydın Karahan, Adem Karbuz, Kadriye Kart Yasar, Ozgur Kasapcopur, Kenichi Kashimada, Sevgi Keles, Yasemin Kendir Demirkol, Yasutoshi Kido, Can Kizil, Ahmet Osman Kılıç, Adam Klocperk, Antonia Koutsoukou, Zbigniew J. Król, Hatem Ksouri, Paul Kuentz, Arthur M.C. Kwan, Yat Wah M. Kwan, Janette S.Y. Kwok, Jean-Christophe Lagier, David S.Y. Lam, Vicky Lampropoulou, Fleur Le Bourgeois, Yee-Sin Leo, Rafael Leon Lopez, Daniel Leung, Michael Levin, Michael Levy, Romain Lévy, Zhi Li, Daniele Lilleri, Edson Jose Adrian Bolanos Lima, Agnes Linglart, Eduardo López-Collazo, José M. Lorenzo-Salazar, Céline Louapre, Catherine Lubetzki, Kwok-Cheung Lung, Charles-Edouard Luyt, David C. Lye, Cinthia Magnone, Enrico Marchioni, Carola Marioli, Majid Marjani, Laura Marques, Jesus Marquez Pereira, Andrea Martín-Nalda, David Martínez Pueyo, Javier Martinez-Picado, Iciar Marzana, Carmen Mata-Martínez, Alexis Mathian, Larissa R.B. Matos, Gail V. Matthews, Julien Mayaux, Raquel McLaughlin-Garcia, Philippe Meersseman, Jean-Louis Mège, Armand Mekontso-Dessap, Isabelle Melki, Federica Meloni, Jean-François Meritet, Paolo Merlani, Özge Metin Akcan, Mehdi Mezidi, Isabelle Migeotte, Maude Millereux, Matthieu Million, Tristan Mirault, Clotilde Mircher, Mehdi Mirsaeidi, Yoko Mizoguchi, Bhavi P. Modi, Francesco Mojoli, Elsa Moncomble, Abián Montesdeoca Melián, Antonio Morales Martinez, Francisco Morandeira, Pierre-Emmanuel Morange, Clémence Mordacq, Guillaume Morelle, Stéphane J. Mouly, Adrián Muñoz-Barrera, Cyril Nafati, Shintaro Nagashima, Yu Nakagama, Bénédicte Neven, João Farela Neves, Yuk-Yung Ng, Hubert Nielly, Yeray Novoa Medina, Esmeralda Nuñez Cuadros, Semsi Nur Karabela, J. Gonzalo Ocejo-Vinyals, Mehdi Oualha, Amani Ouedrani, Tayfun Özçelik, Aslinur Ozkaya-Parlakay, Michele Pagani, Maria Papadaki, Philippe Parola, Tiffany Pascreau, Stéphane Paul, Estela Paz-Artal, Sigifredo Pedraza, Nancy Carolina González Pellecer, Silvia Pellegrini, Rebeca Pérez de Diego, Xosé Luis Pérez-Fernández, Aurélien Philippe, Quentin Philippot, Adrien Picod, Marc Pineton de Chambrun, Antonio Piralla, Laura Planas-Serra, Dominique Ploin, Julien Poissy, Géraldine Poncelet, Garyphallia Poulakou, Marie S. Pouletty, Persia Pourshahnazari, Jia Li Qiu-Chen, Paul Quentric, Thomas Rambaud, Didier Raoult, Violette Raoult, Anne-Sophie Rebillat, Claire Redin, Léa Resmini, Pilar Ricart, Jean-Christophe Richard, Raúl Rigo-Bonnin, Nadia Rivet, Jacques G. Rivière, Gemma Rocamora-Blanch, Mathieu P. Rodero, Carlos Rodrigo, Luis Antonio Rodriguez, Carlos Rodriguez-Gallego, Agustí Rodriguez-Palmero, Carolina Soledad Romero, Anya Rothenbuhler, Damien Roux, Nikoletta Rovina, Flore Rozenberg, Yvon Ruch, Montse Ruiz, Maria Yolanda Ruiz del Prado, Juan Carlos Ruiz-Rodriguez, Joan Sabater-Riera, Kai Saks, Maria Salagianni, Oliver Sanchez, Adrián Sánchez-Montalvá, Silvia Sánchez-Ramón, Laire Schidlowski, Agatha Schluter, Julien Schmidt, Matthieu Schmidt, Catharina Schuetz, Cyril E. Schweitzer, Francesco Scolari, Luis Seijo, Analia Gisela Seminario, Piseth Seng, Sevtap Senoglu, Mikko Seppänen, Alex Serra Llovich, Virginie Siguret, Eleni Siouti, David M. Smadja, Nikaia Smith, Ali Sobh, Xavier Solanich, Jordi Solé-Violán, Catherine Soler, Betül Sözeri, Giulia Maria Stella, Yuriy Stepanovskiy, Annabelle Stoclin, Fabio Taccone, Jean-Luc Taupin, Simon J. Tavernier, Loreto Vidaur Tello, Benjamin Terrier, Guillaume Thiery, Karolina Thorn, Caroline Thumerelle, Imran Tipu, Martin Tolstrup, Gabriele Tomasoni, Julie Toubiana, Josep Trenado Alvarez, Vasiliki Triantafyllia, Jesús Troya, Owen T.Y. Tsang, Liina Tserel, Eugene Y.K. Tso, Alessandra Tucci, Şadiye Kübra Tüter Öz, Matilde Valeria Ursini, Takanori Utsumi, Pierre Vabres, Juan Valencia-Ramos, Ana Maria Van Den Rym, Isabelle Vandernoot, Valentina Velez-Santamaria, Silvia Patricia Zuniga Veliz, Mateus C. Vidigal, Sébastien Viel, Cédric Villain, Marie E. Vilaire-Meunier, Judit Villar-García, Audrey Vincent, Dimitri Van der Linden, Alla Volokha, Fanny Vuotto, Els Wauters, Alan K.L. Wu, Tak-Chiu Wu, Aysun Yahşi, Osman Yesilbas, Mehmet Yildiz, Barnaby E. Young, Ufuk Yükselmiş, Marco Zecca, Valentina Zuccaro, Jens Van Praet, Bart N. Lambrecht, Eva Van Braeckel, Cédric Bosteels, Levi Hoste, Eric Hoste, Fré Bauters, Jozefien De Clercq, Catherine Heijmans, Hans Slabbynck, Leslie Naesens, Benoit Florkin, Mary-Anne Young, Amanda Willis, Paloma Lapuente-Suanzes, Ana de Andrés-Martín, Matilda Berkell, Valerio Carelli, Alessia Fiorentino, Surbhi Malhotra, Alessandro Mattiaccio, Tommaso Pippucci, Marco Seri, Evelina Tacconelli, Michiel van Agtmael, Anne Geke Algera, Brent Appelman, Frank van Baarle, Diane Bax, Martijn Beudel, Harm Jan Bogaard, Marije Bomers, Peter Bonta, Lieuwe Bos, Michela Botta, Justin de Brabander, Godelieve de Bree, Sanne de Bruin, David T.P. Buis, Marianna Bugiani, Esther Bulle, Osoul Chouchane, Alex Cloherty, Mirjam Dijkstra, Dave A. Dongelmans, Romein W.G. Dujardin, Paul Elbers, Lucas Fleuren, Suzanne Geerlings, Theo Geijtenbeek, Armand Girbes, Bram Goorhuis, Martin P. Grobusch, Florianne Hafkamp, Laura Hagens, Jorg Hamann, Vanessa Harris, Robert Hemke, Sabine M. Hermans, Leo Heunks, Markus Hollmann, Janneke Horn, Joppe W. Hovius, Menno D. de Jong, Rutger Koning, Endry H.T. Lim, Niels van Mourik, Jeaninne Nellen, Esther J. Nossent, Frederique Paulus, Edgar Peters, Dan A.I. Pina-Fuentes, Tom van der Poll, Bennedikt Preckel, Jan M. Prins, Jorinde Raasveld, Tom Reijnders, Maurits C.F. J. de Rotte, Michiel Schinkel, Marcus J. Schultz, Femke A.P. Schrauwen, Alex Schuurmans, Jaap Schuurmans, Kim Sigaloff, Marleen A. Slim, Patrick Smeele, Marry Smit, Cornelis S. Stijnis, Willemke Stilma, Charlotte Teunissen, Patrick Thoral, Anissa M. Tsonas, Pieter R. Tuinman, Marc van der Valk, Denise P. Veelo, Carolien Volleman, Heder de Vries, Lonneke A. Vught, Michèle van Vugt, Dorien Wouters, A.H. Zwinderman, Matthijs C. Brouwer, W. Joost Wiersinga, Alexander P.J. Vlaar, Miranda F. Tompkins, Camille Alba, Daniel N. Hupalo, John Rosenberger, Gauthaman Sukumar, Matthew D. Wilkerson, Xijun Zhang, Justin Lack, Andrew J. Oler, Kerry Dobbs, Ottavia M. Delmonte, Jeffrey J. Danielson, Andrea Biondi, Laura Rachele Bettini, Mariella D’Angiò, Ilaria Beretta, Luisa Imberti, Alessandra Sottini, Virginia Quaresima, Eugenia Quiros-Roldan, Camillo Rossi, Riccardo Castagnoli, Daniela Montagna, Amelia Licari, and Gian Luigi Marseglia
Subjects: HLA, association, asymptomatic infection, COVID-19, population stratification, Genetics, QH426-470
Abstract: Summary: Human genetic studies of critical COVID-19 pneumonia have revealed the essential role of type I interferon-dependent innate immunity to SARS-CoV-2 infection. Conversely, an association between the HLA-B∗15:01 allele and asymptomatic SARS-CoV-2 infection in unvaccinated individuals was recently reported, suggesting a contribution of pre-existing T cell-dependent adaptive immunity. We report a lack of association of classical HLA alleles, including HLA-B∗15:01, with pre-omicron asymptomatic SARS-CoV-2 infection in unvaccinated participants in a prospective population-based study in the United States (191 asymptomatic vs. 945 symptomatic COVID-19 cases). Moreover, we found no such association in the international COVID Human Genetic Effort cohort (206 asymptomatic vs. 574 mild or moderate COVID-19 cases and 1,625 severe or critical COVID-19 cases). Finally, in the Human Challenge Characterisation study, the three HLA-B∗15:01 individuals infected with SARS-CoV-2 developed symptoms. As with other acute primary infections studied, no classical HLA alleles favoring an asymptomatic course of SARS-CoV-2 infection were identified.
Published: 2024
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10. Immune response profiles from humans experimentally exposed to Phlebotomus duboscqi bites

Author: Fernanda Fortes de Araujo, Maha Abdeladhim, Clarissa Teixeira, Kelly Hummer, Matthew D. Wilkerson, Roseanne Ressner, Ines Lakhal-Naouar, Michael W. Ellis, Claudio Meneses, Saule Nurmukhambetova, Regis Gomes, W. David Tolbert, George W. Turiansky, Marzena Pazgier, Fabiano Oliveira, Jesus G. Valenzuela, Shaden Kamhawi, and Naomi Aronson
Subjects: P. duboscqi, saliva, antigen, vaccine, immune response, Immunologic diseases. Allergy, RC581-607
Abstract: IntroductionCutaneous leishmaniasis is a neglected vector-borne parasitic disease prevalent in 92 countries with approximately one million new infections annually. Interactions between vector saliva and the human host alter the response to infection and outcome of disease.MethodsTo characterize the human immunological responses developed against saliva of Phlebotomus duboscqi, a Leishmania major (L. major) vector, we repeatedly exposed the arms of 14 healthy U.S volunteers to uninfected P. duboscqi bites. Blood was collected a week after each exposure and used to assess total IgG antibodies against the proteins of P. duboscqi salivary gland homogenate (SGH) and the levels of IFN-gamma and IL-10 from peripheral blood mononuclear cells (PBMCs) stimulated with SGH or recombinant sand fly proteins. We analyzed skin punch biopsies of the human volunteer arms from the insect bite site and control skin site after multiple P. duboscqi exposures (four volunteers) using immunohistochemical staining.ResultsA variety of immediate insect bite skin reactions were observed. Late skin reactions to insect bites were characterized by macular hyperpigmentation and/or erythematous papules. Hematoxylin and eosin staining showed moderate mononuclear skin infiltrate with eosinophils in those challenged recently (within 2 months), eosinophils were not seen in biopsies with recall challenge (6 month post bites). An increase in plasma antigen-specific IgG responses to SGH was observed over time. Western Blot results showed strong plasma reactivity to five P. duboscqi salivary proteins. Importantly, volunteers developed a cellular immunity characterized by the secretion of IFN-gamma upon PBMC stimulation with P. duboscqi SGH and recombinant antigens.DiscussionOur results demonstrate that humans mounted a local and systemic immune response against P. duboscqi salivary proteins. Specifically, PduM02/SP15-like and PduM73/adenosine deaminase recombinant salivary proteins triggered a Th1 type immune response that might be considered in future development of a potential Leishmania vaccine.
Published: 2024
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11. ProteoMixture: A cell type deconvolution tool for bulk tissue proteomic data

Author: Pang-ning Teng, Joshua P. Schaaf, Tamara Abulez, Brian L. Hood, Katlin N. Wilson, Tracy J. Litzi, David Mitchell, Kelly A. Conrads, Allison L. Hunt, Victoria Olowu, Julie Oliver, Fred S. Park, Marshé Edwards, AiChun Chiang, Matthew D. Wilkerson, Praveen-Kumar Raj-Kumar, Christopher M. Tarney, Kathleen M. Darcy, Neil T. Phippen, G. Larry Maxwell, Thomas P. Conrads, and Nicholas W. Bateman
Subjects: Computational bioinformatics, Proteomics, Transcriptomics, Science
Abstract: Summary: Numerous multi-omic investigations of cancer tissue have documented varying and poor pairwise transcript:protein quantitative correlations, and most deconvolution tools aiming to predict cell type proportions (cell admixture) have been developed and credentialed using transcript-level data alone. To estimate cell admixture using protein abundance data, we analyzed proteome and transcriptome data generated from contrived admixtures of tumor, stroma, and immune cell models or those selectively harvested from the tissue microenvironment by laser microdissection from high grade serous ovarian cancer (HGSOC) tumors. Co-quantified transcripts and proteins performed similarly to estimate stroma and immune cell admixture (r ≥ 0.63) in two commonly used deconvolution algorithms, ESTIMATE or ConsensusTME. We further developed and optimized protein-based signatures estimating cell admixture proportions and benchmarked these using bulk tumor proteomic data from over 150 patients with HGSOC. The optimized protein signatures supporting cell type proportion estimates from bulk tissue proteomic data are available at https://lmdomics.org/ProteoMixture/.
Published: 2024
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12. Identification of germline population variants misclassified as cancer-associated somatic variants

Author: Rebecca D. Pollard, Matthew D. Wilkerson, and Padma Sheila Rajagopal
Subjects: germline, somatic, variant classification, misclassification, health disparities, Medicine (General), R5-920
Abstract: IntroductionDatabases used for clinical interpretation in oncology rely on genetic data derived primarily from patients of European ancestry, leading to biases in cancer genetics research and clinical practice. One practical issue that arises in this context is the potential misclassification of multi-ancestral population variants as tumor-associated because they are not represented in reference genomes against which tumor sequencing data is aligned.MethodsTo systematically find misclassified variants, we compared somatic variants in census genes from the Catalogue of Somatic Mutations in Cancer (COSMIC) V99 with multi-ancestral population variants from the Genome Aggregation Databases’ Linkage Disequilibrium (GnomAD). By comparing genomic coordinates, reference, and alternate alleles, we could identify misclassified variants in genes associated with cancer.ResultsWe found 192 of 208 genes in COSMIC’s cancer-associated census genes (92.31%) to be associated with variant misclassifications. Among the 1,906,732 variants in COSMIC, 6,957 variants (0.36%) aligned with normal population variants in GnomAD, concerning for misclassification. The African / African American ancestral population included the greatest number of misclassified variants and also had the greatest number of unique misclassified variants.ConclusionThe direct, systematic comparison of variants from COSMIC for co-occurrence in GnomAD supports a more accurate interpretation of tumor sequencing data and reduces bias related to genomic ancestry.
Published: 2024
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13. Author Correction: Proteogenomic analysis of enriched HGSOC tumor epithelium identifies prognostic signatures and therapeutic vulnerabilities

Author: Nicholas W. Bateman, Tamara Abulez, Anthony R. Soltis, Andrew McPherson, Seongmin Choi, Dale W. Garsed, Ahwan Pandey, Chunqiao Tian, Brian L. Hood, Kelly A. Conrads, Pang-ning Teng, Julie Oliver, Glenn Gist, Dave Mitchell, Tracy J. Litzi, Christopher M. Tarney, Barbara A. Crothers, Paulette Mhawech-Fauceglia, Clifton L. Dalgard, Matthew D. Wilkerson, Mariaelena Pierobon, Emanuel F. Petricoin, Chunhua Yan, Daoud Meerzaman, Clara Bodelon, Nicolas Wentzensen, Jerry S. H. Lee, The APOLLO Research Network, David G. Huntsman, Sohrab Shah, Craig D. Shriver, Neil T. Phippen, Kathleen M. Darcy, David D. L. Bowtell, Thomas P. Conrads, and G. Larry Maxwell
Subjects: Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Published: 2024
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14. Spatial transcriptomics reveals distinct white matter pathology modulated by neutrophil/monocyte signaling following a single, focal cortical contusion injury in mice

Author: Anatomy, Physiology & Genetics (APG), SOM, Savannah K. Kounelis-Wuillaume, Camille Alba, Andrew Frank, Emilie Goguet, William Brooks, Gauthaman Sukumar, Matthew D. Wilkerson, Clifton L. Dalgard, Joseph McCabe, Martin L. Doughty, Anatomy, Physiology & Genetics (APG), SOM, Savannah K. Kounelis-Wuillaume, and Camille Alba, Andrew Frank, Emilie Goguet, William Brooks, Gauthaman Sukumar, Matthew D. Wilkerson, Clifton L. Dalgard, Joseph McCabe, Martin L. Doughty
Abstract: Differential expressed gene (DEG) changes in the WM are consistent with a significant response to trauma in the GM and CC+EC WM but not AC Spatial transcriptomics reveals distinct white matter pathology modulated by neutrophil/monocyte signaling following a single, focal cortical contusion injury in mice Savannah K Kounelis-Wuillaume1, Camille Alba1,2, Andrew Frank3, Emilie Goguet4, William Brooks5Gauthaman Sukumar2, Matthew D. Wilkerson1,6, Clifton L. Dalgard1,2, Joseph McCabe1, Martin L. Doughty1. 1Department of Anatomy, Physiology, & Genetics, Uniformed Services University; 2The American Genome Center; 3Henry M. Jackson Foundation; 4Department Microbiology, Uniformed Services University; 5School of Medicine, Uniformed Services University; 6Center for Military Precision Health The Injured Cortex has a Substantial (Sub)Acute Neuroinflammatory Response Disclaimer. The opinions and assertions expressed herein are those of the author(s) and do not reflect the official policy or position of the Uniformed Services University of the Health Sciences or the Department of Defense. The authors have no conflicts of interest. This work was supported by the Brain Injury Association of America (BIAA) & a Cosmos Club Foundation Scholar Award (Kounelis-Wuillaume), a USU Award (Doughty) and the Department of Defense Program Objective Memorandum HU0001-20-20037 (Dalgard). Comparison 2 days post-injury 7days post-injury CCI Cortex vs Sham Cortex 6143 868 CCI CC+EC vs Sham CC+EC 1197 244 CCI AC vs Sham AC 43 34 CCI CC-EC vs CCI AC 632 1086 Sham CC-EC vs Sham AC 292 167  Damage to grey matter (GM) and white matter (WM) in traumatic brain injury (TBI) initiates spatiotemporally distinct pathophysiological processes  An early modulator of GM and WM injury are peripheral immune cells (PICs) that infiltrate damaged brain tissue during the acute post-injury period  We used Visium Spatial Transcriptomics (10x Genomics) to identify: 1. Gene expression changes in the damaged WM and GM of TB, RITM0038957, Damage to grey matter (GM) and white matter (WM) in traumatic brain injury (TBI) initiates spatiotemporally distinct pathophysiological processes ? An early modulator of GM and WM injury are peripheral immune cells (PICs) that infiltrate damaged brain tissue during the acute post-injury period ? We used Visium Spatial Transcriptomics (10x Genomics) to identify: 1. Gene expression changes in the damaged WM and GM of TBI mice 2. How these gene changes are affected by the infiltration of neutrophils and monocytes into the damaged brain
Published: 2023

15. Tumor microenvironment differences between lung cancer subtypes revealed by spatial transcriptomics

Author: Anatomy, Physiology & Genetics (APG), SOM, Matthew D. Wilkerson, Savannah Kounelis-Wuillaume, Camille Alba, Teri J. Franks, Martin L. Doughty, Robert Kortum, Robert F. Browning, Jr., Clifton L. Dalgard, Craig D. Shriver, Anatomy, Physiology & Genetics (APG), SOM, Matthew D. Wilkerson, and Savannah Kounelis-Wuillaume, Camille Alba, Teri J. Franks, Martin L. Doughty, Robert Kortum, Robert F. Browning, Jr., Clifton L. Dalgard, Craig D. Shriver
Abstract: 1 Center for Military Precision Health, The American Genome Center, Uniformed Services University of the Health Sciences, Bethesda, MD 2 Department of Anatomy Physiology and Genetics, Uniformed Services University, Bethesda MD 3 Henry M. Jackson Foundation for Military Medicine Inc, Bethesda MD 4 Department of Pharmacology, Uniformed Services University of the Health Sciences, Bethesda, MD 5 Pulmonary and Mediastinal Pathology, Department of Defense, Joint Pathology Center, Silver Spring, MD 6 Murtha Cancer Center Research Program, Department of Surgery, Uniformed Services University of the Health Sciences, Bethesda, MD Tumor microenvironment differences between lung cancer subtypes revealed by spatial transcriptomics Matthew D. Wilkerson1,2, Savannah Kounelis-Wuillaume2, Camille Alba1,3, Teri J. Franks5, Martin L. Doughty2, Robert Kortum4, Robert F. Browning, Jr. 5, Clifton L. Dalgard1,2, Craig D. Shriver 6 Introduction Methods: Tissue and Analysis Workflow Lung cancer is a leading cause of cancer deaths worldwide and has complex underlying genetic drivers, subtypes and immune cell types. Molecular analysis of bulk tumors has repeatedly identified key somatic driver genes and subtypes in lung cancer. However, these key molecular strata of bulk lung tumors still contain significant heterogeneity which if characterized in finer detail may reveal new tumor microenvironment factors and lead to improved patient prognostication and therapy options. Here, we sought to compare the tumor microenvironments of lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC) through spatial transcriptomics. We utilized tumor tissues from a cohort of lung cancers from the U.S., as part of the Applied Proteogenomics OrganizationaL Learning and Outcomes (APOLLO) Research Network1. Immune properties of spatial clusters Spatial expression patterns across replicate sections and lung cancer histologies Summary Disclaimer: The contents of this publication are the sole responsibility, RITM0036121, Lung cancer is a leading cause of cancer deaths worldwide and has complex underlying genetic drivers, subtypes and immune cell types. Molecular analysis of bulk tumors has repeatedly identified key somatic driver genes and subtypes in lung cancer. However, these key molecular strata of bulk lung tumors still contain significant heterogeneity which if characterized in finer detail may reveal new tumor microenvironment factors and lead to improved patient prognostication and therapy options. Here, we sought to compare the tumor microenvironments of lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC) through spatial transcriptomics. We utilized tumor tissues from a cohort of lung cancers from the U.S., as part of the Applied Proteogenomics OrganizationaL Learning and Outcomes (APOLLO) Research Network1.
Published: 2023

16. DE-Meta: revealing tumor gene expression by meta-analysis of RNA-Seq and proteomics datasets

Author: Anatomy, Physiology & Genetics (APG), SOM, Xijun Zhang, Clifton L. Dalgard, Matthew D. Wilkerson, Anatomy, Physiology & Genetics (APG), SOM, Xijun Zhang, and Clifton L. Dalgard, Matthew D. Wilkerson
Abstract: Introduction Workflow Summary Detecting differentially expressed genes under different biological conditions is crucial to characterize mechanisms of cancer development and identifying determinants of patient outcome. High throughput technologies such as RNA sequencing and mass spectrometry-based proteomics have been widely used to identify differentially expressed genes (DEG), on a transcript and on a peptide basis, respectively. However, both transcription and translation of genes provide information about gene expression. Thus, leveraging both RNA and protein expression data could potentially produce more accurate results. Various statistical tools have been developed to tackle the differential expression problem for a single platform, such as edgeR, DESeq2, etc. However, a tool that integrates both transcriptome and proteomics data for differential expression analysis has not yet been developed. Meta-analysis can potentially increase statistical power and identify new cancer genes in large sample cohorts and potentially also in small sample cohorts. Here we present DE-Meta, a new tool developed using R, which performs combined meta-analysis of RNA-seq and MS-based proteomics on matched tumor specimens. Lung adenocarcinoma (LUAD) is a primary cause of cancer-related deaths worldwide, despite advances in somatically targeted therapeutics and immune checkpoint therapies. The diagnosis and treatment of LUAD patients pose significant challenges due to the vast morphological and molecular heterogeneity observed both within and between tumors. Two published lung adenocarcinoma datasets were used in this study: APOLLO11,7 and CPTAC2. APOLLO7 is a proteogenomic study seeking to describe the major genome, transcriptome, proteome and phosphoproteome alterations, subtypes, and molecular predictors of patient outcomes. Stratifying LUAD patients using expression subtypes can enhance prediction of clinical outcomes. Expression subtype status of these two cohorts were predicted, RITM0035818, Detecting differentially expressed genes under different biological conditions is crucial to characterize mechanisms of cancer development and identifying determinants of patient outcome. High throughput technologies such as RNA sequencing and mass spectrometrybased proteomics have been widely used to identify differentially expressed genes (DEG), on a transcript and on a peptide basis, respectively. However, both transcription and translation of genes provide information about gene expression. Thus, leveraging both RNA and protein expression data could potentially produce more accurate results. Various statistical tools have been developed to tackle the differential expression problem for a single platform, such as edgeR, DESeq2, etc. However, a tool that integrates both transcriptome and proteomics data for differential expression analysis has not yet been developed. Meta-analysis can potentially increase statistical power and identify new cancer genes in large sample cohorts and potentially also in small sample cohorts. Here we present DE-Meta, a new tool developed using R, which performs combined meta-analysis of RNA-seq and MS-based proteomics on matched tumor specimens.
Published: 2023

17. Whole Genome Sequence Analysis of Candidate Genes Identified Three Loci Potentially Related to Mefloquine Side Effects

Author: Medicine, SOM, Monique Hollis-Perry, Joshua Gray, Dutchabong Shaw, Daniel Hupalo, Heidi Adams, Xijun Zhang, Matthew D. Wilkerson, Lydia D. Hellwig, Clifton Dalgard, Medicine, SOM, Monique Hollis-Perry, and Joshua Gray, Dutchabong Shaw, Daniel Hupalo, Heidi Adams, Xijun Zhang, Matthew D. Wilkerson, Lydia D. Hellwig, Clifton Dalgard
Abstract: Whole Genome Sequence Analysis of Candidate Genes Identified Three Loci Potentially Related to Mefloquine Side Effects Monique Hollis-Perry1, Joshua Gray1, Dutchabong Shaw1,2, Daniel Hupalo1,2, Heidi Adams1,2, Xijun Zhang1,2, Matthew D. Wilkerson1, Lydia D. Hellwig1,2, Clifton Dalgard1, Jeffrey Livezey1, David Saunders1 1Uniformed Services University of Health Sciences Bethesda, MD; 2Henry Jackson Foundation for the Advancement of Military Medicine Bethesda, MD Gene Provided Data RSID Chr loc hg38 Site 1 ref/alt Site 2 ref/alt Site details ORM1 S rs17650,rs1126801 chr9 114323246. ; 114325132 G,G G,G ARG(CGG)20,VAL(GTG)156 ORM1 F1 rs17650,rs1126801 chr9 114323246. ; 114325132 G,A G,G GLN(CAG)20,VAL(GTG)156 ORM1 F2 rs17650,rs1126801 chr9 114323246. ; 114325132 G,A G,A GLN(CAG)20 MET(ATG)156 MTHFR A1298C rs1801131 chr1 11794419 A C p.Glu429Ala MTHFR C677T rs1801133 chr1 11796321 C T p.Ala222Val MDR1 C1236T rs1128503 chr7 87550285 A G p.Gly412Gly MDR1 G2677T rs2032582 chr7 87531302 A C p.Ala893Ser MDR1 C3435T rs1045642 chr7 87509329 A G p.Ile1145Ile PYK2 rs2883490 rs28834970 chr8 27337604 T C intronic HT2A rs7997012 rs7997012 chr13 46837850 A G intronic HT2A rs1928040 rs1928040 chr13 46873101 G A intronic HT2A rs6311 rs6311 chr13 46897343 C T intronic HT2A rs6313 rs6313 chr13 46895805 G A p.Ser34Ser ADA G22A rs73598374 chr20 44651586 C T p.Asp8Tyr ADORA2A (A2A) T1976C rs5751876 chr22 24441333 T C p.Tyr361Tyr ADORA2A (A2A) C2592T rs35320474 chr22 24441942 - T 3' UTR variant METHODS Volunteers with a history of exposure to mefloquine with or without adverse neuropsychiatric symptoms were invited to participate in this case-control cross-sectional study after interviews and medical records review. Investigators searched for potential associations within 7 candidate genes and 16 associated variants for study. Blood samples were collected in Paxgene RNA tubes from 50 volunteers. Mefloquine exposure was defined as: travel to an area with malaria prophylaxis recommendations; w, RITM0040216, Although mefloquine provides effective once-weekly antimalarial prophylaxis, this medication has fallen out of favor due to the risk of neuropsychiatric effects. These can appear after one or two doses, may be mild or severe and commonly include headaches, memory impairment, anxiety or depression, hallucinations, insomnia, and psychosis. Adverse events typically resolve after drug discontinuation, but some patients report long-term complications. While genetic susceptibilities have been identified, pharmacogenomic testing guidance for mefloquine use is not currently available.
Published: 2023

18. Data from Personalized Single-Cell Proteogenomics to Distinguish Acute Myeloid Leukemia from Nonmalignant Clonal Hematopoiesis

Author: Christopher S. Hourigan, Yuesheng Li, Patrick Burr, J. Philip McCoy, Pradeep K. Dagur, Aik Ooi, Shu Wang, Saurabh Gulati, Aaron Llanso, Robert Durruthy-Durruthy, Adam Sciambi, Catherine Lai, Christin B. DeStefano, Janet Valdez, Julie Thompson, Clifton L. Dalgard, Gauthaman Sukumar, Anthony R. Soltis, Matthew D. Wilkerson, Karolyn A. Oetjen, Katherine E. Lindblad, Katherine R. Calvo, Meghali Goswami, Gege Gui, Chidera Nosiri, Jack Ghannam, and Laura W. Dillon
Abstract: Genetic mutations associated with acute myeloid leukemia (AML) also occur in age-related clonal hematopoiesis, often in the same individual. This makes confident assignment of detected variants to malignancy challenging. The issue is particularly crucial for AML posttreatment measurable residual disease monitoring, where results can be discordant between genetic sequencing and flow cytometry. We show here that it is possible to distinguish AML from clonal hematopoiesis and to resolve the immunophenotypic identity of clonal architecture. To achieve this, we first design patient-specific DNA probes based on patient's whole-genome sequencing and then use them for patient-personalized single-cell DNA sequencing with simultaneous single-cell antibody–oligonucleotide sequencing. Examples illustrate AML arising from DNMT3A- and TET2-mutated clones as well as independently. The ability to personalize single-cell proteogenomic assessment for individual patients based on leukemia-specific genomic features has implications for ongoing AML precision medicine efforts.Significance:This study offers a proof of principle of patient-personalized customized single-cell proteogenomics in AML including whole-genome sequencing–defined structural variants, currently unmeasurable by commercial “off-the-shelf” panels. This approach allows for the definition of genetic and immunophenotype features for an individual patient that would be best suited for measurable residual disease tracking.
Published: 2023
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19. Supplementary Data from Personalized Single-Cell Proteogenomics to Distinguish Acute Myeloid Leukemia from Nonmalignant Clonal Hematopoiesis

Author: Christopher S. Hourigan, Yuesheng Li, Patrick Burr, J. Philip McCoy, Pradeep K. Dagur, Aik Ooi, Shu Wang, Saurabh Gulati, Aaron Llanso, Robert Durruthy-Durruthy, Adam Sciambi, Catherine Lai, Christin B. DeStefano, Janet Valdez, Julie Thompson, Clifton L. Dalgard, Gauthaman Sukumar, Anthony R. Soltis, Matthew D. Wilkerson, Karolyn A. Oetjen, Katherine E. Lindblad, Katherine R. Calvo, Meghali Goswami, Gege Gui, Chidera Nosiri, Jack Ghannam, and Laura W. Dillon
Abstract: Supplementary Data
Published: 2023
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20. Data from Integrative Molecular Characterization of Malignant Pleural Mesothelioma

Author: Erik Zmuda, Hongxin Zhang, Hailei Zhang, Jiashan Zhang, Jean C. Zenklusen, Marjorie G. Zauderer, Liming Yang, Shogo Yamamoto, Ye Wu, Tina Wong, Ignacio Wistuba, Lisa Wise, Matthew D. Wilkerson, Daniel J. Weisenberger, John N. Weinstein, Joellen Weaver, Jing Wang, Zhining Wang, Yunhu Wan, Douglas Voet, Luciano S. Viana, Umadevi Veluvolu, Nico van Zandwijk, David J. Van Den Berg, Federico Valdivieso, Tohru Tsujimura, Kane Tse, Anne Tsao, Eric Thompson, Nina Thiessen, Barry S Taylor, Kenji Tatsuno, Roy Tarnuzzer, Donghui Tan, Angela Tam, Qiang Sun, Josh Stuart, Chip Stewart, Paul Spellman, Matthew G. Soloway, Heidi J. Sofia, Tara Skelly, Payal Sipahimalani, Janae V. Simons, Henrique C. S. Silveira, Ilya Shmulevich, Yuichi Shiraishi, Yan Shi, Robert Sheridan, Troy Shelton, Candace Shelton, David T Severson, Tanguy Seiwert, Steven E. Schumacher, Nikolaus Schultz, Jacqueline E. Schein, Cristovam Scapulatempo-Neto, Ayuko Sato, Chris Sander, Gordon Saksena, Sara Sadeghi, Valerie Rusch, Jeffrey Roach, Robert C. Rintoul, William G Richards, David Rice, Sheila M. Reynolds, Rui M. Reis, Glen Reid, Gloria Ravegnini, Doris M. Rassl, Nilsa C. Ramirez, Todd Pihl, Charles M. Perou, Robert Penny, Nathan A. Pennell, Arjun Pennathur, Joseph Paulauskis, Harvey I. Pass, Joel S. Parker, Hatice Osmanbeyoglu, Angelica Ochoa, Yulia Newton, Rashi Naresh, Takashi Nakano, Karen Mungall, Andrew J. Mungall, Lisle E. Mose, Scott Morris, Cesar Moran, Richard A. Moore, Gordon B. Mills, Piotr A. Mieczkowski, Matthew Meyerson, Shaowu Meng, Jonathan Melamed, Sam Meier, Michael Mayo, Marco A. Marra, David Mallory, Dennis T. Maglinte, Yussanne Ma, James Luketich, Yiling Lu, Adhemar Longatto-Filho, Laxmi Lolla, Eric Minwei Liu, Wenbin Liu, Jia Liu, Pei Lin, Tara M. Lichtenberg, Kristen M. Leraas, Darlene Lee, Michael S. Lawrence, Peter W. Laird, Phillip H. Lai, David J. Kwiatkowski, Kozo Kuribayashi, Ritika Kundra, Thomas Krausz, Nobuyuki Kondo, Jaegil Kim, Katayoon Kasaian, Rupa S. Kanchi, Corbin D. Jones, Steven J.M. Jones, Stuart R. Jefferys, Carolyn M. Hutter, Aliya Husain, Alan P. Hoyle, Robert A. Holt, Katherine A. Hoadley, Zachary Heins, David I. Heiman, D. Neil Hayes, David Haussler, Seiki Hasegawa, Guangwu Guo, Benjamin Gross, Chandra Goparaju, Gad Getz, Mark Gerken, Nils Gehlenborg, Julie M. Gastier-Foster, Johanna Gardner, Jianjiong Gao, Françoise Galateau Sallé, Stacey B. Gabriel, Shiro Fukuda, Martin L. Ferguson, Michael Feldman, Rajiv Dhir, Noreen Dhalla, John A. Demchok, Timothy DeFreitas, Assunta De Rienzo, Ludmila Danilova, Erin Curley, Daniel Crain, Leslie Cope, Carrie Cibulskis, Sudha Chudamani, Eric Chuah, Juok Cho, Lucian Chirieac, Dorothy Cheung, Andrew D. Cherniack, Andre L. Carvalho, Rebecca Carlsen, Flávio M. Cárcano, Lauren Averett Byers, Denise Brooks, Moiz S. Bootwalla, Tom Bodenheimer, Craig Bielski, Rameen Beroukhim, Carmen Behrens, Michael Becich, Stephen B. Baylin, Saianand Balu, Miruna Balasundaram, J. Todd Auman, Joshua Armenia, Pavana Anur, Adrian Ally, Marc Ladanyi, Peter Campbell, Bruce W. Robinson, Hiroyuki Aburatani, Ronglai Shen, A. Gordon Robertson, Jonathan A. Fletcher, Michael S. Noble, Lauren A. Byers, Rehan Akbani, Jean Claude Zenklusen, Ina Felau, Jay Bowen, Kristen Leraas, Tara Lichtenberg, Jenette Creaney, Anne S. Tsao, Raphael Bueno, Hedy Kindler, Harvey Pass, Valerie W. Rusch, Henrique C. Silveira, Aliya N. Husain, Junya Fujimoto, Françoise Galateau-Sallé, Lucian R. Chirieac, Sanja Dacic, William D. Travis, Achim A. Jungbluth, Patrice Desmeules, David T. Severson, Havish Kantheti, Lisa Iype, Vesteinn Thorsson, David L. Gibbs, Lixia Diao, Carl M. Gay, Manaswi Gupta, Kiley Graim, Jumpei Takeshita, Yoshitaka Sekido, Hatice U. Osmanbeyoglu, Rupa Kanchi, Reanne Bowlby, Ewan A. Gibb, Esther Drill, Patrick Tarpey, David Heiman, Juliann Shih, Francisco Sanchez-Vega, and Julija Hmeljak
Abstract: Malignant pleural mesothelioma (MPM) is a highly lethal cancer of the lining of the chest cavity. To expand our understanding of MPM, we conducted a comprehensive integrated genomic study, including the most detailed analysis of BAP1 alterations to date. We identified histology-independent molecular prognostic subsets, and defined a novel genomic subtype with TP53 and SETDB1 mutations and extensive loss of heterozygosity. We also report strong expression of the immune-checkpoint gene VISTA in epithelioid MPM, strikingly higher than in other solid cancers, with implications for the immune response to MPM and for its immunotherapy. Our findings highlight new avenues for further investigation of MPM biology and novel therapeutic options.Significance:Through a comprehensive integrated genomic study of 74 MPMs, we provide a deeper understanding of histology-independent determinants of aggressive behavior, define a novel genomic subtype with TP53 and SETDB1 mutations and extensive loss of heterozygosity, and discovered strong expression of the immune-checkpoint gene VISTA in epithelioid MPM.See related commentary by Aggarwal and Albelda, p. 1508.This article is highlighted in the In This Issue feature, p. 1494
Published: 2023
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21. Data from Activation of the PD-1 Pathway Contributes to Immune Escape in EGFR-Driven Lung Tumors

Author: Kwok-Kin Wong, Glenn Dranoff, Peter S. Hammerman, Gordon J. Freeman, Scott J. Rodig, Lynette M. Sholl, Takeshi Shimamura, Geoffrey I. Shapiro, D. Neil Hayes, Matthew Meyerson, Pasi A. Janne, Travis J. Cohoon, Margaret Soucheray, Jacob B. Reibel, Mohit Butaney, Peter E. Fecci, Matthew D. Wilkerson, Trevor J. Pugh, Ellen M. Beauchamp, Andrew D. Cherniack, Oliver R. Mikse, Camilla L. Christensen, Jeremy H. Tchaicha, Abigail Altabef, Julian Carretero, Shohei Koyama, and Esra A. Akbay
Abstract: The success in lung cancer therapy with programmed death (PD)-1 blockade suggests that immune escape mechanisms contribute to lung tumor pathogenesis. We identified a correlation between EGF receptor (EGFR) pathway activation and a signature of immunosuppression manifested by upregulation of PD-1, PD-L1, CTL antigen-4 (CTLA-4), and multiple tumor-promoting inflammatory cytokines. We observed decreased CTLs and increased markers of T-cell exhaustion in mouse models of EGFR-driven lung cancer. PD-1 antibody blockade improved the survival of mice with EGFR-driven adenocarcinomas by enhancing effector T-cell function and lowering the levels of tumor-promoting cytokines. Expression of mutant EGFR in bronchial epithelial cells induced PD-L1, and PD-L1 expression was reduced by EGFR inhibitors in non–small cell lung cancer cell lines with activated EGFR. These data suggest that oncogenic EGFR signaling remodels the tumor microenvironment to trigger immune escape and mechanistically link treatment response to PD-1 inhibition.Significance: We show that autochthonous EGFR-driven lung tumors inhibit antitumor immunity by activating the PD-1/PD-L1 pathway to suppress T-cell function and increase levels of proinflammatory cytokines. These findings indicate that EGFR functions as an oncogene through non–cell-autonomous mechanisms and raise the possibility that other oncogenes may drive immune escape. Cancer Discov; 3(12); 1355–63. ©2013 AACR.See related commentary by Rech and Vonderheide, p. 1330This article is highlighted in the In This Issue feature, p. 1317
Published: 2023
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22. Table S3 from Integrative Molecular Characterization of Malignant Pleural Mesothelioma

Author: Erik Zmuda, Hongxin Zhang, Hailei Zhang, Jiashan Zhang, Jean C. Zenklusen, Marjorie G. Zauderer, Liming Yang, Shogo Yamamoto, Ye Wu, Tina Wong, Ignacio Wistuba, Lisa Wise, Matthew D. Wilkerson, Daniel J. Weisenberger, John N. Weinstein, Joellen Weaver, Jing Wang, Zhining Wang, Yunhu Wan, Douglas Voet, Luciano S. Viana, Umadevi Veluvolu, Nico van Zandwijk, David J. Van Den Berg, Federico Valdivieso, Tohru Tsujimura, Kane Tse, Anne Tsao, Eric Thompson, Nina Thiessen, Barry S Taylor, Kenji Tatsuno, Roy Tarnuzzer, Donghui Tan, Angela Tam, Qiang Sun, Josh Stuart, Chip Stewart, Paul Spellman, Matthew G. Soloway, Heidi J. Sofia, Tara Skelly, Payal Sipahimalani, Janae V. Simons, Henrique C. S. Silveira, Ilya Shmulevich, Yuichi Shiraishi, Yan Shi, Robert Sheridan, Troy Shelton, Candace Shelton, David T Severson, Tanguy Seiwert, Steven E. Schumacher, Nikolaus Schultz, Jacqueline E. Schein, Cristovam Scapulatempo-Neto, Ayuko Sato, Chris Sander, Gordon Saksena, Sara Sadeghi, Valerie Rusch, Jeffrey Roach, Robert C. Rintoul, William G Richards, David Rice, Sheila M. Reynolds, Rui M. Reis, Glen Reid, Gloria Ravegnini, Doris M. Rassl, Nilsa C. Ramirez, Todd Pihl, Charles M. Perou, Robert Penny, Nathan A. Pennell, Arjun Pennathur, Joseph Paulauskis, Harvey I. Pass, Joel S. Parker, Hatice Osmanbeyoglu, Angelica Ochoa, Yulia Newton, Rashi Naresh, Takashi Nakano, Karen Mungall, Andrew J. Mungall, Lisle E. Mose, Scott Morris, Cesar Moran, Richard A. Moore, Gordon B. Mills, Piotr A. Mieczkowski, Matthew Meyerson, Shaowu Meng, Jonathan Melamed, Sam Meier, Michael Mayo, Marco A. Marra, David Mallory, Dennis T. Maglinte, Yussanne Ma, James Luketich, Yiling Lu, Adhemar Longatto-Filho, Laxmi Lolla, Eric Minwei Liu, Wenbin Liu, Jia Liu, Pei Lin, Tara M. Lichtenberg, Kristen M. Leraas, Darlene Lee, Michael S. Lawrence, Peter W. Laird, Phillip H. Lai, David J. Kwiatkowski, Kozo Kuribayashi, Ritika Kundra, Thomas Krausz, Nobuyuki Kondo, Jaegil Kim, Katayoon Kasaian, Rupa S. Kanchi, Corbin D. Jones, Steven J.M. Jones, Stuart R. Jefferys, Carolyn M. Hutter, Aliya Husain, Alan P. Hoyle, Robert A. Holt, Katherine A. Hoadley, Zachary Heins, David I. Heiman, D. Neil Hayes, David Haussler, Seiki Hasegawa, Guangwu Guo, Benjamin Gross, Chandra Goparaju, Gad Getz, Mark Gerken, Nils Gehlenborg, Julie M. Gastier-Foster, Johanna Gardner, Jianjiong Gao, Françoise Galateau Sallé, Stacey B. Gabriel, Shiro Fukuda, Martin L. Ferguson, Michael Feldman, Rajiv Dhir, Noreen Dhalla, John A. Demchok, Timothy DeFreitas, Assunta De Rienzo, Ludmila Danilova, Erin Curley, Daniel Crain, Leslie Cope, Carrie Cibulskis, Sudha Chudamani, Eric Chuah, Juok Cho, Lucian Chirieac, Dorothy Cheung, Andrew D. Cherniack, Andre L. Carvalho, Rebecca Carlsen, Flávio M. Cárcano, Lauren Averett Byers, Denise Brooks, Moiz S. Bootwalla, Tom Bodenheimer, Craig Bielski, Rameen Beroukhim, Carmen Behrens, Michael Becich, Stephen B. Baylin, Saianand Balu, Miruna Balasundaram, J. Todd Auman, Joshua Armenia, Pavana Anur, Adrian Ally, Marc Ladanyi, Peter Campbell, Bruce W. Robinson, Hiroyuki Aburatani, Ronglai Shen, A. Gordon Robertson, Jonathan A. Fletcher, Michael S. Noble, Lauren A. Byers, Rehan Akbani, Jean Claude Zenklusen, Ina Felau, Jay Bowen, Kristen Leraas, Tara Lichtenberg, Jenette Creaney, Anne S. Tsao, Raphael Bueno, Hedy Kindler, Harvey Pass, Valerie W. Rusch, Henrique C. Silveira, Aliya N. Husain, Junya Fujimoto, Françoise Galateau-Sallé, Lucian R. Chirieac, Sanja Dacic, William D. Travis, Achim A. Jungbluth, Patrice Desmeules, David T. Severson, Havish Kantheti, Lisa Iype, Vesteinn Thorsson, David L. Gibbs, Lixia Diao, Carl M. Gay, Manaswi Gupta, Kiley Graim, Jumpei Takeshita, Yoshitaka Sekido, Hatice U. Osmanbeyoglu, Rupa Kanchi, Reanne Bowlby, Ewan A. Gibb, Esther Drill, Patrick Tarpey, David Heiman, Juliann Shih, Francisco Sanchez-Vega, and Julija Hmeljak
Abstract: Table S3 contains the karyotypes of 16 genome-wide LOH MPM cases from the BWH cohort.
Published: 2023
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23. Supplementary Figures from Activation of the PD-1 Pathway Contributes to Immune Escape in EGFR-Driven Lung Tumors

Author: Kwok-Kin Wong, Glenn Dranoff, Peter S. Hammerman, Gordon J. Freeman, Scott J. Rodig, Lynette M. Sholl, Takeshi Shimamura, Geoffrey I. Shapiro, D. Neil Hayes, Matthew Meyerson, Pasi A. Janne, Travis J. Cohoon, Margaret Soucheray, Jacob B. Reibel, Mohit Butaney, Peter E. Fecci, Matthew D. Wilkerson, Trevor J. Pugh, Ellen M. Beauchamp, Andrew D. Cherniack, Oliver R. Mikse, Camilla L. Christensen, Jeremy H. Tchaicha, Abigail Altabef, Julian Carretero, Shohei Koyama, and Esra A. Akbay
Abstract: PDF file 2020K, Supplementary figures 1-11. For the mouse experiments tumor bearing lungs were classified as mildly sick and severely sick based on the tumor burden as determined by right lung lobe weights. Oncogene induced immunosuppressive environment manifested as compromised T cell function, elevation in the levels of tumor promoting cytokines, and changes in lung hematopoietic population was observed in the mildy sick mice in addition to the severely sick EGFR mutant mice. Anti PD-1 antibody treatment did not show efficacy in the Kras driven tumors despite the expression of the PD-1 ligand
Published: 2023
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24. Supplementary Methods from Activation of the PD-1 Pathway Contributes to Immune Escape in EGFR-Driven Lung Tumors

Author: Kwok-Kin Wong, Glenn Dranoff, Peter S. Hammerman, Gordon J. Freeman, Scott J. Rodig, Lynette M. Sholl, Takeshi Shimamura, Geoffrey I. Shapiro, D. Neil Hayes, Matthew Meyerson, Pasi A. Janne, Travis J. Cohoon, Margaret Soucheray, Jacob B. Reibel, Mohit Butaney, Peter E. Fecci, Matthew D. Wilkerson, Trevor J. Pugh, Ellen M. Beauchamp, Andrew D. Cherniack, Oliver R. Mikse, Camilla L. Christensen, Jeremy H. Tchaicha, Abigail Altabef, Julian Carretero, Shohei Koyama, and Esra A. Akbay
Abstract: PDF file 306K, MRI tumor volume quantification, lists for all the antibodies used in the experiments, gating method for Flow cytometry analysis, and supplementary references
Published: 2023
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25. Supplementary Figure Legends from Activation of the PD-1 Pathway Contributes to Immune Escape in EGFR-Driven Lung Tumors

Author: Kwok-Kin Wong, Glenn Dranoff, Peter S. Hammerman, Gordon J. Freeman, Scott J. Rodig, Lynette M. Sholl, Takeshi Shimamura, Geoffrey I. Shapiro, D. Neil Hayes, Matthew Meyerson, Pasi A. Janne, Travis J. Cohoon, Margaret Soucheray, Jacob B. Reibel, Mohit Butaney, Peter E. Fecci, Matthew D. Wilkerson, Trevor J. Pugh, Ellen M. Beauchamp, Andrew D. Cherniack, Oliver R. Mikse, Camilla L. Christensen, Jeremy H. Tchaicha, Abigail Altabef, Julian Carretero, Shohei Koyama, and Esra A. Akbay
Abstract: PDF file 92K, Legends to supplementary figures 1-11
Published: 2023
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26. Supplementary Data from Integrative Molecular Characterization of Malignant Pleural Mesothelioma

Author: Erik Zmuda, Hongxin Zhang, Hailei Zhang, Jiashan Zhang, Jean C. Zenklusen, Marjorie G. Zauderer, Liming Yang, Shogo Yamamoto, Ye Wu, Tina Wong, Ignacio Wistuba, Lisa Wise, Matthew D. Wilkerson, Daniel J. Weisenberger, John N. Weinstein, Joellen Weaver, Jing Wang, Zhining Wang, Yunhu Wan, Douglas Voet, Luciano S. Viana, Umadevi Veluvolu, Nico van Zandwijk, David J. Van Den Berg, Federico Valdivieso, Tohru Tsujimura, Kane Tse, Anne Tsao, Eric Thompson, Nina Thiessen, Barry S Taylor, Kenji Tatsuno, Roy Tarnuzzer, Donghui Tan, Angela Tam, Qiang Sun, Josh Stuart, Chip Stewart, Paul Spellman, Matthew G. Soloway, Heidi J. Sofia, Tara Skelly, Payal Sipahimalani, Janae V. Simons, Henrique C. S. Silveira, Ilya Shmulevich, Yuichi Shiraishi, Yan Shi, Robert Sheridan, Troy Shelton, Candace Shelton, David T Severson, Tanguy Seiwert, Steven E. Schumacher, Nikolaus Schultz, Jacqueline E. Schein, Cristovam Scapulatempo-Neto, Ayuko Sato, Chris Sander, Gordon Saksena, Sara Sadeghi, Valerie Rusch, Jeffrey Roach, Robert C. Rintoul, William G Richards, David Rice, Sheila M. Reynolds, Rui M. Reis, Glen Reid, Gloria Ravegnini, Doris M. Rassl, Nilsa C. Ramirez, Todd Pihl, Charles M. Perou, Robert Penny, Nathan A. Pennell, Arjun Pennathur, Joseph Paulauskis, Harvey I. Pass, Joel S. Parker, Hatice Osmanbeyoglu, Angelica Ochoa, Yulia Newton, Rashi Naresh, Takashi Nakano, Karen Mungall, Andrew J. Mungall, Lisle E. Mose, Scott Morris, Cesar Moran, Richard A. Moore, Gordon B. Mills, Piotr A. Mieczkowski, Matthew Meyerson, Shaowu Meng, Jonathan Melamed, Sam Meier, Michael Mayo, Marco A. Marra, David Mallory, Dennis T. Maglinte, Yussanne Ma, James Luketich, Yiling Lu, Adhemar Longatto-Filho, Laxmi Lolla, Eric Minwei Liu, Wenbin Liu, Jia Liu, Pei Lin, Tara M. Lichtenberg, Kristen M. Leraas, Darlene Lee, Michael S. Lawrence, Peter W. Laird, Phillip H. Lai, David J. Kwiatkowski, Kozo Kuribayashi, Ritika Kundra, Thomas Krausz, Nobuyuki Kondo, Jaegil Kim, Katayoon Kasaian, Rupa S. Kanchi, Corbin D. Jones, Steven J.M. Jones, Stuart R. Jefferys, Carolyn M. Hutter, Aliya Husain, Alan P. Hoyle, Robert A. Holt, Katherine A. Hoadley, Zachary Heins, David I. Heiman, D. Neil Hayes, David Haussler, Seiki Hasegawa, Guangwu Guo, Benjamin Gross, Chandra Goparaju, Gad Getz, Mark Gerken, Nils Gehlenborg, Julie M. Gastier-Foster, Johanna Gardner, Jianjiong Gao, Françoise Galateau Sallé, Stacey B. Gabriel, Shiro Fukuda, Martin L. Ferguson, Michael Feldman, Rajiv Dhir, Noreen Dhalla, John A. Demchok, Timothy DeFreitas, Assunta De Rienzo, Ludmila Danilova, Erin Curley, Daniel Crain, Leslie Cope, Carrie Cibulskis, Sudha Chudamani, Eric Chuah, Juok Cho, Lucian Chirieac, Dorothy Cheung, Andrew D. Cherniack, Andre L. Carvalho, Rebecca Carlsen, Flávio M. Cárcano, Lauren Averett Byers, Denise Brooks, Moiz S. Bootwalla, Tom Bodenheimer, Craig Bielski, Rameen Beroukhim, Carmen Behrens, Michael Becich, Stephen B. Baylin, Saianand Balu, Miruna Balasundaram, J. Todd Auman, Joshua Armenia, Pavana Anur, Adrian Ally, Marc Ladanyi, Peter Campbell, Bruce W. Robinson, Hiroyuki Aburatani, Ronglai Shen, A. Gordon Robertson, Jonathan A. Fletcher, Michael S. Noble, Lauren A. Byers, Rehan Akbani, Jean Claude Zenklusen, Ina Felau, Jay Bowen, Kristen Leraas, Tara Lichtenberg, Jenette Creaney, Anne S. Tsao, Raphael Bueno, Hedy Kindler, Harvey Pass, Valerie W. Rusch, Henrique C. Silveira, Aliya N. Husain, Junya Fujimoto, Françoise Galateau-Sallé, Lucian R. Chirieac, Sanja Dacic, William D. Travis, Achim A. Jungbluth, Patrice Desmeules, David T. Severson, Havish Kantheti, Lisa Iype, Vesteinn Thorsson, David L. Gibbs, Lixia Diao, Carl M. Gay, Manaswi Gupta, Kiley Graim, Jumpei Takeshita, Yoshitaka Sekido, Hatice U. Osmanbeyoglu, Rupa Kanchi, Reanne Bowlby, Ewan A. Gibb, Esther Drill, Patrick Tarpey, David Heiman, Juliann Shih, Francisco Sanchez-Vega, and Julija Hmeljak
Abstract: Supplementary materials and methods, as well as supplementary figures S1-S7.
Published: 2023
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27. Supplementary Table 1 from Activation of the PD-1 Pathway Contributes to Immune Escape in EGFR-Driven Lung Tumors

Author: Kwok-Kin Wong, Glenn Dranoff, Peter S. Hammerman, Gordon J. Freeman, Scott J. Rodig, Lynette M. Sholl, Takeshi Shimamura, Geoffrey I. Shapiro, D. Neil Hayes, Matthew Meyerson, Pasi A. Janne, Travis J. Cohoon, Margaret Soucheray, Jacob B. Reibel, Mohit Butaney, Peter E. Fecci, Matthew D. Wilkerson, Trevor J. Pugh, Ellen M. Beauchamp, Andrew D. Cherniack, Oliver R. Mikse, Camilla L. Christensen, Jeremy H. Tchaicha, Abigail Altabef, Julian Carretero, Shohei Koyama, and Esra A. Akbay
Abstract: PDF file 57K, Supplementary table and legend. Evaluation of the PD-L1 expression in tumor samples carrying EGFR mutations
Published: 2023
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28. Supplementary Figures from Integrative Analysis of miRNAs Identifies Clinically Relevant Epithelial and Stromal Subtypes of Head and Neck Squamous Cell Carcinoma

Author: Yoon Ho Ko, David Neil Hayes, Heejoon Jo, Xiaobei Zhao, Hyo Young Choi, Matthew D. Wilkerson, David Marron, Xiaoying Yin, Vonn Walter, and Jeremiah Holt
Abstract: Supplementary Figures and Legends
Published: 2023
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29. Supplementary Table S7 from Integrative Analysis of miRNAs Identifies Clinically Relevant Epithelial and Stromal Subtypes of Head and Neck Squamous Cell Carcinoma

Author: Yoon Ho Ko, David Neil Hayes, Heejoon Jo, Xiaobei Zhao, Hyo Young Choi, Matthew D. Wilkerson, David Marron, Xiaoying Yin, Vonn Walter, and Jeremiah Holt
Abstract: REporting recommendations for tumour MARKer prognostic studies (REMARK) checklist.
Published: 2023
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30. Supplementary Data from Lung Squamous Cell Carcinoma mRNA Expression Subtypes Are Reproducible, Clinically Important, and Correspond to Normal Cell Types

Author: D. Neil Hayes, Charles M. Perou, Philip S. Bernard, Leigh Thorne, Patrick J. Roberts, Carrie B. Lee, William K. Funkhouser, Alden M. Parsons, Mark A. Socinski, Scott H. Randell, C. Ryan Miller, Kenneth Muldrew, Christopher R. Cabanski, Michele C. Hayward, Yufeng Liu, Katherine A. Hoadley, Xiaoying Yin, and Matthew D. Wilkerson
Abstract: Supplementary Figures S1-S8, Supplementary Materials and Methods, and Supplementary Tables S1-S2.
Published: 2023
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31. Supplementary Figure 1 from High XRCC1 Protein Expression Is Associated with Poorer Survival in Patients with Head and Neck Squamous Cell Carcinoma

Author: D. Neil Hayes, Liza Makowski, Carol G. Shores, Andrew F. Olshan, William K. Funkhouser, Michele C. Hayward, Leigh B. Thorne, C. Ryan Miller, Stephen L. Harris, Bhishamjit S. Chera, Trevor Hackman, Adam M. Zanation, Marion E. Couch, William W. Shockley, Mark C. Weissler, Vonn Walter, Matthew D. Wilkerson, Alex J. Freemerman, Yufeng Liu, Ni Zhao, Karen Fritchie, Sneha Sundaram, Xiao-Ying Yin, Mihir R. Patel, and Mei-Kim Ang
Abstract: PDF file - 157KB
Published: 2023
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32. Supplementary Figure Legend from High XRCC1 Protein Expression Is Associated with Poorer Survival in Patients with Head and Neck Squamous Cell Carcinoma

Author: D. Neil Hayes, Liza Makowski, Carol G. Shores, Andrew F. Olshan, William K. Funkhouser, Michele C. Hayward, Leigh B. Thorne, C. Ryan Miller, Stephen L. Harris, Bhishamjit S. Chera, Trevor Hackman, Adam M. Zanation, Marion E. Couch, William W. Shockley, Mark C. Weissler, Vonn Walter, Matthew D. Wilkerson, Alex J. Freemerman, Yufeng Liu, Ni Zhao, Karen Fritchie, Sneha Sundaram, Xiao-Ying Yin, Mihir R. Patel, and Mei-Kim Ang
Abstract: PDF file - 73KB
Published: 2023
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33. Supplementary Table 1 from High XRCC1 Protein Expression Is Associated with Poorer Survival in Patients with Head and Neck Squamous Cell Carcinoma

Author: D. Neil Hayes, Liza Makowski, Carol G. Shores, Andrew F. Olshan, William K. Funkhouser, Michele C. Hayward, Leigh B. Thorne, C. Ryan Miller, Stephen L. Harris, Bhishamjit S. Chera, Trevor Hackman, Adam M. Zanation, Marion E. Couch, William W. Shockley, Mark C. Weissler, Vonn Walter, Matthew D. Wilkerson, Alex J. Freemerman, Yufeng Liu, Ni Zhao, Karen Fritchie, Sneha Sundaram, Xiao-Ying Yin, Mihir R. Patel, and Mei-Kim Ang
Abstract: PDF file - 68KB
Published: 2023
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34. Data from Lung Squamous Cell Carcinoma mRNA Expression Subtypes Are Reproducible, Clinically Important, and Correspond to Normal Cell Types

Author: D. Neil Hayes, Charles M. Perou, Philip S. Bernard, Leigh Thorne, Patrick J. Roberts, Carrie B. Lee, William K. Funkhouser, Alden M. Parsons, Mark A. Socinski, Scott H. Randell, C. Ryan Miller, Kenneth Muldrew, Christopher R. Cabanski, Michele C. Hayward, Yufeng Liu, Katherine A. Hoadley, Xiaoying Yin, and Matthew D. Wilkerson
Abstract: Purpose: Lung squamous cell carcinoma (SCC) is clinically and genetically heterogeneous, and current diagnostic practices do not adequately substratify this heterogeneity. A robust, biologically based SCC subclassification may describe this variability and lead to more precise patient prognosis and management. We sought to determine if SCC mRNA expression subtypes exist, are reproducible across multiple patient cohorts, and are clinically relevant.Experimental Design: Subtypes were detected by unsupervised consensus clustering in five published discovery cohorts of mRNA microarrays, totaling 382 SCC patients. An independent validation cohort of 56 SCC patients was collected and assayed by microarrays. A nearest-centroid subtype predictor was built using discovery cohorts. Validation cohort subtypes were predicted and evaluated for confirmation. Subtype survival outcome, clinical covariates, and biological processes were compared by statistical and bioinformatic methods.Results: Four lung SCC mRNA expression subtypes, named primitive, classical, secretory, and basal, were detected and independently validated (P < 0.001). The primitive subtype had the worst survival outcome (P < 0.05) and is an independent predictor of survival (P < 0.05). Tumor differentiation and patient sex were associated with subtype. The expression profiles of the subtypes contained distinct biological processes (primitive: proliferation; classical: xenobiotic metabolism; secretory: immune response; basal: cell adhesion) and suggested distinct pharmacologic interventions. Comparison with lung model systems revealed distinct subtype to cell type correspondence.Conclusions: Lung SCC consists of four mRNA expression subtypes that have different survival outcomes, patient populations, and biological processes. The subtypes stratify patients for more precise prognosis and targeted research. Clin Cancer Res; 16(19); 4864–75. ©2010 AACR.
Published: 2023
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35. Data from Integrative Analysis of miRNAs Identifies Clinically Relevant Epithelial and Stromal Subtypes of Head and Neck Squamous Cell Carcinoma

Author: Yoon Ho Ko, David Neil Hayes, Heejoon Jo, Xiaobei Zhao, Hyo Young Choi, Matthew D. Wilkerson, David Marron, Xiaoying Yin, Vonn Walter, and Jeremiah Holt
Abstract: Purpose:The objective of this study is to characterize the role of miRNAs in the classification of head and neck squamous cell carcinoma (HNSCC).Experimental Design:Here, we analyzed 562 HNSCC samples, 88 from a novel cohort and 474 from The Cancer Genome Atlas, using miRNA microarray and miRNA sequencing, respectively. Using an integrative correlations method followed by miRNA expression–based hierarchical clustering, we validated miRNA clusters across cohorts. Evaluation of clusters by logistic regression and gene ontology approaches revealed subtype-based clinical and biological characteristics.Results:We identified two independently validated and statistically significant (P < 0.01) tumor subtypes and named them “epithelial” and “stromal” based on associations with functional target gene ontology relating to differing stages of epithelial cell differentiation. miRNA-based subtypes were correlated with individual gene expression targets based on miRNA seed sequences, as well as with miRNA families and clusters including the miR-17 and miR-200 families. These correlated genes defined pathways relevant to normal squamous cell function and pathophysiology. miRNA clusters statistically associated with differential mutation patterns including higher proportions of TP53 mutations in the stromal class and higher NSD1 and HRAS mutation frequencies in the epithelial class. miRNA classes correlated with previously reported gene expression subtypes, clinical characteristics, and clinical outcomes in a multivariate Cox proportional hazards model with stromal patients demonstrating worse prognoses (HR, 1.5646; P = 0.006).Conclusions:We report a reproducible classification of HNSCC based on miRNA that associates with known pathologically altered pathways and mutations of squamous tumors and is clinically relevant.
Published: 2023
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36. Data from High XRCC1 Protein Expression Is Associated with Poorer Survival in Patients with Head and Neck Squamous Cell Carcinoma

Author: D. Neil Hayes, Liza Makowski, Carol G. Shores, Andrew F. Olshan, William K. Funkhouser, Michele C. Hayward, Leigh B. Thorne, C. Ryan Miller, Stephen L. Harris, Bhishamjit S. Chera, Trevor Hackman, Adam M. Zanation, Marion E. Couch, William W. Shockley, Mark C. Weissler, Vonn Walter, Matthew D. Wilkerson, Alex J. Freemerman, Yufeng Liu, Ni Zhao, Karen Fritchie, Sneha Sundaram, Xiao-Ying Yin, Mihir R. Patel, and Mei-Kim Ang
Abstract: Purpose: We evaluated X-ray repair complementing defective repair in Chinese hamster cells 1 (XRCC1) protein in head and neck squamous cell carcinoma (HNSCC) patients in association with outcome.Experimental Design: XRCC1 protein expression was assessed by immunohistochemical (IHC) staining of pretreatment tissue samples in 138 consecutive HNSCC patients treated with surgery (n = 31), radiation (15), surgery and radiation (23), surgery and adjuvant chemoradiation (17), primary chemoradiation (51), and palliative measures (1).Results: Patients with high XRCC1 expression by IHC (n = 77) compared with patients with low XRCC1 expression (n = 60) had poorer median overall survival (OS; 41.0 months vs. OS not reached, P = 0.009) and poorer progression-free survival (28.0 months vs. 73.0 months, P = 0.031). This association was primarily due to patients who received chemoradiation (median OS of high- and low-XRCC1 expression patients, 35.5 months and not reached respectively, HR 3.48; 95% CI: 1.44–8.38; P = 0.006). In patients treated with nonchemoradiation modalities, there was no survival difference by XRCC1 expression. In multivariable analysis, high XRCC1 expression and p16INK4a-positive status were independently associated with survival in the overall study population (HR = 2.62; 95% CI: 1.52–4.52; P < 0.001 and HR = 0.21; 95% CI: 0.06–0.71; P = 0.012, respectively) and among chemoradiation patients (HR = 6.02; 95% CI: 2.36–15.37; P < 0.001 and HR = 0.26; 95% CI: 0.08–0.92, respectively; P = 0.037).Conclusions: In HNSCC, high XRCC1 protein expression is associated with poorer survival, particularly in patients receiving chemoradiation. Future validation of these findings may enable identification of HNSCC expressing patients who benefit from chemoradiation treatment. Clin Cancer Res; 17(20); 6542–52. ©2011 AACR.
Published: 2023
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37. Supplementary Figure 2 from BRG1/SMARCA4 Inactivation Promotes Non–Small Cell Lung Cancer Aggressiveness by Altering Chromatin Organization

Author: Bernard Weissman, Ian J. Davis, D. Neil Hayes, Michael B. Major, Nisarg Desai, Matthew D. Wilkerson, Joel Parker, Jeremy Simon, Shujie Song, Vonn Walter, Austin Hepperla, and Tess Orvis
Abstract: Supplementary Figure 2. This figure shows additional characterization of global nucleosomal positioning changes in Brg1 KD cell lines.
Published: 2023
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38. Supplementary Table 2 from BRG1/SMARCA4 Inactivation Promotes Non–Small Cell Lung Cancer Aggressiveness by Altering Chromatin Organization

Author: Bernard Weissman, Ian J. Davis, D. Neil Hayes, Michael B. Major, Nisarg Desai, Matthew D. Wilkerson, Joel Parker, Jeremy Simon, Shujie Song, Vonn Walter, Austin Hepperla, and Tess Orvis
Abstract: Supplementary Table 2. Differentially expressed genes were identified between BRG1 mutant and BRG1 wild-type NSCLC cell lines, as described in Materials and Methods. Using an FDR threshold of .025, a total of 135 genes were down-regulated in the BRG1 mutant cell lines.
Published: 2023
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39. Data from Inhibitor-Sensitive FGFR2 and FGFR3 Mutations in Lung Squamous Cell Carcinoma

Author: Peter S. Hammerman, Matthew Meyerson, Robert I. Haddad, Kwok-Kin Wong, Gad Getz, Nathanael S. Gray, D. Neil Hayes, Chandra Sekhar Pedamallu, Trevor J. Pugh, Qingsong Liu, Ellen M. Beauchamp, Andrey Sivachenko, Matthew D. Wilkerson, Jeremy Tchaicha, Joonil Jung, and Rachel G. Liao
Abstract: A comprehensive description of genomic alterations in lung squamous cell carcinoma (lung SCC) has recently been reported, enabling the identification of genomic events that contribute to the oncogenesis of this disease. In lung SCC, one of the most frequently altered receptor tyrosine kinase families is the fibroblast growth factor receptor (FGFR) family, with amplification or mutation observed in all four family members. Here, we describe the oncogenic nature of mutations observed in FGFR2 and FGFR3, each of which are observed in 3% of samples, for a mutation rate of 6% across both genes. Using cell culture and xenograft models, we show that several of these mutations drive cellular transformation. Transformation can be reversed by small-molecule FGFR inhibitors currently being developed for clinical use. We also show that mutations in the extracellular domains of FGFR2 lead to constitutive FGFR dimerization. In addition, we report a patient with an FGFR2-mutated oral SCC who responded to the multitargeted tyrosine kinase inhibitor pazopanib. These findings provide new insights into driving oncogenic events in a subset of lung squamous cancers, and recommend future clinical studies with FGFR inhibitors in patients with lung and head and neck SCC. Cancer Res; 73(16); 5195–205. ©2013 AACR.
Published: 2023
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40. Supplementary Figure 5 from Inhibitor-Sensitive FGFR2 and FGFR3 Mutations in Lung Squamous Cell Carcinoma

Author: Peter S. Hammerman, Matthew Meyerson, Robert I. Haddad, Kwok-Kin Wong, Gad Getz, Nathanael S. Gray, D. Neil Hayes, Chandra Sekhar Pedamallu, Trevor J. Pugh, Qingsong Liu, Ellen M. Beauchamp, Andrey Sivachenko, Matthew D. Wilkerson, Jeremy Tchaicha, Joonil Jung, and Rachel G. Liao
Abstract: PDF file - 159K, Ba/F3 data with six additional inhibitors.
Published: 2023
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41. Supplementary Figure 3 from Inhibitor-Sensitive FGFR2 and FGFR3 Mutations in Lung Squamous Cell Carcinoma

Author: Peter S. Hammerman, Matthew Meyerson, Robert I. Haddad, Kwok-Kin Wong, Gad Getz, Nathanael S. Gray, D. Neil Hayes, Chandra Sekhar Pedamallu, Trevor J. Pugh, Qingsong Liu, Ellen M. Beauchamp, Andrey Sivachenko, Matthew D. Wilkerson, Jeremy Tchaicha, Joonil Jung, and Rachel G. Liao
Abstract: PDF file - 203K, Extracellular domain dimerization studies.
Published: 2023
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42. Supplementary Table 2 from Inhibitor-Sensitive FGFR2 and FGFR3 Mutations in Lung Squamous Cell Carcinoma

Author: Peter S. Hammerman, Matthew Meyerson, Robert I. Haddad, Kwok-Kin Wong, Gad Getz, Nathanael S. Gray, D. Neil Hayes, Chandra Sekhar Pedamallu, Trevor J. Pugh, Qingsong Liu, Ellen M. Beauchamp, Andrey Sivachenko, Matthew D. Wilkerson, Jeremy Tchaicha, Joonil Jung, and Rachel G. Liao
Abstract: PDF file - 74K, FGFR inhibitors profiled in this study.
Published: 2023
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43. Supplementary Table 1 from Inhibitor-Sensitive FGFR2 and FGFR3 Mutations in Lung Squamous Cell Carcinoma

Author: Peter S. Hammerman, Matthew Meyerson, Robert I. Haddad, Kwok-Kin Wong, Gad Getz, Nathanael S. Gray, D. Neil Hayes, Chandra Sekhar Pedamallu, Trevor J. Pugh, Qingsong Liu, Ellen M. Beauchamp, Andrey Sivachenko, Matthew D. Wilkerson, Jeremy Tchaicha, Joonil Jung, and Rachel G. Liao
Abstract: PDF file - 80K, Patient details in lung SqCC patients containing FGFR mutations.
Published: 2023
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44. Supplementary Figure 6 from Inhibitor-Sensitive FGFR2 and FGFR3 Mutations in Lung Squamous Cell Carcinoma

Author: Peter S. Hammerman, Matthew Meyerson, Robert I. Haddad, Kwok-Kin Wong, Gad Getz, Nathanael S. Gray, D. Neil Hayes, Chandra Sekhar Pedamallu, Trevor J. Pugh, Qingsong Liu, Ellen M. Beauchamp, Andrey Sivachenko, Matthew D. Wilkerson, Jeremy Tchaicha, Joonil Jung, and Rachel G. Liao
Abstract: PDF file - 147K, FGFR2-P253R functional data.
Published: 2023
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45. Supplementary Figure 3 from BRG1/SMARCA4 Inactivation Promotes Non–Small Cell Lung Cancer Aggressiveness by Altering Chromatin Organization

Author: Bernard Weissman, Ian J. Davis, D. Neil Hayes, Michael B. Major, Nisarg Desai, Matthew D. Wilkerson, Joel Parker, Jeremy Simon, Shujie Song, Vonn Walter, Austin Hepperla, and Tess Orvis
Abstract: Supplementary Figure 3. This figure shows additional characterization of nucleosome positioning positions changes around transcription start sites in Brg1 KD cell lines.
Published: 2023
Full Text: View/download PDF

46. Supplementary Figure 1 from BRG1/SMARCA4 Inactivation Promotes Non–Small Cell Lung Cancer Aggressiveness by Altering Chromatin Organization

Author: Bernard Weissman, Ian J. Davis, D. Neil Hayes, Michael B. Major, Nisarg Desai, Matthew D. Wilkerson, Joel Parker, Jeremy Simon, Shujie Song, Vonn Walter, Austin Hepperla, and Tess Orvis
Abstract: Supplementary Figure 1. This figure shows validation of H358 and H441 Brg1 knockdown cell lines.
Published: 2023
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47. Supplementary Table and Figure Legends from BRG1/SMARCA4 Inactivation Promotes Non–Small Cell Lung Cancer Aggressiveness by Altering Chromatin Organization

Author: Bernard Weissman, Ian J. Davis, D. Neil Hayes, Michael B. Major, Nisarg Desai, Matthew D. Wilkerson, Joel Parker, Jeremy Simon, Shujie Song, Vonn Walter, Austin Hepperla, and Tess Orvis
Abstract: Supplementary Table and Figure Legends
Published: 2023
Full Text: View/download PDF

48. Supplementary Figure 4 from BRG1/SMARCA4 Inactivation Promotes Non–Small Cell Lung Cancer Aggressiveness by Altering Chromatin Organization

Author: Bernard Weissman, Ian J. Davis, D. Neil Hayes, Michael B. Major, Nisarg Desai, Matthew D. Wilkerson, Joel Parker, Jeremy Simon, Shujie Song, Vonn Walter, Austin Hepperla, and Tess Orvis
Abstract: Supplementary Figure 4. The figure shows kernal-smoothed data for nucleosome positioning about transcription start sites in the Brg1 KD human NSCLC cell line and in mouse SNF5 and Brg1 KO cells.
Published: 2023
Full Text: View/download PDF

49. Supplementary Figure 2 from Inhibitor-Sensitive FGFR2 and FGFR3 Mutations in Lung Squamous Cell Carcinoma

Author: Peter S. Hammerman, Matthew Meyerson, Robert I. Haddad, Kwok-Kin Wong, Gad Getz, Nathanael S. Gray, D. Neil Hayes, Chandra Sekhar Pedamallu, Trevor J. Pugh, Qingsong Liu, Ellen M. Beauchamp, Andrey Sivachenko, Matthew D. Wilkerson, Jeremy Tchaicha, Joonil Jung, and Rachel G. Liao
Abstract: PDF file - 55K, Xenograft tumor images not included in Figure 2.
Published: 2023
Full Text: View/download PDF

50. Supplementary Table 1 from BRG1/SMARCA4 Inactivation Promotes Non–Small Cell Lung Cancer Aggressiveness by Altering Chromatin Organization

Author: Bernard Weissman, Ian J. Davis, D. Neil Hayes, Michael B. Major, Nisarg Desai, Matthew D. Wilkerson, Joel Parker, Jeremy Simon, Shujie Song, Vonn Walter, Austin Hepperla, and Tess Orvis
Abstract: Supplementary Table 1. Differentially expressed genes were identified, as described in Material and Methods. Genes altered by BRG1 KD- Genes whose expression either increased or decreased in the H358 Brg1i.1 and H358 Brgi.2 cell lines; Upregulated and unregulated genes- We identified 316 genes that showed increased expression in both H358 Brg1i.1 and H358 Brg1i.2 cell lines. We also identified 300 genes that did not show altered expression in the Brg1i.2 cell line.
Published: 2023
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