Genomic Correlate of Exceptional Erlotinib Response in Head and Neck Squamous Cell Carcinoma.
Eliezer M. Van Allen,Eliezer M. Van Allen,Vivian Wai Yan Lui,Vivian Wai Yan Lui,Ann Marie Egloff,Eva M. Goetz,Hua Li,Jonas T. Johnson,Umamaheswar Duvvuri,Julie E. Bauman,Nicolas Stransky,Yan Zeng,Breean R. Gilbert,Kelsey P. Pendleton,Lin Wang,Simion I. Chiosea,Carrie Sougnez,Nikhil Wagle,Nikhil Wagle,Fan Zhang,Yu Du,David A Close,Paul A. Johnston,Aaron McKenna,Scott L. Carter,Todd R. Golub,Todd R. Golub,Gad Getz,Gad Getz,Gordon B. Mills,Levi A. Garraway,Levi A. Garraway,Jennifer R. Grandis +32 more
TLDR
Selective erlotinib use in HNSCC may be informed by precision oncology approaches and Hypotheses were formulated regarding enhanced erlot inib response in preclinical models harboring the patient tumor somatic variant MAPK1 E322K following the identification of tumor somatics variants.Abstract:
Importance Randomized clinical trials demonstrate no benefit for epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors in unselected patients with head and neck squamous cell carcinoma (HNSCC). However, a patient with stage IVA HNSCC received 13 days of neoadjuvant erlotinib and experienced a near-complete histologic response. Objective To determine a mechanism of exceptional response to erlotinib therapy in HNSCC. Design, Setting, and Participants Single patient with locally advanced HNSCC who received erlotinib monotherapy in a window-of-opportunity clinical trial (patients scheduled to undergo primary cancer surgery are treated briefly with an investigational agent). Whole-exome sequencing of pretreatment tumor and germline patient samples was performed at a quaternary care academic medical center, and a candidate somatic variant was experimentally investigated for mediating erlotinib response. Intervention A brief course of erlotinib monotherapy followed by surgical resection. Main Outcomes and Measures Identification of pretreatment tumor somatic alterations that may contribute to the exceptional response to erlotinib. Hypotheses were formulated regarding enhanced erlotinib response in preclinical models harboring the patient tumor somatic variant MAPK1 E322K following the identification of tumor somatic variants. Results No EGFR alterations were observed in the pretreatment tumor DNA. Paradoxically, the tumor harbored an activating MAPK1 E322K mutation (allelic fraction 0.13), which predicts ERK activation and erlotinib resistance in EGFR -mutant lung cancer. The HNSCC cells with MAPK1 E322K exhibited enhanced EGFR phosphorylation and erlotinib sensitivity compared with wild-type MAPK1 cells. Conclusions and Relevance Selective erlotinib use in HNSCC may be informed by precision oncology approaches.read more
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The mutational landscape of cutaneous T cell lymphoma and Sezary syndrome
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TL;DR: These analyses identify a distinctive pattern of somatic copy number alterations in Sézary syndrome, including highly prevalent chromosomal deletions involving the TP53, RB1, PTEN, DNMT3A and CDKN1B tumor suppressors and support the development of personalized therapies targeting key oncogenically activated signaling pathways for the treatment of these diseases.
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The Mutational Landscape of Head and Neck Squamous Cell Carcinoma
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Comprehensive genomic characterization of head and neck squamous cell carcinomas
Michael S. Lawrence,Carrie Sougnez,Lee Lichtenstein,Kristian Cibulskis,Eric S. Lander,Stacey Gabriel,Gad Getz,Adrian Ally,Miruna Balasundaram,Inanc Birol,Reanne Bowlby,Denise Brooks,Yaron S.N. Butterfield,Rebecca Carlsen,Dean Cheng,Andy Chu,Noreen Dhalla,Ranabir Guin,Robert A. Holt,Steven J.M. Jones,Darlene Lee,Haiyan I. Li,Marco A. Marra,Michael Mayo,Richard A. Moore,Andrew J. Mungall,A. Gordon Robertson,Jacqueline E. Schein,Payal Sipahimalani,Angela Tam,Nina Thiessen,Tina Wong,Alexei Protopopov,Netty Santoso,Semin Lee,Michael Parfenov,Jianhua Zhang,Harshad S. Mahadeshwar,Jiabin Tang,Xiaojia Ren,Sahil Seth,Psalm Haseley,Dong Zeng,Lixing Yang,Andrew Wei Xu,Xingzhi Song,Angeliki Pantazi,Christopher A. Bristow,Angela Hadjipanayis,Jonathan G. Seidman,Lynda Chin,Peter J. Park,Raju Kucherlapati,Rehan Akbani,Tod D. Casasent,Wenbin Liu,Yiling Lu,Gordon B. Mills,Thomas C. Motter,John N. Weinstein,Lixia Diao,Jing Wang,You Hong Fan,Jinze Liu,Kai Wang,J. Todd Auman,Saianand Balu,Thomas Bodenheimer,Elizabeth Buda,D. Neil Hayes,Katherine A. Hoadley,Alan P. Hoyle,Stuart R. Jefferys,Corbin D. Jones,Patrick K. Kimes,Yufeng Liu,James Stephen Marron,Shaowu Meng,Piotr A. Mieczkowski,Lisle E. Mose,Joel S. Parker,Charles M. Perou,Jan F. Prins,Jeffrey Roach,Yan Shi,Janae V. Simons,Darshan Singh,Matthew G. Soloway,Donghui Tan,Umadevi Veluvolu,Vonn Walter,Scot Waring,Matthew D. Wilkerson,Junyuan Wu,Ni Zhao,Andrew D. Cherniack,Peter S. Hammerman,Aaron D. Tward,Chandra Sekhar Pedamallu,Gordon Saksena,Joonil Jung,Akinyemi I. Ojesina,Scott L. Carter,Travis I. Zack,Steven E. Schumacher,Rameen Beroukhim,Samuel S. Freeman,Matthew Meyerson,Juok Cho,Michael S. Noble,Daniel DiCara,Hailei Zhang,David I. Heiman,Nils Gehlenborg,Doug Voet,Pei Lin,Scott Frazer,Petar Stojanov,Yingchun Liu,Lihua Zou,Jaegil Kim,Donna M. Muzny,Harshavardhan Doddapaneni,Christie Kovar,Jeffrey S. Reid,Donna Morton,Yi Han,Walker Hale,Hsu Chao,Kyle Chang,Jennifer Drummond,Richard A. Gibbs,Nipun Kakkar,David A. Wheeler,Liu Xi,Giovanni Ciriello,Marc Ladanyi,William Lee,Ricardo Ramirez,Chris Sander,Ronglai Shen,Rileen Sinha,Nils Weinhold,Barry S. Taylor,B. Arman Aksoy,Gideon Dresdner,Jianjiong Gao,Benjamin Gross,Anders Jacobsen,Boris Reva,Nikolaus Schultz,S. Onur Sumer,Yichao Sun,Timothy A. Chan,Luc G. T. Morris,Joshua M. Stuart,Stephen C. Benz,Sam Ng,Christopher C. Benz,Christina Yau,Stephen B. Baylin,Leslie Cope,Ludmila Danilova,James G. Herman,Moiz S. Bootwalla,Dennis T. Maglinte,Peter W. Laird,Timothy J. Triche,Daniel J. Weisenberger,David Van Den Berg,Nishant Agrawal,Justin A. Bishop,Paul C. Boutros,Jeff Bruce,Lauren Averett Byers,Joseph A. Califano,Thomas E. Carey,Zhong Chen,Hui Cheng,Simion I. Chiosea,Ezra E.W. Cohen,Brenda Diergaarde,Ann Marie Egloff,Adel K. El-Naggar,Robert L. Ferris,Mitchell J. Frederick,Jennifer R. Grandis,Yan Guo,Robert I. Haddad,Thomas M. Harris,Angela B.Y. Hui,J. Jack Lee,Scott M. Lippman,Fei-Fei Liu,Jonathan B. McHugh,Jeffrey N. Myers,Patrick Kwok Shing Ng,Bayardo Perez-Ordonez,Curtis R. Pickering,Michael B. Prystowsky,Marjorie Romkes,Anthony Saleh,Maureen A. Sartor,Raja R. Seethala,Tanguy Y. Seiwert,Han Si,Carter Van Waes,Daryl Waggott,Maciej Wiznerowicz,Wendell G. Yarbrough,Jiexin Zhang,Zhixiang Zuo,Ken Burnett,Daniel Crain,Johanna Gardner,Kevin Lau,David Mallery,Scott Morris,Joseph Paulauskis,Robert Penny,Candace Shelton,Troy Shelton,Mark E. Sherman,Peggy Yena,Aaron D. Black,Jay Bowen,Jessica Frick,Julie M. Gastier-Foster,Hollie A. Harper,Kristen M. Leraas,Tara M. Lichtenberg,Nilsa C. Ramirez,Lisa Wise,Erik Zmuda,Julien Baboud,Mark A. Jensen,Ari B. Kahn,Todd Pihl,David Pot,Deepak Srinivasan,Jessica Walton,Yunhu Wan,Robert A. Burton,Tanja Davidsen,John A. Demchok,Greg Eley,Martin L. Ferguson,Kenna R. Mills Shaw,Bradley A. Ozenberger,Margi Sheth,Heidi J. Sofia,Roy Tarnuzzer,Zhining Wang,Liming Yang,Jean C. Zenklusen,Charles Saller,Katherine Tarvin,Chu Chen,Roni J. Bollag,Paul M. Weinberger,Wojciech Golusiński,Paweł Golusiński,Matthew Ibbs,Konstanty Korski,Andrzej Mackiewicz,Wiktoria Maria Suchorska,Bartosz Szybiak,Erin Curley,Christina Beard,Colleen Mitchell,George E. Sandusky,Julie Ahn,Zubair Khan,Jonathan C. Irish,John Waldron,William N. William,Sophie C. Egea,Carmen Gomez-Fernandez,Lynn M. Herbert,Carol R. Bradford,Douglas B. Chepeha,Andrea Haddad,Tamara R. Jones,Christine M. Komarck,Mayya Malakh,Jeffrey S. Moyer,Ariane Nguyen,Lisa A. Peterson,Mark E. Prince,Laura S. Rozek,Evan G. Taylor,Heather M. Walline,Gregory T. Wolf,Lori Boice,Bhishamjit S. Chera,William K. Funkhouser,Margaret L. Gulley,Trevor Hackman,Michele C. Hayward,Mei Huang,W. Kimryn Rathmell,Ashley H. Salazar,William W. Shockley,Carol G. Shores,Leigh B. Thorne,Mark C. Weissler,Sylvia Wrenn,Adam M. Zanation,Brandee T. Brown,Michelle Q. Pham +309 more
TL;DR: It is shown that human-papillomavirus-associated tumours are dominated by helical domain mutations of the oncogene PIK3CA, novel alterations involving loss of TRAF3, and amplification of the cell cycle gene E2F1.
Journal ArticleDOI
The Mutational Landscape of Head and Neck Squamous Cell Carcinoma
Nicolas Stransky,Ann Marie Egloff,Aaron D. Tward,Aaron D. Tward,Aaron D. Tward,Aleksandar Kostic,Aleksandar Kostic,Kristian Cibulskis,Andrey Sivachenko,Gregory Kryukov,Gregory Kryukov,Michael S. Lawrence,Carrie Sougnez,Aaron McKenna,Erica Shefler,Alex H. Ramos,Petar Stojanov,Scott L. Carter,Douglas Voet,Maria L. Cortes,Daniel Auclair,Michael F. Berger,Gordon Saksena,Candace Guiducci,Robert C. Onofrio,Melissa Parkin,Marjorie Romkes,Joel L. Weissfeld,Raja R. Seethala,Lin Wang,Claudia Rangel-Escareño,Juan Carlos Fernández-López,Alfredo Hidalgo-Miranda,Jorge Melendez-Zajgla,Wendy Winckler,Kristin Ardlie,Stacey Gabriel,Matthew Meyerson,Eric S. Lander,Eric S. Lander,Eric S. Lander,Gad Getz,Todd R. Golub,Levi A. Garraway,Jennifer R. Grandis +44 more
TL;DR: In this article, the authors analyzed whole-exome sequencing data from 74 tumor-normal pairs and found that at least 30% of cases harbored mutations in genes that regulate squamous differentiation (for example, NOTCH1, IRF6, and TP63), implicating its dysregulation as a major driver of HNSCC carcinogenesis.
Journal ArticleDOI
Exome sequencing of head and neck squamous cell carcinoma reveals inactivating mutations in NOTCH1
Nishant Agrawal,Mitchell J. Frederick,Curtis R. Pickering,Chetan Bettegowda,Kyle Chang,Ryan J. Li,Carole Fakhry,Tong Xin Xie,Jiexin Zhang,Jing Wang,Nianxiang Zhang,Adel K. El-Naggar,Samar A. Jasser,John N. Weinstein,Lisa R. Trevino,Jennifer Drummond,Donna M. Muzny,Yuanqing Wu,Laura D. Wood,Ralph H. Hruban,William H. Westra,Wayne M. Koch,Joseph A. Califano,Joseph A. Califano,Richard A. Gibbs,Richard A. Gibbs,David Sidransky,Bert Vogelstein,Victor E. Velculescu,Nickolas Papadopoulos,David A. Wheeler,Kenneth W. Kinzler,Jeffrey N. Myers +32 more
TL;DR: To explore the genetic origins of head and neck squamous cell carcinoma, whole-exome sequencing and gene copy number analyses were used to study 32 primary tumors and identified mutations in FBXW7 and NotCH1, suggesting that NOTCH1 may function as a tumor suppressor gene rather than an oncogene in this tumor type.
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