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William C. Hahn
Researcher at Harvard University
Publications - 515
Citations - 85047
William C. Hahn is an academic researcher from Harvard University. The author has contributed to research in topics: Cancer & Medicine. The author has an hindex of 130, co-authored 448 publications receiving 72191 citations. Previous affiliations of William C. Hahn include Brigham and Women's Hospital & University of Washington.
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Book ChapterDOI
Contributions of Telomerase to Tumorigenesis
TL;DR: The majority of human tumors exhibit abundant telomerase activity, which protects the chromosome ends to prevent additional genomic instability and confers unlimited replicative potential and presents an ideal target for potential pharmacologic and immunologic therapies.
Journal ArticleDOI
A Ubiquitination Cascade Regulating the Integrated Stress Response and Survival in Carcinomas
Lisa D. Cervia,Tsukasa Shibue,Ashir A. Borah,Benjamin Gaeta,Lin-Juan He,Lisa H. Leung,Na Li,Sydney M. Moyer,Brian H Shim,Nancy Dumont,Alfredo Gonzalez,Mariya Kazachkova,Joshua M. Dempster,John M. Krill-Burger,Federica Piccioni,Namrata D. Udeshi,Meagan E. Olive,Steven A. Carr,David E. Root,James M. McFarland,Francisca Vazquez,William C. Hahn +21 more
TL;DR: It is found that a ubiquitination ligase complex composed of UBA6, BIRC6, KCMF1 and UBR4, which encode an E1, E2 and two heterodimeric E3 subunits is required for the survival of a subset of epithelial tumors, particularly subtypes of breast cancer.
Proceedings ArticleDOI
Abstract 4867: Comparative analysis of RNA sequencing methods for characterization of cancer transcriptomics
Ryan Abo,Ling Lin,Samuel S. Hunter,Deniz N. Dolcen,Rachel R. Paquette,Angelica Laing,Luc de Waal,Aaron R. Thorner,Matthew D. Ducar,Liuda Ziaugra,William C. Hahn,Matthew Meyerson,Laura E. MacConaill,Paul Van Hummelen +13 more
TL;DR: A RNA-seq analysis platform that provides a varied set of library preparations and analytical components for large-scale clinical or research transcriptomics and illustrates the implications of these issues on downstream analysis, such as somatic mutation and fusion calling and differential expression.
Proceedings ArticleDOI
Abstract 433: Triplication of HMGN1 promotes B cell acute lymphoblastic leukemia (B-ALL) through suppression of H3K27me3
Andrew A. Lane,Bjoern Chapuy,Charles Y. Lin,Trevor Tivey,Hubo Li,Elizabeth C. Townsend,Diederik van Bodegom,Tovah A. Day,Shuo-Chieh Wu,Huiyun Liu,Akinori Yoda,Gabriela Alexe,Anna C. Schinzel,Timothy J. Sullivan,Sébastien Malinge,Jordan E. Taylor,Kimberly Stegmaier,Jacob D. Jaffe,Michael Bustin,Geertruy te Kronnie,Shai Izraeli,Marian H. Harris,Kristen E. Stevenson,Donna Neuberg,Lewis B. Silverman,Steven E. Sallan,James E. Bradner,William C. Hahn,John D. Crispino,David Pellman,David M. Weinstock +30 more
TL;DR: In a bone marrow transplant model driven by BCR-ABL, recipients of HMGN1_OE bone marrow developed B-ALL with decreased latency (median 33 days vs not reached) and increased penetrance (17/18 vs 4/17 mice died by 80 days; leukemia-free survival difference), validating the same biology in human disease.
Proceedings ArticleDOI
Abstract 2352: Defining a pediatric cancer dependency map
Neekesh V. Dharia,Clare F. Malone,Amanda Balboni Iniguez,Lillian M. Guenther,Liying Chen,Gabriela Alexe,Adam D. Durbin,Mark W. Zimmerman,Andrew L. Hong,Pratiti Bandopadhayay,Mariella G. Filbin,Thomas P. Howard,Brenton R. Paolella,Iris Fung,Josephine S. Lee,Phil Montgomery,John M. Krill-Burger,Brian J. Abraham,Jennifer Roth,David E. Root,Richard A. Young,A. Thomas Look,Rameen Beroukhim,Jesse S. Boehm,William C. Hahn,Todd R. Golub,Aviad Tsherniak,Francisca Vazquez,Kimberly Stegmaier +28 more
TL;DR: To discover new vulnerabilities in pediatric solid tumors, genome-scale CRISPR-Cas9 loss-of-function screening and deep “omic” characterization in over 60 pediatric cancer cell lines are performed to begin defining a pediatric cancer dependency map.