T
Thomas D. Barber
Researcher at Eli Lilly and Company
Publications - 7
Citations - 4438
Thomas D. Barber is an academic researcher from Eli Lilly and Company. The author has contributed to research in topics: Hepatitis B virus & Gene. The author has an hindex of 5, co-authored 7 publications receiving 4275 citations. Previous affiliations of Thomas D. Barber include Johns Hopkins University.
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PatentDOI
Consensus coding sequences of human breast and colorectal cancers
Tobias Sjöblom,Sian Jones,D. Williams Parsons,Laura D. Wood,Jimmy Lin,Thomas D. Barber,Diana Mandelker,Bert Vogelstein,Kenneth W. Kinzler,Victor E. Velculesu +9 more
TL;DR: In this paper, the authors analyzed 13,023 genes in 11 breast and 11 colorectal cancers and found that individual tumors accumulate an average of 90 mutant genes but only a subset of these contribute to the neoplastic process.
Journal ArticleDOI
Genome-wide survey of recurrent HBV integration in hepatocellular carcinoma
Wing-Kin Sung,Hancheng Zheng,Shuyu Li,Ronghua Chen,Xiao Liu,Yingrui Li,Nikki P. Lee,Wah Heng Lee,Pramila N. Ariyaratne,Chandana Tennakoon,Fabianus Hendriyan Mulawadi,Kwong F. Wong,Angela M. Liu,Ronnie T.P. Poon,Sheung Tat Fan,KL Chan,Zhuolin Gong,Yujie Hu,Zhao Lin,Guan Wang,Qinghui Zhang,Thomas D. Barber,Wen-Chi Chou,Amit Aggarwal,Ke Hao,Wei Zhou,Chunsheng Zhang,James S. Hardwick,James S. Hardwick,Carolyn A. Buser,Jiangchun Xu,Zhengyan Kan,Hongyue Dai,Mao Mao,Mao Mao,Christoph Reinhard,Jun Wang,Jun Wang,John M. Luk +38 more
TL;DR: Evidence is reported that suggests that the number of HBV integrations is associated with patient survival and copy-number variations were significantly increased at HBV breakpoint locations where chromosomal instability was likely induced.
Journal ArticleDOI
Whole-genome sequencing identifies recurrent mutations in hepatocellular carcinoma
Zhengyan Kan,Hancheng Zheng,Xiao Liu,Shuyu Li,Thomas D. Barber,Zhuolin Gong,Huan Gao,Ke Hao,Melinda D. Willard,Jiangchun Xu,Robert Hauptschein,Paul A. Rejto,Julio Fernandez,Guan Wang,Qinghui Zhang,Bo Wang,Ronghua Chen,Jian Wang,Nikki P. Lee,Wei Zhou,Zhao Lin,Zhiyu Peng,Kang Yi,Shengpei Chen,Lin Li,Xiaomei Fan,Jie Yang,Rui Ye,Jia Ju,Kai Wang,Heather Estrella,Shibing Deng,Ping Wei,Ming Qiu,Isabella H. Wulur,Jiangang Liu,Mariam Ehsani,Chunsheng Zhang,Andrey Loboda,Wing-Kin Sung,Wing-Kin Sung,Amit Aggarwal,Ronnie T.P. Poon,Sheung Tat Fan,Jun Wang,James S. Hardwick,James S. Hardwick,Christoph Reinhard,Hongyue Dai,Yingrui Li,John M. Luk,John M. Luk,John M. Luk,Mao Mao,Mao Mao +54 more
TL;DR: Findings from a whole-genome sequencing study of 88 matched HCC tumor/normal pairs, 81 of which are Hepatitis B virus (HBV) positive, find beta-catenin to be the mostrequently mutated oncogene and TP53 the most frequently mutated tumor suppressor.
Journal ArticleDOI
Somatic Mutations in GRM1 in Cancer Alter Metabotropic Glutamate Receptor 1 Intracellular Localization and Signaling
Jessica L. Esseltine,Melinda D. Willard,Isabella H. Wulur,Mary E. Lajiness,Thomas D. Barber,Stephen S. G. Ferguson +5 more
TL;DR: The present study investigated the intracellular localization and G protein–dependent and –independent signaling of eight GRM1 (mGluR1a) somatic mutations and suggested that mGlu R1a signaling in cancer is disrupted by somatics mutations with multiple downstream consequences.
Journal ArticleDOI
Somatic mutations in CCK2R alter receptor activity that promote oncogenic phenotypes.
Melinda D. Willard,Mary E. Lajiness,Isabella H. Wulur,Bo Feng,Bo Feng,Michelle L. Swearingen,Mark T. Uhlik,Kenneth W. Kinzler,Victor E. Velculescu,Tobias Sjöblom,Tobias Sjöblom,Sanford D. Markowitz,Steven M. Powell,Bert Vogelstein,Thomas D. Barber +14 more
TL;DR: It is suggested that somatic mutations in CCK2R may promote tumorigenesis through deregulated receptor activity and highlight the importance of evaluating CCK 2R inhibitors to block both the normal and mutant forms of the receptor.