V
Vijay Yajnik
Researcher at Harvard University
Publications - 111
Citations - 6272
Vijay Yajnik is an academic researcher from Harvard University. The author has contributed to research in topics: Inflammatory bowel disease & Crohn's disease. The author has an hindex of 33, co-authored 105 publications receiving 5334 citations. Previous affiliations of Vijay Yajnik include Cleveland Clinic & Columbia University Medical Center.
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Journal ArticleDOI
Hedgehog is an early and late mediator of pancreatic cancer tumorigenesis
Sarah P. Thayer,Marina Pasca di Magliano,Patrick W. Heiser,Corinne M. Nielsen,Drucilla J. Roberts,Gregory Y. Lauwers,Yan Ping Qi,Stephan Gysin,Carlos Fernandez-del Castillo,Vijay Yajnik,Bozena Antoniu,Martin McMahon,Andrew L. Warshaw,Matthias Hebrok +13 more
TL;DR: It is reported that sonic hedgehog, a secreted hedgehog ligand, is abnormally expressed in pancreatic adenocarcinoma and its precursor lesions: pancreatic intraepithelial neoplasia (PanIN), and that maintenance of hedgehog signalling is important for aberrant proliferation and tumorigenesis.
Journal ArticleDOI
Treg cells expressing the coinhibitory molecule TIGIT selectively inhibit proinflammatory Th1 and Th17 cell responses.
Nicole Joller,Ester Lozano,Patrick R. Burkett,Bonny Patel,Sheng Xiao,Chen Zhu,Junrong Xia,Tze Guan Tan,Esen Sefik,Vijay Yajnik,Arlene H. Sharpe,Arlene H. Sharpe,Francisco J. Quintana,Diane Mathis,Christophe Benoist,David A. Hafler,Vijay K. Kuchroo +16 more
TL;DR: TIGIT expression identifies a Treg cell subset that demonstrates selectivity for suppression of Th1 and Th17 cell but not Th2 cell responses.
Journal ArticleDOI
Inflammatory bowel disease and cancer: The role of inflammation, immunosuppression, and cancer treatment.
TL;DR: The characteristics and risks of cancer in patients with IBD are explored, including management of IBD after a diagnosis of cancer, the effects of cancer treatment on IBD, and the effect of I BD and medications for IBD on cancer outcomes are evaluated.
Journal ArticleDOI
DOCK4, a GTPase activator, is disrupted during tumorigenesis.
Vijay Yajnik,Charles Paulding,Raffaella Sordella,Andrea I. McClatchey,Mako Saito,Doke C.R. Wahrer,Paul A. Reynolds,Daphne W. Bell,Robert J. Lake,Sander van den Heuvel,Jeff Settleman,Daniel A. Haber +11 more
TL;DR: A deletion targeting DOCK4, a member of the CDM gene family encoding regulators of small GTPases, is described, which encodes a CDM family member that regulates intercellular junctions and is disrupted during tumorigenesis.