Presence of Somatic Mutations in Most Early-Stage Pancreatic Intraepithelial Neoplasia
By M. Kanda, H. Matthaei, Jian Wu, Seung‐Mo Hong, Jun Yu, Michael Borges, R. Hruban, A. Maitra, Kenneth W. Kinzler, Bert Vogelstein and 1 more. Gastroenterology, 2012
724 citations recorded by the source corpus.
More information is needed about genetic factors that initiate development of pancreatic intraepithelial neoplasms (PanINs)—the most common precursors of pancreatic ductal adenocarcinoma. We show that >99% of the earliest stage, lowest-grade, PanIN-1 lesions contain mutations in KRAS, p16/CDKN2A, GNAS, or BRAF. These findings could improve our understanding the development and progression of these pre-malignant lesions.
Subfields: Cancer Research, Oncology, Surgery
View Paper: https://www.semanticscholar.org/paper/a6650c8b2b50463661e14c084bde8a736aedd508
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Citations in the corpus
- KRAS: The Critical Driver and Therapeutic Target for Pancreatic Cancer (2018, background): “Greater than 90% frequency of KRAS mutations are found in PanIN-1 lesions (Kanda et al. 2012).”
- KRAS: feeding pancreatic cancer proliferation (2014, neutral): “In PDAC, KRAS mutation is an early and initiating event as it has been shown that over 90% of low-grade pancreatic intraepithelial neoplasia (PanIN) lesions (Figure 3) harbor oncogenic KRAS mutations [7].”