Notch mediates TGF alpha-induced changes in epithelial differentiation during pancreatic tumorigenesis.

By Y. Miyamoto, A. Maitra, B. Ghosh, U. Zechner, P. Argani, C. Iacobuzio-Donahue, V. Sriuranpong, T. Iso, I. Meszoely, M. Wolfe and 4 more. Cancer Cell, 2003

704 citations recorded by the source corpus.

Subfields: Oncology, Surgery

View Paper: https://www.semanticscholar.org/paper/9b04459b21bbdc87b77786938852231cfd43ad1b

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In Oncology

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Citations in the corpus

• Chronic pancreatitis is essential for induction of pancreatic ductal adenocarcinoma by K-Ras oncogenes in adult mice. (2007, background): “Finally, these PanINs were also positive for Hes1, a marker for the Notch pathway also identified in human pancreatic tumors (Figure 3H) (Miyamoto et al., 2003).”
• Preinvasive and invasive ductal pancreatic cancer and its early detection in the mouse. (2003, background): “…were seen only in the context of an additional mutation in a cyclin- served transdifferentiation of acinar-like cells occurred within 3–4 days (Miyamoto et al., 2003).dependent kinase, CDK4R24C (Cdk4R24C has a markedly decreased binding affinity for p16INK4a and thereby resists its tumor We…”
• Genetics and biology of pancreatic ductal adenocarcinoma. (2006, background): “TGF- signaling may also contribute to tumorigenesis in an autocrine manner since PDACs often overexpress the type II TGF- receptor relative to normal pancreas (Wagner et al. 1999; for review, see Rane et al. 2006) while experimental blockade of TGFsignaling by expression of soluble type II TGF- rece”
• A phase I trial of the γ-secretase inhibitor MK-0752 in combination with gemcitabine in patients with pancreatic ductal adenocarcinoma (2018, background): “Notch signalling is relatively inactive in the normal adult pancreas; however, it becomes activated in damaged and dysplastic pancreatic tissue (Miyamoto et al, 2003).”