Loss of expression of Dpc4 in pancreatic intraepithelial neoplasia: evidence that DPC4 inactivation occurs late in neoplastic progression.
By R. Wilentz, C. Iacobuzio-Donahue, P. Argani, D. McCarthy, Jennifer Parsons, C. Yeo, S. Kern, R. Hruban. Cancer Research, 2000
621 citations recorded by the source corpus.
View Paper: https://www.semanticscholar.org/paper/c835a7945c3db78d99265ea37a94fdc814b3dbf7
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Citations in the corpus
- Activated Kras and Ink4a/Arf deficiency cooperate to produce metastatic pancreatic ductal adenocarcinoma. (2003, background): “Finally, mutations in SMAD4/ DPC4 and p53—encountered in >50% of tumors—are late events, implying a role in full malignant progression, including acquisition of an invasive phenotype (DiGiuseppe et al. 1994; Wilentz et al. 2000; Luttges et al. 2001).”
- An Illustrated Consensus on the Classification of Pancreatic Intraepithelial Neoplasia and Intraductal Papillary Mucinous Neoplasms (2004, background): “The term neoplasia is used to reflect the observation that these lesions are clonal prol i fe ra t ions wi th a l te ra t ions in cancer -assoc ia ted genes.(12,20,23,25,38,40,50,52,55,56,60,80,81,85,88,90,91,93) PanINs-1 and -2 are typically incidental findings and are of unproved clinical signific”
- Progression model for pancreatic cancer. (2000, background): “gene), loss of DPC4gene expression, abnormalities of p53gene expression, and biallelic inactivation of the BRCA2tumor suppressor gene have all also been reported in pancreatic duct lesions (22, 26, 27, 32, 33).”
- Genetics and biology of pancreatic ductal adenocarcinoma. (2006, background): “At the same time, while PanINs may appear to arise from differentiated ducts, it is worth noting that the targeting of activated Kras to mature ductal cells using the cytokeratin-19 promoter failed to produce PanINs or PDAC, resulting, instead, in periductal inflammation (Brembeck et al. 2003).”