Progression model for pancreatic cancer.

By R. Hruban, M. Goggins, Jennifer Parsons, S. Kern. Clinical Cancer Research, 2000

909 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/7fe77a16d1172002a06074f36ec17ab20c503d81

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Citations in the corpus

• Preinvasive and invasive ductal pancreatic cancer and its early detection in the mouse. (2003, methodology): “Similar to long-established models for other epithelial malignancies, such as breast, colon, and prostate, a progression model for the precursor lesions of PDA has been elaborated (Cubilla and Fitzgerald, 1975, 1976; Hruban et al., 2000a; Klimstra and Longnecker, 1994).”
• Genetics and biology of pancreatic ductal adenocarcinoma. (2006, background): “2; Klimstra and Longnecker 1994; Moskaluk et al. 1997; Heinmoller et al. 2000; Hruban et al. 2000b, 2001; Wilentz et al. 2000; Yamano et al. 2000; Luttges et al. 2001; Maitra et al. 2003).”
• Dynamics of the immune reaction to pancreatic cancer from inception to invasion. (2007, background): “all the histologic stages described for the human disease (26).”
• Mutations in the p53 Tumor Suppressor Gene: Important Milestones at the Various Steps of Tumorigenesis. (2011, methodology): “In this model, the TP53 gene was suggested to be lost late in the development of pancreatic neoplasia.(22) In addition, examination of breast cancers reveals that TP53 mutations are rare at T1 stage tumors, which are less than 2 cm in diameter and significantly more frequent in T3 stage tumors, whic”
• An Illustrated Consensus on the Classification of Pancreatic Intraepithelial Neoplasia and Intraductal Papillary Mucinous Neoplasms (2004, background): “entire spectrum of PanINs represent a continuum of intraductal neoplastic progression.(28) Most of the genetic alterations pre-”
• KRAS: The Critical Driver and Therapeutic Target for Pancreatic Cancer (2018, background): “In early-stage PanIN formation, flat pancreatic epithelial cells take on a cuboidal appearance, increase mucin production, and acquire atypical cytological andmorphological features (Hruban et al. 2000, 2004; Distler et al. 2014).”
• DNA replication stress as a hallmark of cancer. (2015, result): “Similar studies in other tumor types suggest that, generally, mutations in oncogenes precede TP53 mutations (50).”
• Mutant p53 drives metastasis and overcomes growth arrest/senescence in pancreatic cancer (2010, background): “PDAC arises from precursor lesions called pancreatic intraepithelial neoplasms (PanINs), which are characterized by the sequential accumulation of alterations in the KRAS oncogene and loss of the CDKN2A, TP53, and/or SMAD4 tumor suppressors in many cases (3).”