Journal
ANNUAL REVIEW OF PATHOLOGY-MECHANISMS OF DISEASE
Volume 3, Issue -, Pages 157-188Publisher
ANNUAL REVIEWS
DOI: 10.1146/annurev.pathmechdis.3.121806.154305
Keywords
pancreas; carcinoma; adenocarcinoma; precursor; genetics; stem cell; mouse model; targeted therapy
Categories
Funding
- NATIONAL CANCER INSTITUTE [R01CA113669, P50CA062924] Funding Source: NIH RePORTER
- NCI NIH HHS [R01 CA113669-05, R01 CA113669, R01CA113669, R01 CA113669-03, R01 CA113669-04, P50 CA062924-140016, P50CA062924, P50 CA062924, R01 CA113669-01, P50 CA062924-150016, R01 CA113669-02] Funding Source: Medline
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The past two decades have witnessed an explosion in Our understanding of pancreatic cancer, and it is now clear that pancreatic cancer is a disease of inherited (germ-line) and somatic gene mutations. The genes mutated in pancreatic cancer include KRAS2, p16/CDKN2A, TP53, and SMAD4/DPC4, and these are accompanied by a substantial compendium of genomic and transcriptomic alterations that facilitate cell cycle deregulation, cell survival, invasion, and metastases. Pancreatic cancers do not arise de novo, and three distinct precursor lesions have been identified. Experimental models of pancreatic cancer have been developed in genetically engineered mice, which recapitulate the multistep progression of the cognate human disease. Although the putative cell of origin for pancreatic cancer remains elusive, minor populations of cells with stem-like properties have been identified that appear responsible for tumor initiation, metastases, and resistance of Pancreatic cancer to conventional therapies.
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