Molecular pathogenesis of pancreatic cancer.
Our understanding of the biology of pancreatic carcinoma has greatly benefited from studies of the genetic alterations in this tumor type. The p16-CDK4-cyclinD-Rb pathway, the p53 tumor suppressor pathway, and the DPC4/Smad4 pathway are genetically inactivated in the majority of sporadic pancreatic carcinomas, whereas oncogenic K-ras signaling is almost ubiquitously activated. These genetic data have provided the basis to shape a first genetic progression model of this tumor type. Furthermore, a number of well defined genetic syndromes which are associated with an inherited risk for pancreatic carcinoma have been identified recently.
Hilgers
Werner
W
Department of Medical Oncology, Hopital Saint Louis, 1 Avenue Claude Vellefaux, 75475 Paris, France. whilgers@free.fr
Rosty
Christophe
C
Hahn
Stephan A
SA
D000230:Adenocarcinoma / Q000235:genetics*; D002471:Cell Transformation, Neoplastic / Q000235:genetics; D002869:Chromosome Aberrations; D002877:Chromosomes, Human / Q000235:genetics / Q000648:ultrastructure; D004252:DNA Mutational Analysis; D004272:DNA, Mitochondrial / Q000235:genetics; D018450:Disease Progression; D016147:Genes, Tumor Suppressor; D020022:Genetic Predisposition to Disease; D006801:Humans; D007621:Karyotyping; D009363:Neoplasm Proteins / Q000235:genetics; D009386:Neoplastic Syndromes, Hereditary / Q000235:genetics; D009857:Oncogenes; D010190:Pancreatic Neoplasms / Q000235:genetics*; D012042:Registries
D004272:DNA, Mitochondrial; D009363:Neoplasm Proteins