Molecular pathogenesis of pancreatic cancer.
Pancreatic cancer is fundamentally a disease of inherited and acquired mutations in cancer-related genes. The genes targeted in pancreatic cancer include tumor-suppressor genes (p16/CDKN2A, TP53 and SMAD4), oncogenes (KRAS, BRAF, AKT2, MYB, and AIB1), and genome-maintenance genes (MLH1, MSH2, BRAC2 and other Fanconi anemia genes). An understanding of the cancer-related genes that are altered in pancreatic cancer has a number of clinical applications including genetic counseling for individuals with a family history of cancer, early detection of pancreatic neoplasia, and mechanism-based therapies for patients with advanced disease. This chapter will provide an overview of the molecular pathogenesis of pancreatic cancer with emphasis on clinical applications.
Maitra
Anirban
A
Department of Pathology, The Sol Goldman Pancreatic Cancer Research Center, The Johns Hopkins Medical Institutions, Baltimore, MD 21231, USA. amaitra1@jhmi.edu
Kern
Scott E
SE
Hruban
Ralph H
RH
D002278:Carcinoma in Situ / Q000235:genetics / Q000473:pathology / Q000628:therapy; D021441:Carcinoma, Pancreatic Ductal / Q000235:genetics / Q000473:pathology / Q000628:therapy; D015870:Gene Expression; D016147:Genes, Tumor Suppressor; D042822:Genomic Instability; D006801:Humans; D008403:Mass Screening; D009857:Oncogenes; D010190:Pancreatic Neoplasms / Q000235:genetics* / Q000473:pathology / Q000628:therapy; D016615:Telomere