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Although the group of exocrine pancreatic cancers is heterogeneous in terms of clinical presentation, histological features, and treatment response, the biology of the majority of pancreatic cancers remains unknown. Most of the information on the genetics of these tumors can be obtained through genomic studies of familial pancreatic cancer. Using a whole-genome approach to genome-wide screens, a few families and sporadic individuals have been identified to have pathogenic mutations in genes involved in three distinct molecular pathways of pancreatic tumorigenesis: the cell cycle (cyclin-dependent kinases, tumor suppressors, proto-oncogenes, and retinoblastoma protein), the WNT pathway (beta-catenin, the wingless proto-oncogene), and mismatch repair. A majority of these molecularly oriented studies have focused on one or two genes, which leaves many questions about the molecular pathogenesis of pancreatic tumors unanswered. The present review summarises current knowledge about the molecular genetics of pancreatic cancers, focusing on the genes involved in the three above-mentioned pathways.104 F.3d 356
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