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The average number of somatic mutations in pancreatic is considerably less than that in breast cancer or colorectal cancers,even though fewer genes were sequenced in the latter two tumor types.One plausible explanation for this lower rate is that the cells that initiates pancreatic tumorigenesis have gone through fewer divisions than colorectal or breast cancer cells.It has been previously shown that the majority of mutations observed in colorectal cancers are likely to have occurred in the normal stem cells that gave rise to the initiating neoplastic cell.Our data are thus consistent with observations showing that normal pancreatic epithelial cells divide infrequently.
We further evaluated 39 genes that were mutated in more than one of the 24 discovery screen cancers in a prevalence screen consisting of 90 pancreatic cancers.In the screen,we detected 255 nonsilent somatic mutations among 23 genes.The nonsilent mutation rate of the genes in the prevalence screen was higher than that in the discovery screen (3.6 versus 1.47 nonsilent mutations per Mbase,P