Abstract
Very long-term survival in pancreatic cancer.
Highlights
Editorial atypical clinical course of this particular subgroup of patients with Pancreatic ductal adenocarcinoma (PDAC)
A total of 301 somatic mutations were identified in 274 genes, only 5 genes (KRAS, TP53, SMAD4, CDKN2A, and RNF43) were altered in more than one of the eight PDACs
Inactivating mutations in this gene have been reported in intraductal papillary mucinous neoplasm (IPMN), a non-invasive pancreatic cystic neoplasm which has the potential to progress to PDAC [6]
Summary
Editorial atypical clinical course of this particular subgroup of patients with PDAC. A total of 301 somatic mutations were identified in 274 genes (mean of 37.6 non-synonymous somatic mutations per carcinoma), only 5 genes (KRAS, TP53, SMAD4, CDKN2A, and RNF43) were altered in more than one of the eight PDACs. Of these KRAS, TP53, SMAD4, and CDKN2A are previously described commonly mutated driver genes in this tumor type.
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