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Sequencing of acinar cell carcinomas found that they do not carry the KRAS mutation that drives ordinary pancreatic cancer; instead about a quarter have fusions activating BRAF or RAF1, which MEK-blocking drugs can shut down in the laboratory, and almost half have broken DNA repair genes that may make them sensitive to platinum and PARP inhibitors.
Targeted sequencing of 44 pancreatic acinar cell carcinomas. Recurrent gene fusions involving BRAF or RAF1 (including SND1-BRAF and HERPUD1-BRAF) were found in about 23 percent of tumours, with mutual exclusivity from other MAPK alterations, and cell lines expressing the fusions were sensitive to MEK inhibition.
About 45 percent of tumours carried inactivating alterations in DNA repair genes such as BRCA2, PALB2, ATM and MSH2, and KRAS mutations were rare. The genomic landscape was distinct from ductal adenocarcinoma, with high mutational heterogeneity and few recurrent point mutations.
Acinar cell carcinoma should be sequenced: RAF fusions and DNA repair defects offer targeted and platinum or PARP inhibitor options that ductal adenocarcinoma rarely has.
Shares Pancreatic acinar cell carcinoma, Pancreatic ductal adenocarcinoma.
Shares Pancreatic acinar cell carcinoma, Pancreatic ductal adenocarcinoma.
Shares Pancreatic acinar cell carcinoma, Pancreatic ductal adenocarcinoma.
Shares Pancreatic acinar cell carcinoma, Pancreatic ductal adenocarcinoma.