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Screening 3,170 pancreatic cancers found five with an ALK gene fusion, all in patients under 50 and none with a KRAS mutation, and three of four treated with ALK inhibitors benefited.
Comprehensive genomic profiling of 3,170 pancreatic ductal adenocarcinomas identified 5 cases (0.16%) with an ALK fusion: exon 6 EML4-exon 20 ALK (3), exon 13 EML4-exon 20 ALK (1) and exon 3 STRN-exon 20 ALK (1). Activating KRAS mutations were absent in all 5, who were under 50; among patients under 50, ALK translocations were 1.3% of cancers. Four of 5 were treated with an ALK inhibitor and 3 showed stable disease, radiographic response and/or CA 19-9 normalisation.
ALK is the reason young, KRAS wild-type patients should have fusion testing even though the overall rate is one in six hundred.
Shares ALK fusion (ALK-positive), KRAS wild-type pancreatic ductal adenocarcinoma, ALK, Receptor tyrosine kinase activation.
Shares ALK fusion (ALK-positive), ALK.
Shares KRAS wild-type pancreatic ductal adenocarcinoma, Receptor tyrosine kinase activation, Pancreatic ductal adenocarcinoma.
Shares KRAS wild-type pancreatic ductal adenocarcinoma, Receptor tyrosine kinase activation, Pancreatic ductal adenocarcinoma.
Shares ALK, Receptor tyrosine kinase activation.
Shares ALK fusion (ALK-positive), Crizotinib.
Shares Alectinib, Crizotinib, ALK.