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Whole-genome and RNA sequencing of pancreatic cancers in younger patients found that most of the tumours without a KRAS mutation instead carried a fusion of the NRG1 gene, and two patients given a HER-family blocker responded. It established NRG1 fusions as the driver to look for in KRAS wild-type pancreatic cancer.
Report from the German NCT/DKTK MASTER precision oncology programme on whole-genome and transcriptome sequencing of pancreatic ductal adenocarcinomas from young patients (50 or under). Among the tumours without a KRAS mutation, most harboured an NRG1 gene fusion, whereas no KRAS-mutant tumour did.
Two patients with NRG1 fusion-positive tumours treated with the ERBB inhibitor afatinib had clinical and radiological responses, providing the first evidence that these fusions are actionable in pancreatic cancer and that RNA-level analysis is needed to find them.
KRAS wild-type status should trigger fusion testing, ideally by RNA sequencing, because NRG1 fusions can be targeted by HER-family inhibitors and now by zenocutuzumab.
Shares Zenocutuzumab, NRG1, Afatinib, Wild-type (WT).
Shares Zenocutuzumab, NRG1, Wild-type (WT), HER3.
Shares Zenocutuzumab, NRG1, HER3, KRAS wild-type pancreatic ductal adenocarcinoma.
Shares NRG1, Wild-type (WT), KRAS wild-type pancreatic ductal adenocarcinoma, Receptor tyrosine kinase activation.
Shares Wild-type (WT), Cancer Discovery, Receptor tyrosine kinase activation, RAS / RAF / MEK / ERK (MAPK).
Shares Zenocutuzumab, NRG1, HER3, Receptor tyrosine kinase activation.
Shares NRG1, Cancer Discovery, Receptor tyrosine kinase activation, RNA sequencing & expression profiling.
Shares Wild-type (WT), KRAS wild-type pancreatic ductal adenocarcinoma, RNA sequencing & expression profiling, Whole-exome & whole-genome sequencing.