KRAS Loss of Heterozygosity Promotes MAPK-Dependent Pancreatic Ductal Adenocarcinoma Initiation and Induces Therapeutic Sensitivity to MEK Inhibition.

doi:10.1158/0008-5472.CAN-23-2709

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KRAS Loss of Heterozygosity Promotes MAPK-Dependent Pancreatic Ductal Adenocarcinoma Initiation and Induces Therapeutic Sensitivity to MEK Inhibition.

Cancer research - 15 Jan 2025

Fey Sigrid K, Najumudeen Arafath K, Watt Dale M, Millett Laura M, Ford Catriona A, Gilroy Kathryn, Simpson Rosalin J, McLay Kathy, Upstill-Goddard Rosanna, Chang David, Clark William, Nixon Colin, Birch Joanna L, Barry Simon T, Morton Jennifer P, Campbell Andrew D, Sansom Owen J

Abstract excerpt

Pancreatic cancer is characterized by the prevalence of oncogenic mutations in KRAS. Previous studies have reported that altered KRAS gene dosage drives progression and metastasis in pancreatic cancer. Whereas the role of oncogenic KRAS mutations is well characterized, the relevance of the partnering wild-type (WT) KRAS allele in pancreatic cancer is less well understood and controversial. Using in vivo mouse...

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KRAS Loss of Heterozygosity Promotes MAPK-Dependent Pancreatic Ductal Adenocarcinoma Initiation and Induces Therapeutic Sensitivity to MEK Inhibition.

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