The KRAS-G12D mutation drives venous thromboembolism (VTE) and colorectal cancer progression via MAPK/ERK signaling.

ABSTRACT:

Objective

KRAS mutations occur in nearly 50 % of colorectal cancer (CRC) cases, with G12D representing the most frequent variant. While CRC is recognized as a moderate risk factor for venous thromboembolism (VTE), the thrombogenic potential of KRAS-G12D mutations remains poorly understood.

Methods

We established a KRAS-G12D-associated coagulation gene (KMCG) prognostic model through integrative analysis of clinical data from CRC patients. Mechanistic investigations combining in vitro and in vivo models revealed that KRAS-G12D potentiates thrombotic risk through MAPK/ERK pathway activation.

Results

Integrating TCGA data, we constructed a KRAS-G12D-associated coagulation gene (PLCG2/MAPK12/C4B)-based prognostic model, where high-risk patients exhibited significantly red

SUBMITTER: Mao J 

PROVIDER: S-EPMC12481119 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature