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Loss of <i>Kmt2c</i> / <i>d</i> promotes gastric cancer initiation and confers vulnerability to mTORC1 inhibition and anti-PD1 immunotherapy

2025-04-01

Abstract excerpt

KMT2C and KMT2D ( KMT2C/D ) are frequently mutated in gastric adenocarcinoma, yet their function in cancer initiation remains poorly understood. In this study, based on the observation that loss-of-function mutations of KMT2C and KMT2D are enriched and co-occur in gastric adenocarcinoma, we developed genetically engineered mouse models to selectively knock out Kmt2c and Kmt2d in gastric epithelial cells with...

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Identifiers and source

Literature Corpus work
0f6b3e2b-0790-55c8-83a5-95d42357d66f
DOI
10.1101/2025.03.27.645747
Open publication

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Loss of <i>Kmt2c</i> / <i>d</i> promotes gastric cancer initiation and confers vulnerability to mTORC1 inhibition and anti-PD1 immunotherapyDOI 10.1101/2025.03.27.645747
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