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Article

DDR1/2 enhance KIT activation and imatinib resistance of primary and secondary KIT mutants in gastrointestinal stromal tumors.

Molecular carcinogenesis - 1 Jan 2024

Liu Anbu, Zhang Shaoting, Wang Ming, Zhang Liangying, Xu Shidong, Nasimian Ahmad, Li Shujing, Zhao Sien, Cao Xu, Tian Jinhai, Yu Yuanyuan, Fan Zhaoyang, Xiao Kun, Zhao Hui, Kazi Julhash U, Ma Lijun, Sun Jianmin

Abstract excerpt

Gastrointestinal stromal tumors (GISTs) are predominantly initiated by KIT mutations. In this study, we observed that discoidin domain receptors 1 and 2 (DDR1 and DDR2) exhibited high expression in GISTs, were associated with KIT, and enhanced the activation of both wild-type KIT and primary KIT mutants. Inhibition of DDR1/2 led to a reduction in the activation of KIT and its downstream signaling molecules,...

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Share to Gastrointestinal Stromal Tumors
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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Source

Identifiers

PMID: 37737519
DOI: 10.1002/mc.23637

Genes

KIT
DDR1
DDR2

Variants

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026.

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