Associated Papers
Clinicopathological characteristics of progressive gastrointestinal stromal tumors and heterogeneity analyses of secondary mutations.
Li J et al.
The Oncologist, 2025
Broad spectrum of regorafenib activity on mutant KIT and absence of clonal selection in gastrointestinal stromal tumor (GIST): correlative analysis from the GRID trial.
Jeffers M et al.
Gastric Cancer : Official Journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association, 2022
35050442 (PubMed )
Supplement: 10120_2021_1274_MOESM1_ESM.docx
Loss of PI3 kinase association improves the sensitivity of secondary mutation of KIT to Imatinib.
Zhu G et al.
Cell & Bioscience, 2020
SF3B1, NRAS, KIT, and BRAF Mutation; CD117 and cMYC Expression; and Tumoral Pigmentation in Sinonasal Melanomas: An Analysis With Newly Found Molecular Alterations and Some Population-Based Molecular Differences.
Wroblewska JP et al.
The American Journal of Surgical Pathology, 2019
Assessment of computational methods for predicting the effects of missense mutations in human cancers.
Gnad F et al.
Bmc Genomics, 2013
23819521 (PubMed )
Supplement: 1471-2164-14-S3-S7-S1.xlsx › COSMIC
Secondary mutations in the kinase domain of the KIT gene are predominant in imatinib-resistant gastrointestinal stromal tumor.
Nishida T et al.
Cancer Science, 2008
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