Associated Papers
Germ cell immunoprofile and KIT exon 17 mutation guide rectification of seminoma misclassified as epithelioid gastrointestinal stromal tumor: A case report.
Zhang X et al.
Biomedical Reports, 2026
Clinicopathological characteristics of progressive gastrointestinal stromal tumors and heterogeneity analyses of secondary mutations.
Li J et al.
The Oncologist, 2025
The Utility of NGS Analysis in Homologous Recombination Deficiency Tracking.
Tsantikidi A et al.
Diagnostics (basel, Switzerland), 2023
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
Monitoring Circulating Tumor DNA During Surgical Treatment in Patients with Gastrointestinal Stromal Tumors.
Johansson G et al.
Molecular Cancer Therapeutics, 2021
Landscape of drug-resistance mutations in kinase regulatory hotspots.
Kim P et al.
Briefings in Bioinformatics, 2021
Mutational spectrum and precision oncology for biliary tract carcinoma.
Lin J et al.
Theranostics, 2021
The V654A second-site KIT mutation increases tumor oncogenesis and STAT activation in a mouse model of gastrointestinal stromal tumor.
Zhang JQ et al.
Oncogene, 2020
Secondary Resistant Mutations to Small Molecule Inhibitors in Cancer Cells.
Hamid AB et al.
Cancers, 2020
Identifying Secondary Mutations in Chinese Patients with Imatinib-Resistant Gastrointestinal Stromal Tumors (GISTs) by Next Generation Sequencing (NGS).
Du J et al.
Pathology Oncology Research : Por, 2020
Loss of PI3 kinase association improves the sensitivity of secondary mutation of KIT to Imatinib.
Zhu G et al.
Cell & Bioscience, 2020
The Immunogenic Potential of Recurrent Cancer Drug Resistance Mutations: An In Silico Study.
Punta M et al.
Frontiers in Immunology, 2020
FGFR1 and NTRK3 actionable alterations in "Wild-Type" gastrointestinal stromal tumors.
Shi E et al.
Journal of Translational Medicine, 2016
Acquired Resistance to the TRK Inhibitor Entrectinib in Colorectal Cancer.
Russo M et al.
Cancer Discovery, 2016
[Role of molecular subtypes in gastrointestinal stromal tumors in a clinical setting].
Pan Z et al.
Zhonghua Wei Chang Wai Ke Za Zhi = Chinese Journal of Gastrointestinal Surgery, 2014
Flumatinib, a selective inhibitor of BCR-ABL/PDGFR/KIT, effectively overcomes drug resistance of certain KIT mutants.
Zhao J et al.
Cancer Science, 2014
Assessment of computational methods for predicting the effects of missense mutations in human cancers.
Gnad F et al.
Bmc Genomics, 2013
Fresh surgical specimens yield breast stem/progenitor cells and reveal their oncogenic abnormalities.
Pommier SJ et al.
Annals of Surgical Oncology, 2012
Mechanisms of resistance to imatinib and sunitinib in gastrointestinal stromal tumor.
Wang WL et al.
Cancer Chemotherapy and Pharmacology, 2011
Disruption of the EGFR E884-R958 ion pair conserved in the human kinome differentially alters signaling and inhibitor sensitivity.
Tang Z et al.
Oncogene, 2009
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
Clonal evolution of resistance to imatinib in patients with metastatic gastrointestinal stromal tumors.
Desai J et al.
Clinical Cancer Research : an Official Journal of the American Association for Cancer Research, 2007
Surgical management after neoadjuvant imatinib therapy in gastrointestinal stromal tumours (GISTs) with respect to imatinib resistance caused by secondary KIT mutations.
Haller F et al.
Annals of Surgical Oncology, 2007
Lack of Response to Imatinib in Melanoma Carrying Rare KIT Mutation p.T632I.
Orlova KV et al.
Case Reports in Oncology, 0