NDLI: Secondary mutations of c-KIT contribute to acquired resistance to imatinib and decrease efficacy of sunitinib in Chinese patients with gastrointestinal stromal tumors.

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Secondary mutations of c-KIT contribute to acquired resistance to imatinib and decrease efficacy of sunitinib in Chinese patients with gastrointestinal stromal tumors.

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Secondary mutations of c-KIT contribute to acquired resistance to imatinib and decrease efficacy of sunitinib in Chinese patients with gastrointestinal stromal tumors.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Gao, Jing Tian, Ye Li, Jian Sun, Naiping Yuan, Jiajia Shen, Lin
Description	Country affiliation: China Author Affiliation: Gao J ( Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Department of GI Oncology, Peking University Cancer Hospital and Institute, No. 52, Fucheng Road, Haidian District, Beijing 100142, China.)
Abstract	The aim of this study was to investigate the associations between secondary mutations of c-KIT/PDGFR and acquired imatinib resistance or efficacy of sunitinib in Chinese patients with gastrointestinal stromal tumors (GISTs). Mutations of c-KIT (exons 9, 11, 13, 14, 17, and 18) and PDGFR (exons 12 and 18) in tumor samples of 50 patients were analyzed by direct sequencing. A total of 50 samples before imatinib and 52 samples after imatinib were collected. Among 52 samples after imatinib, 38 samples were imatinib resistant and 14 samples were imatinib sensitive. All patients before imatinib treatment had primary mutations of c-KIT exon 11 (n = 45) or exon 9 (n = 5), and no PDGFR mutations were found in these patients. After imatinib treatment, 25 of 38 (65.8 %) resistant tumors had secondary mutations in c-KIT exon 13 (n = 10), exon 14 (n = 1), exon 17 (n = 12) and exon 18 (n = 2), while no secondary mutations of c-KIT were found in 14 sensitive tumors (P < 0.001), indicating the close association of c-KIT secondary mutations with imatinib-acquired resistance. In our study, 19 patients received sunitinib treatment after the failure of imatinib, and it seemed that the median progression-free survival (7 vs. 19 months, P = 0.244) in patients with secondary mutations (n = 13) was lower than that in patients without secondary mutations (n = 6). Secondary mutations of c-KIT were significantly associated with acquired resistance to imatinib in Chinese GIST patients, and whether secondary mutations of c-KIT could influence the efficacy of sunitinib needed to be further investigated.
File Format	HTM / HTML
ISSN	13570560
Issue Number	2
Volume Number	30
e-ISSN	1559131X
Journal	Medical Oncology
Language	English
Publisher	Springer
Publisher Date	2013-06-01
Publisher Place	United States
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Research Support, Non-u.s. Gov't Gastrointestinal Neoplasms Humans Middle Aged Pyrroles Molecular Sequence Data Drug Resistance, Neoplasm Male Journal Article Young Adult Pyrimidines Genetics Adult Female Retrospective Studies Indoles Trends Discipline Oncology Amino Acid Sequence Piperazines Mortality Drug Therapy Antineoplastic Agents Survival Rate Treatment Outcome Imatinib Mesylate Therapeutic Use Asian Continental Ancestry Group Aged Benzamides Mutation Proto-oncogene Proteins C-kit Gastrointestinal Stromal Tumors
Content Type	Text
Resource Type	Article
Subject	Hematology Cancer Research Oncology

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