Study on the mechanism of imatinib-induced resistance in gastrointestinal stromal tumors / 中华肿瘤杂志
Chinese Journal of Oncology
;
(12): 597-601, 2009.
Article
in Chinese
| WPRIM
| ID: wpr-295241
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the mechanism of imatinib mesylate (IM) induced-resistance in the patients with gastrointestinal stromal tumors (GISTs) and treated with imatinib.</p><p><b>METHODS</b>Eight patients with GIST treated with IM developed secondary IM resistance. A total of 16 tumor samples (pre-IM therapy) and 11 tumor samples (post-IM treatment) were available. Exon 9, 11, 13, and 17 of c-kit gene as well as exon 12 and exon 18 of PDGFRA gene were sequenced.</p><p><b>RESULTS</b>In addition to the changes of baseline genotype, the IM-induced gene changes were concentrated in the kinase domain of c-kit gene in all 8 patients, 2 of them were located in the exon 13 of c-kit gene presenting with V654A, while 6 in exon 17 involving 816 and 820 to 823 codons.</p><p><b>CONCLUSION</b>The mechanism of imatinib mesylate resistance after initial treatment with this agent in gastrointestinal stromal tumors is a novel mutation development in kinase domain of c-kit.</p>
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Pathology
/
Piperazines
/
Pyrimidines
/
General Surgery
/
Benzamides
/
Protein-Tyrosine Kinases
/
Codon
/
Exons
/
Follow-Up Studies
/
Proto-Oncogene Proteins c-kit
Type of study:
Observational study
/
Prognostic study
Limits:
Adult
/
Aged
/
Female
/
Humans
/
Male
Language:
Chinese
Journal:
Chinese Journal of Oncology
Year:
2009
Type:
Article
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