Recurrent gastrointestinal stromal tumor (GIST) of the stomach associated with a novel c-kit mutation after imatinib treatment.
Recurrent gastrointestinal stromal tumor (GIST) of the stomach associated with a novel c-kit mutation after imatinib treatment.
复制标题
DOI：
10.1007/s10120-006-0368-5
复制
发表时间：
2006-01-01
期刊：
影响因子：
--
通讯作者：
Yanaga, Katsuhiko
中科院分区：
文献类型：
--
作者：
Koyama, Tomoki;Nimura, Hiroshi;Yanaga, Katsuhiko
一名57岁男子患有胃肠道间质瘤（GIST）并腹膜扩散，接受了胃切除术。手术后，他接受了400 mg/天的伊马替尼治疗，26个月没有复发。在26个月时，由于恶心而减少伊马替尼剂量，在剂量减少后4个月，检测到GIST复发，再次进行手术切除。第一个手术标本在c-kit受体基因的第11外显子有突变。有趣的是，第二个手术标本在c-kit受体基因中，除了上述突变外，还有一个外显子17的新突变。根据分子生物学分析结果，长期化疗诱导的外显子17的新突变被判定为是复发的原因，这可能是由伊马替尼剂量减少引发的。
A 57-year-old man with gastrointestinal stromal tumor (GIST) of the stomach with peritoneal dissemination underwent gastrectomy. After surgery, he was treated with 400 mg/day of imatinib, without recurrence, for 26 months. At 26 months, the imatinib dose was reduced because of nausea, and 4 months after the dose reduction, recurrence of GIST was detected, for which surgical resection was performed again. The first surgical specimen had a mutation of exon 11 in the c-kit receptor gene. Intriguingly, the second surgical specimen had a novel mutation of exon 17, in addition to the above-mentioned mutation, in the c-kit receptor gene. Based on the result of molecular analysis, the novel mutation of exon 17, induced by longterm chemotherapy, was judged to have been responsible for the recurrence, which perhaps was triggered by the dose reduction of imatinib.