期刊文献+

野生型胃肠间质瘤分子机制研究进展 被引量:3

Progress in understanding of molecular mechanisms of wild-type gastrointestinal stromal tumors
下载PDF
导出
摘要 胃肠道间质瘤(gastrointestinal stromal tumor,GIST)是消化系最常见的间叶源性肿瘤,80%-95%GIST存在KIT或PDGFRA基因突变,未突变者称为野生型GIST(WT-GIST).目前证实,突变型GIST对酪氨酸激酶抑制剂(tyrosine kinase inhibitor,TKI)分子靶向治疗有效.但WT-GIST通常对TKI类药物不敏感,其分子理论基础、发生机制需明确阐述. Gastrointestinal stromal tumors (GIST) are the most frequent mesenchymal tumors of the gastrointestinal tract, 80%-95% of which have KIT and PDGFRA gene mutations. GISTs without gene mutations, including KIT and PDGFRA gene mutations, are called wild- type GISTs (WT-GISTs). The development of a molecular drug targeting tyrosine kinase inhibitor (TKI) has changed the therapeutic of GISTs with gene mutations; however, WT- GISTs are not sensitive to TKI. The molecular basis and mechanism of these characteristics should be elucidated.
出处 《世界华人消化杂志》 CAS 2017年第13期1166-1172,共7页 World Chinese Journal of Digestology
关键词 野生型胃肠间质瘤 分子机制 基因突变 Wild type gastrointestinal stromaltumor Molecular mechanism Genetic mutation
  • 相关文献

参考文献2

二级参考文献38

  • 1Nilsson B, Bumming P, Meis-Kindblom JM, et al. Gastrointestinal stromal tumor: the incidence, prevalence, clinical course, and prognostication in the prcimatinib mesylate era-a population-based study in western Sweden [ J ]. Cancer, 2005, 103(4): 821-829.
  • 2Agaimy A, Wunsch PH, Hofstaedter F, et al. Minute gastric sclerosing stromal tumors (GIST tumorlets) are common in adults and frequently show c-KIT mutations [ J ] . Am J Surg Pathol, 2007, 31(1 ) :113-120.
  • 3Rossi S, Gasparotto D, Toffolatti L, et al. Molecular and clinicopathologic characterization of gastrointestinal stromal tumors (GIST) of small size[J]. Am J Surg. Pathol, 2010, 34 (10) : 1480-1491.
  • 4Pauwels P, Debiec-Rychter M, Stul M, et al. Changing phenotype of gastrointestinalstromal tumours under imatinib mesylate treatment: a potential diagnostic pitfall [ J ]. Histopathology, 2005, 47 ( 1 ) :41-47.
  • 5Antonescu CR, Romeo S, Zhang L, et al. Dedifferentiation in gastrointestinal stromal tumor to an anaplastic KIT-negative phenotype: a diagnostic pitfall: morphologic and molecular characterization of 8 cases occurring either de novo or after imatinib therapy[J]. Am J Surg Pathol, 2013, 37(3) :385-392.
  • 6Agaram NP, Wong GC, Guo T, et al. Novel V600E BRAF mutations in imatinib-naive and imatinib-resistant gastrointestinal stromal tumors[ J]. Genes Chromosom Cancer, 2008, 47 (10) : 853-859.
  • 7Liegl B, Homiek JL, Antonescu CR, et al. Rhabdomyosarcomatous differentiation in gastrointestinal stromal tumors after tyrosine kinase inhibitor therapy: a novel form of tumor progression [ J]. Am J Surg Pathol, 2009, 33 (2) : 218- 226.
  • 8Huizinga JD, Thuneberg L, Kluppel M, et al. W/kit gene required for interstitial ceils of Cajal and for intestinal pacemaker activity[J]. Nature, 1995, 373(6512): 347-349.
  • 9Chi P, Chen Y, Zhang L, et al. ETV1 is a lineage survival factor that cooperates with KIT in gastrointestinal stromal tumours [ J ]. Nature, 2010, 467(7317) :849-853.
  • 10Hirota S, Isozaki K, Moriyama Y, et al. Gain-of-function mutations of c-kit in human gastrointestinal stromal tumors [ J ]. Science, 1998, 279(5350) :577-580.

共引文献12

同被引文献14

引证文献3

二级引证文献11

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部