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通过促进增殖和抑制凋亡来评论 c-KIT  基因突变与胃肠道间质肿瘤的发展

 

Authors Ma YY, Yu S, He XJ, Xu Y, Wu F, Xia YJ, Guo K, Wang HJ, Ye ZY, Zhang W, Tao HQ

Published Date May 2014 Volume 2014:7 Pages 637—643

DOI http://dx.doi.org/10.2147/OTT.S60458

Received 10 January 2014, Accepted 26 February 2014, Published 2 May 2014

Abstract: The aim of this study was to discuss the role of  c-KIT  mutation in the pathogenesis of gastrointestinal stromal tumors (GISTs) and analyze its correlation with proliferation and apoptosis.  c-KIT  and PDGFRA  genotypes were examined by deoxyribonucleic acid sequencing. Immunohistochemistry was performed to determine the expression levels of Kit, Ki-67 (proliferation marker), and apoptotic protease-activating factor (APAF)-1 (apoptosis marker) and the relationship between their three genes. In the 68 cases examined, 44 cases (64.7%) showed mutations in one of the four exons of c-KIT . The mutations were most frequently found in exon 11 (30 cases [44.1%]), followed by exon 9 (ten cases [14.7%]) and exon 13 (four cases [5.9%]). c-KIT  mutation showed no association with prognostic factors using the classification of risk of aggressive behavior in GIST proposed by Fletcher et al. No cases had mutated exon 17 of c-KIT , and neither did exon 12, 14, or 18 of PDGFRA  in our present study. There was a positive correlation between the expression level of Kit and Ki-67 (R =0.282, P =0.020). Conversely, a negative correlation was found between the expression levels of Kit and APAF1 (R =−0.243, P =0.046). In conclusion, most GISTs with Kit expression showed c-KIT  mutation. Kit expression has a positive correlation with Ki-67 and a negative correlation with APAF1, showing that c-KIT  is involved in GIST occurrence and development through proliferation promotion and apoptosis inhibition.
Keywords: gastrointestinal stromal tumors, c-KIT , mutation, proliferation, apoptosis


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