CAJ | 학술논문

目的通过检测结直肠腺癌中神经内分泌(NE)细胞微卫星改变和p53基因突变,探讨结直肠腺癌中NE细胞的克隆性起源.方法采用激光捕获显微切割(LCM)技术,应用DNA抽提和全基因组扩增,在全基因组范围内选取26个微卫星位点,使用聚合酶链反应-单链构象多态性(PCR-SSCP)-银染色检测30例伴NE分化的结直肠腺癌中腺癌细胞和NE细胞的微卫星不稳定(MSI)、杂合性缺失(LOH)改变情况,联合PCR测序检测p53基因突变发生情况.结果 30例样本MSI总发生率为16.9％,LOH总发生率为8.5％,腺癌细胞与NE细胞的MSI和LOH发生率差异无统计学意义.30例样本中6例微卫星改变完全一致,23例微卫星改变一致性大于不一致性,1例微卫星改变一致性与不一致性相同.微卫星改变一致性与不一致性的差异有统计学意义(t=11.138,P=0.000).p53基因突变发生率为16.7％,腺癌细胞与NE细胞发生一致性改变.结论结直肠腺癌中腺癌细胞与NE细胞具有相似的微卫星改变和完全一致的p53基因突变,推测两种细胞起源具有一致性.
목적 통과검측결직장선암중신경내분비(NE)세포미위성개변화p53기인돌변,탐토결직장선암중NE세포적극륭성기원.방법 채용격광포획현미절할(LCM)기술,응용DNA추제화전기인조확증,재전기인조범위내선취26개미위성위점,사용취합매련반응-단련구상다태성(PCR-SSCP)-은염색검측30례반NE분화적결직장선암중선암세포화NE세포적미위성불은정(MSI)、잡합성결실(LOH)개변정황,연합PCR측서검측p53기인돌변발생정황.결과 30례양본MSI총발생솔위16.9％,LOH총발생솔위8.5％,선암세포여NE세포적MSI화LOH발생솔차이무통계학의의.30례양본중6례미위성개변완전일치,23례미위성개변일치성대우불일치성,1례미위성개변일치성여불일치성상동.미위성개변일치성여불일치성적차이유통계학의의(t=11.138,P=0.000).p53기인돌변발생솔위16.7％,선암세포여NE세포발생일치성개변.결론 결직장선암중선암세포여NE세포구유상사적미위성개변화완전일치적p53기인돌변,추측량충세포기원구유일치성.
Objective To study the possible clonal origin of neuroendocrine cells in colorectal adenocarcinoma.Methods Twenty-six microsatellite loci were screened using laser capture microdissection,DNA extraction and whole genome amplification.Microsatellite instability (MSI) and loss of heterozygosity (LOH) in adenocarcinoma cells and neuroendocrine cells amongst 30 cases of colorectal carcinoma with neuroendocrine differentiation were detected using polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP)-silver staining.The mutation status of p53 was evaluated by PCR-sequencing.The clonal origin of neuroendocrine cells in colorectal adenocarcinoma was determined.Results Amongst the 30 cases studied,the prevalence of MSI was 16.9％ while that of LOH was 8.5％.The rate showed no statistically significant difference between adenocarcinoma cells and neuroendocrine cells.In 6 cases,the microsatellite alteration was entirely consistent.In 23 cases,the rate of microsatellite alteration consistency was greater than that of inconsistency.In 1 case,the consistency and inconsistency rates were identical.There was statistically significant difference between consistency and inconsistency of microsatellite alteration.The prevalence of p53 mutation was 16.7％ which was the same for both adenocarcinoma cells and neuroendocrine cells.Conclusions Adenocarcinoma cells and neuroendocrine cells in colorectal adenocarcinoma with neuroendocrine differentiation have similar biologic changes.It is likely that they are of identical origin.