肿瘤研究与临床
腫瘤研究與臨床
종류연구여림상
CANCER RESEARCH AND CLINIC
2008年
10期
690-694
,共5页
食管肿瘤%等位基因%杂合性,丢失
食管腫瘤%等位基因%雜閤性,丟失
식관종류%등위기인%잡합성,주실
Esophageal neoplasms%Alleles%Heterozygosity,loss of
目的 探讨食管鳞状细胞癌(ESCC)发生、发展过程中基因的变化及多位点之间的相关性,发现9号染色体上与ESCC密切相关的抑癌基因.方法 通过手工显微切割、PCR扩增、变性聚丙烯酰胺凝胶电泳、AgNO3染色等技术,对照正常组织,检测不典型增生及癌组织在9号染色体上6个微卫星位点的杂合性缺失(LOH)的情况,同时分析该6个位点之间的相关性.结果 在有信息的病例中,正常组织未发生LOH,不典型增生总LOH率为17.2%(25/145),ESCC总LOH率为24.9%(43/173);不典型增生和ESCC组织中,6个微卫星位点的LOH率依次分别为D9S162(20.8%、36.7%)、D9S171(33.3%、36%)、D9S753(34.8%、46.2%)、D9S1748(4.2%、13.8%)、D9S242(14.3%、21.2%)、D9S43(0、0).无论在不典型增生还是在癌组织中,其LOH在9号染色体的各位点之间差异有统计学意义(x2=17.26,P<0.005;X3=22.66,P<0.005).结论 从正常组织到不典型增生再到癌变的过程中,存在染色体改变的累积.D9S171、D9S162、D9S242、D9S753位点存在较高的等位基因LOH,均>20%,各位点或其附近可能存在与ESCC发展相关的抑癌基因.
目的 探討食管鱗狀細胞癌(ESCC)髮生、髮展過程中基因的變化及多位點之間的相關性,髮現9號染色體上與ESCC密切相關的抑癌基因.方法 通過手工顯微切割、PCR擴增、變性聚丙烯酰胺凝膠電泳、AgNO3染色等技術,對照正常組織,檢測不典型增生及癌組織在9號染色體上6箇微衛星位點的雜閤性缺失(LOH)的情況,同時分析該6箇位點之間的相關性.結果 在有信息的病例中,正常組織未髮生LOH,不典型增生總LOH率為17.2%(25/145),ESCC總LOH率為24.9%(43/173);不典型增生和ESCC組織中,6箇微衛星位點的LOH率依次分彆為D9S162(20.8%、36.7%)、D9S171(33.3%、36%)、D9S753(34.8%、46.2%)、D9S1748(4.2%、13.8%)、D9S242(14.3%、21.2%)、D9S43(0、0).無論在不典型增生還是在癌組織中,其LOH在9號染色體的各位點之間差異有統計學意義(x2=17.26,P<0.005;X3=22.66,P<0.005).結論 從正常組織到不典型增生再到癌變的過程中,存在染色體改變的纍積.D9S171、D9S162、D9S242、D9S753位點存在較高的等位基因LOH,均>20%,各位點或其附近可能存在與ESCC髮展相關的抑癌基因.
목적 탐토식관린상세포암(ESCC)발생、발전과정중기인적변화급다위점지간적상관성,발현9호염색체상여ESCC밀절상관적억암기인.방법 통과수공현미절할、PCR확증、변성취병희선알응효전영、AgNO3염색등기술,대조정상조직,검측불전형증생급암조직재9호염색체상6개미위성위점적잡합성결실(LOH)적정황,동시분석해6개위점지간적상관성.결과 재유신식적병례중,정상조직미발생LOH,불전형증생총LOH솔위17.2%(25/145),ESCC총LOH솔위24.9%(43/173);불전형증생화ESCC조직중,6개미위성위점적LOH솔의차분별위D9S162(20.8%、36.7%)、D9S171(33.3%、36%)、D9S753(34.8%、46.2%)、D9S1748(4.2%、13.8%)、D9S242(14.3%、21.2%)、D9S43(0、0).무론재불전형증생환시재암조직중,기LOH재9호염색체적각위점지간차이유통계학의의(x2=17.26,P<0.005;X3=22.66,P<0.005).결론 종정상조직도불전형증생재도암변적과정중,존재염색체개변적루적.D9S171、D9S162、D9S242、D9S753위점존재교고적등위기인LOH,균>20%,각위점혹기부근가능존재여ESCC발전상관적억암기인.
Objective To investigate the gene variation and the dependability and to evaluate the possible tumor suppressor genes on chromosome 9 in the development and progression of EC. Methods LOH was detected in normal esophageal mucosa, high-grade squamous dysplasia and esophageal squamous cell carcinoma by microdissection, polymerase chain reaction, denaturing polyacrylamide gel eleetrophoresis and silver nitrate staining technology. The changes of LOH at six microsatellite markers and the relationship between LOH rate were analyzed. Results In the informative cases, total frequency of LOH was 17.2 % in high-grade squamous dysplasia and 24.9 % in esophageal squamous cell carcinoma. In high grade squamous dysplasia and squamous cell carcinoma, LOH was detected at marker D9S162 (20.8 %, 36.7 %), D9S171 (33.3 %, 36 %), D9S753(34.8 %, 46.2 %), D9S1748(4.2 %, 13.8 %), D9S242(14.3 %, 21.2 %), D9S43(0, 0). The frequency of LOH showed significant difference among the six microsatellite markers (X2=17.26, P< 0.005; X2=22.66,P<0.005). Conclusion The progression from normal squamous epithelium to high-grade Squamous dysplasia and subsequently to squamous cell carcinoma of the esophagus is associated with accumulation of chromosomal change. The situs of D9S171, D9S162, D9S242, D9S753 exist higher LOH and all exceed 20 %. Possible tumor suppressor genes at or near D9S171, D9S162, D9S242, D9S753 may be related to the progression of esophageal squamous cell carcinoma.
