中国现代医学杂志
中國現代醫學雜誌
중국현대의학잡지
CHINA JOURNAL OF MODERN MEDICINE
2007年
9期
1028-1032
,共5页
马萍%王睿%赵艳%宋敏%宋继谒
馬萍%王睿%趙豔%宋敏%宋繼謁
마평%왕예%조염%송민%송계알
乳腺导管非典型增生%乳腺癌%端粒酶%凋亡%基因表达
乳腺導管非典型增生%乳腺癌%耑粒酶%凋亡%基因錶達
유선도관비전형증생%유선암%단립매%조망%기인표체
mammary ductal atypical hyperplasia%breast tumor%telomerase%apoptosis%gene expression
目的 观察端粒酶基因(hTR、hTRT)、凋亡相关基因(p53、bcl-2)在乳腺癌及癌前病变中的表达及相互关系.方法 应用原位杂交方法检测端粒酶基因(hTR、hTRT)和凋亡相关基因(p53、bcl-2)mRNA在44例乳腺导管非典型增生组织中的表达,应用免疫组化方法检测p53基因蛋白在上述病例中的表达,并与6例乳腺良性乳腺增生及26例乳腺癌病例进行了比较.结果 端粒酶基因(hTR、hTRTmRNA)在乳腺导管重度非典型增生组织中表达增强(60.9%,52.1%),其表达与在轻、中度非典型增生中(分别为22.2%,11.1%和33.3%,25.0%)和乳腺癌组织中(88.5%,80.8%)的表达差异显著(P<0.05).p53mRNA在乳腺导管非典型增生组织中的表达随着异型性的增加而下降,而p53基因蛋白则相应增加.Bcl-2在乳腺导管非典型增生组织中呈中度表达,其中以在重度中表达明显.结论 端粒酶基因hTR、hTRT的表达与乳腺非典型增生细胞的恶性转化密切相关,同时可检测到p53mRNA的表达缺失、p53蛋白突变及bcl-2mRNA的过表达,且表达水平与端粒酶活性有相关关系.
目的 觀察耑粒酶基因(hTR、hTRT)、凋亡相關基因(p53、bcl-2)在乳腺癌及癌前病變中的錶達及相互關繫.方法 應用原位雜交方法檢測耑粒酶基因(hTR、hTRT)和凋亡相關基因(p53、bcl-2)mRNA在44例乳腺導管非典型增生組織中的錶達,應用免疫組化方法檢測p53基因蛋白在上述病例中的錶達,併與6例乳腺良性乳腺增生及26例乳腺癌病例進行瞭比較.結果 耑粒酶基因(hTR、hTRTmRNA)在乳腺導管重度非典型增生組織中錶達增彊(60.9%,52.1%),其錶達與在輕、中度非典型增生中(分彆為22.2%,11.1%和33.3%,25.0%)和乳腺癌組織中(88.5%,80.8%)的錶達差異顯著(P<0.05).p53mRNA在乳腺導管非典型增生組織中的錶達隨著異型性的增加而下降,而p53基因蛋白則相應增加.Bcl-2在乳腺導管非典型增生組織中呈中度錶達,其中以在重度中錶達明顯.結論 耑粒酶基因hTR、hTRT的錶達與乳腺非典型增生細胞的噁性轉化密切相關,同時可檢測到p53mRNA的錶達缺失、p53蛋白突變及bcl-2mRNA的過錶達,且錶達水平與耑粒酶活性有相關關繫.
목적 관찰단립매기인(hTR、hTRT)、조망상관기인(p53、bcl-2)재유선암급암전병변중적표체급상호관계.방법 응용원위잡교방법검측단립매기인(hTR、hTRT)화조망상관기인(p53、bcl-2)mRNA재44례유선도관비전형증생조직중적표체,응용면역조화방법검측p53기인단백재상술병례중적표체,병여6례유선량성유선증생급26례유선암병례진행료비교.결과 단립매기인(hTR、hTRTmRNA)재유선도관중도비전형증생조직중표체증강(60.9%,52.1%),기표체여재경、중도비전형증생중(분별위22.2%,11.1%화33.3%,25.0%)화유선암조직중(88.5%,80.8%)적표체차이현저(P<0.05).p53mRNA재유선도관비전형증생조직중적표체수착이형성적증가이하강,이p53기인단백칙상응증가.Bcl-2재유선도관비전형증생조직중정중도표체,기중이재중도중표체명현.결론 단립매기인hTR、hTRT적표체여유선비전형증생세포적악성전화밀절상관,동시가검측도p53mRNA적표체결실、p53단백돌변급bcl-2mRNA적과표체,차표체수평여단립매활성유상관관계.
[Objective] To investigate the expression and the relationship between telomerase genes(hTR,hTRT)and apoptosis related genes(p53, bcl-2) in breast ductal cancer and precancerous lession. [Methods] Expressions of telomerase genes (hTR,hTRT), p53, and bcl-2 genes mRNA were detected by in situ hybridization, and the expression of the p53 protein was detected by immunohistochemistry. 44 patients with ductal atypical hyperplasia were selected and compared with 6 of benign hyperplasia and 26 of breast ductal cancer. [Results] The expression of telomerase genes (hTR, hTRT mRNA) in severe ductal atypical hyperplasia was enhanced (60.9%,52.1%), and significantly different from those in mild-medium ductal atypical hyperplasia (22.2%, 11.1%; 33.3%, 25.0%)and breast ductal cancer(88.5%, 80.8%) (P <0.05). With the upgrading of atypia of atypia of ductal hyperplasia, expression of wild p53 mRNA (mild: 55.6%; medium: 41.7%; severe: 26.1%) decreased while expression of the p53 protein (mild:11.1%: medium: 25.0%; severe: 34.8%) increased. As for bcl-2 mRNA, it showed moderate expression more obviously in severe atypical hyperplasia. [Conclusion] There is a significant correlation between the expression of telomerase genes(hTR, hTRT) and the state of malignant transformation in ductal atypical hyperplasia. The absence of p53 mRNA, the mutation of p53 protein and the overexpression of bcl-2 mRNA, which associate with telomerase activation, can be detected.