CAJ | 학술논문

目的观察端粒酶基因在乳腺癌前病变-乳腺导管非典型增生及乳腺癌中的表达,探讨其与恶性转化的关系.方法应用原位杂交方法评价端粒酶基因hTR和hTRT在50例乳腺增生组织(其中乳腺单纯性增生6例,轻度非典型增生9例,中度非典型增生12例,重度非典型增生23例)及26例乳腺癌中的表达.结果在乳腺导管单纯性增生组织中端粒酶基因(hTR、hTRTmRNA)呈弱表达(16.6%)或表达阴性.在乳腺导管轻、中度非典型增生组织中端粒酶基因(hTR、hTRTmRNA)呈弱表达(22.2%,11.1%;33.3%,25.0%),在乳腺导管重度非典型增生组织中端粒酶基因(hTR、hTRTmRNA)表达增强(60.9%,52.1%),在乳腺癌组织中端粒酶基因(hTR、hTRTmRNA)呈较强阳性表达(88.5%,80.8%).乳腺导管重度非典型增生组织中的端粒酶基因表达与在轻中度非典型增生、乳腺浸润性导管癌组织中的表达比较差异显著(P<0.05),但与导管内癌表达无显著差异(P>0.05).结论端粒酶基因hTR、hTRT的表达与乳腺导管非典型增生细胞的恶性转化有关,端粒酶的重新激活可能在乳腺癌的组织发生中起作用.
목적관찰단립매기인재유선암전병변-유선도관비전형증생급유선암중적표체,탐토기여악성전화적관계.방법응용원위잡교방법평개단립매기인hTR화hTRT재50례유선증생조직(기중유선단순성증생6례,경도비전형증생9례,중도비전형증생12례,중도비전형증생23례)급26례유선암중적표체.결과재유선도관단순성증생조직중단립매기인(hTR、hTRTmRNA)정약표체(16.6%)혹표체음성.재유선도관경、중도비전형증생조직중단립매기인(hTR、hTRTmRNA)정약표체(22.2%,11.1%;33.3%,25.0%),재유선도관중도비전형증생조직중단립매기인(hTR、hTRTmRNA)표체증강(60.9%,52.1%),재유선암조직중단립매기인(hTR、hTRTmRNA)정교강양성표체(88.5%,80.8%).유선도관중도비전형증생조직중적단립매기인표체여재경중도비전형증생、유선침윤성도관암조직중적표체비교차이현저(P<0.05),단여도관내암표체무현저차이(P>0.05).결론단립매기인hTR、hTRT적표체여유선도관비전형증생세포적악성전화유관,단립매적중신격활가능재유선암적조직발생중기작용.
Objective To investigate telomerase gene expression in precancerous mammary lesion, such as atypical ductal hyperplasia and breast cancer and to study the relationship between expression and malignant transformation.Methods Expression of human telomerase genes (hTR) and human reverse transcriptase gene (hTRT) in 76 cases of mammary tissue was evaluated using in situ hybridization and included 50 cases of mammary hyperplasia, 6 of which were benign hyperplasia, 9 were mild atypical hyperplasia, 12 were moderate atypical hyperplasia, 23 were severe atypical hyperplasia and 26 were mammary cancer. Results The expressions of hTR and hTRT mRNA were much weaker or negative in benign hyperplasia (16.6%, 0), weak to mild-moderate in atypical hyperplasia (22.2%, 11.1%, 33.3%, 25.0%), strong in severe atypical hyperplasia (60.9%, 52.1%), and significantly strong in mammary cancer (88.5%, 80.8%).The difference between mild-moderate atypical hyperplasia, invasive ductal carcinoma and severe atypical hyperplasia was significant (P<0.05) and the difference between severe atypical hyperplasia and intraductal carcinoma was not significant (P>0.05). Conclusion Telomerase genes (hTR and hTRT) expressions are related to the transformation of atypical hyperplasia. Activated telomerase may play a role in mammary cancer development.