CAJ | 학술논문

目的：研究上皮细胞黏附分子E-钙黏蛋白( E-cadherin)在乳腺癌组织中的表达和临床意义。方法回顾性分析2009年11月至2014年10月在河南科技大学第一附属医院接受改良根治术的303例乳腺癌病例资料,应用免疫组织化学染色法检测癌组织中 E-cadherin 和 HER-2的表达,分析E-cadherin在不同分子分型乳腺癌中的表达特点及与临床病理特征的相关性。计数资料采用χ2检验或Fisher 确切概率法,相关性分析采用 Pearson 相关分析,并用Logistic回归分析影响E-cadherin表达的独立因素。结果303例乳腺癌组织中 E-cadherin 和 HER-2阳性表达率分别为71．9%(218/303)和16．2%(49/303)。 E-cadherin与患者年龄、月经状态、TNM 分期及腋窝淋巴结转移有关(χ2=4．854、8．277、8．757、10．614,P 均<0．050),HER-2表达与组织学分级有关(χ2=0．002,P<0．050)。 Pearson相关分析显示,乳腺癌组织中E-cadherin与HER-2、ER及PR呈正相关( r=0．135、0．206、0．135,P=0．019、0．000、0．019),而与 Ki67表达强度无关；HER-2与 ER、PR 呈负相关(r=-0．160、-0．118,P=0．005、0．040),与Ki67表达呈正相关(r=0．228,P=0．000)。 Logistic回归多因素分析显示年龄、肿瘤直径、TNM分期为影响E-cadherin表达的临床病理因素,而HER-2和ER是影响E-cadherin表达的分子病理因素。 E-cadherin阳性表达率在不同分子分型间差异有统计学意义(χ2=24．816,P=0．000),而三阴性乳腺癌( TNBC)为51．3%,显著低于luminal B型及HER-2过表达型( P均<0．008)。结论 E-cadherin 表达缺失与 TNBC 更容易发生侵袭转移密切相关,而HER-2和ER可能参与E-cadherin表达缺失的调控机制。
목적：연구상피세포점부분자E-개점단백( E-cadherin)재유선암조직중적표체화림상의의。방법회고성분석2009년11월지2014년10월재하남과기대학제일부속의원접수개량근치술적303례유선암병례자료,응용면역조직화학염색법검측암조직중 E-cadherin 화 HER-2적표체,분석E-cadherin재불동분자분형유선암중적표체특점급여림상병리특정적상관성。계수자료채용χ2검험혹Fisher 학절개솔법,상관성분석채용 Pearson 상관분석,병용Logistic회귀분석영향E-cadherin표체적독립인소。결과303례유선암조직중 E-cadherin 화 HER-2양성표체솔분별위71．9%(218/303)화16．2%(49/303)。 E-cadherin여환자년령、월경상태、TNM 분기급액와림파결전이유관(χ2=4．854、8．277、8．757、10．614,P 균<0．050),HER-2표체여조직학분급유관(χ2=0．002,P<0．050)。 Pearson상관분석현시,유선암조직중E-cadherin여HER-2、ER급PR정정상관( r=0．135、0．206、0．135,P=0．019、0．000、0．019),이여 Ki67표체강도무관；HER-2여 ER、PR 정부상관(r=-0．160、-0．118,P=0．005、0．040),여Ki67표체정정상관(r=0．228,P=0．000)。 Logistic회귀다인소분석현시년령、종류직경、TNM분기위영향E-cadherin표체적림상병리인소,이HER-2화ER시영향E-cadherin표체적분자병리인소。 E-cadherin양성표체솔재불동분자분형간차이유통계학의의(χ2=24．816,P=0．000),이삼음성유선암( TNBC)위51．3%,현저저우luminal B형급HER-2과표체형( P균<0．008)。결론 E-cadherin 표체결실여 TNBC 경용역발생침습전이밀절상관,이HER-2화ER가능삼여E-cadherin표체결실적조공궤제。
Objective To study the expression of epithelial cellular adhesion molecule ( E-cadherin) in different molecular subtypes of breast cancer and its clinical significance. Methods A total of 303 cases of breast cancer treated with modified radical mastectomy were retrospectively collected in the First Affiliated Hospital, Henan University of Science and Technology from November 2009 to October 2014. The expressions of E-cadherin and HER-2 in breast cancer tissues were detected by immunohistochemical staining to analyze the expression pattern of E-cadherin in different molecular subtypes of breast cancer and its association with clinico-pathological features of the patients. Numeration data was processed using χ2 test or Fisher ’ s exact test, correlation analysis was performed using Pearson method, and Logistic regression was used to analyze the independent factors in E-cadherin expression. Results The positive rates of E-cadherin and HER-2 in 303 cases of breast cancer were 71. 9% (218/303) and 16. 2% (49/303) respectively. E-cadherin expression was correlated with patients ’ age, menopausal status, TNM staging, and axillary lymph node metastasis (χ2 =4. 854,8. 277,8. 757,10. 614, all P<0. 050 );and HER-2 expression was associated with histological grade (χ2=0. 002,P<0. 050). Pearson correlation analysis showed that E-cadherin was positively correlated with HER-2, ER, and PR in breast cancer tissue (r=0. 135, 0. 206, 0. 135, P=0. 019, 0. 000, 0. 019), and not correlated with Ki67. HER-2 was negatively correlated with ER and PR ( r=-0. 160, -0. 118, P=0. 005, 0. 040), and positively correlated with Ki67 (r=0. 228, P=0. 000). Logistic regression showed that patients’ age, tumor size, and TNM staging, clinico pathological and HER-2 and ER were molecular pathological factors influencing E-cadherin expression in breast cancer. There was a significant difference in E-cadherin expression between different molecular subtypes of breast cancer (χ2 = 24. 816, P = 0. 000 ). The positive rate of E-cadherin expression was 51. 3% in triple-negative breast cancer ( TNBC ) , significantly lower than that in luminal B or HER-2-riched ( all P<0. 008 ) . Conclusion The deficiency of E-cadherin expression is associated with the biological behaviors of invasion and metastasis in TNBC, while HER-2 and ER may be involved in the regulatory mechanism of E-cadherin expression deficiency.