摘要
目的研究肿瘤细胞凋亡抑制基因bcl-2与血管内皮生长因子(VEGF)在乳腺癌中的表达情况及二者间的相关性,探讨其在乳腺癌中的预后价值。方法应用免疫组织化学法检测64例乳腺癌组织bcl-2与VEGF。结果bcl-2的阳性表达率为66%,VEGF的阳性表达率为62%。bcl-2的表达与腋淋巴结转移、组织学分级,同时还与雌激素受体(ER)、孕激素受体(PR)的表达呈正相关;腋淋巴结转移组与非转移组之bcl-2表达差异有统计学意义,提示bcl-2的表达可能与肿瘤的进展有关。VEGF与肿瘤的大小、TNM分期、组织学分级、腋淋巴结转移呈正相关。VEGF阳性患者的预后明显差于VEGF阴性患者。bcl-2与VEGF有显著的相关性,呈正相关。结论①bcl-2表达失调导致乳腺癌细胞凋亡调控紊乱,促进乳腺癌细胞的生长和腋淋巴结转移,进而影响乳腺癌的生物学行为。②VEGF通过促进肿瘤微血管生成和血管通透性增加,参与恶性肿瘤的侵袭、转移。③VEGF与bcl-2相互作用,共同参与乳腺癌的发生和发展。④通过对VEGF及bcl-2表达的研究,为肿瘤基因靶向治疗、抗血管生成治疗策略提供了理论依据。
Objectives To investigate the expression of bcl-2,vascular endothelial growth factor(VEGF) in breast cancer, and the relationship of these two factors. Method Sixty-four women of primary breast carcinoma were studied for the expression of bcl-2 and VEGF proteins with the method of automated immunohistochemical assay.Results Forty-two(66%) and forty(62%)breast cancer cases were found positive for bcl-2 and VEGF.A statistically significant association was found between the bcl-2 expression and the high grading,positive lymph nodes,estrogen receptor(ER) positivity,progestin receptor(PR) positivity.Bcl-2 may extend the viability of cells containing genetic alterations,and facilitate tumor progression.The VEGF expression is negatively related to the ER and PR;VEGF is positivily related to tumor size,lymph nodes,high grading;besides bcl-2 and VEGF themselves also have a positive correlation. Conclutions ①Disorder of bcl-2 expression made the breast cancer cells have a disorder in apoptosis′ modulation,so promoting the cancer cell′s growth and axillary lymphnode metastasis,even affecting their biological behavior;②VEGF,via its enhancing the cancer cells′ microvascularization and raising their permeability,takes part in the cancer′s invasion and metastasis;③The interaction of VEGF and bcl-2 participates in the genesis and development of breast cancer;④Researching the VEGF and bcl-2 expression offered a theoretical basis for the gene-targeted therapy and antivascularization.
出处
《中国药物与临床》
CAS
2005年第6期427-430,共4页
Chinese Remedies & Clinics
基金
太原市科技启明星基金资助项目(0202103)
