男性生殖细胞肿瘤p53、PCNA、bcl-2表达及临床病理学意义

目的:探讨男性生殖细胞肿瘤发生的可能分子生物学机制。 方法 :应用免疫组化 L SAB法检测 5 8例男性恶性生殖细胞肿瘤组织 (精原细胞瘤 36例 ,性腺外精原细胞瘤 6例 ,胚胎性癌 16例 )和 15例正常睾丸组织标本的 p5 3、PCNA和 bcl- 2的表达 ,并与临床病理资料进行比较。 结果:p5 3、PCNA在肿瘤组织中阳性表达率 (81.1%、10 0 .0 % )均明显高于正常睾丸组织的阳性表达率 (4 0 .0 %、5 3.3% ) ,P <0 .0 5 ;但在肿瘤组织各类型、组织分级和临床分期之间 p5 3、PCNA表达差异无统计学意义。在正常睾丸组织中 bcl- 2阳性表达率 (5 3.3% )明显高于肿瘤组织 (18.9% ) ,P <0 .0 5 ;在肿瘤组织各类型之间及相关的临床病理指标间 bcl- 2表达差异无统计学意义。 结论:(1)p5 3、PCNA的表达可能是参与生殖细胞肿瘤发生的重要分子生物学机制。 (2 ) bcl- 2癌基因在肿瘤组织中低表达 ,可能反映了 bcl- 2基因抗凋亡效应并未参与了睾丸肿瘤的发生、发展 ,在肿瘤发生过程中可能呈“丢失现象”。

Expressions of p53、PCNA and bcl-2 protein in germ cell tumors of male patients and the clinicopathologic significance

Objective: The possible molecular mechanisms of human male germ cell tumorigenesis was studied by detecting the altered oncogene expression and compared with some clinicopathological parameters. Methods: Expressions of p53?PCNA and bcl-2 protein in tumor tissues of 58 male patients with malignant germ cell tumors (seminoma 42, embryonic carcinoma 16) and 15 specimens of normal testicle tissues were detected by immunohistochemical (LSAB) technique. Some clinicopathological parameters was also analysed with the immunohistological results. Results: The positive frequency of p53 and PCNA protein was significant high in tumor tissues (81.1% and 100.0%) than in normal testicular tissues (40.0% and 53.3%) respectively, (P<0.05); but no statistic differences were found among different types of tumor? histologic gradings? clinical stagings. The expression of bcl-2 protein in normal testicular tissues was significant high (53.3%) than in tumor tissues (18.9%) (P<0.05), and no statistical significance among tumor types and related clinicopathological parameters. Conclusions: (1) The expression of the mutated p53 and PCNA oncoprotein in male germinomas may involve the molecular mechanisms of germ cell tumorigenesis. (2) The low positive frequency of bcl-2 oncogene expression, especially in high grading germionomas may reflect that the anti-apoptosis effects of bcl-2 oncogene was not involved the male germ cell tumor genesis and progression, probably it was loss or deleting in tumorigenesis processing.