Rukstalis D B
Department of Surgery and Pathology, Medical College of Pennsylvania, Philadelphia 19129, USA.
World J Urol. 1996;14(5):347-52. doi: 10.1007/BF00184608.
Molecular investigations into the neoplastic transformation of a normal spermatogenic precursor cell into a germ-cell malignancy have implicated a wide array of DNA and RNA alterations. Previous epidemiologic and familial patterns of cancer presentation had suggested that testicular cancer developed from one or more genetic alterations. In particular, mutations in cellular oncogenes such as c-kit and tumor-suppressor genes such as the retinoblastoma gene product have been identified as putative etiologic agents in the development and progression of testicular germ-cell tumors. Additionally, alterations in the transcription of RNA that are regulated through a process of genomic imprinting have been identified in human testis cancers. This report provides a framework for integrating this growing literature on the molecular biology of testicular germ-cell tumors into a potential etiologic hypothesis.
对正常生精前体细胞向生殖细胞恶性肿瘤的肿瘤转化进行的分子研究表明,存在大量DNA和RNA改变。先前癌症表现的流行病学和家族模式表明,睾丸癌是由一种或多种基因改变发展而来的。特别是,细胞癌基因(如c-kit)和肿瘤抑制基因(如视网膜母细胞瘤基因产物)中的突变已被确定为睾丸生殖细胞肿瘤发生和发展的假定病因。此外,在人类睾丸癌中已发现通过基因组印记过程调节的RNA转录改变。本报告提供了一个框架,用于将有关睾丸生殖细胞肿瘤分子生物学的不断增长的文献整合到一个潜在的病因假说中。