Lamm D L, Gittes R F
Invest Urol. 1977 Mar;14(5):366-8.
Recent immunologic and microbiologic evidence suggests that urothelial tumors may be caused by "C" type oncogenic viruses. Such viruses may exert their oncogenic potential in responce to stimulation by known chemical carcinogens. By means of a unique enzyme, reverse transcriptase, these viruses are able to incorporate genetic information into that of the host, and can thereby be transmitted vertically from generation to generation. An evaluation of the specific antiviral agents dimethylbenzyldemethl-rifampicin and streptovaricin-comples, which inhibit the enzyme reverse transcriptase, revealed no depay in the induction of bladder tumors by the chemical carcinogen, 2-formylamino-4-(5-nitro-2-furyl) thiazole (FANFT) in C3H mice. This observation suggests that the reproduction and release of virus may not be essential in the malignant transformation of bladder epithelial cells, but does not preclude the possiblity that inherited viral genetic information may be involved in the oncogenesis of bladder tumors.
最近的免疫学和微生物学证据表明,尿路上皮肿瘤可能由“C”型致癌病毒引起。这类病毒可能在已知化学致癌物的刺激下发挥其致癌潜力。借助一种独特的酶——逆转录酶,这些病毒能够将遗传信息整合到宿主的遗传信息中,从而实现代代垂直传播。对抑制逆转录酶的特异性抗病毒药物二甲基苄基去甲基利福平及链黑菌素复合物进行评估后发现,在C3H小鼠中,化学致癌物2-甲酰氨基-4-(5-硝基-2-呋喃基)噻唑(FANFT)诱发膀胱肿瘤的过程中,这两种药物并无作用。这一观察结果表明,病毒的复制和释放可能并非膀胱上皮细胞恶性转化所必需,但并不排除遗传性病毒遗传信息可能参与膀胱肿瘤发生的可能性。