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劳舍尔白血病病毒疫苗对小鼠化学致癌作用的影响。

Effect of a Rauscher leukemia virus vaccine upon chemical oncogenesis in the mouse.

作者信息

Basombrío M A, Pasqualini C D

出版信息

Arch Geschwulstforsch. 1976;46(8):630-3.

PMID:1021012
Abstract

The concept that type-C RNA viruses serve as determinants of chemically induced cancer would be supported if immunization against such viruses reduced the incidence of methylcholanthrene-induced sarcomas. A formalin vaccine was employed which was able to protect mice against the development of virus-induced Rauscher leukemia: 8/12 vaccinated mice survived versus 1/12 controls. When mice so immunized were challenged with near-threshold doses of chemical carcinogen, sarcoma incidence and death latency did not differ between vaccinated and control groups: within 10 months, a 320 mug dose of methylcholanthrene induced 100% sarcomas in both groups, while a 64 mug dose induced 62% and 65% tumors in vaccinated and control mice respectively. Thus, a relevant postulate of the oncogene hypothesis could not be supported by these studies. Formalin treatment neutralizes the oncogenic effect of mouse leukemia viruses yiwlding preparations that are immunogenic and can be successfully used as vaccines to protect against virus-induced leukemia (5). The finding of murine leukemia viruses in chemically induced tumors (1, 2) poses the question of whether these viruses are present in the tumors as passengers, or whether they are etiologically involved in the process of tumor induction. An approach to answering this question would be to challenge with chemical carcinogens mice which have been vaccinated with leukemia virus. If the virus were somehow involved in tumor induction, antiviral immunization might conceivably interfere with chemical carcinogenesis. Whitmire and Huebner (9) have reported that mice immunized with formalin-treated leukemia viruses, become resistant to sarcomagenesis by methylcholanthrene. Repetition of this experiment by Gericke and Chandra (6) gave non-significant differences between experimental and control groups. The present paper deals with the effect of immunization against Rauscher leukemia virus upon tumor induction by near-threshold doses of methylcholanthrene.

摘要

如果针对此类病毒的免疫接种能降低甲基胆蒽诱导的肉瘤发病率,那么C型RNA病毒作为化学诱导癌症的决定因素这一概念将得到支持。使用了一种福尔马林疫苗,它能够保护小鼠免受病毒诱导的劳斯氏白血病的发展:12只接种疫苗的小鼠中有8只存活,而对照组12只中只有1只存活。当用接近阈值剂量的化学致癌物对如此免疫的小鼠进行攻击时,接种疫苗组和对照组之间的肉瘤发病率和死亡潜伏期没有差异:在10个月内,320微克剂量的甲基胆蒽在两组中均诱导出100%的肉瘤,而64微克剂量在接种疫苗的小鼠和对照小鼠中分别诱导出62%和65%的肿瘤。因此,这些研究无法支持癌基因假说的一个相关假设。福尔马林处理可中和小鼠白血病病毒的致癌作用,产生具有免疫原性的制剂,可成功用作预防病毒诱导白血病的疫苗(5)。在化学诱导的肿瘤中发现鼠白血病病毒(1,2)提出了一个问题,即这些病毒是以过客形式存在于肿瘤中,还是在肿瘤诱导过程中病因学上相关。回答这个问题的一种方法是用白血病病毒接种过的小鼠用化学致癌物进行攻击。如果病毒以某种方式参与肿瘤诱导,抗病毒免疫可能会干扰化学致癌作用。惠特迈尔和休伯纳(9)报道,用福尔马林处理的白血病病毒免疫的小鼠对甲基胆蒽诱导的肉瘤发生具有抗性。杰里克和钱德拉(6)重复了这个实验,实验组和对照组之间没有显著差异。本文探讨了针对劳斯氏白血病病毒的免疫接种对接近阈值剂量的甲基胆蒽诱导肿瘤的影响。

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