Gaudillière J P
Hôpital des Enfants malades, Pavillon Archkambault, Paris, France.
Rev Hist Sci Paris. 1994 Jan-Mar;47(1):57-89.
After World War II, in the United States,viral explanation of cancer replaced a vision of the disease emphasizing genetic factors. From the mid 1950s onwards, experimental oncologists favored the notion that cancer was initiated by infectious agents passed from one generation to the next. In order to analyze this displacement, the present paper focuses on the part played by new experimental systems, i.e. mice showing tumors induced by viruses. Since animal models are agencies which "represent" human diseases, and mediate between different social worlds, their uses often result in opposing views. Mouse models thus provided tractable resources which favored the alternation between heredity and infection. The paper describes the emergence, in the late 1930s, at the Jackson Memorial Laboratory, of an agent enhancing the formation of mammary tumors in mice. This laboratory was then involved in the production of marketable inbred mice as well as in research concerned with genetic factors that may cause cancer. After World War II, loose theories and conflicting results helped turn the agent into a virus. At the National Cancer Institute, the virus was associated with a whole range of particles causing leukemia in mice. Owing to the Virus Cancer Program, the value of mouse tumor viruses increased in the late 1960s. This research effort then aimed at finding human tumor viruses, and at crafting cancer vaccines. It was modeled after the experience of the NCI chemotherapy program stemming from war research. In addition to the fact that biomedical research became a state enterprise, the study emphasizes three parameters. First, loose practices--both theoretical and experimental--helped manage the variability of animal models. Secondly, the standardization and mass production of animals and reagents encouraged the stabilization of research programs. Thirdly, private biotechnology companies working under NCI contracts implemented preclinical work, and mediated between virology laboratories and clinical settings.
第二次世界大战后,在美国,癌症的病毒学解释取代了强调遗传因素的疾病观念。从20世纪50年代中期起,实验肿瘤学家倾向于认为癌症是由代代相传的传染因子引发的。为了分析这种转变,本文聚焦于新实验系统所起的作用,即那些显示出由病毒诱发肿瘤的小鼠。由于动物模型是“代表”人类疾病并在不同社会领域之间起媒介作用的媒介物,它们的使用常常导致相反的观点。小鼠模型因此提供了便于操作的资源,有利于在遗传与感染之间交替。本文描述了20世纪30年代末在杰克逊纪念实验室出现的一种促进小鼠乳腺肿瘤形成的因子。该实验室当时既参与可销售的近交系小鼠的生产,也参与与可能引发癌症的遗传因素相关的研究。第二次世界大战后,不严谨的理论和相互矛盾的结果促使该因子被认定为一种病毒。在国家癌症研究所,这种病毒与一系列导致小鼠白血病的粒子联系在一起。由于病毒癌症计划,小鼠肿瘤病毒的价值在20世纪60年代末有所增加。这项研究工作随后旨在寻找人类肿瘤病毒并研制癌症疫苗。它是以源于战时研究的美国国家癌症研究所化疗计划的经验为蓝本的。除了生物医学研究成为国家事业这一事实外,该研究还强调了三个参数。首先,不严谨的做法——理论上的和实验上的——有助于应对动物模型的变异性。其次,动物和试剂的标准化及大规模生产促进了研究计划的稳定。第三,根据美国国家癌症研究所合同开展工作的私营生物技术公司进行临床前工作,并在病毒学实验室和临床环境之间起媒介作用。