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过去认为,只要有单个或多个协同的癌基因激活,就可导致细胞癌变;活动癌基因的作用是显性作用(“domi-nantly acting”)。但是早年设计的“恶性—正常”体细胞融合试验却提示,在正常细胞中存在某种抑制性基因,可以阻止恶性性状的表达。近年人们用细胞遗传学和 DNA限制性片段长度多态性分析(RFLP)技术,进一步证明某些基因的遗传性缺失可以作为癌变的关键性因素。这类基因被称为“肿瘤抑制基因”(tumor suppressov gene)。二年多前克隆得到的视网膜母细胞瘤抑制基因(Rb-1),为肿瘤抑制基因假说提供了有力证据。目前已经在小细胞肺癌,乳癌和结直肠癌等其它人类肿瘤中发现了肿瘤抑制
In the past, it was thought that single or multiple coordinated oncogene activation could lead to cell canceration; the role of active oncogenes was a dominant effect (“domi-nantly acting”). However, the “malignant-normal” somatic fusion experiment designed in early years suggests that there is an inhibitory gene in normal cells that can prevent the expression of malignant traits. In recent years, cytogenetics and DNA-restriction fragment length polymorphism (RFLP) techniques have been used to further prove that genetic loss of certain genes can be a key factor in canceration. This type of gene is called a tumor suppressov gene. The retinoblastoma suppressor gene (Rb-1) cloned more than two years ago provides strong evidence for the tumor suppressor hypothesis. Tumor inhibition has been found in other human tumors such as small cell lung cancer, breast cancer and colorectal cancer.