Malkin D, Li F P, Strong L C, Fraumeni J F, Nelson C E, Kim D H, Kassel J, Gryka M A, Bischoff F Z, Tainsky M A
Division of Molecular Genetics, Massachusetts General Hospital Cancer Center, Charlestown 02129.
Science. 1990 Nov 30;250(4985):1233-8. doi: 10.1126/science.1978757.
Familial cancer syndromes have helped to define the role of tumor suppressor genes in the development of cancer. The dominantly inherited Li-Fraumeni syndrome (LFS) is of particular interest because of the diversity of childhood and adult tumors that occur in affected individuals. The rarity and high mortality of LFS precluded formal linkage analysis. The alternative approach was to select the most plausible candidate gene. The tumor suppressor gene, p53, was studied because of previous indications that this gene is inactivated in the sporadic (nonfamilial) forms of most cancers that are associated with LFS. Germ line p53 mutations have been detected in all five LFS families analyzed. These mutations do not produce amounts of mutant p53 protein expected to exert a trans-dominant loss of function effect on wild-type p53 protein. The frequency of germ line p53 mutations can now be examined in additional families with LFS, and in other cancer patients and families with clinical features that might be attributed to the mutation.
家族性癌症综合征有助于明确肿瘤抑制基因在癌症发生过程中的作用。显性遗传的李-佛美尼综合征(LFS)尤其引人关注,因为受影响个体中会出现多种儿童期和成人期肿瘤。LFS的罕见性和高死亡率使得进行正式的连锁分析变得不可能。另一种方法是选择最有可能的候选基因。由于之前有迹象表明该基因在大多数与LFS相关的散发性(非家族性)癌症形式中失活,因此对肿瘤抑制基因p53进行了研究。在分析的所有五个LFS家族中都检测到了种系p53突变。这些突变不会产生预期会对野生型p53蛋白产生反式显性功能丧失效应的突变p53蛋白量。现在可以在更多的LFS家族以及其他癌症患者和具有可能归因于该突变的临床特征的家族中检查种系p53突变的频率。