作者: Marc S. Mendonca , Clare L. Fasching , Eri S. Srivatsan , Eric J. Stanbridge , J. Leslie Redpath
DOI: 10.2307/3578923
关键词: Chromosome 、 Neoplastic transformation 、 Chromosome 13 、 Locus (genetics) 、 HeLa 、 Tumor suppressor gene 、 Molecular biology 、 Fibroblast 、 Genetics 、 Biology 、 Carcinogenesis
摘要: The nontumorigenic HeLa x skin fibroblast hybrid cell line, CGL1, can be induced to re-express tumor-associated surface antigen, p75-IAP (intestinal alkaline phosphatase), with resulting neoplastic transformation, by exposure gamma radiation. This has allowed the human system developed into a quantitative in vitro model for radiation-induced transformation of cells. Recently, several gamma-ray-induced IAP-expressing mutants (GIMs) CGL1 were isolated and all tumorigenic when injected subcutaneously nude mice (Mendonca et al., Cancer Res. 51, 4455-4462, 1991). Control lines which negative (CONs) also from irradiated populations, none found tumorigenic. We have now begun investigate molecular basis this studying potential genetic linkage between p75/IAP expression, tumorigenicity damage putative tumor suppressor locus on chromosome 11. Previous analysis rare spontaneous segregants indicated that is involved regulation expression marker intestinal phosphatase (p75-IAP) system. Therefore, restriction fragment length polymorphism painting been performed 11, 13 as control, p75/IAP-positive GIM p75/IAP-negative CON lines. report five eight GIMs large-scale 11's evident (four lost one complete copy 11 both copies heavily damaged). None CONs, however (0/5), either No control 13's was detected or CONs. data further suggest contain an active loss will result conclude it responsible at least part these