Liang J C, Pinkel D P, Bailey N M, Trujillo J M
Division of Laboratory Medicine, University of Texas M.D. Anderson Cancer Center, Houston 77030.
Cancer. 1989 Oct 1;64(7):1474-9. doi: 10.1002/1097-0142(19891001)64:7<1474::aid-cncr2820640719>3.0.co;2-s.
A cancer-prone family was studied to determine if certain chromosomal abnormalities might have predisposed members to develop diverse types of malignancies. The types of neoplasia that occurred in this family included cancers of the breast and stomach, multiple myeloma, dermatofibrosarcoma, Wilm's tumor, and leukemia; the latter three occurred in children at an early age. Peripheral lymphocytes from 13 family members were examined for the presence of constitutional chromosomal abnormalities, fragile sites, and mutagen sensitivity. Our data shows that all living members of this family who had cancers were hypersensitive to chromosome breakage induced by bleomycin. In contrast, neither constitutional chromosomal abnormality nor heritable type of folate-sensitive fragile site was observed in any member. The above findings suggest that genetic defects affecting chromosomal breakage and repair may be contributing factors for cancer development in several members of this family.
对一个癌症易感家族进行了研究,以确定某些染色体异常是否可能使家族成员易患多种类型的恶性肿瘤。该家族发生的肿瘤类型包括乳腺癌、胃癌、多发性骨髓瘤、皮肤纤维肉瘤、威尔姆斯瘤和白血病;后三种肿瘤在儿童早期就出现了。对13名家族成员的外周淋巴细胞进行了检查,以确定是否存在先天性染色体异常、脆性位点和诱变敏感性。我们的数据表明,这个家族中所有患癌的在世成员对博来霉素诱导的染色体断裂都高度敏感。相比之下,在任何成员中都未观察到先天性染色体异常或遗传性叶酸敏感脆性位点。上述发现表明,影响染色体断裂和修复的遗传缺陷可能是这个家族中几名成员患癌的促成因素。