Bale A E, Gailani M R, Leffell D J
Department of Genetics, Yale University School of Medicine, New Haven, Connecticut 06510.
J Invest Dermatol. 1994 Nov;103(5 Suppl):126S-130S. doi: 10.1111/1523-1747.ep12399438.
The nevoid basal cell carcinoma syndrome is an autosomal dominant disorder that predisposes to basal cell carcinomas of the skin, ovarian fibromas, and medulloblastomas. Unlike other hereditary disorders associated with cancer, it features widespread developmental defects. Laboratory studies of radiation sensitivity and chromosome instability over the past 20 years have generally yielded negative or inconclusive results. Recently, screening for allelic loss in sporadic and hereditary basal cell carcinomas, hereditary ovarian fibromas, and sporadic medulloblastomas provided evidence for a tumor suppressor gene on chromosome 9q, important in all three tumor types. Demonstration of a chromosome 9q deletion in an unusual patient with this syndrome and genetic linkage studies in large kindreds indicated that the nevoid basal cell carcinoma syndrome gene maps to the exact same location lost in tumors. These data show that tumors arise with homozygous inactivation of the gene and imply that it normally functions as a tumor suppressor. In contrast, hemizygous germ-line mutations lead to multiple congenital anomalies.
痣样基底细胞癌综合征是一种常染色体显性疾病,易引发皮肤基底细胞癌、卵巢纤维瘤和髓母细胞瘤。与其他与癌症相关的遗传性疾病不同,它具有广泛的发育缺陷。在过去20年中,关于辐射敏感性和染色体不稳定性的实验室研究通常得出阴性或不确定的结果。最近,对散发性和遗传性基底细胞癌、遗传性卵巢纤维瘤和散发性髓母细胞瘤的等位基因缺失筛查,为9号染色体长臂上的一个肿瘤抑制基因提供了证据,该基因在所有这三种肿瘤类型中都很重要。在一名患有该综合征的特殊患者中发现9号染色体长臂缺失,以及在大家族中的基因连锁研究表明,痣样基底细胞癌综合征基因定位于肿瘤中缺失的同一确切位置。这些数据表明,肿瘤是由于该基因的纯合失活而产生的,这意味着它通常作为肿瘤抑制因子发挥作用。相比之下,半合子种系突变会导致多种先天性异常。