Mathew C G
King's College London School of Medicine, Division of Genetics and Molecular Medicine, Guy's Hospital, London, UK.
Oncogene. 2006 Sep 25;25(43):5875-84. doi: 10.1038/sj.onc.1209878.
Fanconi anaemia (FA) is a rare recessive disorder associated with chromosomal fragility, aplastic anaemia, congenital abnormalities and a high risk of cancer, including acute myeloid leukaemia and squamous cell carcinomas. The identification of 11 different FA genes has revealed a complex web of interacting proteins that are involved in the recognition or repair of DNA interstrand crosslinks and perhaps other forms of DNA damage. Bi-allelic mutations in BRCA2 are associated with a rare and highly cancer-prone form of FA, and the DNA helicase BRIP1 (formerly BACH1) is mutated in FA group J. There is little convincing evidence that FA heterozygotes are at increased risk of cancer, but larger studies are needed to address the possibility of modest risk effects. Somatic inactivation of the FA pathway by mutation or epigenetic silencing has been observed in several different types of sporadic cancer, and this may have important implications for targeted chemotherapy. Inhibition of this pathway represents a possible route to sensitization of tumours to DNA crosslinking drugs such as cisplatin.
范可尼贫血(FA)是一种罕见的隐性疾病,与染色体脆性、再生障碍性贫血、先天性异常以及包括急性髓系白血病和鳞状细胞癌在内的高癌症风险相关。11种不同的FA基因的鉴定揭示了一个复杂的相互作用蛋白网络,这些蛋白参与DNA链间交联的识别或修复,或许还参与其他形式的DNA损伤。BRCA2的双等位基因突变与一种罕见且高度易患癌症的FA形式相关,DNA解旋酶BRIP1(原名BACH1)在J组FA中发生突变。几乎没有令人信服的证据表明FA杂合子患癌风险增加,但需要更大规模的研究来探讨存在适度风险效应的可能性。在几种不同类型的散发性癌症中已观察到通过突变或表观遗传沉默使FA通路发生体细胞失活,这可能对靶向化疗具有重要意义。抑制该通路是使肿瘤对顺铂等DNA交联药物敏感的一条可能途径。