Lyakhovich Alex, Surralles Jordi
Group of Mutagenesis, Department of Genetics and Microbiology, Universitat Autònoma de Barcelona, 08193 Bellaterra, Barcelona, Spain.
Cancer Lett. 2006 Jan 28;232(1):99-106. doi: 10.1016/j.canlet.2005.07.038. Epub 2005 Oct 21.
An increasing number of studies provide evidences linking disruption of Fanconi anemia/BRCA cascade with sporadic cancers. Given that this pathway plays essential roles in response to the DNA interstrand cross-links, these cancers are expected to be chemosensitive to cross-link based therapy. In the present mini-review we expand the spectrum of possibilities for FA/BRCA disruption and review some works describing functional upstream and downstream events linking disruption of the FA/BRCA pathway to sporadic cancer. This may involve but not limited to epigenetic silencing of the FA-core complex or BRCA1/2, mutations of one or several FA-BRCA genes or modification of encoded products. All this may serve as a platform for occurrence, development and treatment of sporadic cancers and therefore deserves to be in the focus of new research directions.
越来越多的研究提供证据表明范可尼贫血/乳腺癌易感基因（Fanconi anemia/BRCA）级联反应的破坏与散发性癌症有关。鉴于该途径在应对DNA链间交联中起关键作用，这些癌症预计对基于交联的治疗具有化学敏感性。在本综述中，我们扩展了范可尼贫血/乳腺癌易感基因（FA/BRCA）破坏的可能性范围，并回顾了一些描述将FA/BRCA途径破坏与散发性癌症联系起来的功能性上游和下游事件的研究。这可能涉及但不限于FA核心复合物或BRCA1/2的表观遗传沉默、一个或几个FA-BRCA基因的突变或编码产物的修饰。所有这些都可能成为散发性癌症发生、发展和治疗的平台，因此值得成为新研究方向的重点。
