Lehmann Ulrich, Brakensiek Kai, Kreipe Hans
Institute of Pathology, Medizinische Hochschule Hannover, Carl-Neuberg-Str.1, 30625, Hannover, Germany.
Ann Hematol. 2004 Mar;83(3):137-52. doi: 10.1007/s00277-003-0798-7. Epub 2003 Dec 2.
Inactivation of tumor suppressor genes is an important event contributing to the development of neoplasia. In addition to the classic genetic mechanisms of deletion or inactivating point mutations, growth regulatory genes can be functionally inactivated without alterations of the primary sequence by methylation of cytosine residues in the promoter regions of the genes. After introducing epigenetic phenomena in general and the molecular basis of DNA methylation in more detail, this review will present the broad spectrum of alterations in DNA methylation patterns found in hematopoietic malignancies. In addition, the implications for therapy and prognosis will be discussed.
肿瘤抑制基因的失活是促成肿瘤形成的一个重要事件。除了缺失或失活性点突变等经典遗传机制外,生长调节基因可通过基因启动子区域胞嘧啶残基的甲基化在不改变一级序列的情况下发生功能失活。在总体介绍表观遗传现象并更详细地阐述DNA甲基化的分子基础后,本综述将呈现造血系统恶性肿瘤中发现的DNA甲基化模式的广泛改变。此外,还将讨论其对治疗和预后的影响。