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越来越多的研究发现,肿瘤的发生与抑癌基因及癌基因的异常表达直接相关。如果抑癌基因突变或缺失失去活性,细胞就会在无控制状态下反复复制,最终形成肿瘤并发生转移。例如,抑癌基因SHP-1酪氨酸磷酸酶在造血细胞信号传导中发挥负调节作用,SHP-1表达的减少和缺失对肿瘤的发生起关键性作用。如果癌基因在白血病患者中失去了抑癌基因的负调控作用,多数就会表现为异常高表达,如癌基因c-kit,在多种白血病细胞中表达活跃。研究表明,启动子区的高甲基化导致了抑癌基因失活及癌基因表达活跃,因此恢复启动子区的正常甲基化有助于恢复基因的正常表达,从而达到基因治疗白血病的目的。本文就甲基化,甲基化异常与白血病,甲基化抑制剂与白血病治疗作了简明的综述。
More and more studies have found that the occurrence of tumors is directly related to the abnormal expression of tumor suppressor genes and oncogenes. If the tumor suppressor gene mutations or deletions loss of activity, the cells will be copied repeatedly in the uncontrolled state, eventually forming a tumor and metastasis. For example, the tumor suppressor SHP-1 tyrosine phosphatase plays a negative regulatory role in hematopoietic cell signaling, and the reduction and deletion of SHP-1 expression play a key role in tumorigenesis. If oncogenes loses the negative regulatory effect of tumor suppressor genes in patients with leukemia, most of them display abnormally high expression, such as the oncogene c-kit, which is highly expressed in many leukemia cells. Studies have shown that hypermethylation of the promoter region leads to inactivation of tumor suppressor genes and active expression of oncogenes, thus restoring the normal methylation of the promoter region helps to restore the normal gene expression so as to achieve gene therapy for leukemia. This article provides a brief overview of methylation, methylation abnormalities and leukemia, methylation inhibitors and leukemia.