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在多种类型的急性白血病中,常发生MLL蛋白节段与其他多种非相关蛋白融合的现象。目前认为,这种融合引起MLL的激活直接促成了正常骨髓细胞向白血病癌细胞的转变。然而,此过程发生的机制目前尚不清楚。最近我们发现白血病MLL的融合可以消除肿瘤抑制蛋白P53的抑癌作用,后者则是通过引导受损细胞自毁来发挥抗癌作用的,与大多数癌症中p53基因的高突变率相比,在白血病中仅有少量p53基因的突变,提示白血病中MLL融合蛋白通过对P53功能的抑制,至少部分加速了疾病的进展。这一点如果被证实,则可能为白血病细胞中P53通路的重新激活提供一条新的途径,从而为那些检测出有MLL融合的白血病人处理提供一种合理的治疗方法。
In many types of acute leukemia, the phenomenon that MLL protein segments fuse with a variety of other non-related proteins often occurs. It is currently believed that this fusion causes the activation of MLL directly contribute to the transformation of normal bone marrow cells to leukemia cancer cells. However, the mechanism by which this process occurs is not yet clear. Recently, we found that the fusion of leukemia MLL can eliminate the tumor suppressor protein P53 tumor suppressor effect, which is through the destruction of damaged cells to play a role in anti-cancer self-destruction, and most of the cancer p53 gene mutation rate compared to high, Only a small number of mutations in the p53 gene are found in leukemias, suggesting that MLL fusion proteins in leukemia at least partially accelerate the progression of the disease by inhibiting the function of P53. This, if confirmed, may provide a new pathway for the re-activation of the P53 pathway in leukemic cells, thus providing a reasonable treatment for leukemia patients detected with MLL fusion.