论文部分内容阅读
尽管酪氨酸激酶抑制剂(TKIs)伊马替尼(IM)可抑制Bcr-Abl激酶活性,在慢性期慢性粒细胞白血病治疗中有效,但很难达分子学缓解(MR),提示存在酪氨酸激酶抑制剂耐药的白血病细胞(如肿瘤干细胞),致微小残留病长期存在,最终复发。目前,IM耐药的机制不明,有BCR-ABL依赖与非依赖途径两种假说,前者包括BCR-ABL表达增高、激酶点突变等,但单用IM不能治愈疾病,提示需要寻求新的治疗方案以清除肿瘤干细胞。药物联用有望有效作用于肿瘤干细胞,不失为有价值的选择之一。
Although imatinib (IM), a tyrosine kinase inhibitor (TKIs), inhibits Bcr-Abl kinase activity and is effective in the treatment of chronic myeloid leukemia, it is difficult to achieve molecular remission (MR) Leukemic cells (such as cancer stem cells) that are resistant to the kinase inhibitor of arginine kinase cause minimal residual disease that lasts longer and eventually relaps. At present, the mechanism of IM resistance is unknown. There are two hypotheses about BCR-ABL dependence and non-dependence. The former includes the increase of BCR-ABL expression and kinase point mutation. However, IM alone can not cure the disease, suggesting that a new treatment plan should be sought To clear tumor stem cells. Drug combination is expected to effectively act on cancer stem cells, after all, one of the valuable options.