威尼斯人
髓系白血病
医学
白血病
肿瘤科
内科学
癌症研究
阿糖胞苷
细胞凋亡
髓样
化疗
免疫学
生物
遗传学
慢性淋巴细胞白血病
作者
Abhishek Maiti,Michael Andreeff,Marina Konopleva
标识
DOI:10.1016/s2152-2650(21)01190-3
摘要
Introduction BCL-2 inhibition has transformed the therapeutic landscape of acute myeloid leukemia (AML). However, 10–50% of newly diagnosed patients with AML may not respond to venetoclax and HMA or LDAC, and 3–15% patients may not respond to venetoclax with intensive or non-intensive chemotherapy.1–6 In addition, up to 40% of responding patients may relapse with low rates of response of 20% to salvage therapy and poor overall survival of 2 months after relapse.7 Clinical and biological factors associated with primary and acquired resistance to venetoclax include secondary AML, monocytic differentiation, complex cytogenetics, mutations in TP53, BAX, dependence on other anti-apoptotic proteins, altered metabolism of nicotinamide, fatty acids, and oxidative phosphortylation.3,8–14
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