Univ. Lille, CNRS, Inserm, CHU Lille, UMR9020-U1277-CANTHER-Cancer Heterogeneity Plasticity and Resistance to Therapies, F-59000 Lille, France.
Univ. Lille, Inserm, U1003-PHYCEL-Physiologie Cellulaire, F-59000 Lille, France.
Cells. 2022 Feb 4;11(3):543. doi: 10.3390/cells11030543.
Acute myeloid leukemia (AML) is a clonal disorder characterized by genetic aberrations in myeloid primitive cells (blasts) which lead to their defective maturation/function and their proliferation in the bone marrow (BM) and blood of affected individuals. Current intensive chemotherapy protocols result in complete remission in 50% to 80% of AML patients depending on their age and the AML type involved. While alterations in calcium signaling have been extensively studied in solid tumors, little is known about the role of calcium in most hematologic malignancies, including AML. Our purpose with this review is to raise awareness about this issue and to present (i) the role of calcium signaling in AML cell proliferation and differentiation and in the quiescence of hematopoietic stem cells; (ii) the interplay between mitochondria, metabolism, and oxidative stress; (iii) the effect of the BM microenvironment on AML cell fate; and finally (iv) the mechanism by which chemotherapeutic treatments modify calcium homeostasis in AML cells.
急性髓系白血病 (AML) 是一种以髓系原始细胞（白血病细胞）遗传异常为特征的疾病，导致其成熟/功能缺陷，并在受影响个体的骨髓 (BM) 和血液中增殖。目前，根据患者的年龄和 AML 类型，强化化疗方案可使 50%至 80%的 AML 患者获得完全缓解。虽然钙信号转导在实体肿瘤中已经得到广泛研究，但对于钙在大多数血液恶性肿瘤（包括 AML）中的作用知之甚少。我们撰写这篇综述的目的是提高对这一问题的认识，并介绍（i）钙信号在 AML 细胞增殖和分化以及造血干细胞静止中的作用；（ii）线粒体、代谢和氧化应激之间的相互作用；（iii）BM 微环境对 AML 细胞命运的影响；最后（iv）化疗治疗改变 AML 细胞钙稳态的机制。
