期刊
CELLS
卷 11, 期 3, 页码 -出版社
MDPI
DOI: 10.3390/cells11030543
关键词
acute myeloid leukemia; calcium signaling; leukemic stem cells; cell metabolism; microenvironment; chemotherapies
类别
资金
- Inserm
- CNRS
- Contrat de Plan Etat-Region (CPER) 2015-2020
- Ligue contre le cancer (Septentrion)
- Ligue nationale contre le cancer
- Fondation ARC
- Institut de Recherche sur le Cancer de Lille (IRCL)
- Lille Hospital
- Hauts de France Region
Acute myeloid leukemia (AML) is a clonal disorder characterized by genetic aberrations in myeloid primitive cells, resulting in their defective maturation/function and proliferation. The role of calcium signaling in AML cell proliferation and differentiation, as well as in the quiescence of hematopoietic stem cells, is significant but still not well understood.
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.
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