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Put in a “Ca2+ll” to Acute Myeloid Leukemia

Abstract : 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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https://www.hal.inserm.fr/inserm-03562726
Contributor : Thierry Idziorek Connect in order to contact the contributor
Submitted on : Wednesday, February 9, 2022 - 11:11:53 AM
Last modification on : Wednesday, March 23, 2022 - 3:51:30 PM
Long-term archiving on: : Tuesday, May 10, 2022 - 6:32:52 PM

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Clara Lewuillon, Marie-Océane Laguillaumie, Bruno Quesnel, Thierry Idziorek, Yasmine Touil, et al.. Put in a “Ca2+ll” to Acute Myeloid Leukemia. Cells, MDPI, 2022, 11 (3), pp.543. ⟨10.3390/cells11030543⟩. ⟨inserm-03562726⟩

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