TY  - JOUR
AU  - Bordron, Anne
AU  - Tempescul, Adrian
AU  - Christophe Ianotto, Jean
AU  - Guillerm, Gaelle
AU  - H Brooks, Wesley
AU  - Couturier, Marie-Anne
AU  - Zdrenghea, Mihnea
AU  - Berthou, Christian
AU  - Renaudineau, Yves
AU  - Bagacean, Cristina
PY  - 2018
DA  - 2018/12/14
TI  - Distinct Mechanisms of Alterations in DNA Methylation/Demethylation Leading to Myelodysplastic Syndromes/Acute Myeloid Leukemia and Chronic Lymphocytic Leukemia
JO  - OBM Genetics
SP  - 054
VL  - 02
IS  - 04
AB  - Myelodysplastic syndromes (MDS) represent malignant myeloid disorders characterized by ineffective hematopoiesis, peripheral cytopenias, and an increased risk of progression to acute myeloid leukemia (AML). AML is a highly heterogeneous disease characterized by the presence of large chromosomal translocations, gene fusions as well as mutations in the genes involved in hematopoietic proliferation and differentiation resulting in the accumulation of poorly differentiated myeloid cells. Chronic lymphocytic leukemia (CLL) is the most frequent type of leukemia, and is characterized by the clonal proliferation and accumulation of mature, long-lived CD5+ B cells. Epigenetic dysregulations are present in both myeloid disorders and in CLL, but, in contrast to MDS and AML that present gene fusions (TET1/LCX) and somatic mutations in epigenetic regulators (DNMT3A, TET2, IDH1/2), in CLL, epigenetic modifications are not qualitative but mostly quantitative (DNMT3A, TET2) and associated with disease progression. As a consequence, in MDS, AML and CLL, the focal or global DNA methylation/demethylation process is altered.
In conclusion, a better qualitative and quantitative understanding of epigenetic regulators during myeloid/lymphoid differentiation, their localization and the co-recruitment of other proteins at specific DNA target sites, could offer us the possibility to modulate hematopoiesis, restore the initial balance, and control disease progression.
SN  - 2577-5790
UR  - https://doi.org/10.21926/obm.genet.1804054
DO  - 10.21926/obm.genet.1804054
ID  - Bordron2018
ER  -