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Epigenetic therapy of hematological malignancies: where are we now?

Epigenetic therapy of hematological malignancies: where are we now?

http://www.wikidata.org/entity/Q38101042

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Epimutational profile of hematologic malignancies as attractive target for new epigenetic therapies Genomics of lymphoid malignancies reveal major activation pathways in lymphocytes.Epigenetic regulation of cell signaling pathways in acute lymphoblastic leukemia.Regulation of protein stability of DNA methyltransferase 1 by post-translational modifications Hydralazine-valproate: a repositioned drug combination for the epigenetic therapy of cancer.miR-29s: a family of epi-miRNAs with therapeutic implications in hematologic malignancies.Selective HDAC6 inhibition decreases early stage of lupus nephritis by down-regulating both innate and adaptive immune responses.Harmine, a Novel DNA Methyltransferase 1 Inhibitor in the Leukemia Cell Line.Epigenetic therapies - a new direction in clinical medicine.Oncogenic Y641 mutations in EZH2 prevent Jak2/β-TrCP-mediated degradation.Markers as mediators: A review and synthesis of epigenetics literature Activation of viral defense signaling in cancer

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Epigenetic therapy of hematological malignancies: where are we now?

http://www.wikidata.org/entity/Q38101042

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Epigenetic therapy of hematological malignancies: where are we now?

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Epigenetic therapy of hematological malignancies: where are we now?

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Epigenetic therapy of hematological malignancies: where are we now?

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2040620712466864

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Therapeutic advances in hematology

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Epigenetic therapy of hematological malignancies: where are we now?

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Jonathan D Licht

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Mrinal Y Shah

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Relja Popovic

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The Polycomb group protein EZH2 directly controls DNA methylation

Hydroxylation of 5-methylcytosine by TET1 promotes active DNA demethylation in the adult brain

Impaired hydroxylation of 5-methylcytosine in myeloid cancers with mutant TET2

Conversion of 5-methylcytosine to 5-hydroxymethylcytosine in mammalian DNA by MLL partner TET1

Efficacy of azacitidine compared with that of conventional care regimens in the treatment of higher-risk myelodysplastic syndromes: a randomised, open-label, phase III study

The genetic basis of early T-cell precursor acute lymphoblastic leukaemia.

The common feature of leukemia-associated IDH1 and IDH2 mutations is a neomorphic enzyme activity converting alpha-ketoglutarate to 2-hydroxyglutarate

Oncometabolite 2-hydroxyglutarate is a competitive inhibitor of α-ketoglutarate-dependent dioxygenases

Recurring mutations found by sequencing an acute myeloid leukemia genome

Genetic characterization of TET1, TET2, and TET3 alterations in myeloid malignancies

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10.1177/2040620712466864

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