Λέξεις-κλειδιά:
azacitidine; decitabine; DNA; DNA methyltransferase 1; DNA methyltransferase 3A; histone deacetylase; romidepsin; vorinostat; DNA, acute myeloblastic leukemia; cancer chemotherapy; cancer combination chemotherapy; cancer growth; cancer prognosis; cancer recurrence; cancer risk; cancer survival; clinical outcome; clinical trial (topic); cutaneous T cell lymphoma; demethylation; DNA methylation; drug mechanism; drug response; Editorial; enzyme inhibition; epigenetics; evidence based practice; gene expression regulation; gene identification; gene inactivation; gene silencing; human; jurkat cell line; leukemogenesis; malignant transformation; multiple myeloma; mycosis fungoides; myelodysplastic syndrome; peripheral T cell lymphoma; priority journal; pyrosequencing; Sezary syndrome; T cell leukemia; T-cell leukemia cell line; tumor suppressor gene; DNA methylation; gene silencing; genetics; methylation; promoter region; T cell leukemia, DNA; DNA Methylation; Gene Silencing; Humans; Leukemia, T-Cell; Methylation; Promoter Regions, Genetic
