| Abstract: |
In recent years, the therapeutic landscape of myeloid malignancies has been completely revolutionized by the introduction of several new drugs, targeting molecular alterations or pathways crucial for leukemia cells survival. Particularly, many agents targeting apoptosis have been investigated in both pre-clinical and clinical studies. For instance, venetoclax, a pro-apoptotic agent active on BCL-2 signaling, has been successfully used in the treatment of acute myeloid leukemia (AML). The impressive results achieved in this context have made the apoptotic pathway an attractive target also in other myeloid neoplasms, translating the experience of AML. Therefore, several drugs are now under investigation either as single or in combination strategies, due to their synergistic efficacy and capacity to overcome resistance. In this paper, we will review the mechanisms of apoptosis and the specific drugs currently used and under investigation for the treatment of myeloid neoplasia, identifying critical research necessities for the upcoming years. © 2023 Elsevier Ltd |
| Keywords: |
cancer survival; protein expression; treatment outcome; myeloproliferative disorders; gene mutation; myeloproliferative disorder; leukemia, myeloid, acute; fludarabine; drug tolerability; fatigue; review; placebo; cancer combination chemotherapy; diarrhea; drug efficacy; antineoplastic agents; drug targeting; cytarabine; outcome assessment; antineoplastic agent; cell proliferation; metabolism; cell survival; dna repair; protein bcl 2; apoptosis; multiple cycle treatment; multiple myeloma; anemia; nausea; thrombocytopenia; vomiting; chronic myeloid leukemia; protein p53; drug dose escalation; febrile neutropenia; hypokalemia; ubiquitination; drug mechanism; cell damage; drug response; vorinostat; single drug dose; oxidative stress; idarubicin; obatoclax; oblimersen; drug protein binding; azacitidine; antileukemic activity; myeloid neoplasia; navitoclax; neddylation; acute myeloid leukemia; bone marrow cancer; decitabine; ruxolitinib; ponatinib; humans; human; venetoclax; gilteritinib; [2 (4 tert butyl 2 ethoxyphenyl) 4,5 bis(4 chlorophenyl) 4,5 dihydro 4,5 dimethyl 1h imidazol 1 yl][4 [3 (methylsulfonyl)propyl] 1 piperazinyl]methanone; pevonedistat; idasanutlin; ivuxolimab; alvocidib; therapeutic vulnerability; aeg 35156; birinapant; murizatoclax; tapotoclax
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