Targeting epigenetic mechanisms to overcome venetoclax resistance

• Published in: Biochimica et biophysica acta. Molecular cell research Vol. 1868; no. 8; p. 119047
• Main Authors: Prado, Gabriel, Kaestner, Charlotte L., Licht, Jonathan D., Bennett, Richard L.
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 01.07.2021
• Subjects: Antineoplastic Agents - chemistry; Antineoplastic Agents - pharmacology; Azacytidine; Bridged Bicyclo Compounds, Heterocyclic - chemistry; Bridged Bicyclo Compounds, Heterocyclic - pharmacology; Decitabine; Drug Resistance, Neoplasm - drug effects; Drug Resistance, Neoplasm - genetics; Enzyme Inhibitors - chemistry; Enzyme Inhibitors - pharmacology; Epigenesis, Genetic - drug effects; Epigenesis, Genetic - genetics; EZH2; Humans; JQ1; Neoplasms - drug therapy; Neoplasms - metabolism; Neoplasms - pathology; Sulfonamides - chemistry; Sulfonamides - pharmacology; Venetoclax; Azacytidine; Decitabine; JQ1; Venetoclax; EZH2

The BH-3 mimetic venetoclax overcomes apoptosis and therapy resistance caused by high expression of BCL2 or loss of BH3-only protein function. Although a promising therapy for hematologic malignancies, increased expression of anti-apoptotic MCL-1 or BCL-XL, as well as other resistance mechanisms pre...