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September 17, 2025Molecular OncologyOpen Access

Inhibition of CDK9 enhances AML cell death induced by combined venetoclax and azacitidine

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Authors

SWShuangshuang WuNanjing Medical UniversityJZJianlei ZhaoPingdingshan UniversityAAAsfar S. AzmiThe Barbara Ann Karmanos Cancer Institute

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Implication

Combination therapy with AZD4573 improves outcomes in AML by targeting c-MYC and MCL-1, suggesting new treatment avenues.

Key Points

  • Combination of AZD4573, venetoclax, and azacitidine substantially increases AML cell death.
  • AZD4573 significantly downregulates c-MYC and MCL-1, contributing to enhanced efficacy against relapsed AML.
  • The treatment shows effectiveness even at lower concentrations of venetoclax, indicating potential for safer dosing.
  • Normal hematopoietic progenitor cells remain unaffected, suggesting a targeted treatment approach.

Cite This Study

Wu et al. (2025) studied this question.

synapsesocial.com/papers/68d45e4e31b076d99fa5e4b5https://doi.org/10.1002/1878-0261.70124
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Reduced duration and dosage of venetoclax is efficient in newly diagnosed patients with acute myeloid leukemia2023 · 20 citations
  2. 2Venetoclax therapy and emerging resistance mechanisms in acute myeloid leukaemia2024 · 76 citations
  3. 3c-Myc regulates expression of NKG2D ligands ULBP1/2/3 in AML and modulates their susceptibility to NK-mediated lysis2014 · 69 citations
  4. 4Inhibition of Bcl-2 Synergistically Enhances the Antileukemic Activity of Midostaurin and Gilteritinib in Preclinical Models of FLT3-Mutated Acute Myeloid Leukemia2019 · 181 citations
  5. 5A Novel MCL1 Inhibitor Combined with Venetoclax Rescues Venetoclax-Resistant Acute Myelogenous Leukemia2018 · 386 citations