Evidence map›Paper›PMID 32319019›Full record

ReviewTargeted oncology2020

Targeting Apoptosis in Acute Myeloid Leukemia: Current Status and Future Directions of BCL-2 Inhibition with Venetoclax and Beyond.

Jun H Choi, James M Bogenberger, Raoul Tibes

Registry-linked trialAbstract readReview
PubMed Publisher
In one paragraph

Review in Targeted oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07507825 (A Prospective, Multicenter, Exploratory Study of Venetoclax, Homoharringtonine, and Azacitidine Combined With G-CSF in Elderly or Unfit Patients With Newly Diagnosed Acute Myeloid Leukemia), which is not on this map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.5field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

NCT07507825 phase2not yet recruitingnot on this mapstarted 2026, after this paper: background citation

A Prospective, Multicenter, Exploratory Study of Venetoclax, Homoharringtonine, and Azacitidine Combined With G-CSF in Elderly or Unfit Patients With Newly Diagnosed Acute Myeloid Leukemia

TypeinterventionalSponsorFirst People's Hospital of HangzhouRan2026 to 2029Enrolled61ConditionsAcute Myeloid Leukemia (AML)ArmsIntervention for Venetoclax, Intervention for Homoharringtonine, Intervention for Azacitidine, Intervention for G-CSF
3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
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  9. Design of rigid protein-protein interaction inhibitors enables targeting of undruggable Mcl-1.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  10. Review
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  19. Enhanced cytarabine-induced killing in OGG1-deficient acute myeloid leukemia cells.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  20. Frontiers in oncology · 2021
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Jun H ChoiDivision of Hematology and Medical Oncology, New York University School of Medicine and Perlmutter Comprehensive Cancer Center, New York University Langone Health, New York, NY, USA.
James M BogenbergerMayo Clinic, Scottsdale, AZ, USA.
Raoul TibesDivision of Hematology and Medical Oncology, New York University School of Medicine and Perlmutter Comprehensive Cancer Center, New York University Langone Health, New York, NY, USA. Raoul.Tibes@nyulangone.org.
NYU Langone Health · USMayo Clinic in Arizona · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute myeloid leukemia (AML) is a disease of the hematopoietic system that remains a therapeutic challenge despite advances in our understanding of the underlying cancer biology over the past decade. Recent developments in molecular targeting have shown promising results in treating leukemia, paving the way for novel treatment strategies. The discovery of drugs that promote apoptosis in leukemic cells has translated to encouraging activity in clinical trials. B-cell lymphoma (BCL)-2 inhibition has been at the center of drug development efforts to target apoptosis in AML. Remarkable clinical success with venetoclax has revolutionized the ways we treat hematological malignancies. Several landmark trials have demonstrated the potent antitumor activity of venetoclax, and it is now frequently combined with traditional cytotoxic agents to treat AML. However, resistance to BCL-2 inhibition is emerging, and alternative strategies to address resistance mechanisms have become an important focus of research. A number of clinical trials are now underway to investigate a plurality of novel agents that were shown to overcome resistance to BCL-2 inhibition in preclinical models. Some of the most promising data come from studies on drugs that downregulate myeloid cell leukemia (MCL)-1, such as cyclin-dependent kinases (CDK) inhibitors. Furthermore, innovative approaches to target apoptosis via extrinsic pathways and p53 regulation have added new cytotoxic agents to the arsenal, including drugs that inhibit inhibitor of apoptosis protein (IAP) family proteins and murine double minute 2 (MDM2). This review provides a perspective on past and current treatment strategies harnessing various mechanisms of apoptosis to target AML and highlights some important promising treatment combinations in development.

Indexed as

Antineoplastic AgentsApoptosisBridged Bicyclo Compounds, HeterocyclicHumansLeukemia, Myeloid, AcuteProto-Oncogene Proteins c-bcl-2SulfonamidesAntineoplastic AgentsBridged Bicyclo Compounds, HeterocyclicProto-Oncogene Proteins c-bcl-2Sulfonamidesvenetoclax

Identifiers

PMID32319019
OpenAlexW3017304578

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.