Evidence map›Paper›PMID 41030943›Full record

ReviewFrontiers in oncology2025

Factors affecting response and resistance to venetoclax in acute myeloid leukemia.

Michael D Diamantidis

Abstract readReview
In one paragraph

Review in Frontiers in oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

5 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Review
  5. 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

1 author.

Michael D DiamantidisThalassemia and Sickle Cell Disease Unit, Department of Hematology, General Hospital of Larissa, Larissa, Greece.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The use of the BCL2 inhibitor venetoclax in combination with hypomethylating agents (HMA) is a revolution for the treatment of frail and elderly acute myeloid leukemia (AML) patients. This effective treatment strategy is increasingly more and more applicable for other subsets of AML patients and is currently being tested in numerous clinical trials in combination with other drugs in all treatment lines. In particular, venetoclax combinations can also serve as a definitive therapy or as an effective bridge to allogeneic hematopoietic stem cell transplantation (HSCT). However, the factors affecting response to venetoclax in the abovementioned AML patients are not completely clear and understood until today. The aim of this review is to describe the molecular and clinical patterns of response and durable remission of venetoclax-based combinations in AML patients. Hence, mutations in IDH1, IDH2, ASXL1, NPM1, DDX41, chromatin-cohesin complex and splicing-factor genes predict superior response to venetoclax, while inferior response to the drug has been observed for FLT3-ITD, KRAS, NRAS and TP53 gene mutations. Intriguingly, the achievement of measurable residual disease (MRD) negativity in the first four cycles of venetoclax administration characterizes a subgroup of NPM1-mutated AML patients with a more favorable outcome. Even though focus will be given on factors influencing response to the drug in this review, the main mechanisms of resistance to venetoclax in AML patients will also be discussed.

Indexed as

acute myeloid leukemia (AML)azacitidine (AZA)BCL2 (B-cell lymphoma 2) inhibitionhypomethylating agents (HMAs)MCL1 (myeloid cell leukemia sequence 1) overexpressionresistanceresponsevenetoclax (VEN)

Identifiers

PMID41030943
PMCPMC12476996

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Registered trials

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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.