Evidence map›Paper›PMID 40757392›Full record

ArticleBlood neoplasia2025

PPARγ-induced upregulation of fatty acid metabolism confers resistance to venetoclax and decitabine therapy in AML.

Kotoko Yamatani, Tatsuro Watanabe, Kaori Saito, Abdullah Khasawneh, Abhishek Maiti, Zhihong Zeng, Kala Hayes, Shinya Kimura, Courtney D DiNardo, Xiaoping Su and 5 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Blood neoplasia, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. Review
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

15 authors.

Kotoko YamataniDepartment of Clinical Laboratory Medicine, Juntendo University Graduate School of Medicine, Tokyo, Japan.
Tatsuro WatanabeDepartment of Drug Discovery and Biomedical Sciences, Faculty of Medicine, Saga University, Saga, Japan.
Kaori SaitoDepartment of Clinical Laboratory Medicine, Juntendo University Graduate School of Medicine, Tokyo, Japan.
Abdullah KhasawnehDepartment of Clinical Laboratory Medicine, Juntendo University Graduate School of Medicine, Tokyo, Japan.
Abhishek MaitiDepartment of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX.
Zhihong ZengDepartment of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX.
Kala HayesDepartment of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX.
Shinya KimuraDepartment of Drug Discovery and Biomedical Sciences, Faculty of Medicine, Saga University, Saga, Japan.
Courtney D DiNardoDepartment of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX.
Xiaoping SuDepartment of Bioinformatics and Computational Biology, The University of Texas MD Anderson Cancer Center, Houston, TX.
Shuko NojiriMedical Technology Innovation Center, Juntendo University Graduate School of Medicine, Tokyo, Japan.
Yasushi OkazakiDiagnostics and Therapeutic of Intractable Diseases, Juntendo University Graduate School of Medicine, Tokyo, Japan.
Michael AndreeffDepartment of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX.
Marina KonoplevaDepartment of Oncology and Molecular Pharmacology, Einstein Cancer Center, Albert Einstein College of Medicine, Bronx, NY.
Yoko TabeDepartment of Clinical Laboratory Medicine, Juntendo University Graduate School of Medicine, Tokyo, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The combination of the B-cell lymphoma 2 (BCL2) inhibitor venetoclax (VEN) and the hypomethylating agent decitabine (DEC; VEN/DEC) constitutes a primary therapeutic strategy for treating older adults with acute myeloid leukemia (AML). However, a notable subset of patients exhibits resistance to VEN/DEC, demonstrating either no disease response or relapse after initial remission. This study aimed to elucidate the molecular mechanisms underlying this resistance through analyses of gene expression and DNA methylation profiles. We conducted comprehensive RNA sequencing analysis and DNA methylation profiling on AML samples from 35 patients undergoing VEN/DEC therapy. The RNA sequencing analysis revealed that several genes related to fatty acid metabolism were significantly upregulated in leukemia cells from patients who received VEN/DEC treatment and relapsed or failed to respond. Increased expression of

Identifiers

PMID40757392
PMCPMC12318265

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.