Evidence map›Paper›PMID 40890352›Full record

ReviewNature reviews. Clinical oncology2025

Apoptosis-targeting BH3 mimetics: transforming treatment for patients with acute myeloid leukaemia.

Antonino Glaviano, Ellen Weisberg, Hiu Y Lam, Donavan J J Tan, Andrew J Innes, Yubin Ge, Catherine E Lai, Wendy Stock, Christina Glytsou, Linda Smit and 12 more

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Clinical oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

  1. Pediatric AML CAR T cell therapy.Molecular therapy. Oncology · 2026
    Review
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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

22 authors.

Antonino GlavianoDepartment of Biological, Chemical and Pharmaceutical Sciences and Technologies, University of Palermo, Palermo, Italy.
Ellen WeisbergDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.
Hiu Y LamDepartment of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
Donavan J J TanDepartment of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
Andrew J InnesCentre for Haematology, Department of Immunology and Inflammation, Faculty of Medicine, Imperial College London, London, UK.
Yubin GeKarmanos Cancer Institute, Wayne State University School of Medicine, Detroit, MI, USA.ORCID http://orcid.org/0000-0002-8748-716X
Catherine E LaiDivision of Hematology/Oncology, Department of Medicine, University of Pennsylvania, Philadelphia, PA, USA.
Wendy StockDepartment of Hematology and Oncology, Medical Center, University of Chicago, Chicago, IL, USA.
Christina GlytsouDepartment of Chemical Biology, Ernest Mario School of Pharmacy, Rutgers, The State University of New Jersey, Piscataway, NJ, USA.ORCID http://orcid.org/0000-0002-6260-338X
Linda SmitDepartment of Hematology, Cancer Center Amsterdam, Amsterdam UMC, VU Medical Center, Amsterdam, Netherlands.
Tatsushi YoshidaDepartment of Biochemistry and Molecular Biology, Kyoto Prefectural University of Medicine, Kyoto, Japan.ORCID http://orcid.org/0000-0002-0634-5160
Tian Y ZhangDepartment of Medicine, Division of Hematology, Stanford Cancer Institute, Stanford University, Stanford, CA, USA.
Vanessa E KennedyDepartment of Medicine, Division of Blood and Marrow Transplantation and Cellular Therapy, Stanford University, Stanford, CA, USA.
B Douglas SmithDivision of Hematologic Malignancies, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, MD, USA.
Thomas MercherOPALE Carnot Institute, Gustave Roussy Cancer Campus, Université Paris-Saclay, Paris, France.
Stéphane de BottonDepartment of Hematology, Gustave Roussy Cancer Campus, Université Paris-Saclay, Paris, France.
Patrizia DianaDepartment of Biological, Chemical and Pharmaceutical Sciences and Technologies, University of Palermo, Palermo, Italy.
Marina KonoplevaDepartment of Molecular Pharmacology, Albert Einstein College of Medicine, New York City, NY, USA.ORCID http://orcid.org/0000-0002-9347-2212
Michael J MauroMyeloproliferative Neoplasms Program, Memorial Sloan Kettering Cancer Center, New York City, NY, USA.
James D GriffinDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.
Courtney D DiNardoDepartment of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX, USA. cdinardo@mdanderson.org.ORCID http://orcid.org/0000-0001-9003-0390
Alan P KumarDepartment of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore. apkumar@nus.edu.sg.ORCID http://orcid.org/0000-0002-3754-5712

Funding

TYROSINE KINASE ONCOGENESIS IN MYELOID LEUKEMIAP01CA066996 · NCI · DANA-FARBER CANCER INSTITUTE · PI SCOTT A ARMSTRONG · 1996 to 2026
$52.5M
NCI NIH HHS P01 CA066996
6 · The paper itself

Abstract

Acute myeloid leukaemia (AML) remains a challenging haematological malignancy, with most patients developing resistance to standard-of-care (SOC) treatments. This resistance is often attributed to the overexpression of anti-apoptotic BCL-2 family proteins, which regulate the intrinsic apoptotic pathway by inhibiting pro-apoptotic effector proteins such as BAX and BAK. AML cells exploit this imbalance to evade apoptosis and sustain survival, necessitating the development of novel therapeutic strategies. BH3 mimetics are small-molecule inhibitors targeting the pro-survival BCL-2 family proteins and have emerged as promising agents in patients with AML who are unable to receive high-intensity induction chemotherapy. Co-treatment with the BCL-2-specific inhibitor venetoclax and various SOC therapies has been proven effective, with several combinations now approved by the US Food and Drug Administration for adults with AML who are ≥75 years of age and/or are ineligible for intensive induction chemotherapy, on the basis of improved response rates and survival outcomes compared with the previous SOC. In this Review, we highlight the transformative potential of BH3 mimetics in AML therapy, including ongoing studies investigating novel combination regimens and efforts to further refine treatment strategies, with the ultimate goal of improving outcomes for patients with AML.

Indexed as

Antineoplastic AgentsApoptosisLeukemia, Myeloid, AcuteProto-Oncogene Proteins c-bcl-2Antineoplastic Combined Chemotherapy ProtocolsBridged Bicyclo Compounds, HeterocyclicHumansPeptide FragmentsProto-Oncogene ProteinsSulfonamidesAntineoplastic AgentsBax protein (53-86)Bridged Bicyclo Compounds, HeterocyclicPeptide FragmentsProto-Oncogene ProteinsProto-Oncogene Proteins c-bcl-2Sulfonamidesvenetoclax

Identifiers

PMID40890352

What OpenQuestion holds

Textmetadata
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.