Evidence map›Paper›PMID 40341460›Full record

ReviewAnnals of hematology2025

"Galectin-9: A double-edged sword in Acute Myeloid Leukemia".

Omolbanin Sargazi Aval, Ali Ahmadi, Ali Jihad Hemid Al-Athari, Hamed Soleimani Samarkhazan, Fatemeh Sotudeh Chafi, Marjan Asadi, Mohammad Hossein Mohammadi, Mojtaba Aghaei

Abstract readReview
In one paragraph

Review in Annals of hematology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
–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

29 citing papers in PubMed, 1 synthesis or guideline pooled it.

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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

8 authors.

Omolbanin Sargazi AvalDepartment of Hematology, Faculty of Allied Medical Sciences, Zabol University of Medical Sciences, Zabol, Iran.ORCID http://orcid.org/0000-0003-3325-5125
Ali AhmadiDepartment of Hematology and Blood Banking, School of Allied Medical Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran.ORCID http://orcid.org/0009-0003-4779-6077
Ali Jihad Hemid Al-AthariCollege of Pharmacy, Al- Mustaqbal University, Babylon, 51001, Iraq.
Hamed Soleimani SamarkhazanStudent Research Committee, Department of Hematology and Blood Banking, School of Allied Medical Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran.ORCID http://orcid.org/0000-0003-1045-7613
Fatemeh Sotudeh ChafiDepartment of Hematology and Blood Banking, School of Allied Medical Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran.ORCID http://orcid.org/0009-0008-6689-2888
Marjan AsadiHSCT research center, Bone Marrow Transplantation and Cell Therapy Lab, Taleghani hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran.ORCID http://orcid.org/0000-0003-2789-8271
Mohammad Hossein MohammadiDepartment of Hematology and Blood Banking, School of Allied Medical Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Drmohammadi@sbmu.ac.ir.ORCID http://orcid.org/0009-0005-4884-5218
Mojtaba AghaeiStudent Research Committee, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. mojtabaaghaei745@gmail.com.ORCID http://orcid.org/0000-0002-6382-6657

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute Myeloid Leukemia (AML) presents a formidable challenge in the realm of hematologic malignancies, characterized by the unregulated proliferation of myeloid progenitor cells, leading to severe disruptions in normal hematopoiesis. This review examines the multifaceted role of Galectin-9, a crucial glycan-binding protein in the pathophysiology of AML, emphasizing its potential as both a prognostic biomarker and a therapeutic target. Recent insights into the molecular underpinnings of AML, particularly those involving genetic mutations and cytogenetic abnormalities, illuminate the complex landscape of this disease, where patient outcomes are significantly influenced by individual biological markers. Galectin-9, initially recognized for its involvement in fundamental biological processes such as cell proliferation and immune modulation, has emerged as a pivotal molecule in AML, with expression levels correlating with leukemic cell behavior and clinical prognosis. This review consolidates the extensive literature on Galectin-9, elucidating its role in leukemic transformation and the therapeutic implications of manipulating this pathway. By investigating the intricate relationship between Galectin-9 and AML, we aim to provide a comprehensive understanding that could lead to innovative strategies for managing this aggressive malignancy, offering hope for improved survival outcomes through targeted therapeutic interventions.

Indexed as

GalectinsLeukemia, Myeloid, AcuteNeoplasm ProteinsAnimalsBiomarkers, TumorGene Expression Regulation, LeukemicHumansPrognosisBiomarkers, TumorGalectinsLGALS9 protein, humanNeoplasm ProteinsAcute myeloid leukemiaGalectin-9ImmunomodulationLeukemic stem cellTargeted therapy

Identifiers

PMID40341460
PMCPMC12283773

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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.