Evidence map›Paper›PMID 41550719›Full record

ArticleiScience2026

Regulatory role of mTORC1 signaling in osteoblasts in acute myeloid leukemia progression and steady-state hematopoiesis.

Kazuya Fukasawa, Kazuya Tokumura, Makoto Yoshimoto, Koki Sadamori, Ioanna Mosialou, Yoshiaki Harakawa, Kazuto Isawa, Shohei Tsuji, Haruhiko Inufusa, Atsushi Hirao and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in iScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

12 authors.

Kazuya FukasawaDepartment of Bioactive Molecules, Pharmacology, Gifu Pharmaceutical University, Gifu 501-1196, Japan.
Kazuya TokumuraDepartment of Bioactive Molecules, Pharmacology, Gifu Pharmaceutical University, Gifu 501-1196, Japan.
Makoto YoshimotoDepartment of Bioactive Molecules, Pharmacology, Gifu Pharmaceutical University, Gifu 501-1196, Japan.
Koki SadamoriDepartment of Bioactive Molecules, Pharmacology, Gifu Pharmaceutical University, Gifu 501-1196, Japan.
Ioanna MosialouDepartment of Physiology and Cellular Biophysics, Columbia University Medical Center, New York, NY 10032, USA.
Yoshiaki HarakawaDivision of Anti-Oxidant Research, Life Science Research Center, Gifu University, Gifu 501-1194, Japan.
Kazuto IsawaDepartment of Bioactive Molecules, Pharmacology, Gifu Pharmaceutical University, Gifu 501-1196, Japan.
Shohei TsujiDepartment of Bioactive Molecules, Pharmacology, Gifu Pharmaceutical University, Gifu 501-1196, Japan.
Haruhiko InufusaDivision of Anti-Oxidant Research, Life Science Research Center, Gifu University, Gifu 501-1194, Japan.
Atsushi HiraoWPI Nano Life Science Institute (WPI-Nano LSI), Kanazawa University, Kanazawa, Ishikawa, Japan.
Stavroula KousteniDepartment of Physiology and Cellular Biophysics, Columbia University Medical Center, New York, NY 10032, USA.
Eiichi HinoiDepartment of Bioactive Molecules, Pharmacology, Gifu Pharmaceutical University, Gifu 501-1196, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute myeloid leukemia (AML) is widely recognized for its intrinsic leukemic-cell-driven regulation as well as its extrinsic niche-driven regulation. Despite mounting evidence that bone-forming osteoblasts provide an endosteal niche for AML cells, the precise mechanism remains to be elucidated. The cell-autonomous mammalian target of rapamycin complex 1 (mTORC1) is involved in the onset and progression of AML. Here, we found that mTORC1 signaling was activated in the osteoblasts of an AML murine model and clinical AML specimens. Osteoblast-specific mTORC1 activation in mice promotes AML growth, whereas mTORC1 inactivation suppresses it. Interleukin-6 (IL-6) was identified through screening as a downstream factor in mTORC1-regulated AML progression. Genetic ablation of the IL-6 receptor in AML cells significantly attenuated AML growth in osteoblast-specific mTORC1-activated mice. Collectively, our results suggest that the mTORC1/IL-6 axis in osteoblastic niche non-autonomously contributes to the AML progression, suggesting a viable therapeutic target for AML.

Indexed as

cancercell biology

Identifiers

PMID41550719
PMCPMC12808893

What OpenQuestion holds

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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.