Evidence map›Paper›PMID 40927635›Full record

ArticleEJHaem2025

SGLT-2 Inhibitors Are Potent to Suppress Aggressive Transformation From Indolent Type of Adult T-Cell Leukemia/Lymphoma: Unique Insight Into Therapeutics for Diabetes-Related Hematological Malignancy.

Kazuho Morichika, Keita Tamaki, Takuya Fukushima, Hiroaki Masuzaki

Abstract read
In one paragraph

Article in EJHaem, 2025. 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. 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

4 authors.

Kazuho MorichikaDivision of Endocrinology Diabetes and Metabolism, Hematology and Rheumatology, Second Department of Internal Medicine Graduate School of Medicine University of the Ryukyus Ryukyus Japan.
Keita TamakiDivision of Endocrinology Diabetes and Metabolism, Hematology and Rheumatology, Second Department of Internal Medicine Graduate School of Medicine University of the Ryukyus Ryukyus Japan.
Takuya FukushimaLaboratory of Immunohematology School of Health Sciences Faculty of Medicine University of the Ryukyus Ryukyus Japan.
Hiroaki MasuzakiDivision of Endocrinology Diabetes and Metabolism, Hematology and Rheumatology, Second Department of Internal Medicine Graduate School of Medicine University of the Ryukyus Ryukyus Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: We previously reported that sodium-glucose co-transporter 2 (SGLT-2) was ectopically overexpressed in adult T-cell leukemia (ATL) cells notably in aggressive type but in indolent type, and widely-used anti-diabetic SGLT-2 inhibitors (SGLT-2i) considerably attenuated proliferation of leukemic cells. Methods: We performed retrospective analyses for 10 years to see whether SGLT-2i would prevent aggressive transformation in patients with indolent type ATL accompanied by diabetes. Nucleosome occupancy in the promotor region of the Results: In patients of indolent ATL with diabetes, the cumulative progression rate in the non-SGLT-2i-treated group was 71%, while no patients developed aggressive transformation in the SGLT-2i treated group. ATL cells showed an apparent trend to decrease nucleosome occupancy in the promotor region of the Conclusion: Our data suggest that SGLT-2i is advantageous for preventing aggravative transformation in indolent ATL. Trial Registration: Authors confirmed that clinical trial registration was not requested for the present study and this manuscript.

Indexed as

adult T‐cell leukemia/lymphomadiabetes‐associated malignancySGLT‐2 inhibitors

Identifiers

PMID40927635
PMCPMC12416307

What Socratic holds

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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 Socratic graph.