GREM1 deficiency induced bone marrow adipose niche promotes B-cell acute lymphoblastic leukemia disease progression.
Song L., Zhang R., Pan L., Mi Q., Yang Y., Wang X.
Animal Study, published in Int J Cancer (2025) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Animal Study
- Journal
- Int J Cancer (2025)
- Country
- United States
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 40285538
- DOI
- 10.1002/ijc.35418
Abstract (original English)
Relapse and disease progression are the primary causes of treatment failure and subsequent mortality in children with B-cell acute lymphocytic leukemia (B-ALL). At diagnosis and during treatment, dyslipidemia and the bone marrow adipose microenvironment are commonly observed in pediatric leukemia. However, the intricate connection between these factors and disease progression remains largely unexplored. We found that abnormal triglyceride accumulation increased the risk of death. Further investigation into the adipogenic potential of BM-MSCs revealed a correlation between higher adipogenicity and elevated serum TG levels, which subsequently led to the rapid proliferation of leukemia cells and heightened the risk of post-relapse mortality. Through RNA sequencing, Gremlin1 (GREM1) was identified as an important factor affecting adipogenicity. Silencing of GREM1 in BM-MSCs induced adipogenic differentiation, partly through the BMP/SMAD signaling pathway. In an in vitro co-culture model, shGREM1-MSCs promoted B-ALL cell proliferation and induced drug resistance to dexamethasone, while increasing sensitivity to L-asparaginase. Furthermore, GREM1-deficient BM-MSCs promoted B-ALL disease progression in xenograft models. This study provides new insights into overcoming drug resistance, relapse, and death by elucidating the novel mechanism by which GREM1 deficiency induces adipogenic di
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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