ArticleFrontiers in immunology2025
A comprehensive prognostic and immune analysis of
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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.
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.
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Who cites it
2 citing papers in PubMed.
- LAPTM proteins in neurological disorders - Autophagy-lysosome dysfunction and therapeutic targets: A review.Biomolecules & biomedicine · 2026Review
- Toward a chemotherapy and allo-HSCT free future: the evolution of treatment for Philadelphia chromosome-positive acute lymphoblastic leukemia.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Lysosomal-associated protein transmembrane-4 beta (LAPTM4B) protein expression was increased in solid tumors, whereas few studies were performed in hematologic malignancies. We aimed to study the effect of the LAPTM4B gene in pan-cancer and Philadelphia chromosome-positive acute B cell lymphoblastic leukemia (Ph+ B-ALL). Methods: The differential expression, diagnosis, prognosis, genetic and epigenetic alterations, tumor microenvironment, stemness, immune infiltration cells, function enrichment, single-cell analysis, and drug response across cancers were conducted based on multiple computational tools. Additionally, Ph+ B-ALL transgenic mouse model with Laptm4b knockout was used to analyze the function of LAPTM4B Results: We identified that LAPTM4B expression was increased in various cancers, with significant associations with clinical outcomes. LAPTM4B expression correlated with DNA and RNA methylation patterns and was associated with drug resistance. It also influenced the tumor immune microenvironment, with implications for immunotherapy response. In leukemia, LAPTM4B was expressed in stem cells and associated with specific subtypes. Knockout of LAPTM4B impeded B-ALL progression in mice and reduced cell proliferation and caused G0/G1 arrest Discussion: Our study elucidated the role LAPTM4B that promoted the development and progression in Ph+ B-ALL. Furthermore, LAPTM4B played a diagnostic, prognostic, and immunological factor.
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