# A comprehensive prognostic and immune analysis of LAPTM4B in pan-cancer and Philadelphia chromosome-positive acute lymphoblastic leukemia

## TL;DR

This study explores how the LAPTM4B gene affects cancer progression and immune response in various cancers and leukemia.

## Contribution

The study is the first to comprehensively analyze LAPTM4B's role in Ph+ B-ALL and pan-cancer, linking it to prognosis, immunity, and drug resistance.

## Key findings

- LAPTM4B expression is elevated in various cancers and correlates with poor clinical outcomes.
- LAPTM4B influences tumor immune microenvironment and drug resistance patterns.
- Knocking out LAPTM4B in mice reduced B-ALL progression and cell proliferation.

## Abstract

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).

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 in vivo. BrdU incorporation method, flow cytometry, and Witte-lock Witte culture were used to evaluate the roles of LAPTM4B in vitro.

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 in vitro.

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.