Related Experiment Video
Updated: Feb 1, 2026
06:48
In Ovo Xenografting of Patient-Derived Acute Lymphoblastic Leukemia (ALL) Cells (PDX-ALL)
Published on: August 1, 2025
517
mTOR Modulation Affects Galectin-1 Expression in KMT2A-rearranged Acute Lymphoblastic Leukemia Cells
Bartłomiej Pawlik1,2, Joanna Madzio1, Zuzanna Rydzyńska1
1Department of Pediatrics, Oncology and Hematology, Medical University of Lodz, Lodz, Poland.
Anticancer Research
|January 30, 2026
Summary
Targeting the mTOR pathway can regulate Galectin-1, an immune checkpoint protein, in KMT2A-rearranged Acute Lymphoblastic Leukemia (KMT2A r-ALL). This finding suggests mTOR inhibition as a potential strategy against immune evasion in KMT2A r-ALL.
Area of Science:
- Oncology
- Immunology
- Molecular Biology
Background:
- Acute Lymphoblastic Leukemia (ALL) is a common pediatric cancer.
- KMT2A-rearranged ALL (KMT2A r-ALL) has poor outcomes and immune evasion challenges.
- Galectin-1 is a highly expressed immune checkpoint protein in KMT2A r-ALL, indicating its therapeutic potential.
Purpose of the Study:
- To investigate the role of the mTOR signaling pathway in regulating Galectin-1 expression in KMT2A r-ALL.
- To explore potential therapeutic strategies targeting the mTOR-Galectin-1 axis in KMT2A r-ALL.
Main Methods:
- Bioinformatic analysis of gene expression data from B-cell ALL subtypes.
- In vitro studies using leukemia cell lines treated with the mTOR inhibitor everolimus.
- Quantitative PCR (qPCR) and immunoblotting to assess Galectin-1 mRNA and protein levels.
- Computational tools to analyze transcription factor binding on the Galectin-1 promoter.
Main Results:
- Galectin-1 mRNA and protein were selectively upregulated in KMT2A r-ALL cells.
- Inhibition of the mTOR pathway with everolimus modulated Galectin-1 expression.
- SP1 was identified as a putative transcription factor binding to the Galectin-1 promoter, potentially regulated by mTOR.
Conclusions:
- mTOR signaling pathway plays a role in regulating Galectin-1 immune checkpoint activity in KMT2A r-ALL.
- Inhibiting mTOR may offer a therapeutic strategy to overcome immune evasion in KMT2A r-ALL.
- Targeting the mTOR-Galectin-1 axis presents a promising avenue for KMT2A r-ALL treatment.
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