ArticleOncotarget2015
B-cell precursor acute lymphoblastic leukemia and stromal cells communicate through Galectin-3.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
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Who cites it
63 citing papers in PubMed, 95 citations in OpenAlex.
- Expression, Localization and Actions of Galectin-3: Implications in the Pathophysiology and Therapy of Cardiovascular Disease.International journal of molecular sciences · 2026Review
- Extracellular vesicle cargo dynamics in the bone marrow microenvironment: from hematopoietic homeostasis to malignant transformation.Extracellular vesicle · 2026Article
- Drug resistance in chronic myeloid leukemia: the involvement of Galectin-1 and Galectin-3.Molecular biology reports · 2026Review
- Galectin-3 Release in the Bone Marrow Microenvironment Promotes Drug Resistance and Relapse in Acute Myeloid Leukemia.Life (Basel, Switzerland) · 2025Review
- Dysregulation of the Bone Marrow Microenvironment in Pediatric Tumors: The Role of Extracellular Vesicles in Acute Leukemias and Neuroblastoma.International journal of molecular sciences · 2025Review
- Harnessing the power of exosomes for diagnosis, prognosis, and treatment of hematological malignancies.Stem cell research & therapy · 2025Review
- Galectins-1, -3 and -9 in leukemia: mechanistic insights and therapeutic translation.Frontiers in immunology · 2025Review
- ActivinA modulates B-acute lymphoblastic leukaemia cell communication and survival by inducing extracellular vesicles production.Scientific reports · 2024Article
- Intracellular galectin interactions in health and disease.Seminars in immunopathology · 2024Review
- Extracellular Vesicles in Pathophysiology: A Prudent Target That Requires Careful Consideration.Cells · 2024Review
- Article
- Exosome derived from tumor-associated macrophages: biogenesis, functions, and therapeutic implications in human cancers.Biomarker research · 2023Review
- Stromal-induced epithelial-mesenchymal transition induces targetable drug resistance in acute lymphoblastic leukemia.Cell reports · 2023Article
- The Role of Extracellular Vesicles in the Pathogenesis of Hematological Malignancies: Interaction with Tumor Microenvironment; a Potential Biomarker and Targeted Therapy.Biomolecules · 2023Review
- Integrins and the Metastasis-like Dissemination of Acute Lymphoblastic Leukemia to the Central Nervous System.Cancers · 2023Review
- Article
- Tumour‑derived exosomes and their emerging roles in leukaemia (Review).Experimental and therapeutic medicine · 2023Review
- Contribution of the TIME in BCP-ALL: the basis for novel approaches therapeutics.Frontiers in immunology · 2023Review
- The role of microenvironment in the initiation and evolution of B-cell precursor acute lymphoblastic leukemia.Frontiers in oncology · 2023Review
- Extracellular vesicles in hematological malignancies: EV-dence for reshaping the tumoral microenvironment.Frontiers in immunology · 2023Review
3 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
The molecular interactions between B-cell precursor acute lymphoblastic leukemia (pre-B ALL) cells and stromal cells in the bone marrow that provide microenvironmentally-mediated protection against therapeutic drugs are not well-defined. Galectin-3 (Lgals3) is a multifunctional galactose-binding lectin with reported location in the nucleus, cytoplasm and extracellular space in different cell types. We previously reported that ALL cells co-cultured with stroma contain high levels of Galectin-3. We here establish that, in contrast to more mature B-lineage cancers, Galectin-3 detected in and on the ALL cells originates from stromal cells, which express it on their surface, secrete it as soluble protein and also in exosomes. Soluble and stromal-bound Galectin-3 is internalized by ALL cells, transported to the nucleus and stimulates transcription of endogenous LGALS3 mRNA. When human and mouse ALL cells develop tolerance to different drugs while in contact with protective stromal cells, Galectin-3 protein levels are consistently increased. This correlates with induction of Galectin-3 transcription in the ALL cells. Thus Galectin-3 sourced from stroma becomes supplemented by endogenous Galectin-3 production in the pre-B ALL cells that are under continuous stress from drug treatment. Our data suggest that stromal Galectin-3 may protect ALL cells through auto-induction of Galectin-3 mRNA and tonic NFκB pathway activation. Since endogenously synthesized Galectin-3 protects pre-B ALL cells against drug treatment, we identify Galectin-3 as one possible target to counteract the protective effects of stroma.
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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 OpenQuestion graph.