ArticleCell death & disease2014
Galectin-3 is a marker of favorable prognosis and a biologically relevant molecule in neuroblastic tumors.
Article in Cell death & disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 23 citations in OpenAlex.
- SGSS05-NS3, a covalent SETD8 inhibitor that activates p53 pathway in neuroblastoma.Journal of experimental & clinical cancer research : CR · 2025Article
- Causal Relationship Between Galectins With Neuroblastoma: A Mendelian Randomization Study.Molecular neurobiology · 2025Article
- Harnessing B7-H6 for Anticancer Immunotherapy: Expression, Pathways, and Therapeutic Strategies.International journal of molecular sciences · 2024Review
- BAP31 Promotes Angiogenesis via Galectin-3 Upregulation in Neuroblastoma.International journal of molecular sciences · 2024Article
- Targeting galectin-driven regulatory circuits in cancer and fibrosis.Nature reviews. Drug discovery · 2023Review
- Clinical significance of galectin-3 expression in malformed hepatic venous tissue.The Indian journal of medical research · 2018Article
- Microenvironment in neuroblastoma: isolation and characterization of tumor-derived mesenchymal stromal cells.BMC cancer · 2018Article
- MRE11 inhibition highlights a replication stress-dependent vulnerability of MYCN-driven tumors.Cell death & disease · 2018Article
- TrkB-Target Galectin-1 Impairs Immune Activation and Radiation Responses in Neuroblastoma: Implications for Tumour Therapy.International journal of molecular sciences · 2018Review
- Galectin-3: One Molecule for an Alphabet of Diseases, from A to Z.International journal of molecular sciences · 2018Review
- PARP inhibitors enhance replication stress and cause mitotic catastrophe in MYCN-dependent neuroblastoma.Oncogene · 2017Article
- Overexpression of ezrin and galectin-3 as predictors of poor prognosis of cervical cancer.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2017Article
- Epigenetic siRNA and Chemical Screens Identify SETD8 Inhibition as a Therapeutic Strategy for p53 Activation in High-Risk Neuroblastoma.Cancer cell · 2017Article
- mRNA Transcriptomics of Galectins Unveils Heterogeneous Organization in Mouse and Human Brain.Frontiers in molecular neuroscience · 2016Article
- NKp30 and its ligands: emerging players in tumor immune evasion from natural killer cells.Annals of translational medicine · 2015Article
- Galectin-1, -3 and -9 Expression and Clinical Significance in Squamous Cervical Cancer.PloS one · 2015Article
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Authors and funding
14 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Childhood neuroblastic tumors are characterized by heterogeneous clinical courses, ranging from benign ganglioneuroma (GN) to highly lethal neuroblastoma (NB). Although a refined prognostic evaluation and risk stratification of each tumor patient is becoming increasingly essential to personalize treatment options, currently only few biomolecular markers (essentially MYCN amplification, chromosome 11q status and DNA ploidy) are validated for this purpose in neuroblastic tumors. Here we report that Galectin-3 (Gal-3), a β-galactoside-binding lectin involved in multiple biological functions that has already acquired diagnostic relevance in specific clinical settings, is variably expressed in most differentiated and less aggressive neuroblastic tumors, such as GN and ganglioneuroblastoma, as well as in a subset of NB cases. Gal-3 expression is associated with the INPC histopathological categorization (P<0.001) and Shimada favorable phenotype (P=0.001), but not with other prognostically relevant features. Importantly, Gal-3 expression was associated with a better 5-year overall survival (P=0.003), and with improved cumulative survival in patient subsets at worse prognosis, such as older age at diagnosis, advanced stages or NB histopathological classification. In vitro, Gal-3 expression and nuclear accumulation accompanied retinoic acid-induced cell differentiation in NB cell lines. Forced Gal-3 overexpression increased phenotypic differentiation and substrate adherence, while inhibiting proliferation. Altogether, these findings suggest that Gal-3 is a biologically relevant player for neuroblastic tumors, whose determination by conventional immunohistochemistry might be used for outcome assessment and patient's risk stratification in the clinical setting.
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