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Therapeutic:

Current focus of our research is on the galectin-3, a member of the beta-galactoside-binding lectin family.

  • Galectin-3 has emerged as an important mediator of various diseases including cancer. It promotes angiogenesis, tumor-endothelial cell interactions, and metastasis of many cancers. Galectin-3 also participates in the nicotine-induced promotion of cancer progression and enrichment of cancer stem-cell like properties.
  • Galectin-3 has been shown to manipulate immune systems of the cancer patients. For example, it is involved in inactivation and silencing of NK and T cells in cancer patients compromising their immune systems.
  • Galectin-3 also regulates chronic inflammation and fibrogenesis through direct effects on tissue myofibroblasts and by mediating cross talk between the innate immune system and fibroblast populations in various organs.
  • Blocking of galectin-3 activity using carbohydrate inhibitors may have clinical utility in the treatment of patients with cancers and fibrotic diseases.

Relevant Publications:

    1. Liu FT, Rabinovich GA: Galectins as modulators of tumor progression. Nat Rev Cancer 2005, 5: 29-41[PubMed]
    2. Johnson KD, Glinskii OV et al: Galectin-3 as a potential therapeutic target in tumors arising from malignant endothelia. Neoplasia 2007, 9: 662-670. [PubMed]
    3. Guha P, Bandyopadhyaya G et al: Nicotine promotes apoptosis resistance of breast cancer cells and enrichment of side population cells with cancer stem cell like properties via a signaling cascade involving galectin-3, α9 nicotinic acetylcholine receptor and STAT3. Breast Cancer Res Treat 2014, 145: 5-22. [PubMed]
    4. Glinskii OV, Sud S et al: Inhibition of prostate cancer bone metastasis by synthetic TF antigen mimic/galectin-3 inhibitor lactulose-l-leucine. Neoplasia 2012, 14: 65-73. [PubMed]
    5. Guha P, Kaptan E et al: Cod glycopeptides with picomolar affinity to galectin-3 suppresses T-cell apoptosis and prostate cancer metastasis. Proc Natl Acad Sci USA 2013, 110: 5052-5057. [PubMed]
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