|Support type:||Scholarships in Brazil - Doctorate|
|Effective date (Start):||February 01, 2012|
|Effective date (End):||March 31, 2015|
|Field of knowledge:||Biological Sciences - Genetics - Human and Medical Genetics|
|Principal Investigator:||Roger Chammas|
|Grantee:||Camila Morais Melo|
|Home Institution:||Instituto do Câncer do Estado de São Paulo Octavio Frias de Oliveira (ICESP). Coordenadoria de Serviços de Saúde (CSS). Secretaria da Saúde (São Paulo - Estado). São Paulo , SP, Brazil|
Melanoma is the most aggressiveness of skin cancers. This cancer often presents itself resistant to therapeutic approaches. The tumor-associated angiogenesis is a critical step in tumorigenesis and results on action of various cytokines and growth factors such as VEGF produced in the tumor microenvironment. The extracellular galectins participate in multiple biological processes including tumor angiogenesis and metastasis. The interaction with galectins and cells present in the tumor microenvironment may occur via Toll-like receptors suggesting its involvement in the pro-inflammatory processes and cytokine secretion. Have recently shown that the absence of gal-3 in the stroma and tumor parenchyma decreases angiogenesis by interfering with the macrophage response by VEGF and / or TGF²1. However, the involvement of extracellular galectins in angiogenesis and modulation of the immune system in the tumor microenvironment is not clear. Thus, this study aims to find answers to the involvement of galectins on tumor growth and angiogenesis contributes to the fight against malignant melanoma. Our results show in wild-type mice, inoculated with murine melanoma cells and treatment with galectin functional inhibitor show lower tumor growth than the control group. However, by inhibiting galectins in MyD88 knockout mice observed a higher tumor growth. Our preliminary results indicate that these galectins as potential molecules involved in tumor growth, angiogenesis and promoting conferring resistance. We suggest that this response to galectins occurs via Toll-like receptors as shown by the experiments with MyD88 knockout mice.