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Reduction of tumor activity through different therapeutic strategies in head and neck cancer cells.

Abstract

Head and neck cancer (HNC) is one of the tumor types with the highest incidence in the world, consisting of a heterogeneous group of malignant neoplasms, which include tumors of the oral cavity, pharynx, larynx, and paranasal sinuses. Despite the treatments used, the prognosis is poor, with a survival of approximately 5 years for approximately 90% of patients. A protein commonly expressed in several epithelial tumors, including CCP, is the Epithelial Growth Factor Receptor (EGFR), a tyrosine kinase receptor that, after binding with the growth factor, initiates a cascade that can activate different proteins and cell signaling pathways. that lead to events such as cell proliferation and differentiation, drug resistance, resistance to apoptosis, increased cell migration and angiogenesis. EGFR activates Kirsten Rat Sarcoma (Kras), a GTPase highly expressed in several types of cancer, which, when activated, converts GTP into GDP and this energy is used to initiate an important cell signaling pathway, Phosphatidylinositol-3-Kinase (PI3K/AKT). Activation of the PI3K/AKT/mTOR pathway, as well as EGFR activation, is related to important cellular processes, such as anabolic reactions, nutrient absorption, motility, growth, proliferation and cell survival. Therefore, the main objective of this study is to evaluate new therapeutic strategies that reduce cell proliferation, angiogenesis, drug resistance and inhibition of apoptosis in HNC, through the modulation of these signaling pathways. (AU)

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VEICULO: TITULO (DATA)
VEICULO: TITULO (DATA)