Henrique Duarte

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Glicosilação de células de cancro gástrico como modulador do receptor oncogénico ErbB2

Autores e Afiliações:

Henrique O. Duarte1,2,3, Meritxell Balmaña1,2, Stefan Mereiter1,2, Hugo Osório1,2,4, Joana Gomes1,2 and Celso A. Reis1,2,3,4

1Institute for Research and Innovation in Health (i3S), University of Porto, 4200-135 Porto, Portugal

2Institute of Molecular Pathology and Immunology of the University of Porto (IPATIMUP), 4200-135 Porto, Portugal

Gastric Cancer Cell Glycosylation as a Modulator od the ErbB2 Oncogenic Receptor

Cell surface receptor tyrosine kinases (RTKs) play a central role in the initiation, promotion and progression of multiple human cancers, by triggering the aberrant activation of downstream signaling pathways implicated in malignant cell phenotype and behavior. In particular, overexpression of the human epidermal growth factor 2 (ErbB2) RTK constitutes a well-established molecular driver of carcinogenesis. RTK maturation is tightly regulated by protein N-linked glycosylation.