Expression of fatty acid synthase, ErbB2 and Ki-67 in head and neck squamous cell carcinoma. A clinicopathological study

Autor(es)

Silva, Sabrina D. ; Agostini, Michelle ; Nishimoto, Inês N. ; Coletta, Ricardo D. ; Alves, Fábio A. ; Lopes, Márcio A. ; Kowalski, Luiz Paulo ^[7] ; Graner, Edgard

• Tipo de documento: Artigo Científico
• Fonte: Oral Oncology; v. 40, n. 7, p. 688-696, Aug. 2004.
• Área do conhecimento: Ciências da Saúde - Medicina
• Assunto(s): Anatomia patológica Neoplasias de cabeça e pescoço Carcinoma de células escamosas

Resumo

Fatty acid synthase (FAS) is a multifunctional enzyme responsible for the synthesis of saturated fatty acids using acetyl-CoA and malonyl-CoA as substrates. Overexpression of FAS has been reported in several human malignancies and suggested as a potential prognostic factor. ErbB2 (Her-2/neu), a transmembrane tyrosine kinase member of the ErbB receptor family, is known to be overexpressed in a variety of tumors and was recently shown to regulate FAS production in breast epithelial cell lines. Herein we analyzed by immunohistochemistry the expression of FAS, ErbB2, and the proliferation marker Ki-67 in 62 head and neck squamous cell carcinoma (HNSCC) samples. Approximately 78% of the cases were positive for FAS or ErbB2 at the cell membrane and 70% of the tumors that showed a high expression of FAS were also strongly positive for ErbB2 (Fisher's exact test, p=0.01). The immunolabeling for both FAS and ErbB2 was stronger in histologically well-differentiated lesions. Additionally, Ki-67 expression was significantly associated with a poor prognosis (log-rank test, p=0.03). Taken together, the results presented here suggest that ErbB2 regulates FAS expression in HNSCC and point out Ki-67 as a useful prognostic marker for these tumors. (AU)

• Processo FAPESP: 02/08030-1 - Estudo das enzimas desubiquitinantes Ubp-45(USP9) e Ubp-69 (USP2) no controle da proliferação de linhagens celulares de carcinoma bucal e de fibromatose gengival hereditária
• Beneficiário: Edgard Graner
• Modalidade de apoio: Auxílio à Pesquisa - Regular