A biologia molecular no prognóstico do carcinoma da tireóide

• Autor(a) principal: Rodrigues,Aluizio Soares de Souza
• Data de Publicação: 2003
• Tipo de documento: Artigo
• Idioma: por
• Título da fonte: Revista do Colégio Brasileiro de Cirurgiões
• Texto Completo: http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0100-69912003000600012
• topic: Molecular biology; Thyroid neoplasms; Prognosis; Oncogenes

This overview examines some selected genetic mechanisms of cancer development. Strong evidence has been accumulated suggesting that alteration in either the struture or activity of proto-oncogene contributes to the development and for the maintenance of the malignant phenotype. Many factors are known to interfere with both normal and pathological controls of growth and differentiation of thyroid cells. Among them, some are oncogenes, like those encoding g-proteins (ras, gsp, TSH-R), encoding thyrosino kinases receptors (RET, trk, c-met, c-erb, BRAF) and encoding nuclear proteins (c-myc, e-fós). Others are anti-oncogenes (p53, p15, RB), by loss of the growth suppression ativity of the suppressive gene. Cancer cell invasion and metastasis are the major causes of morbidity and mortality in cancer patients. Many genes are involved in the mechanism of invasion and metastasis of thyroid tumors, like Nis, b-catenina, E-caderina, galectina-3, GLUT, telomerase, VEGT, nm-23. All these oncogenes, antioncogenes and tumor invasion and metastasis-related genes are analysed. Several clinical and prognostic factors have been proposed to identify patients at risk for the development of metastasis and death. The role of molecular genetics in this issue is discussed. However, other studies are needed to validate molecular alterations as an independent prognostic factor in thyroid cancer.