Expressions of Raf-1 kinase, phosphorylated mitogen extracellular kinase 1, and phosphorylated extracellular signal-regulated protein kinase 1/2 in hepatocellular carcinoma and their relationship with prognosis / 中国医学科学院学报
Acta Academiae Medicinae Sinicae
;
(6): 424-428, 2010.
Artículo
en Chino
| WPRIM
| ID: wpr-322758
ABSTRACT
<p><b>OBJECTIVE</b>To explore the prognostic values of Raf-1 kinase (Raf-1), phosphorylated mitogen extracellular kinase 1 (pMEK1), and phosphorylated extracellular signal-regulated protein kinase 1/2(pERK1/2) in hepatocellular carcinoma (HCC) patients.</p><p><b>METHODS</b>We assessed the expressions of Raf-1, pMEK1, and pERK1/2 in HCC using immunohistochemical techniques. The relationships between the expressions of Raf-1, pMEK1, and pERK1/2 and the prognosis were explored.</p><p><b>RESULTS</b>The over-expression rates of Raf-1, pMEK1, and pERK1/2 in HCC were 38.3%, 46.7%, and 38.3%, respectively. The over-expressions of Raf-1, pMEK1, and pERK1/2 were positively correlated with each other (P>0.05), but had no significant correlation with sex, age, α-fetoprotein, hepatitis B surface antigen status, the TNM stage, size,differentiation and vascular invasion of tumor, and liver cirrhosis (P>0.05). Univariate survival analysis and COX proportional hazard regression model showed that Raf-1 over-expression was an independent prognostic factor of poor survival (P<0.05).</p><p><b>CONCLUSION</b>Raf-1 over-expression is an independent marker for the patients of HCC, which may provide new clue in the future targeted therapy.</p>
Texto completo:
Disponible
Índice:
WPRIM (Pacífico Occidental)
Asunto principal:
Fosforilación
/
Pronóstico
/
Carcinoma Hepatocelular
/
Proteínas Proto-Oncogénicas c-raf
/
MAP Quinasa Quinasa 1
/
Quinasas MAP Reguladas por Señal Extracelular
/
Diagnóstico
/
Neoplasias Hepáticas
/
Metabolismo
Tipo de estudio:
Estudio diagnóstico
/
Estudio pronóstico
Límite:
Adulto
/
Anciano
/
Femenino
/
Humanos
/
Masculino
Idioma:
Chino
Revista:
Acta Academiae Medicinae Sinicae
Año:
2010
Tipo del documento:
Artículo
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