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A Case of Granulocyte-Colony Stimulating Factor-Producing Hepatocellular Carcinoma Confirmed by Immunohistochemistry
Artigo em Inglês | WPRIM (Pacífico Ocidental) | ID: wpr-199408
Biblioteca responsável: WPRO
ABSTRACT
Granulocyte-colony stimulating factor (G-CSF) is a naturally occurring glycoprotein that stimulates the proliferation and maturation of precursor cells in the bone marrow into fully differentiated neutrophils. Several reports of G-CSF-producing malignant tumors have been published, but scarcely any in the hepatobiliary system, such as in hepatocellular carcinoma (HCC). Here, we encountered a 69-yr-old man with a hepatic tumor who had received right hepatic resection. He showed leukocytosis of 25,450/microL along with elevated serum G-CSF. Histological examination of surgical samples demonstrated immunohistochemical staining for G-CSF, but not for G-CSF receptor. The patient survived without recurrence for four years, but ultimately passed away with multiple bone metastases. In light of the above, clinicians may consider G-CSF-producing HCC when encountering patients with leukocytosis and a hepatic tumor. More cases are needed to clarify the clinical picture of G-CSF-producing HCC.
Assuntos

Texto completo: Disponível Base de dados: WPRIM (Pacífico Ocidental) Assunto principal: Neoplasias Ósseas / Fator Estimulador de Colônias de Granulócitos / Receptores de Fator Estimulador de Colônias de Granulócitos / Evolução Fatal / Carcinoma Hepatocelular / Neoplasias Hepáticas Limite: Idoso / Humanos / Masculino Idioma: Inglês Revista: Journal of Korean Medical Science Ano de publicação: 2010 Tipo de documento: Artigo
Texto completo: Disponível Base de dados: WPRIM (Pacífico Ocidental) Assunto principal: Neoplasias Ósseas / Fator Estimulador de Colônias de Granulócitos / Receptores de Fator Estimulador de Colônias de Granulócitos / Evolução Fatal / Carcinoma Hepatocelular / Neoplasias Hepáticas Limite: Idoso / Humanos / Masculino Idioma: Inglês Revista: Journal of Korean Medical Science Ano de publicação: 2010 Tipo de documento: Artigo
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