The association of TGF beta1 and AT1R gene polymorphisms with hereditary susceptibility and clinical phenotype of HBV-induced liver cirrhosis / 中华医学遗传学杂志
Chinese Journal of Medical Genetics
;
(6): 298-301, 2007.
Artigo
em Chinês
| WPRIM
| ID: wpr-247331
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the association of TGF beta1 and AT1R gene polymorphisms with hereditary susceptibility and clinical phenotype of HBV-induced liver cirrhosis.</p><p><b>METHODS</b>Peripheral blood samples were collected from 102 patients with HBV-induced liver cirrhosis and 106 healthy blood donors. The polymorphisms of the promoter site -509C/T of TGF beta1 and 1166A/C of AT1R gene were determined by PCR-RFLP.</p><p><b>RESULTS</b>The frequency of the homozygote CC of -509C/T of TGF beta1 gene in the group of liver cirrhosis was higher than that the control group (P<0.05); and the frequency rate of homozygote CC was higher in group C than in group A and group B of liver cirrhosis (P<0.05), but there was no significant difference in allele frequency among these group (P>0.05). There was no significant difference in genotypes and allele frequency of AT1R gene 1166A/C between the liver cirrhosis group and the control group (P>0.05).</p><p><b>CONCLUSION</b>The polymorphism of the promoter site -509C/T of TGF beta1 gene is associated with hereditary susceptibility to liver cirrhosis and severity of HBV-induced liver cirrhosis; the polymorphism of AT1R gene 1166A/C is not associated with hereditary susceptibility to HBV-induced liver cirrhosis.</p>
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Fenótipo
/
Polimorfismo Genético
/
Virologia
/
Estudos de Casos e Controles
/
Predisposição Genética para Doença
/
Receptor Tipo 1 de Angiotensina
/
Alelos
/
Fator de Crescimento Transformador beta1
/
Genética
/
Genótipo
Tipo de estudo:
Estudo observacional
/
Fatores de risco
Limite:
Adulto
/
Feminino
/
Humanos
/
Masculino
Idioma:
Chinês
Revista:
Chinese Journal of Medical Genetics
Ano de publicação:
2007
Tipo de documento:
Artigo
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