A Polymorphism (rs1801018, Thr7Thr) of BCL2 is Associated with Papillary Thyroid Cancer in Korean Population
Clinical and Experimental Otorhinolaryngology
;
: 149-154, 2011.
Artigo
em Inglês
| WPRIM
| ID: wpr-78184
ABSTRACT
OBJECTIVES:
Among the apoptosis signals, B-cell CLL/lymphoma 2 (BCL2) is a well-known regulator of apoptosis with anti-apoptotic properties. We investigated here whether single nucleotide polymorphisms (SNPs) of the BCL2 were associated with host susceptibility of papillary thyroid cancer (PTC) occurrence and clinicopathologic parameters.METHODS:
Ninety-two PTC patients and 222 control subjects were recruited. One promoter SNP (rs2279115, -938A/C) and one synonymous SNP (rs1801018, Thr7Thr) in the BCL2 gene were selected and genotyped using direct sequencing. Multiple logistic regression models were performed to evaluate odds ratios, 95% confidence intervals, and P-values.RESULTS:
rs1801018 of the BCL2 gene was not associated with the development of PTC. In the clinicopathologic features, rs1801018 SNP was associated with the number and location. The G allele frequency of rs1801018 in PTC patients with multifocality (13.3%) was about four-fold higher than that in PTC patients with unifocality (3.4%). The G allele frequency of rs1801018 in PTC patients with both lobes (15.4%) was increased by about five-fold, compared to PTC patients with one lobe (3.2%).CONCLUSION:
The results suggest that synonymous SNP rs1801018 and the G allele of the BCL2 gene may be associated with the multifocality and bilaterality of PTC in Korean population.
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Glândula Tireoide
/
Haplótipos
/
Fator IX
/
Neoplasias da Glândula Tireoide
/
Linfócitos B
/
Modelos Logísticos
/
Razão de Chances
/
Apoptose
/
Polimorfismo de Nucleotídeo Único
/
Alelos
Tipo de estudo:
Estudo de etiologia
/
Estudo prognóstico
/
Fatores de risco
Limite:
Humanos
Idioma:
Inglês
Revista:
Clinical and Experimental Otorhinolaryngology
Ano de publicação:
2011
Tipo de documento:
Artigo
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