Overexpression of TFIIB-related factor 2 is significantly correlated with tumor angiogenesis and poor survival in patients with esophageal squamous cell cancer.
Med Oncol
; 30(2): 553, 2013 Jun.
Article
em En
| MEDLINE
| ID: mdl-23550276
Studies have shown that genetic activation of TFIIB-related factor 2 (BRF2) represents a unique mechanism of tumorigenesis through the increase in Pol III-mediated transcription. Several studies have shown that BRF2 is overexpressed in several types of cancer and suggest the oncogenic role of BRF2. This study aimed to examine the expression of TFIIB-related factor 2 (BRF2) in patients with esophageal squamous cell cancer (ESCC) and explore the relationship of BRF2 expression with clinicopathologic factors, tumor angiogenesis and prognosis. We found that increased BRF2 protein expression was prevalent in esophageal squamous cell cancer and was significantly associated with deeper tumor invasion (P = 0.039) and microvessel density (P = 0.007). Additionally, expression of BRF2 was found to be an independent prognostic factor in ESCC patients. Furthermore, a significant correlation between high BRF2 expression and shorter overall survival time was found in different subgroups of ESCC patients stratified by the clinical stage, T classification and lymph node metastasis. High expression of BRF2 protein is closely associated with tumor progression and angiogenesis and poor survival of ESCC. BRF2 is a promising biomarker to identify individuals with poor prognostic potential and concludes the possibility of its use as a prognostic marker in patients with ESCC.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Neoplasias Esofágicas
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Biomarcadores Tumorais
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Regulação Neoplásica da Expressão Gênica
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Neoplasias de Células Escamosas
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Fator de Transcrição TFIIIB
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Neovascularização Patológica
Tipo de estudo:
Diagnostic_studies
/
Observational_studies
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Prognostic_studies
/
Risk_factors_studies
Limite:
Aged
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Female
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Humans
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Male
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Middle aged
Idioma:
En
Revista:
Med Oncol
Ano de publicação:
2013
Tipo de documento:
Article