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Strong NFκB Expression is Associated With High-grade Dysplasia in Barrett's Esophagus.
El Jamal, Siraj M; Yaseen, Alae A; Alatassi, Houda; Slone, Stephen; Bishop, Barbara J; Fraig, Mostafa.
Afiliação
  • El Jamal SM; *Department of Pathology, University of Mississippi Medical Center, Jackson, MS †Department of Pathology, University of Louisville, Louisville, KY.
Appl Immunohistochem Mol Morphol ; 25(5): 329-333, 2017.
Article em En | MEDLINE | ID: mdl-26990751
ABSTRACT
Nuclear factor kappa B (NFκB) is a transcription factor that regulates the activation of genes involved in proinflammatory response and growth. In this study, we utilized immunohistochemical stains for 2 of the NFκB molecules (RELA and NFκB-1) to evaluate the expression of NFκB in Barrett's esophagus (BE). Forty-three cases of BE [17 cases with no dysplasia, 16 cases with low-grade dysplasia (LGD), and 10 cases with high-grade dysplasia (HGD)], 10 normal esophageal biopsies, and 9 cases of esophageal adenocarcinoma were evaluated. Expression of NFκB-1 and RELA did not occur in normal esophageal squamous mucosa. BE without dysplasia showed weak expression of RELA and NFκB-1 in 35% and 65% of cases, respectively. BE with LGD showed weak expression of RELA and NFκB-1 in 50% and 75% of cases, respectively. Strong expression of RELA and NFκB-1 did not occur in BE without dysplasia or with LGD. BE with HGD showed strong expression of RELA and NFκB-1 in 80% and 90% of cases, respectively. All cases of adenocarcinoma showed strong expression of both RELA and NFκB-1. There was a progressive increase in staining intensity of RELA and NFκB-1 along the metaplasia-dysplasia-adenocarcinoma pathway. Strong expression of NFκB is associated with HGD and adenocarcinoma (P<0.0001). We showed that strong expression of NFκB-1 and RELA correlates highly with BE with HGD and adenocarcinoma.
Assuntos

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Tipo de estudo: Diagnostic_studies / Risk_factors_studies Limite: Humans Idioma: En Ano de publicação: 2017 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Tipo de estudo: Diagnostic_studies / Risk_factors_studies Limite: Humans Idioma: En Ano de publicação: 2017 Tipo de documento: Article