Hornerin Is Involved in Breast Cancer Progression / 한국유방암학회지
Journal of Breast Cancer
; : 142-147, 2016.
Article
en En
| WPRIM
| ID: wpr-166640
Biblioteca responsable:
WPRO
ABSTRACT
PURPOSE: The S100 gene family, which comprises over 20 members, including S100A1, S100A2, S100A8, S100A9, profilaggrin, and hornerin encodes low molecular weight calcium-binding proteins with physiological and pathological roles in keratinization. Recent studies have suggested a link between S100 proteins and human cancer progression. The purpose of the present study was to determine the expression levels of hornerin, S100A8, and S100A9 and evaluate their roles in the progression of invasive ductal carcinoma (IDC). METHODS: Seventy cases of ductal carcinoma in situ (DCIS), IDC, and metastatic carcinoma in lymph nodes (MCN) were included. Tissue microarrays were constructed from lesions of DCIS, IDC, and MCN from the same patients. Expression of hornerin, S100A8, and S100A9 was analyzed using immunohistochemistry. RESULTS: The expression of hornerin was associated with the estrogen receptor-negative (p=0.003) and the human epidermal growth factor receptor 2-positive (p=0.002) groups. The expression of S100A8 was associated with a higher pT stage (p=0.017). A significant (p0.050) different. The expression of hornerin increased in a stepwise manner (DCISPalabras clave
Texto completo:
1
Índice:
WPRIM
Asunto principal:
Mama
/
Neoplasias de la Mama
/
Proteínas de Unión al Calcio
/
Inmunohistoquímica
/
Proteínas S100
/
Carcinoma Intraductal no Infiltrante
/
Carcinoma Ductal
/
Estrógenos
/
Receptores ErbB
/
Ganglios Linfáticos
Límite:
Humans
Idioma:
En
Revista:
Journal of Breast Cancer
Año:
2016
Tipo del documento:
Article
Texto completo:
1
Índice:
WPRIM
Asunto principal:
Mama
/
Neoplasias de la Mama
/
Proteínas de Unión al Calcio
/
Inmunohistoquímica
/
Proteínas S100
/
Carcinoma Intraductal no Infiltrante
/
Carcinoma Ductal
/
Estrógenos
/
Receptores ErbB
/
Ganglios Linfáticos
Límite:
Humans
Idioma:
En
Revista:
Journal of Breast Cancer
Año:
2016
Tipo del documento:
Article