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1.
Braz. oral res. (Online) ; 38: e018, 2024. tab, graf
Artículo en Inglés | LILACS-Express | LILACS, BBO | ID: biblio-1550152

RESUMEN

Abstract The aim of this study was to evaluate the expression of the EZH2 protein and describe the clinical and microscopic characteristics of adenoid cystic carcinoma (ACC) and pleomorphic adenoma (PA). The study included 16 ACC cases and 12 PA. All ACC and PA cases were positive for EZH2 and the ACC samples showed significantly higher EZH2 expression. The clinical and microscopic covariates were described in relation to EZH2 staining in ACC samples. The highest mean values of EZH2 were observed in cases with local metastasis, recurrence, perineural invasion, and predominantly cribriform growth pattern without solid areas. EZH2 is a potential marker of malignancy.

2.
J. appl. oral sci ; 28: e20190532, 2020. tab, graf
Artículo en Inglés | BBO, LILACS | ID: biblio-1101257

RESUMEN

Abstract Oral leukoplakia (OL) is a white lesion of an indeterminate risk not related to any excluded (other) known diseases or disorders that carry no increased risk for cancer. Many biological markers have been used in an attempt to predict malignant transformation; however, no reliable markers have been established so far. Objective To evaluate cell proliferation and immortalization in OL, comparing non-dysplastic (Non-dys OL) and dysplastic OL (Dys OL). Methodology This is a cross-sectional observational study. Paraffin-embedded tissue blocks of 28 specimens of Non-dys OL, 33 of Dys OL, 9 of normal oral mucosa (NOM), 17 of inflammatory hyperplasia (IH), and 19 of oral squamous cell carcinomas (OSCC) were stained for Ki-67 and BMI-1 using immunohistochemistry. Results A gradual increase in BMI-1 and K-i67 expression was found in oral carcinogenesis. The immunolabeling for those markers was higher in OSCC when compared with the other groups (Kruskal-Wallis, p<0.05). Ki-67 expression percentage was higher in OL and in IH when compared with NOM (Kruskal-Wallis/Dunn, p<0.05). Increased expression of BMI-1 was also observed in OL when compared with NOM (Kruskal-Wallis/Dunn, p<0.05). No differences were observed in expression of both markers when non-dysplastic and dysplastic leukoplakias were compared. A significant positive correlation between Ki-67 and BMI-1 was found (Spearman correlation coefficient, R=0.26, p=0.01). High-grade epithelial dysplasia was associated with malignant transformation (Chi-squared, p=0.03). Conclusions These findings indicate that BMI-1 expression increases in early oral carcinogenesis and is possibly associated with the occurrence of dysplastic changes. Furthermore, our findings indicate that both Ki-67 and BMI-1 are directly correlated and play a role in initiation and progression of OSCC.


Asunto(s)
Humanos , Animales , Masculino , Adulto , Persona de Mediana Edad , Anciano , Anciano de 80 o más Años , Leucoplasia Bucal/patología , Neoplasias de la Boca/patología , Carcinoma de Células Escamosas/patología , Antígeno Ki-67/análisis , Complejo Represivo Polycomb 1/análisis , Mucosa Bucal/patología , Inmunohistoquímica , Estudios Transversales , Factores de Riesgo , Estadísticas no Paramétricas , Progresión de la Enfermedad , Proliferación Celular , Carcinogénesis/patología
3.
São Paulo; s.n; 2005. 123 p. ilus, tab, graf. (BR).
Tesis en Portugués | LILACS, BBO | ID: lil-436118

RESUMEN

o carcinoma epidermóide bucal é uma doença genética que faz uso de diversos mecanismos de sinalização molecular para crescer, invadir e metastatizar. Profundas alterações genéticas e protéicas podem ser observadas durante este processo que implicam não somente na sinalização intracelular, como em uma intensa comunicação entre as células neoplásicas e modulação do meio ambiente num processo conhecido como sinalização parácrina e autócrina. A presença dos altos níveis de expressão de NFKB nas linhagens de carcinomas epidermóides bucais foi demonstrada, assim como a direta correlação entre esta superexpressão e o aumento na ativação de IL6. A capacidade da via de sinalização do NFKB em estabelecer uma sinalização parácrina diretamente através da IL6 foi provada com a ativação do STAT3 em células epiteliais normais. Fazendo uso da técnica de microarray diversos genes conhecidamente associados a esta via de sinalização assim como genes totalmente desconhecidos foram apontados


Asunto(s)
Carcinoma de Células Escamosas , Patología Bucal
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