RESUMEN
Experimental evidence suggests that in lung cancer, development, progression and an increased proliferation rate can be linked to apoptosis-related factors. The objective of this study is to evaluate the status of Neu, signal transducer and activator of transcription (STAT)-3, STAT5 and Bcl-xL expression in non-small-cell lung cancer. We investigated the immunohistochemical expression of these proteins in 92 non-small-cell lung cancer specimens to establish their role in lung cancer pathogenesis. Neu was overexpressed in 65% of cases, and although STAT3 was overexpressed in 52.1% in cytoplasm, it was expressed in nucleus (activated) in 60.8%. Meanwhile, STAT5 was found overexpressed in 41.3% in cytoplasm and 32.6% in nucleus. Thus, Bcl-xL was overexpressed in cytoplasm in 81.5%. Interestingly, we found nuclear expression of Bcl-xL in 30.4% of cases. Finally, we found correlation among histological types of lung cancer and nuclear expression of both STAT5 (P=0.005) and nuclear Bcl-xL (P=0.003). Besides, nuclear expression of Bcl-xL was correlated with TNM stage IV (distant metastasis) (P=0.02). These results suggest for the first time, a relevant role for STAT5 and Bcl-xL as apoptosis-regulatory proteins in the pathogenesis of lung cancer, and overexpression of both Neu and activated STAT3, could be related with the proliferation rate in lung carcinoma cells.
Asunto(s)
Neoplasias Pulmonares/metabolismo , Receptor ErbB-2/metabolismo , Factor de Transcripción STAT3/metabolismo , Factor de Transcripción STAT5/metabolismo , Proteína bcl-X/metabolismo , Adenocarcinoma/metabolismo , Adenocarcinoma/patología , Adulto , Anciano , Anciano de 80 o más Años , Apoptosis , Carcinoma de Células Grandes/metabolismo , Carcinoma de Células Grandes/patología , Carcinoma de Pulmón de Células no Pequeñas/metabolismo , Carcinoma de Pulmón de Células no Pequeñas/patología , Carcinoma de Células Escamosas/metabolismo , Carcinoma de Células Escamosas/patología , Proliferación Celular , Femenino , Regulación Neoplásica de la Expresión Génica , Humanos , Neoplasias Pulmonares/patología , Masculino , Persona de Mediana Edad , Estadificación de Neoplasias , Estudios RetrospectivosRESUMEN
En este trabajo se presenta la influencia de la variabilidad genética sobre el metabolismo el etanol, hecho que puede generalizarse a prácticamente todos los procesos porque, en mayor a menor proporción, existen variaciones genéticas que influyen de manera importante en la respuesta individual a un estímulo dado; sólo que en la respuesta metabólica a la ingestión aguda o crónica de etanol esto es particularmente claro, porque las principales enzimas que participan en su degradación presentan formas polimórficas con actividades diferentes. Factores como la edad, sexo, raza, etc., contribuyen en la obsorción, la distribución y el metabolismo del etanol. la deshidrogenasa alcohólica y el sistema microsomal oxidante del etanol son los principales sistemas de oxidación del etanol a acetaldehído. formas múltiples de la deshidrogenasa alcohólica han sido caracterizadas y permiten explicar la base molecular del polimorfismo enzimático. La siguiente oxidación del acetaldehído a acetato está catalizada por la deshidrogenasa aldehídica, cuyo polimorfismo influye en el control del alcoholismo, saobre todo en poblaciones de origen monogoloide (chinos, japoneses). Resta determinar el papel de un perfil específico de deshidrogenasa aldehídica en el desarrollo de una hepatopatía
Asunto(s)
Humanos , Etanol/metabolismo , Enzimas/metabolismo , Absorción , Etnicidad , Etanol/síntesis químicaRESUMEN
An inverse relationship has been found between high density lipoprotein cholesterol (HDL-C) and the incidence of coronary disease. A controversy exists in the international literature as to which sub-fraction, HDL2-C or DHL-C, rises after ethanol ingestion. This paper studies a comparison of the levels of circulating cholesterol, HDL-C, HDL2-C and HDL3-C in two groups: a control group of 44 healthy subjects who had no ethanol in over a year, and a second one made up off 40 chronic alcoholics, who consumed between 80 and 160 gr. of ethanol per day. The alcoholic population showed lower levels of cholesterol and higher levels of HDL-C, HDL2-C and HDL3-C. When compared with the control group, the increase was in alcoholics 58% for HDL2-C and 29% for HDL3-C. An analysis of the different age groups shows an increase of 110% in HDL2-C, in alcoholics between ages 31 and 40, as compared with their control group. An increase of 81% occurred between ages 51 and 60, but rarely rose 20% between ages 21 and 30, as well as between 51 and 60. The maximum rise of HDL3-C in drinkers, related to their control group, was 38% during the fourth decade of life. The conclusion is that the HDL2-C subfraction rises in chronic alcoholics, and the changes in other HDL-C subfractions are more useful when they are placed at the different individual's decades of age, than when taken from complete population samples.