Publication: Análisis comparativo de las vías de carcinogénesis colorrectal entre dos grupos de edades diferenciados
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2017-08-23
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Universidad Complutense de Madrid
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Abstract
El cáncer colorrectal (CCR) es la segunda neoplasia maligna más frecuente en los países desarrollados y ocupa el primer lugar como causa de muerte por tumor. Su prevalencia en España supera los 26.500 casos al año. El cáncer de colon representa dos tercios de todos los CCR. El 97% de los CCR son adenocarcinomas. El CCR tiene formas de presentación variables. La mayoría de los cánceres son esporádicos. Sin embargo, entre un 5 y 10% tiene un componente hereditario y el restante 20 a 25% presenta agregación familiar. Las alteraciones en el genoma que dan origen al cáncer son genéticas (cambios en la secuencia del ADN) y epigenéticas (afectan la expresión genética sin afectación estructural del gen). La descripción de carcinogénesis original de Fearon y Vogelstein ha servido de base para comprender el desarrollo tumoral. Posteriormente se han identificado tres grandes vías de carcinogénesis: la vía supresora o de la inestabilidad cromosómica (IC), la mutadora o de la inestabilidad de microsatélites (IMS) y la vía metiladora o del fenotipo metilador (FM) también llamada vía serrada. Estas tres vías no son mutuamente excluyentes. Por este motivo, el CCR no se comporta de manera uniforme y aunque exista una vía preferente, la acumulación de cambios mutacionales y el solapamiento de las vías de carcinogénesis hacen que el fenotipo tumoral sea variable...
Colorectal cancer (CRC) is the second most common malignancy in developed countries and the first cause of death by tumor. In Spain, its prevalence is estimated around 26,500 cases per year. Colon cancer represents two thirds of all CRC. 97% of CRC are adenocarcinomas. About 75% of patients with CRC have sporadic disease. However, between 5 and 10% have a hereditary component and the remaining 20-25% have a familial history of CRC. Genome alterations that give rise to cancer are genetic (changes in DNA sequence) and epigenetic (gene expression is altered but there is not a structural involvement of the gene). The genetic model for colorectal tumorigenesis proposed by Fearon and Vogelstein constituted a basis for understanding cancer development. Over time, three main carcinogenetic pathways have been identified: the suppressor pathway or chromosomal instability (CIN), the mutator phenotype or microsatellite instability pathway (MSI) and the CpG island methylator phenotype (CIMP) also called serrated pathway. These pathways are not mutually exclusive. Therefore, CRC is heterogeneous and although a preferred pathway may exist, the accumulation of mutational changes and the overlapping between carcinogenetic pathways make every tumor phenotype unique...
Colorectal cancer (CRC) is the second most common malignancy in developed countries and the first cause of death by tumor. In Spain, its prevalence is estimated around 26,500 cases per year. Colon cancer represents two thirds of all CRC. 97% of CRC are adenocarcinomas. About 75% of patients with CRC have sporadic disease. However, between 5 and 10% have a hereditary component and the remaining 20-25% have a familial history of CRC. Genome alterations that give rise to cancer are genetic (changes in DNA sequence) and epigenetic (gene expression is altered but there is not a structural involvement of the gene). The genetic model for colorectal tumorigenesis proposed by Fearon and Vogelstein constituted a basis for understanding cancer development. Over time, three main carcinogenetic pathways have been identified: the suppressor pathway or chromosomal instability (CIN), the mutator phenotype or microsatellite instability pathway (MSI) and the CpG island methylator phenotype (CIMP) also called serrated pathway. These pathways are not mutually exclusive. Therefore, CRC is heterogeneous and although a preferred pathway may exist, the accumulation of mutational changes and the overlapping between carcinogenetic pathways make every tumor phenotype unique...
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Tesis inédita de la Universidad Complutense de Madrid, Facultad de Medicina, leída el 25-01-2016