Mecanismos moleculares diferenciales en la carcinogénesis del carcinoma colorrectal

Edith Illescas; Pedro Politti; Daniel Lewi

doi:10.56969/oc.v20i1.107

Autores/as

Edith Illescas Laboratorio de Biología Molecular, Universidad Maimónides, Buenos Aires
Pedro Politti Cátedra de Farmacología, Facultad de Medicina, UBA
Daniel Lewi Departmento de Oncología, Hospital Dr. Juan A. Fernández

DOI:

https://doi.org/10.56969/oc.v20i1.107

Palabras clave:

cáncer de colon, vías de carcinogénesis, inestabilidad cromosomal, inestabilidad de microsatélites, fenotipo mutador, fenotipo supresor, colon cancer, carcinogenesis pathway, chromosomal instability, microsatellite instability, mutator phenotype, suppressor phenotype

Resumen

La mayoría de los carcinomas colorrectales (CRCs - colorectal cancer) se originan de lesiones pre-neoplásicas desde una hiperplasia y/o adenoma que inicialmente son benignos, pero muchos de ellos progresan a carcinoma. Esta transformación, de un adenoma progresar a carcinoma, implica la acumulación de múltiples alteraciones genéticas en diferentes vías de señalización. Dos modelos complementarios en el mecanismo de carcinogénesis del CRC, son revisados en este trabajo, uno de ellos llamado vía “canónica o supresora” la cual involucra inestabilidad cromosomal (Chromosome Instability-CIN) y la vía “mutadora” que involucra la inestabilidad de microsatélites (MSI) (Microsatellite Instability). Esta creciente precisión descriptiva de las cascadas de señalización molecular oncogénica en CRC, apoya expectativas de desarrollos terapéuticos selectivos, dirigidos contra dianas moleculares claramente definidas.

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