Biología molecular del cáncer de próstata
Molecular biology of prostate cancer
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Esta obra está bajo una licencia internacional Creative Commons Atribución-NoComercial-SinDerivadas 4.0.
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Introducción: el cáncer de próstata (CaP) es la neoplasia maligna más frecuente en hombres y una causa relevante de mortalidad oncológica mundial. Su heterogeneidad, desde tumores indolentes hasta formas agresivas, dificulta la estratificación del riesgo y la selección terapéutica, pero los avances en biología molecular han aclarado las alteraciones genómicas y epigenéticas implicadas en la tumorogénesis, progresión y resistencia, impulsando la medicina de precisión.
Métodos: se realizó una revisión narrativa de la literatura sobre vías moleculares clave, alteraciones genómicas clínicamente relevantes y estrategias terapéuticas emergentes basadas en biomarcadores en CaP localizado y metastásico.
Resultados: las mutaciones germinales y somáticas en genes de reparación del ADN, como BRCA1, BRCA2 y ATM, se relacionan con mayor susceptibilidad, fenotipos agresivos y sensibilidad a inhibidores PARP y esquemas con platino. La pérdida de genes supresores tumorales (PTEN, TP53, RB1) favorece la inestabilidad genómica, la resistencia a la castración y un pronóstico desfavorable. Los clasificadores genómicos (Oncotype DX, Decipher) refinan la estratificación del riesgo y orientan la intensificación o desescalamiento terapéutico en enfermedad localizada, mientras que el testeo genético reflejo y los estudios clínicos dirigidos por biomarcadores ejemplifican la integración clínica de la información molecular. En enfermedad avanzada, terapias dirigidas al receptor androgénico, a la reparación del ADN y al PSMA están transformando el manejo del CaP.
Conclusiones: la caracterización molecular del CaP permite intervenciones guiadas por biomarcadores que optimizan las decisiones terapéuticas y los desenlaces clínicos. La incorporación sistemática del perfil genómico será esencial para consolidar la medicina de precisión en el tratamiento.
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