Contribución de la vía PI3k/Akt-PTEN y sus blancos corriente abajo en iniciación y progresión de glioblastoma multiforme
Palabras clave:
Neoplasmas del sistema nervioso central, glioblastoma, proteinas oncogénicas virales, Fosfatidilinositoles, hexoquinasa, mTOR, telomerasa, proteina oncogénica AktResumen
Los tumores malignos del sistema nervioso central constituyen un problema importante en oncología debido a que son de difícil tratamiento y tienen un alto porcentaje de resistencia a la terapia, además de que su pronóstico es muy pobre. El análisis de los cambios genéticos y moleculares asociados a la iniciación y progresión del proceso tumoral constituye una herramienta importante para establecer grupos de tratamiento específico, para reducir la incidencia de resistencia al mismo y para establecer nuevos blancos terapéuticos.
Este artículo busca analizar diversos aspectos genéticos y moleculares subyacentes a la iniciación y progresión del tumor cerebral maligno más frecuente, el glioblastoma multiforme, procesos que siguen siendo poco conocidos. El análisis se centrará en la vía de supervivencia neuronal mediada por los receptores tirosina quinasa (RTK) y sus blancos corriente abajo: PTEN, PI3K, Akt, mTOR y hexoquinasa. Poco se sabe, sin embargo, acerca de cómo cambios genéticos y moleculares en estas vías de señalización celular se interrelacionan temporal y funcionalmente para determinar la progresión maligna y la resistencia a la terapia en glioblastoma multiforme. En la actualidad se está desarrollando un estudio in vivo e in vitro utilizando especímenes quirúrgicos y líneas celulares de glioblastoma, para analizar sus cambios genéticos y moleculares asociados a la vía PI3K/Akt-PTEN, y realizar una correlación con la expresión de hexoquinasa, mTOR y telomerasa, y su importancia en cuanto a resistencia a la terapia.
Biografía del autor/a
Gonzalo Arboleda, Instituto Nacional de Cancerología
Instituto Nacional de Cancerología, E.S.E., Grupo de Investigación en Biología del Cáncer, Laboratorio de Genética, Bogotá, D.C., Colombia.
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