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La inestabilidad cromosómica inducida por Mad2 conduce a la recaída del tumor pulmonar después de la retirada de
Rocio Sotillo1, Juan-Manuel Schvartzman, Nicholas D Socci
1Cancer Biology and Genetics Program, Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA.
Nature
|February 23, 2010
Resumen
La inestabilidad cromosómica, inducida por la sobreexpresión de Mad2, no impidió la regresión tumoral inicial, pero aumentó significativamente las tasas de recurrencia. Esto sugiere que la inestabilidad temprana impulsa la recaída después del tratamiento del cáncer.
Área de la Ciencia:
- Oncología Oncología.
- Biología del cáncer Biología del cáncer.
- Genética La genética.
Sus antecedentes:
- La adicción oncogénica describe la muerte de las células tumorales por inhibición oncogénica, lo que impulsa el desarrollo de terapias dirigidas contra el cáncer.
- Los tumores sólidos con frecuencia exhiben inestabilidad cromosómica debido a la desregulación de la vía del punto de control mitótico.
- El impacto de la inestabilidad cromosómica en la adicción oncogénica sigue siendo inexplorado.
Objetivo del estudio:
- Para investigar el efecto de la inestabilidad cromosómica en la adicción oncogénica en los tumores de pulmón impulsados por Kras.
- Para determinar si la sobreexpresión del gen del punto de control mitótico transitorio influye en la recurrencia del tumor después de la inhibición oncogénica.
Principales métodos:
- La sobreexpresión del gen del punto de control mitótico Mad2 en ratones para inducir la inestabilidad cromosómica.
- Inhibición de Kras en tumores de pulmón impulsados por Kras para evaluar la regresión inicial.
- Monitorear las tasas de recurrencia tumoral y analizar la ploidia y la activación de la vía de los tumores recurrentes.
Principales resultados:
- La sobreexpresión de Mad2 y la inestabilidad cromosómica inducida no afectaron la regresión inicial de los tumores pulmonares impulsados por Kras tras la inhibición de Kras.
- Los tumores que experimentan una sobreexpresión Mad2 transitoria e inestabilidad cromosómica mostraron tasas de recurrencia notablemente elevadas.
- Los tumores recurrentes eran altamente aneuploides con una activación diversa de las vías pro-proliferativas.
Conclusiones:
- La inestabilidad cromosómica temprana puede no impedir la respuesta inicial al tratamiento, pero contribuye significativamente a la recaída del tumor.
- La aneuploidía y la activación variada de la vía pro-proliferativa en tumores recurrentes sugieren mecanismos para superar la terapia dirigida.
- Este estudio destaca la inestabilidad cromosómica como un factor crítico en el fracaso del tratamiento del cáncer y la recaída.
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