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Los clones mutantes somáticos colonizan el esófago humano con la edad
Iñigo Martincorena1, Joanna C Fowler2, Agnieszka Wabik2
1Wellcome Sanger Institute, Hinxton, Cambridgeshire CB10 1SA, UK. im3@sanger.ac.uk pj3@sanger.ac.uk.
Science (New York, N.Y.)
|October 20, 2018
Resumen
Las mutaciones somáticas se acumulan con la edad en las células esofágicas normales, impulsadas por procesos intrínsecos. Los clones con mutaciones asociadas al cáncer, como NOTCH1 y TP53, se expanden significativamente, afectando el envejecimiento y el desarrollo del cáncer.
Área de la Ciencia:
- La genética
- Biología del cáncer
- Investigación sobre el envejecimiento
Sus antecedentes:
- La comprensión de la acumulación de mutaciones somáticas en los tejidos normales es crucial para el envejecimiento y la investigación del cáncer.
- Los estudios anteriores no han aclarado completamente el alcance y los factores de la expansión clonal en tejidos adultos sanos.
Objetivo del estudio:
- Para mapear y caracterizar los clones mutantes en el epitelio esofágico humano normal.
- Investigar la relación entre la edad, las mutaciones somáticas y la expansión clonal.
- Identificar genes específicos bajo selección positiva en el epitelio esofágico normal.
Principales métodos:
- Secuenciación del genoma de epitelio esofágico normal de nueve donantes en un amplio rango de edad (20-75 años).
- Análisis de la acumulación de mutaciones somáticas y patrones de expansión clonal.
- Identificación de genes con mutaciones bajo selección positiva.
Principales resultados:
- Las mutaciones somáticas se acumulan con la edad, principalmente debido a procesos mutacionales intrínsecos.
- Se observó una selección positiva significativa para los clones con mutaciones en 14 genes de cáncer.
- En los donantes mayores, los clones con mutaciones asociadas al cáncer (NOTCH1, TP53) ocupaban porciones sustanciales del epitelio.
- La prevalencia de la mutación NOTCH1 en el esófago normal excedió la de los cánceres de esófago.
Conclusiones:
- El epitelio esofágico normal alberga clones en expansión con mutaciones asociadas al cáncer, influenciadas por la edad y los procesos mutacionales intrínsecos.
- La alta prevalencia de mutaciones NOTCH1 en el tejido normal sugiere funciones complejas en el desarrollo del cáncer y el envejecimiento.
- Estos hallazgos requieren una reevaluación de los eventos mutacionales tempranos en la patogénesis del cáncer y el envejecimiento.
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