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Expansión clonal de células acinares en la homeostasis del páncreas y la carcinogénesis
Patrick Neuhöfer1,2,3, Caitlin M Roake1,2,3, Stewart J Kim1,2,3
1Stanford Cancer Institute, Stanford University School of Medicine, Stanford, CA, USA.
Nature
|September 16, 2021
Resumen
Las células pancreáticas raras que expresan altos niveles de telomerasa transcriptasa inversa (TERT) impulsan el inicio del cáncer de páncreas. Estas células altas en TERT, cuando mutan, forman lesiones precancerosas, ofreciendo nuevos conocimientos sobre el desarrollo del adenocarcinoma ductal pancreático (PDAC).
Área de la Ciencia:
- Biología celular
- Investigación sobre el cáncer
- Gastroenterología
Sus antecedentes:
- El adenocarcinoma ductal pancreático (PDAC) es una de las principales causas de cáncer en todo el mundo.
- Los mecanismos de renovación celular pancreática y la iniciación de PDAC no se comprenden completamente.
- Las células madre del cáncer están implicadas en el desarrollo de tumores para muchos tipos de cáncer.
Objetivo del estudio:
- Identificar los tipos de células responsables de la renovación pancreática y el inicio de la PDAC.
- Investigar el papel de subpoblaciones celulares específicas en la tumorigénesis pancreática.
- Para aclarar las vías de señalización involucradas en el desarrollo temprano de PDAC.
Principales métodos:
- Rastreo del linaje utilizando el locus de la telomerasa inversa (Tert) en modelos de ratón.
- Análisis de las poblaciones de células acinares durante la homeostasis y en respuesta a mutaciones oncogénicas.
- Detección de mutaciones fosfo-ERK y KRAS en neoplasias pancreáticas humanas resecadas.
Principales resultados:
- Se identificó una subpoblación rara de células acinares pancreáticas positivas para TERT (TERThigh).
- Las células acinares TERThigh renuevan el páncreas durante la homeostasis y forman clones en expansión.
- La expresión de Kras mutante en las células acinares TERThigh acelera la formación de clones e induce la transdiferenciación a lesiones preinvasivas a través de la señalización Ras-MAPK/ERK.
- Los focos de células acinares fosfo-ERK positivas con mutaciones KRAS son comunes en las neoplasias pancreáticas humanas, lo que sugiere una lesión precursora temprana.
Conclusiones:
- Las células acinares raras con alto contenido de TERT son actores clave en la renovación pancreática y la iniciación de PDAC.
- El mantenimiento de las mutaciones KRAS en las células acinares TERThigh impulsa la expansión de las células acinares e inicia la tumorigénesis.
- Las células acinares de alta TERT representan un origen celular potencial para el cáncer de páncreas.
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