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Adquisición somática y señalización de TGFBR1*6A en el cáncer

Boris Pasche¹, Thomas J Knobloch, Yansong Bian

¹Cancer Genetics Program, Division of Hematology/Oncology, Department of Medicine, The Feinberg School of Medicine, Northwestern, University, Chicago, Ill 60611, USA. b-pasche@northwestern.edu

|October 6, 2005

Resumen

El polimorfismo común TGFBR1 * 6A es adquirido por metástasis de cáncer colorrectal, lo que potencialmente promueve el crecimiento tumoral al alterar la señalización de TGF-beta. Esto sugiere TGFBR1 * 6A como un objetivo terapéutico en el desarrollo del cáncer.

Área de la Ciencia:

Oncología Oncología.
Biología Molecular Biología Molecular
Genética del cáncer Genética del cáncer.

Sus antecedentes:

El polimorfismo del receptor beta del factor de crecimiento transformador de tipo I (TGFBR1), TGFBR1 * 6A, está relacionado con la susceptibilidad al cáncer.
Los mecanismos precisos por los cuales TGFBR1*6A contribuye al desarrollo del cáncer siguen siendo en gran parte sin aclarar.

Objetivo del estudio:

Para investigar la adquisición somática de TGFBR1*6A en tumores primarios y metástasis.
Para determinar si la distintiva deleción de 3 aminoácidos en TGFBR1*6A es parte del receptor maduro o de la secuencia de señales.
Explorar el impacto funcional de la señalización TGFBR1*6A en las células cancerosas.

Principales métodos:

Análisis de tejidos tumorales y de la línea germinal de 531 pacientes con cáncer (cabeza y cuello, colorrectal, mama).
Ensayos de traducción in vitro y transfección estable de líneas celulares cancerosas (MCF-7, DLD-1, SW48) con las variantes TGFBR1*6A.
Evaluación de la proliferación celular dependiente de TGF-beta y la adquisición somática de TGFBR1*6A.

Principales resultados:

TGFBR1*6A se adquirió somáticamente en el 29,5% de las metástasis de cáncer colorrectal y en un porcentaje menor de tumores primarios.
La adquisición somática de TGFBR1*6A no se relacionó con los marcadores de inestabilidad genética.
Los receptores maduros TGFBR1 y TGFBR1 * 6A eran idénticos, con secuencias de señal escindidas en el mismo sitio.
TGFBR1*6A parecía convertir las señales inhibidoras del TGF-beta en señales estimulantes del crecimiento en las células cancerosas.

Conclusiones:

TGFBR1*6A se adquiere somáticamente en una proporción significativa de las metástasis del cáncer colorrectal, lo que le confiere una ventaja potencial de crecimiento.
Los efectos funcionales de TGFBR1*6A en el cáncer parecen estar mediados por su secuencia de señales, no por el receptor maduro.
TGFBR1*6A representa un aspecto novedoso de la señalización de TGF-beta en el cáncer y un objetivo terapéutico potencial.

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