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Yeast As a Chassis for Developing Functional Assays to Study Human P53
Published on: August 4, 2019
La mutación clonal p53 en el cáncer cervical primario: asociación con tumores negativos para el virus del papiloma
1Ludwig Institute for Cancer Research, St Mary's Hospital Medical School, London, UK.
Lancet (London, England)
|May 2, 1992
Resumen
La infección por el virus del papiloma humano (VPH) está inversamente correlacionada con las mutaciones del gen p53 en los cánceres de cuello uterino. Los tumores positivos para el VPH muestran predominantemente p53 de tipo salvaje, lo que sugiere un mecanismo diferente para la inactivación del gen supresor tumoral.
Área de la Ciencia:
- Oncología Oncología.
- Virología Virología.
- Biología Molecular Biología Molecular
Sus antecedentes:
- Se ha observado una correlación inversa entre el virus del papiloma humano (VPH) y las mutaciones del gen supresor de tumores p53 en cánceres anales y líneas celulares.
- El cáncer de cuello uterino está fuertemente asociado con la infección por VPH, y el gen p53 es un supresor tumoral crítico frecuentemente alterado en el cáncer.
Objetivo del estudio:
- Investigar la asociación entre la infección por VPH y las mutaciones somáticas del gen p53 en tumores cervicales primarios.
- Comprender el papel de las alteraciones del gen p53 en la patogénesis del cáncer cervical en relación con el estado del VPH.
Principales métodos:
- Análisis de 28 muestras de tumores cervicales primarios para la presencia de ADN de VPH utilizando Southern blot y reacción en cadena de la polimerasa (PCR).
- Detección de los tipos 16 y 18 del VPH.
- Evaluación de las mutaciones del gen p53 mediante la secuenciación de toda la región codificante utilizando PCR asimétrica.
- Análisis de la deleción alélica en el brazo corto del cromosoma 17 utilizando polimorfismo de longitud de fragmento de restricción (RFLP).
Principales resultados:
- Se detectaron secuencias de VPH en 25 de 28 (89%) tumores cervicales, con 20 positivos para el VPH16 y 5 para el VPH18.
- No se encontró evidencia de deleción alélica en el brazo corto del cromosoma 17 en 17 tumores analizados.
- Solo 3 tumores negativos para el VPH exhibieron mutaciones puntuales heterocigóticas en el gen p53.
- En contraste, 21 cánceres de cuello uterino positivos para el VPH mostraron secuencias p53 de tipo salvaje en toda la región analizada.
Conclusiones:
- La pérdida de la función p53 de tipo salvaje es crucial en la patología del cáncer cervical.
- En los cánceres de cuello uterino positivos para el VPH, las proteínas codificadas por el VPH probablemente median la pérdida de la función de la p53, lo que evita la necesidad de la mutación somática de la p53.
- Se requiere una mutación somática del gen p53 para la inactivación de p53 en ausencia de mecanismos mediados por el VPH.
- Los distintos patrones de la mutación p53 en los cánceres de cuello uterino HPV-positivos versus HPV-negativos pueden contribuir a las diferencias en el pronóstico de los pacientes.
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