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Áreas de investigación Ciencias Biológicas La genética Expresión génica (incluido el microarray y otros enfoques de todo el genoma)
Áreas de investigación
Ciencias Biológicas
La genética
Expresión génica (incluido el microarray y otros enfoques de todo el genoma)
Evolución genómica-transcriptómica en el cáncer de pulmón y las metástasis

Evolución genómica-transcriptómica en el cáncer de pulmón y las metástasis

Carlos Martínez-Ruiz ^1,2, James R M Black ^1,2, Clare Puttick ^1,2,3, Mark S Hill ³, Jonas Demeulemeester ^4,5,6, Elizabeth Larose Cadieux ^4,7, Kerstin Thol ^1,2, Thomas P Jones ^1,2, Selvaraju Veeriah ¹, Cristina Naceur-Lombardelli ¹, Antonia Toncheva ¹, Paulina Prymas ¹, Andrew Rowan ³, Sophia Ward ^1,3,8, Laura Cubitt ⁸, Foteini Athanasopoulou ^1,3,8, Oriol Pich ³, Takahiro Karasaki ^1,3,9, David A Moore ^1,3,10, Roberto Salgado ^11,12, Emma Colliver ³, Carla Castignani ^4,7, Michelle Dietzen ^1,2,3, Ariana Huebner ^1,2,3, Maise Al Bakir ^1,3, Miljana Tanić ^7,13, Thomas B K Watkins ³, Emilia L Lim ^1,3, Ali M Al-Rashed ¹⁴, Danny Lang ¹⁵, James Clements ¹⁵, Daniel E Cook ³, Rachel Rosenthal ³, Gareth A Wilson ³, Alexander M Frankell ^1,3, Sophie de Carné Trécesson ¹⁶, Philip East ¹⁷, Nnennaya Kanu ¹, Kevin Litchfield ^1,18, Nicolai J Birkbak ^1,3,19,20,21, Allan Hackshaw ²², Stephan Beck ⁷, Peter Van Loo ^4,23,24, Mariam Jamal-Hanjani ^1,9,25, , Charles Swanton ^26,27,28, Nicholas McGranahan ^29,30

Carlos Martínez-Ruiz ^1,2, James R M Black ^1,2, Clare Puttick ^1,2,3

¹Cancer Research UK Lung Cancer Centre of Excellence, University College London Cancer Institute, London, UK.
²Cancer Genome Evolution Research Group, Cancer Research UK Lung Cancer Centre of Excellence, University College London Cancer Institute, London, UK.
³Cancer Evolution and Genome Instability Laboratory, The Francis Crick Institute and University College London Cancer Institute, London, UK.
⁴Cancer Genomics Laboratory, The Francis Crick Institute, London, UK.
⁵Integrative Cancer Genomics Laboratory, Department of Oncology, KU Leuven, Leuven, Belgium.
⁶VIB-KU Leuven Center for Cancer Biology, Leuven, Belgium.
⁷Medical Genomics, University College London Cancer Institute, London, UK.
⁸Advanced Sequencing Facility, The Francis Crick Institute, London, UK.
⁹Cancer Metastasis Laboratory, University College London Cancer Institute, London, UK.
¹⁰Department of Cellular Pathology, University College London Hospitals, London, UK.
¹¹Department of Pathology, ZAS Hospitals, Antwerp, Belgium.
¹²Division of Research, Peter MacCallum Cancer Centre, Melbourne, Victoria, Australia.
¹³Experimental Oncology, Institute for Oncology and Radiology of Serbia, Belgrade, Serbia.
¹⁴Centre for Nephrology, Division of Medicine, University College London, London, UK.
¹⁵Scientific Computing STP, Francis Crick Institute, London, UK.
¹⁶Oncogene Biology Laboratory, The Francis Crick Institute, London, UK.
¹⁷Bioinformatics and Biostatistics, The Francis Crick Institute, London, UK.
¹⁸Tumour Immunogenomics and Immunosurveillance Laboratory, University College London Cancer Institute, London, UK.
¹⁹Department of Molecular Medicine, Aarhus University Hospital, Aarhus, Denmark.
²⁰Department of Clinical Medicine, Aarhus University, Aarhus, Denmark.
²¹Bioinformatics Research Centre, Aarhus University, Aarhus, Denmark.
²²Cancer Research UK & UCL Cancer Trials Centre, London, UK.
²³Department of Genetics, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
²⁴Department of Genomic Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
²⁵Department of Medical Oncology, University College London Hospitals, London, UK.
²⁶Cancer Research UK Lung Cancer Centre of Excellence, University College London Cancer Institute, London, UK. Charles.Swanton@crick.ac.uk.
²⁷Cancer Evolution and Genome Instability Laboratory, The Francis Crick Institute and University College London Cancer Institute, London, UK. Charles.Swanton@crick.ac.uk.
²⁸Department of Medical Oncology, University College London Hospitals, London, UK. Charles.Swanton@crick.ac.uk.
²⁹Cancer Research UK Lung Cancer Centre of Excellence, University College London Cancer Institute, London, UK. nicholas.mcgranahan.10@ucl.ac.uk.
³⁰Cancer Genome Evolution Research Group, Cancer Research UK Lung Cancer Centre of Excellence, University College London Cancer Institute, London, UK. nicholas.mcgranahan.10@ucl.ac.uk.

⁰Cancer Research UK Lung Cancer Centre of Excellence, University College London Cancer Institute, London, UK.

Nature +

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12 de abril de 2023

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12 de abril de 2023

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Ver abstracta en PubMed

Resumen

Este resumen es generado por máquina.

La heterogeneidad intratumoral impulsa la evolución del cáncer de pulmón y la resistencia al tratamiento. Este estudio revela el transcriptoma

Área De La Ciencia

En el campo de la oncología
La genómica
Las transcripciones

Sus Antecedentes

La heterogeneidad intratumoral (ITH) es un factor clave de la progresión del cáncer de pulmón, la evasión inmune y la resistencia terapéutica.
Comprender la base molecular del ITH es crucial para desarrollar tratamientos efectivos para el cáncer de pulmón.

Objetivo Del Estudio

Investigar la diversidad transcriptómica intratumoral en el cáncer de pulmón de células no pequeñas (CPNM).
Explorar la relación entre la expresión génica, la ITH y la evolución del tumor.
Identificar los mecanismos basados en el ARN que contribuyen a la progresión y metástasis del cáncer.

Principales Métodos

Secuenciación emparejada de todo el exoma y el ARN de 354 tumores de CPNM y 96 tejidos normales adyacentes del estudio TRACERx.
Análisis de 947 regiones tumorales (primarias y metastásicas) para evaluar la variación transcriptómica.
Aplicación del aprendizaje automático para vincular los datos genómicos y transcriptómicos con el potencial de metástasis.

Principales Resultados

El transcriptoma contribuye significativamente a la variación fenotípica y al ITH en el NSCLC.
La expresión específica del alelo, a menudo independiente de los cambios en el número de copias, está vinculada a la disfunción epigenómica y la evolución paralela genómica-transcriptómica.
Las firmas de sustitución de ARN de una sola base implican la actividad de ADAR y APOBEC3A, revelando la actividad de APOBEC en curso.
El potencial de metástasis se asocia con el contexto evolutivo de las mutaciones y el aumento de la proliferación en los tumores primarios.

Conclusiones

La interacción entre el genoma y el transcriptoma es fundamental para dar forma a la ITH e impulsar la evolución del cáncer de pulmón.
La diversidad transcriptómica y la edición del ARN juegan un papel importante en la progresión del cáncer de pulmón y la resistencia terapéutica.
Los análisis genómicos y transcriptómicos proporcionan información sobre los mecanismos de metástasis y las posibles dianas terapéuticas.

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