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Los tumores cerebrales pueden surgir de una lesión no curada adecuadamente, debido a la inflamación

Los tumores cerebrales pueden surgir de una lesión que no se curar adecuadamente, según han descubierto científicos canadienses.

Las investigaciones detectaron un aumento de los marcadores de inflamación típicos de la respuesta a la lesión en las células que dan lugar al glioblastoma, la forma más común y agresiva de cáncer de cerebro, lo que indica el papel potencial de las células cancerosas en la curación de tejidos.

Estos inesperados hallazgos abren nuevas ideas sobre cómo se desarrollan los tumores cerebrales y sugieren que los medicamentos antiinflamatorios podrían beneficiar a algunos pacientes con glioblastoma, según apuntan los investigadores de la Universidad de Toronto (Canadá) en la revista ‘Nature Cancer’.

El proceso de curación que sigue a una lesión cerebral, sea un trauma, una infección o un derrame cerebral, podría estimular el crecimiento del tumor cuando las nuevas células generadas para reemplazar las perdidas por la lesión se desvían por mutaciones.

Los hallazgos fueron realizados por un equipo interdisciplinario de investigadores de la Universidad de Toronto, el Hospital para Niños Enfermos (SickKids) y el Centro Oncológico Princess Margaret, que también forman parte del Dream Team pancanadiense de Stand Up To Cancer Canada que se centra en un objetivo común cáncer de cerebro conocido como glioblastoma.

«Nuestros datos sugieren que el cambio mutacional correcto en células particulares en el cerebro podría ser modificado por una lesión para dar lugar a un tumor», explica Peter Dirks, líder del Dream Team que es el Jefe de la División de Neurocirugía y Científico Senior en el programa de Biología de células madre y desarrollo en SickKids.

Gary Bader, profesor de genética molecular en el Centro Donnelly de Investigación Celular y Biomolecular de la Facultad de Medicina Temerty de la Universidad de Toronto, y el doctor Trevor Pugh, científico principal del Princess Margaret, también dirigieron la investigación cuyos hallazgos podrían conducir a una nueva terapia para los pacientes con glioblastoma que actualmente tienen opciones de tratamiento limitadas con una vida promedio de 15 meses después del diagnóstico.

«El glioblastoma se puede considerar como una herida que nunca deja de cicatrizar –explica Dirks–. Estamos entusiasmados con lo que esto nos dice sobre cómo se origina y crece el cáncer y abre ideas completamente nuevas sobre el tratamiento al enfocarse en la respuesta a la lesión y la inflamación».

Los investigadores aplicaron las últimas tecnologías de secuenciación de ARN unicelular y aprendizaje automático para mapear la composición molecular de las células madre del glioblastoma (GSC), que el equipo de Dirks demostró anteriormente que son responsables del inicio y la recurrencia del tumor después del tratamiento.

Encontraron nuevas subpoblaciones de GSC que llevan el sello molecular de la inflamación y que se combinan con otras células madre cancerosas dentro de los tumores de los pacientes. Ello sugiere que algunos glioblastomas comienzan a formarse cuando el proceso normal de curación del tejido, que genera nuevas células para reemplazar las perdidas por la lesión, se descarrila por mutaciones, posiblemente incluso muchos años antes de que los pacientes se vuelvan sintomáticos, señala Dirks.

Una vez que una célula mutante se dedica a la curación de heridas, no puede dejar de multiplicarse porque los controles normales se rompen y esto estimula el crecimiento del tumor, según el estudio.

«El objetivo es identificar un fármaco que matará las células madre del glioblastoma –resalta Bader, cuyo estudiante graduado Owen Whitley contribuyó al análisis de datos computacionales–. Pero primero necesitábamos comprender la naturaleza molecular de estas células para poder apuntarlos de manera más eficaz».

El equipo recogió GSC de los tumores de 26 pacientes y las expandió en el laboratorio para obtener una cantidad suficiente de estas células raras para su análisis. Se analizaron casi 70.000 células mediante secuenciación de ARN unicelular que detecta qué genes están activados en células individuales, un esfuerzo dirigido por Laura Richards, una estudiante de posgrado en el laboratorio de Pugh.

Los datos confirmaron una amplia heterogeneidad de la enfermedad, lo que significa que cada tumor contiene múltiples subpoblaciones de células madre cancerosas molecularmente distintas, lo que hace que la recurrencia sea probable, ya que la terapia existente no puede eliminar todos los diferentes subclones.

Una mirada más cercana reveló que cada tumor tiene uno de los dos estados moleculares distintos, denominados «desarrollo» y «respuesta a la lesión», o en algún lugar de un gradiente entre los dos.

El estado de desarrollo es un sello distintivo de las células madre del glioblastoma y se asemeja al de las células madre que se dividen rápidamente en el cerebro en crecimiento antes del nacimiento.

Pero el segundo estado fue una sorpresa. Los investigadores lo denominaron ‘Respuesta a las lesiones’ porque mostraba una regulación positiva de las vías inmunitarias y los marcadores de inflamación, como el interferón y el TNFalpha, que son indicativos de los procesos de cicatrización de heridas.

Estas firmas inmunes solo se detectaron gracias a la nueva tecnología unicelular después de que los métodos más antiguos las pasaran por alto para las mediciones de células a granel.

Mientras tanto, los experimentos dirigidos por el laboratorio de Stephane Angers, de la Facultad de Farmacia de Leslie Dan, establecieron que los dos estados son vulnerables a diferentes tipos de eliminación de genes, revelando una serie de dianas terapéuticas relacionadas con la inflamación que no se habían considerado previamente para el glioblastoma.

Finalmente, se encontró que la combinación relativa de los dos estados era específica del paciente, lo que significa que cada tumor estaba sesgado hacia el desarrollo o la respuesta a la lesión final del gradiente. Los investigadores ahora buscan apuntar a estos sesgos para terapias personalizadas.

«Ahora estamos buscando fármacos que sean eficaces en diferentes puntos de este gradiente –apunta Pugh, también director de Genómica del Instituto de Ontario para la Investigación del Cáncer–. Aquí existe una oportunidad real para la medicina de precisión: diseccionar los tumores de los pacientes a nivel de una sola célula y diseñar un cóctel de fármacos que pueda eliminar más de un subclon de células madre cancerosas al mismo tiempo».

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