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SoMuKT

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SOmatic MUtagenesis in Kidney Tubule is enhanced by specific metabolic pathways

An important factor favoring cancer initiation is the lifelong accumulation of somatic mutations in the genome. In agreement, somatic mutations in a specific set of driver genes has been shown to drive the transition from a health... ver más

26/09/2022

OSR

183K€

Presupuesto del proyecto: 183K€

Líder del proyecto

OSPEDALE SAN RAFFAELE SRL No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Fecha límite participación Sin fecha límite de participación.

Financiación concedida El organismo H2020 notifico la concesión del proyecto el día 2022-09-26

MSCA-IF-2019: Individual Fellowships

I+D

Cerrada hace 5 años

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No hay información privada compartida para este proyecto. Habla con el coordinador.

1 Participantes

OSR

183.47K€ | Lider

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Duración del proyecto: 29 meses Fecha Inicio: 2020-04-09
Fecha Fin: 2022-09-26

Líder del proyecto

OSPEDALE SAN RAFFAELE SRL No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Presupuesto del proyecto 183K€

Fecha límite de participación Sin fecha límite de participación.

Descripción del proyecto An important factor favoring cancer initiation is the lifelong accumulation of somatic mutations in the genome. In agreement, somatic mutations in a specific set of driver genes has been shown to drive the transition from a healthy cell to a tumorigenic clone in the kidney. The vast majority of kidney tumors originate from a specific segment of the kidney nephron, named proximal tubule (PT). However, the rate of somatic mutation accumulation before tumorigenic transformation in the kidney PT and the causes underlying this phenomenon are unexplored. Somatic mutation data can be used as a footprint to track the mutational processes that occurred in a specific cell during an individual´s lifetime. I established a protocol for reliable detection of somatic mutations in non-cancer human cells. I obtained whole genome data from clonally expanded single cells from skeletal muscle, kidney, fat and skin of healthy donors. My preliminary data point to an increased rate of somatic mutation accumulation during adult life in kidney PT compared to other kidney and non-kidney cells. PT cells showed a unique mutation pattern and distribution that enhances the chances of acquiring a driver mutation and tumorigenic traits. The very homogeneous pattern of somatic mutations in PT cells leads me to the hypothesis that the kidney PT is exposed to genotoxic compounds that are endogenously produced during physiological cellular activities. In particular, my data point to specific metabolic pathways, including 1) ammonia production, 2) aminoacid metabolism /reabsorption from the urine and 3) response to hypoxia. I will use cellular models to perturb the metabolic homeostasis of the kidney PT and test the effect on somatic mutagenesis and underlining mechanisms. My project will shed light on a mostly unexplored topic: how cellular metabolism can damage the genome over time and may have important implications for tumor prevention.

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