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Onco-inflammation

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Origin of genomic instability Understanding the biological influence of inflamm...

Origin of genomic instability Understanding the biological influence of inflammation in the initiation of pancreatic tumorigenesis Inflammation is suspected to be the first step leading to cancer due to alcohol consumption or tobacco smoking between others. Little is known of how inflammation triggers genetic changes leading to tumorigenesis. Recently, I show... ver más

31/08/2024

FUNDACION PUBLICA...

173K€

Presupuesto del proyecto: 173K€

Líder del proyecto

FUNDACION PUBLICA ANDALUZA PROGRESO Y SALUD No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5 | 14M€

Fecha límite participación Sin fecha límite de participación.

Financiación concedida El organismo H2020 notifico la concesión del proyecto el día 2024-08-31

MSCA-IF-2020: Individual Fellowships

I+D

Cerrada hace 4 años

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

1 Participantes

FUNDACION PUBLICA ANDALUZA P...

172.93K€ | Lider

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Duración del proyecto: 40 meses Fecha Inicio: 2021-04-23
Fecha Fin: 2024-08-31

Líder del proyecto

FUNDACION PUBLICA ANDALUZA PROGRESO Y SALUD No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5 | 14M€

Presupuesto del proyecto 173K€

Fecha límite de participación Sin fecha límite de participación.

Descripción del proyecto Inflammation is suspected to be the first step leading to cancer due to alcohol consumption or tobacco smoking between others. Little is known of how inflammation triggers genetic changes leading to tumorigenesis. Recently, I show that TGFb, a cytokine present during inflammation, is able to generate aneuploidy, polyploidy and plausible chromosomal rearrangements in breast cells. Such effects were mediated through the induction of the epigenetic reprogramming EMT. In view to understand how inflammatory signaling can affect the genome integrity, I design the project Onco-Inflammation, to study one of the most lethal cancer, the pancreatic ductal adenocarcinoma (PDAC), where therapeutic options are greatly limited. Using several mice models of pancreatitis, we will follow the establishment of genomic insults, and in particular focusing in whole genome doubling, nuclear envelope disruption and micronuclei. I will evaluate the genetic diversity present under pancreatitis and weigh the roles of the epigenetic re-programming Acinar-Dutual-Metaplasia as well as the oncogene KRAS, using high-resolution 3D imaging, as well as single cell CNV analysis (Aim1). I will also study the common pathways activated in newly aneuploid cells, in view to find some specific therapeutic target. (Aim2). Several pathways will be tested in an attempt to block cancer initiation and progression. Results will be tested and validated using human samples (Aim 3). At the Host Institution, I will greatly benefit and learn from the scientific guidance from my supervisor, expert in pancreas biology as well as experts in mitosis, genetic instability and bioinformatics. MSCA-IF will be instrumental to develop this initial hypothesis into deeper biological understanding the inflammation and cell plasticity’s roles on genomic instability and represent a crucial support to transition into an independent academic career.

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