Hola,
¿eres nuevo aquí?

Regístrate gratis y conecta tu empresa con financiación pública, partners y proyectos.

Tengo cuenta

Regístrate

Ver video

DSBR AND CLUSTERS

Financiado

Cerrado

Processing of oxidatively induced clustered DNA lesions under a double strand br...

Processing of oxidatively induced clustered DNA lesions under a double strand break repair deficiency in human tumor cells Although a number of risk factors associated with cancer have been well established for many years, there is an emerging need for delineation of the role of DNA repair factors relative to cancer risk, and especially the discovery... ver más

31/05/2016

NATIONAL TECHNICAL...

100K€

Presupuesto del proyecto: 100K€

Líder del proyecto

ETHNICON METSOVION POLYTECHNION 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 FP7 notifico la concesión del proyecto el día 2016-05-31 No tenemos la información de la convocatoria

0% 100% 100%

Información adicional privada

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

1 Participantes

NATIONAL TECHNICAL UNIVERSIT...

0.00€ | Lider

Conecta tu I+D

¿Tienes un proyecto y buscas un partner? Gracias a nuestro motor inteligente podemos recomendarte los mejores socios y ponerte en contacto con ellos. Te lo explicamos en este video

Proyectos interesantes

ChroSoDSB Chromatin Study of DNA Double Strand Breaks 200K€ Cerrado

SAF2009-10023 LA REGULACION DE LA INTEGRIDAD DEL APOPTOSIS Y DEL CROMOSOMA... 182K€ Cerrado

BFU2012-38171 MECANISMOS Y REGULACION POR CICLO CELULAR DE LA RESPUESTA A... 173K€ Cerrado

RSHEALTH Investigating the causes and consequences of replication str... 2M€ Cerrado

SAF2013-43255-P REGULACION DEL PROCESAMIENTO DE LOS CORTES DE DOBLE CADENA E... 157K€ Cerrado

SAF2010-14877 MODULACION EN EL CONTEXTO DEL CICLO CELULAR DEL TIPO DE REPA... 182K€ Cerrado

Líder del proyecto

ETHNICON METSOVION POLYTECHNION No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Presupuesto del proyecto 100K€

Fecha límite de participación Sin fecha límite de participación.

Descripción del proyecto Although a number of risk factors associated with cancer have been well established for many years, there is an emerging need for delineation of the role of DNA repair factors relative to cancer risk, and especially the discovery and quantification of risks associated with gene mutations in double strand break (DSB) repair factors (e.g. BRCA1, DNA-PK, Lig4, XRCC4). In addition, higher levels of oxidative stress (reactive oxygen species, ROS), DNA damage and/or defective DNA repair have been reported in different malignancies and tumors. The long term objective of this project is to identify the role(s) of BRCA1 (homologous recombination-HR) and DNA-PK (non-homologous end joining-NHEJ) two key double strand break repair (DSBR) proteins in the processing of non-DSB oxidatively induced single and clustered DNA lesions (OCDLs) in human gamma-irradiated tumor cells. In addition, chromosomal instability and apoptosis will be measured in each case. There are very limited and only fragmentary data on this specific field. Based also on preliminary data, our central hypothesis is that a compromised DSB repair pathway will also lead to deficient OCDL repair and accumulation of oxidatively-generated DNA lesions when DSBR deficient cells are challenged by various oxidizing agents like ionizing radiation. These studies are expected to provide meaningful mechanistic insights into DNA repair pathways involved in the processing of non-DSB clusters and therefore advance the field. They will also contribute to cancer etiology associated with complex DNA damage since accumulation of OCDLs is associated with increased mutation rate and chromosomal instability. Fingerprinting the molecular identity of these DNA modifications can be utilized in designing more efficient cancer therapeutic strategies based on the concept of selective apoptotic activation in malignant cells after exposure to therapeutic sources of oxidative stress like radiation and chemotherapy drugs

Conecta tu I+D

Entra hoy

¿Olvidé mi contraseña?

Financiación

Empresas

CTIs/Universidades

Proyectos

Investigadores