Hola,
¿eres nuevo aquí?

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

Tengo cuenta

Regístrate

Ver video

NKG2D

Financiado

Cerrado

CO OPTION OF THE NKG2D LYMPHOCYTE RECEPTOR AS AN ONCOPROTEIN PROMOTING CANCER ST...

CO OPTION OF THE NKG2D LYMPHOCYTE RECEPTOR AS AN ONCOPROTEIN PROMOTING CANCER STEM CELL TRANSDIFFERENTIATION AND CANCER AUTONOMY The stimulatory NKG2D lymphocyte receptor expressed on natural killer cells and T cells and its tumor-associated ligands enable the immune system to recognize and destroy cancer cells. This role of NKG2D is well recognized and eff... ver más

01/01/2018

MEDICAL UNIVERSITY...

261K€

Presupuesto del proyecto: 261K€

Líder del proyecto

MEDIZINISCHE UNIVERSITAT GRAZ 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 2018-01-01 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

MEDICAL UNIVERSITY OF GRAZ

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

SAF2014-58752-R LA BIOLOGIA DE LOS RECEPTORES ACTIVADORES DE LOS LINFOCITOS... 169K€ Cerrado

NKG2D in T-cells Memory Control The role of NKG2D and the T cell receptor in... 173K€ Cerrado

SAF2012-32293 INMUNIDAD TUMORAL: BIOQUIMICA DEL RECONOCIMIENTO MEDIADO POR... 140K€ Cerrado

ELIMINATESENESCENT The Role of Elimination of Senescent Cells in Cancer Develop... 2M€ Cerrado

DIEAML Deciphering immune evasion of Acute Myeloid Leukemia 163K€ Cerrado

BFU2015-65625-P REGULACION ESPACIO-TEMPORAL Y DINAMICA DE ACTIVACION DE ONCO... 142K€ Cerrado

Líder del proyecto

MEDIZINISCHE UNIVERSITAT GRAZ No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Presupuesto del proyecto 261K€

Fecha límite de participación Sin fecha límite de participación.

Descripción del proyecto The stimulatory NKG2D lymphocyte receptor expressed on natural killer cells and T cells and its tumor-associated ligands enable the immune system to recognize and destroy cancer cells. This role of NKG2D is well recognized and efforts are underway to target NKG2D and its ligands for cancer therapy. However, cancers adopt diverse strategies to safeguard their survival. With advanced human cancers, NKG2D ligand expression favors tumor progression, which has been ascribed to ligand-induced immune evasion. In a surprising conceptual twist, Dr. Spies’ laboratory at the Fred Hutchinson Cancer Research Center has found that cancer cells themselves express NKG2D together with its DAP10 signaling adaptor. Above-threshold expression of NKG2D–DAP10 in ligand-bearing tumor lines activates oncogenic signaling cascades and induces differentiation changes characteristic of the epithelial-mesenchymal transition (EMT), a cellular reprogramming process that leads to increased cancer cell motility and metastatic dissemination. Intertwined with EMT is the generation of self-renewing cancer stem cells (CSCs), which are main culprits of failed cancer therapies. These findings challenge current concepts as cancer cells may co-opt NKG2D as an oncoprotein serving their own benefit. In a preliminary assessment, this role is supported by significant correlations between proportions of cancer cells that are positive for surface NKG2D and criteria of tumor progression. This proposal seeks to establish that cancer cell NKG2D has a major role in the development of CSCs. The experimental approach involves tissue culture-based studies using model tumor cell lines and functional testing of patient-derived NKG2D bearing CSCs for their tumor forming capacity in a mouse model. The results may have profound biomedical implications by establishing a previously unrecognized mechanism that promotes tumor autonomy, and may impact translational approaches targeting NKG2D or its ligands for cancer therapy.

Conecta tu I+D

Entra hoy

¿Olvidé mi contraseña?

Financiación

Empresas

CTIs/Universidades

Proyectos

Investigadores