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NKG2D

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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

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Este proyecto no cuenta con búsquedas de partenariado abiertas en este momento.

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1 Participantes

MEDICAL UNIVERSITY OF GRAZ

0.00€ | Lider

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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.

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