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Tolltum

Role, regulation and targeting of nucleic acid-sensing TLRs within the tumour microenvironment

Total Cost €

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EC-Contrib. €

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Partnership

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Project "Tolltum" data sheet

The following table provides information about the project.

Coordinator
THE CHANCELLOR, MASTERS AND SCHOLARS OF THE UNIVERSITY OF OXFORD 

Organization address
address: WELLINGTON SQUARE UNIVERSITY OFFICES
city: OXFORD
postcode: OX1 2JD
website: www.ox.ac.uk

contact info
title: n.a.
name: n.a.
surname: n.a.
function: n.a.
email: n.a.
telephone: n.a.
fax: n.a.

 Coordinator Country United Kingdom [UK]
 Project website https://www.rdm.ox.ac.uk/about/our-divisions/investigative-medicine-division/investigative-medicine-division-research/cerundolo-group
 Total cost 195˙454 €
 EC max contribution 195˙454 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2014
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2015
 Duration (year-month-day) from 2015-10-01   to  2017-09-30

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    THE CHANCELLOR, MASTERS AND SCHOLARS OF THE UNIVERSITY OF OXFORD UK (OXFORD) coordinator 195˙454.00

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 Project objective

Inflammation is an integral part of carcinogenesis. Several different cells of myeloid, lymphoid and non-hematopoietic origin contribute to the strong link between cancer and inflammation and maintain a pro-tumoral environment. The complexity of this environment and the diversity of tumours lead to distinct responses during tumour immunotherapies. Nucleic acid-sensing (NAS) TLR ligands are an essential component of anti-tumour strategies to induce efficient tumour-specific adaptive immune responses. NAS TLRs can also detect nucleic acid released during tumour necrosis, thereby modulating the tumour microenvironment. Interestingly, NAS TLR signalling can induce cell death via apoptosis or induce pro-tumoral survival and proliferation of cancer cells. These opposing effects of NAS TLR ligands may be due to the differential response of distinct tumour-associated cells to TLR ligands. Indeed, the individual response of subsets of tumour-associated cells remains unclear, thus making it difficult to predict the outcome of tumour immunotherapies. Furthermore, the expression and regulation of NAS TLRs in tumour-associated cells remains unknown. Using ex vivo cultures from adenocarcinomas and melanomas, we will systematically analyze the expression of all NAS TLRs on sorted cells. Using cutting edge technologies, we will dissect the role of TLRs in modulating the tumour microenvironment, which will provide novel insights into our ability to modulate cellular inflammation in the tumour. This proposal has the potential not only to reveal novel aspects of NAS TLR regulation, but also to provide new targets for the modulation of the tumour stroma and the infiltrating cells during carcinogenesis.

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