#	Pagina
attuale pagina	/open-h2020/projects/209672/index.html

Opendata, web and dolomites

DSMT16 SIGNED

Deciphering causes and consequences of inflammation in subtypes of sporadic intestinal cancer

Total Cost €

EC-Contrib. €

Partnership

Views

DSMT16 project word cloud

Explore the words cloud of the DSMT16 project. It provides you a very rough idea of what is the project "DSMT16" about.

generate dictate tumourigenic g12d braf systematic signalling manner immune mechanistically preliminary mice chronic v637e intestine tumourigenesis tumours epithelium recombinase transplantation determines survival cancers immunophenotyping basis anti microenvironment endoscopic drs mutation il2rg cell infiltrating personalised therapies conversely pro genetically inflammatory suggest pik3ca unclear mechanisms intestinal serrated mimics cancer mechanistic stroma models insights mutational h1047r abrogated faithfully data rag2 decipher humans immunodeficient oncogenic subtypes characterise sporadic organoids mediators house association dependent elucidate carcinogenesis reconstruct tumour wild vivo detection oncogenes turn oncogene notably inflammation expression kras an cells dual experimentally

Project "DSMT16" data sheet

The following table provides information about the project.

Coordinator	KLINIKUM RECHTS DER ISAR DER TECHNISCHEN UNIVERSITAT MUNCHEN Organization address address: ISMANINGER STRASSE 22 city: MUENCHEN postcode: 81675 website: http://www.med.tu.muenchen.de 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	Germany [DE]
Total cost	159˙460 €
EC max contribution	159˙460 € (100%)
Programme	1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
Code Call	H2020-MSCA-IF-2016
Funding Scheme	MSCA-IF-EF-ST
Starting year	2018
Duration (year-month-day)	from 2018-02-15 to 2020-02-14

Partnership

Take a look of project's partnership.

#	participants	country	role	EC contrib. [€]
1	KLINIKUM RECHTS DER ISAR DER TECHNISCHEN UNIVERSITAT MUNCHEN KLINIKUM RECHTS DER ISAR DER TECHNISCHEN UNIVERSITAT MUNCHEN Organization address address: ISMANINGER STRASSE 22 city: MUENCHEN postcode: 81675 website: http://www.med.tu.muenchen.de contact info title: n.a. name: n.a. surname: n.a. function: n.a. email: n.a. telephone: n.a. fax: n.a.	DE (MUENCHEN)	coordinator	159˙460.00

Map

Project objective

An association between inflammation and carcinogenesis is well established, however, how they are related mechanistically in subtypes of sporadic intestinal tumours remains unclear. This study aims to decipher how oncogenes determine the inflammatory microenvironment (stroma) and how this affects tumour development and survival. Notably, intestinal epithelium-specific expression of oncogenic Kras(G12D), Braf(V637E) and Pik3ca(H1047R) in mice mimics serrated intestinal cancers in humans faithfully. Preliminary data suggest that the mutational make-up of the tumour may dictate the pro- and anti-tumourigenic immune response, which in turn determines tumour development and survival. This study therefore aims to characterise the tumour-infiltrating immune cells by systematic immunophenotyping and to decipher the involved inflammatory signalling mechanisms in a cell-type and mutation-specific manner. Moreover, we aim to reconstruct the formation of the oncogene-specific inflammatory microenvironment, which we will determine via endoscopic transplantation of intestinal organoids derived from Kras(G12D), Braf(V637E) and Pik3ca(H1047R) mice into the large intestine of wild-type mice. Importantly, detection of involved inflammatory mediators and immune cell-subtypes will allow us to genetically target them in vivo using novel in-house generated dual-recombinase systems (DRS). In order to investigate the consequences of inflammation on sporadic intestinal tumourigenesis, models with genetically or experimentally induced chronic inflammation will be applied. Conversely, immunodeficient Rag2;Il2rg–/– mice will be used to elucidate if sporadic intestinal carcinogenesis in Kras(G12D), Braf(V637E) and Pik3ca(H1047R) mice is dependent on inflammation and can be abrogated. This study will generate new mechanistic insights into the microenvironment of cancer subtypes, which could provide a basis for the development of new personalised immune therapies.

Publications

List of publications.
year	authors and title	journal	last update
2018	Markus Tschurtschenthaler, Timon Erik Adolph The Selective Autophagy Receptor Optineurin in Crohnâ€™s Disease published pages: , ISSN: 1664-3224, DOI: 10.3389/fimmu.2018.00766	Frontiers in Immunology 9	2019-05-29

Are you the coordinator (or a participant) of this project? Plaese send me more information about the "DSMT16" project.

For instance: the website url (it has not provided by EU-opendata yet), the logo, a more detailed description of the project (in plain text as a rtf file or a word file), some pictures (as picture files, not embedded into any word file), twitter account, linkedin page, etc.

Send me an email (fabio@fabiodisconzi.com) and I put them in your project's page as son as possible.

Thanks. And then put a link of this page into your project's website.

The information about "DSMT16" are provided by the European Opendata Portal: CORDIS opendata.