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TRANSREAD SIGNED

Restoration of tumor suppressor function by induction of translational read-through of premature termination codons - a strategy for improved cancer therapy

Total Cost €

EC-Contrib. €

Partnership

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Outcomes and
results

TRANSREAD project word cloud

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

efficient pten tp53 inherited sporadic translational induce hits tumors mechanism effect characterization protein patients molecular cells human tested read truncated frequently fraction premature generate techniques clinical ex molecules compounds functional length proteins primary therapy expression preclinical codons mutations termination unstable hit vivo translation action full knock trials mouse rb1 tumor p53 cetsa suppressor models genes elucidate nonsense inactivated apc mutant

Project "TRANSREAD" data sheet

The following table provides information about the project.

Coordinator	KAROLINSKA INSTITUTET Organization address address: Nobels Vag 5 city: STOCKHOLM postcode: 17177 website: www.ki.se 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	Sweden [SE]
Total cost	2˙480˙889 €
EC max contribution	2˙480˙889 € (100%)
Programme	1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
Code Call	ERC-2015-AdG
Funding Scheme	ERC-ADG
Starting year	2016
Duration (year-month-day)	from 2016-09-01 to 2021-08-31

Partnership

Take a look of project's partnership.

#	participants	country	role	EC contrib. [€]
1	KAROLINSKA INSTITUTET KAROLINSKA INSTITUTET Organization address address: Nobels Vag 5 city: STOCKHOLM postcode: 17177 website: www.ki.se contact info title: n.a. name: n.a. surname: n.a. function: n.a. email: n.a. telephone: n.a. fax: n.a.	SE (STOCKHOLM)	coordinator	2˙480˙889.00

Map

Project objective

Tumor suppressor genes such as TP53, RB1, PTEN and APC are frequently inactivated in sporadic and inherited human tumors. A significant fraction of the mutations in these genes are nonsense mutations that lead to premature termination of translation and expression of truncated unstable and non-functional proteins. We will identify and characterize novel molecules that can induce translational read-through of premature termination codons in nonsense mutant TP53 and expression of full length p53 protein. Hits will be tested for their effect on nonsense mutant RB1, PTEN and APC. We will also elucidate the molecular mechanism of action of the identified compounds by CETSA and other techniques. Moreover, we will test hit compounds on primary tumor cells from patients ex vivo, and generate mouse knock-in tumor models with nonsense mutant tumor suppressor genes for further characterization of hits. We will take the most promising hits through preclinical development towards clinical trials. Our aim is to develop novel and efficient targeted therapy for tumors with nonsense mutations in the TP53, RB1, PTEN and/or APC tumor suppressor genes.

Publications

List of publications.
year	authors and title	journal	last update
2018	Meiqiongzi Zhang, Angelos Heldin, Mireia Palomar-Siles, Susanne Ã–hlin, Vladimir J. N. Bykov, Klas G. Wiman Synergistic Rescue of Nonsense Mutant Tumor Suppressor p53 by Combination Treatment with Aminoglycosides and Mdm2 Inhibitors published pages: , ISSN: 2234-943X, DOI: 10.3389/fonc.2017.00323	Frontiers in Oncology 7	2019-06-13

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