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ONCOMECHAML SIGNED

Common Oncogenic Mechanisms in Multi-Partner Translocation Families in Acute Myeloid Leukemia

Total Cost €

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EC-Contrib. €

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Partnership

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 Outcomes and results

 ONCOMECHAML project word cloud

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

unknown    molecular    gene    representative    networks    hypothesize    cancer    majority    conserved    genes    proteins    clinically    myeloid    interactomes    hits    encoded    models    leukemia    straightforward    gt    mechanism    genetic    fused    protein    screens    arising    blood    transforming    diagnostic    denominators    significance    strategies    fusion    found    pipeline    acute    recurrently    interaction    validated    mortality    modular    80    therapeutic    complexity    complicated    chromosomal    effectors    delineate    loci    families    decisions    clinical    cells    patients    mpt    mouse    model    shrna    frequent    oncogenic    critical    aml    act    functional    recipient    transformation    runx1    relevance    pooled    driver    nup98    architecture    cellular    mechanisms    diagnosis    unclear    confidence    oncogenes    contribution    physical    primary    characterization    informative    mll    aberrations    experimental    expression    translocation    datasets    despite    generate    basic    translocations   

Project "ONCOMECHAML" data sheet

The following table provides information about the project.

Coordinator		 VETERINAERMEDIZINISCHE UNIVERSITAET WIEN 

Organization address
address: Veterinaerplatz 1
city: VIENNA
postcode: 1210
website: www.vetmeduni.ac.at

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 Austria [AT]
 Total cost 1˙499˙500 €
 EC max contribution 1˙499˙500 € (100%)
 Programme 1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
 Code Call ERC-2014-STG
 Funding Scheme ERC-STG
 Starting year 2015
 Duration (year-month-day) from 2015-06-01   to  2020-05-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    VETERINAERMEDIZINISCHE UNIVERSITAET WIEN AT (VIENNA) coordinator 513˙990.00
2    LUDWIG BOLTZMANN GESELLSCHAFT GMBH AT (WIEN) participant 985˙509.00

Map

 Project objective

Acute Myeloid Leukemia (AML) is the most frequent cancer of the blood system, with >80% mortality within 5 years of diagnosis. Straightforward clinical decisions are complicated by the genetic complexity of AML. In particular, fusion proteins arising from chromosomal aberrations are recurrently found in AML and often act as strong driver oncogenes. In “Multi-Partner Translocation” (MPT) families, one specific gene is fused to many recipient loci. Due to this modular architecture, MPT families are of particular interest to comparative studies of oncogenic mechanisms. The three most common MPT families in AML represent translocations of the MLL, RUNX1 and NUP98 genes. Despite their clinical significance, the molecular mechanism of transformation remains unknown for the majority of fusion proteins and it is unclear if transforming mechanisms are conserved within and across different MPT families. We hypothesize that common oncogenic mechanisms of fusion proteins are encoded in physical and genetic cellular interaction networks that are specific to MPT families. We propose to delineate critical common effectors of oncogenic mechanisms in AML driven by MPT families through a comprehensive, comparative, functional analysis of 20 clinically representative MLL-, RUNX1- and NUP98-fusion proteins using a unique experimental pipeline. Characterization of protein interactomes and their effects on gene expression will identify common cellular denominators of MPT families, whose functional contribution will be assessed through pooled shRNA screens in clinically relevant model systems. High-confidence hits will be validated in mouse models and primary cells from AML patients. This project will generate large informative datasets and novel experimental systems that are of relevance for basic and clinical cancer research. It will contribute to improved understanding of oncogenic mechanisms, which may directly impact on diagnostic and therapeutic strategies in the management of AML.

 Publications

year authors and title journal last update
List of publications.
2016 Thomas Eder, Florian Grebien, Thomas Rattei
NVT: a fast and simple tool for the assessment of RNA-seq normalization strategies
published pages: btw521, ISSN: 1367-4803, DOI: 10.1093/bioinformatics/btw521 		Bioinformatics 2019-05-27
2017 Katrin Noack, Nisintha Mahendrarajah, Dorle Hennig, Luisa Schmidt, Florian Grebien, Dagmar Hildebrand, Markus Christmann, Bernd Kaina, Andreas Sellmer, Siavosh Mahboobi, Katharina Kubatzky, Thorsten Heinzel, Oliver H. Krämer
Analysis of the interplay between all-trans retinoic acid and histone deacetylase inhibitors in leukemic cells
published pages: 2191-2208, ISSN: 0340-5761, DOI: 10.1007/s00204-016-1878-5 		Archives of Toxicology 91/5 2019-05-27
2016 Tahereh Javaheri, Zahra Kazemi, Jan Pencik, Ha TT Pham, Maximilian Kauer, Rahil Noorizadeh, Barbara Sax, Harini Nivarthi, Michaela Schlederer, Barbara Maurer, Maximillian Hofbauer, Dave NT Aryee, Marc Wiedner, Eleni M Tomazou, Malcolm Logan, Christine Hartmann, Jan P Tuckermann, Lukas Kenner, Mario Mikula, Helmut Dolznig, Aykut Üren, Günther H Richter, Florian Grebien, Heinrich Kovar, Richard Moriggl
Increased survival and cell cycle progression pathways are required for EWS/FLI1-induced malignant transformation
published pages: e2419, ISSN: 2041-4889, DOI: 10.1038/cddis.2016.268 		Cell Death and Disease 7/10 2019-05-27
2016 Jan Pencik, Ha Thi Thanh Pham, Johannes Schmoellerl, Tahereh Javaheri, Michaela Schlederer, Zoran Culig, Olaf Merkel, Richard Moriggl, Florian Grebien, Lukas Kenner
JAK-STAT signaling in cancer: From cytokines to non-coding genome
published pages: 26-36, ISSN: 1043-4666, DOI: 10.1016/j.cyto.2016.06.017 		Cytokine 87 2019-05-27
2018 Ha Thi Thanh Pham, Barbara Maurer, Michaela Prchal-Murphy, Reinhard Grausenburger, Eva Grundschober, Tahereh Javaheri, Harini Nivarthi, Auke Boersma, Thomas Kolbe, Mohamed Elabd, Florian Halbritter, Jan Pencik, Zahra Kazemi, Florian Grebien, Markus Hengstschläger, Lukas Kenner, Stefan Kubicek, Matthias Farlik, Christoph Bock, Peter Valent, Mathias Müller, Thomas Rülicke, Veronika Sexl, Richard Moriggl
STAT5BN642H is a driver mutation for T cell neoplasia
published pages: 387-401, ISSN: 0021-9738, DOI: 10.1172/JCI94509 		Journal of Clinical Investigation 128/1 2019-05-27

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