Opendata, web and dolomites


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

Total Cost €


EC-Contrib. €






 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.

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

Project "ONCOMECHAML" data sheet

The following table provides information about the project.


Organization address
address: Veterinaerplatz 1
city: VIENNA
postcode: 1210

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


Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 


 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.


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

Are you the coordinator (or a participant) of this project? Plaese send me more information about the "ONCOMECHAML" 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 ( 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 "ONCOMECHAML" are provided by the European Opendata Portal: CORDIS opendata.

More projects from the same programme (H2020-EU.1.1.)

EVOMENS (2020)

The evolution of menstruation in primates

Read More  


RNA regulation during viral infection

Read More  

DimorphicCircuits (2019)

Elucidating the development of sexually-dimorphic circuits: from molecular mechanisms to synapses and behavior

Read More