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ContraNPM1AML SIGNED

Dissecting to hit the therapeutic targets in nucleophosmin (NPM1)-mutated acute myeloid leukemia

Total Cost €

0

EC-Contrib. €

0

Partnership

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 ContraNPM1AML project word cloud

Explore the words cloud of the ContraNPM1AML project. It provides you a very rough idea of what is the project "ContraNPM1AML" about.

hereto    hypothesis    hematologic    drug    group    relies    screenings    libraries    revisited    screening    clinical    heterogeneity    frequent    therapy    genome    crispr    missing    strategies    models    aml    vulnerabilities    mechanisms    succumb    antracyclinecytarabine    issue    myeloid    patients    either    interference    leukemogenesis    somatic    avail    mutations    genes    improvements    neoplasms    insights    laboratories    analyzing    network    50    intracellular    genomics    landscape    therapeutic    acute    entity    drugs    leukemia    deciphering    complementary    synthetic    cured    alteration    genetic    30    adult    gained    despite    advantage    young    nucleophosmin    unravel    uncovered    molecular    subtype    scheme    pharmacological    trials    place    discoveries    sequencing    generation    npm1    mutated    whilst    recurrent    concurrent    classify    lethal    difficult    disease    soon    classification    discovered    malignancies    context    chemical    throughput    treat    interactions    elderly   

Project "ContraNPM1AML" data sheet

The following table provides information about the project.

Coordinator
UNIVERSITA DEGLI STUDI DI PERUGIA 

Organization address
address: PIAZZA DELL UNIVERSITA 1
city: PERUGIA
postcode: 6123
website: www.unipg.it

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 Italy [IT]
 Total cost 1˙883˙749 €
 EC max contribution 1˙883˙749 € (100%)
 Programme 1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
 Code Call ERC-2016-COG
 Funding Scheme ERC-COG
 Starting year 2017
 Duration (year-month-day) from 2017-04-01   to  2022-03-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    UNIVERSITA DEGLI STUDI DI PERUGIA IT (PERUGIA) coordinator 1˙883˙749.00

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 Project objective

Acute myeloid leukemia (AML) is a group of hematologic malignancies which, due to their molecular and clinical heterogeneity, have been traditionally difficult to classify and treat. Recently, next-generation, whole-genome sequencing has uncovered several recurrent somatic mutations that better define the landscape of AML genomics. Despite these advances in deciphering AML molecular subsets, there have been no concurrent improvements in AML therapy which still relies on the ‘antracyclinecytarabine’ scheme. Hereto, only about 40-50% of adult young patients are cured whilst most of the elderly succumb to their disease. Therefore, new therapeutic approaches which would take advantage of the new discoveries are clearly needed. In the past years, we discovered and characterized nucleophosmin (NPM1) mutations as the most frequent genetic alteration (about 30%) in AML, and today NPM1-mutated AML is a new entity in the WHO classification of myeloid neoplasms. However, mechanisms of leukemogenesis and a specific therapy for this leukemia are missing. Here, I aim to unravel the complex network of molecular interactions that take place in this distinct genetic subtype, and find their vulnerabilities to identify new targets for therapy. To address this issue, I will avail of relevant pre-clinical models developed in our laboratories and propose two complementary strategies: 1) a screening-based approach, focused either on the target, by analyzing synthetic lethal interactions through CRISPR-based genome-wide interference, or on the drug, by high-throughput chemical libraries screenings; 2) a hypothesis-driven approach, based on our recent gained novel insights on the role of specific intracellular pathways/genes in NPM1-mutated AML and on pharmacological studies with ‘old’ drugs, which we have revisited in the specific AML genetic context. I expect our discoveries will lead to find novel therapeutic approaches and make clinical trials available to patients as soon as possible.

 Publications

year authors and title journal last update
List of publications.
2018 Lorenzo Brunetti, Michael C. Gundry, Daniele Sorcini, Anna G. Guzman, Yung-Hsin Huang, Raghav Ramabadran, Ilaria Gionfriddo, Federica Mezzasoma, Francesca Milano, Behnam Nabet, Dennis L. Buckley, Steven M. Kornblau, Charles Y. Lin, Paolo Sportoletti, Maria Paola Martelli, Brunangelo Falini, Margaret A. Goodell
Mutant NPM1 Maintains the Leukemic State through HOX Expression
published pages: 499-512.e9, ISSN: 1535-6108, DOI: 10.1016/j.ccell.2018.08.005
Cancer Cell 34/3 2019-11-26
2019 Paolo Sportoletti, Letizia Celani, Emanuela Varasano, Roberta Rossi, Daniele Sorcini, Chiara Rompietti, Francesca Strozzini, Beatrice Del Papa, Valerio Guarente, Giulio Spinozzi, Debora Cecchini, Oxana Bereshchenko, Torsten Haferlach, Maria Paola Martelli, Franca Falzetti, Brunangelo Falini
GATA1 epigenetic deregulation contributes to the development of AML with NPM1 and FLT3-ITD cooperating mutations
published pages: 1827-1832, ISSN: 0887-6924, DOI: 10.1038/s41375-019-0399-7
Leukemia 33/7 2019-11-26

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