ContraNPM1AML SIGNED
Dissecting to hit the therapeutic targets in nucleophosmin (NPM1)-mutated acute myeloid leukemia
Total Cost €
0EC-Contrib. €
0Partnership
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Project "ContraNPM1AML" data sheet
The following table provides information about the project.
| Coordinator |
UNIVERSITA DEGLI STUDI DI PERUGIA
Organization address contact info |
| 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.
| # | ||||
|---|---|---|---|---|
| 1 | UNIVERSITA DEGLI STUDI DI PERUGIA | IT (PERUGIA) | coordinator | 1˙883˙749.00 |
Map
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 |
|---|---|---|---|
| 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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