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MAMLE SIGNED

Understanding the mechanisms of human acute myeloid leukaemia (AML) evolution

Total Cost €

EC-Contrib. €

Partnership

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Outcomes and
results

MAMLE project word cloud

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

biology aid describe starts europeans diagnosed elderly prel suited malignancies stages treatment myeloid cancers serially 100 carry human until vision single patients historical blood health naive mechanism integrate healthy somatic structure stem tools relapses individuals deadly preleukemic acute collected cells hematopoietic hspcs genetics evolution spanning fraction molecular unravel tends aml half n cell diagnosis followed mutations understand clearer leukemia genetic discoveries population progenitor root evolutionary clonal disease cohort relapse small million

Project "MAMLE" data sheet

The following table provides information about the project.

Coordinator	WEIZMANN INSTITUTE OF SCIENCE Organization address address: HERZL STREET 234 city: REHOVOT postcode: 7610001 website: www.weizmann.ac.il 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	Israel [IL]
Total cost	1˙750˙000 €
EC max contribution	1˙750˙000 € (100%)
Programme	1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
Code Call	ERC-2016-STG
Funding Scheme	ERC-STG
Starting year	2017
Duration (year-month-day)	from 2017-02-01 to 2022-01-31

Partnership

Take a look of project's partnership.

#	participants	country	role	EC contrib. [€]
1	WEIZMANN INSTITUTE OF SCIENCE WEIZMANN INSTITUTE OF SCIENCE Organization address address: HERZL STREET 234 city: REHOVOT postcode: 7610001 website: www.weizmann.ac.il contact info title: n.a. name: n.a. surname: n.a. function: n.a. email: n.a. telephone: n.a. fax: n.a.	IL (REHOVOT)	coordinator	1˙750˙000.00

Map

Project objective

Acute myeloid leukemia (AML) is one of the most deadly cancers. Currently, we do not fully understand how and why AML starts or why it tends to relapse after treatment. Recent discoveries by the applicant and others have identified preleukemic stem and progenitor cells (preL-HSPCs) as the root of AML evolution. Many healthy elderly individuals carry the preleukemic mutations in their preL-HSPCs and yet, do not develop AML. It is also becoming clearer that leukemia evolution is spanning over many years but most research is focused on the late stages of the disease. Population genetics tools are specifically suited for the study of historical evolution however such tools are not well developed in the field of somatic evolution. This proposal will integrate population genetics, stem cell and leukemia biology in order to unravel human leukemia evolution from the very early preleukemic phase to relapse. Novel single cell population genetics tools will be used to describe the naive clonal structure of the human hematopoietic system in both health and disease. A unique cohort of half a million Europeans, who have been followed for years, will be used to understand why only a small fraction of the individuals carrying preleukemic mutations develop AML. Novel genetic analysis will be developed to study the clonal structure of blood cells, years before AML was diagnosed. A large cohort (N=100) of AML patients were collected serially over a year and will be collected until relapse. Detailed molecular and population genetics of this cohort will aid in understanding the mechanism of AML relapse and in developing novel molecular methodologies, that will allow early relapse diagnosis. AML like many other malignancies is diagnosed late in its evolutionary path. In this proposal the evolution of AML before diagnosis and before it relapses will be studied by novel population genetic tools so that the vision of early diagnosis and treatment will become reality.

Publications

List of publications.
year	authors and title	journal	last update
2018	Sagi Abelson, Grace Collord, Stanley W. K. Ng, Omer Weissbrod, Netta Mendelson Cohen, Elisabeth Niemeyer, Noam Barda, Philip C. Zuzarte, Lawrence Heisler, Yogi Sundaravadanam, Robert Luben, Shabina Hayat, Ting Ting Wang, Zhen Zhao, Iulia Cirlan, Trevor J. Pugh, David Soave, Karen Ng, Calli Latimer, Claire Hardy, Keiran Raine, David Jones, Diana Hoult, Abigail Britten, John D. McPherson, Mattias Johansson, Faridah Mbabaali, Jenna Eagles, Jessica K. Miller, Danielle Pasternack, Lee Timms, Paul Krzyzanowski, Philip Awadalla, Rui Costa, Eran Segal, Scott V. Bratman, Philip Beer, Sam Behjati, Inigo Martincorena, Jean C. Y. Wang, Kristian M. Bowles, J. RamÃ³n QuirÃ³s, Anna Karakatsani, Carlo La Vecchia, Antonia Trichopoulou, Elena Salamanca-FernÃ¡ndez, JosÃ© M. Huerta, Aurelio Barricarte, Ruth C. Travis, Rosario Tumino, Giovanna Masala, Heiner Boeing, Salvatore Panico, Rudolf Kaaks, Alwin KrÃ¤mer, Sabina Sieri, Elio Riboli, Paolo Vineis, Matthieu Foll, James McKay, Silvia Polidoro, NÃºria Sala, Kay-Tee Khaw, Roel Vermeulen, Peter J. Campbell, Elli Papaemmanuil, Mark D. Minden, Amos Tanay, Ran D. Balicer, Nicholas J. Wareham, Moritz Gerstung, John E. Dick, Paul Brennan, George S. Vassiliou, Liran I. Shlush Prediction of acute myeloid leukaemia risk in healthy individuals published pages: 400-404, ISSN: 0028-0836, DOI: 10.1038/s41586-018-0317-6	Nature 559/7714	2019-06-13

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