Although standard chemotherapy induces disease remission in the majority of Acute Myeloid Leukemia (AML) patients, most of them relapse and eventually die since they do not respond to therapy anymore. Therefore, there is an urgent medical need to identify disease markers predicting relapse or response to treatment.
Currently, resistance to treatment is associated mainly to the selection of rare tumor cells harboring specific DNA mutations (relapse-specific mutations) that cause resistance to drugs. More recently, however, a complementary possibility emerged, that envisions alterations of the “epigenome” as involved in the determination of resistance to drugs. Initial findings hint at the possibility that those alterations exist, and they affect the genome architecture both locally and at a more global level.
This project aims to explore drug resistance in AML as the result of functional alterations in the epigenome, and to analyze both local and global changes in the epigenome. The initial discovery phase will be followed by a validation phase to assess the functional significance of the epigenetic alterations identified. This study will enable identifying markers predicting cure or relapse after treatment, ready to be tested in clinical trials.
Identification of drug resistance associated epigenetic alterations in AMLs
CRG, Spain (2x 1 month):
Computational analyses and functional studies.
CURIE, France (1 month):
Preliminary characterisation of histone H3.3 spatial organisation in AML samples.
ELISAVA, Spain (2 weeks):
Learning new design features to represent AM drug resistance.
Enrolment in doctoral programs
PhD in Systems Medicine (curriculum of Molecular Oncology) from University of Milan
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