Yu , Jiangyan
Ms. Jiangyan Yu 

PhD Candidate



Relapse is the major cause of treatment failure in pediatric acute lymphoblastic leukemia (ALL). In the treatment of B-cell precursor ALL (BCP-ALL), the incidence of relapse varies between 15 and 25%, dependent on the protocol. We and others previously demonstrated that the presence at diagnosis of deletions inIKZF1is a strong risk factor for relapse. Furthermore, preliminary results show that these deletions can be present at subclonal levels, often undetectable by routine methodologies. These findings are in line with recent studies, which have shown a complex, dynamic architecture of clonal diversity in ALL and other leukemia subtypes, both at diagnosis and at relapse. This multiclonal diversity follows a Darwinian model of evolution, and likely contributes to the selective outgrowth of therapy-resistant leukemic cells during or after chemotherapy treatment, resulting in relapse. However, the clinical importance for subclonal genetic abnormalities for relapse risk is still poorly defined.

I am investigating the multiclonal architecture of ALL in relation to therapy resistance and the origin of relapse using comprehensive genetic characterization of diagnosis-relapse pairsand backtracking of relapse-specific aberrations in diagnosis samples in order to identify relapse-initiating clones. Furthermore, I am studying the clinical relevance of subclonal aberrations in recently identified prognostic markers (including e.g.IKZF1) at time of diagnosis using both retrospective and prospective approaches. We expect that these studies will yield new valuable insight into the properties of relapse-initiating cells in leukemia, and will provide novel strategies for future routine diagnostics and relapse prediction at diagnosis.

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