Sven Turkalj

I am an MRC WIMM-funded DPhil student working in the Vyas group. I obtained my Bachelor's Degree  at the University of Trieste, where I studied the inhibitors of apoptotic and B-cell receptor pathways in the context of B-cell malignancies, supervised by Prof. Dimitar Efremov. I obtained my Master's Degree in functional genomics and then genetics from the University of Paris. There, I worked on a novel mutant of the transcription factor PU.1, under the supervision of Dr. Olivier Bernard at the Institute Gustave Roussy. 

My current work is focused on the molecular mechanisms leading to clonal expansion of haematopoietic stem cells and early progenitors, in the context of clonal haematopoiesis, a state associated with higher risk of developing Acute Myeloid Leukemia (AML), and other diseases. In particular, I am interested in how somatic mutations in epigenetic regulators, such as TET2, DNMT3A and ASXL1, confer clonal advantage during haematopoietic differentiation, and which pathways are corrupted in the process. Defining the direct and indirect targets of these proteins, and how these targets regulate self-renewal and lineage specification, remains a largely unresolved question in the field. Importantly, understanding these mechanisms would contribute in elucidating the earliest steps of leukemia stem cell formation, the fuel of haematopoietic transformation.

I am also involved in a project studying the clonal evolution of AML and the mechanisms of relapse following the combined treatment with Venetoclax and the IDH1 inhibitor Ivosidenib, using multi-omic approaches at the single cell level. 

Mechanisms of B Cell Receptor Activation and Responses to B Cell Receptor Inhibitors in B Cell Malignancies

Journal article

Efremov D, Turkalj S, and Laurenti L., 2020, Cancers

https://doi.org/10.3390/cancers12061396

Inhibition of SYK or BTK augments venetoclax sensitivity in SHP1-negative/BCL-2-positive diffuse large B-cell lymphoma

Journal article

Sasi BK, Martines C, Xerxa E, et al., 2019, Leukemia 

10.1038/s41375-019-0442-8

SHP1 Deficiency Is Responsible for the Constitutive Activation of the BCR Pathway in GCB DLBCL

Conference paper

Sasi BK, Turkalj S, Kalkan H, et al., 2018, Blood (ASH)

10.1182/blood-2018-99-118120