T-cell acute lymphoblastic leukemia (T-ALL) results from the malignant transformation of thymocytes.
Although prognosis has improved with combination chemotherapy, a significant number of T-ALL patients relapse and become refractory to intensive treatment, indicating the need for improved and targeted therapy.
Our research focuses on modeling different oncogenes and tumor suppressor genes (including PHF6) in zebrafish, a well suited model to study T-ALL, and analyse their tumor initiating capacity and their possible cooperation with other T-ALL linked genes.
The resulting T-ALLs are characterized on genome, transcriptome (including single cell) and epigenome level and compared to human T-ALLs.
I obtained a Master in Biomedical Sciences with a major in Genetics (UGent, 2014).
I immediately became a full-time doctoral fellow (from 2014 until 2019, FWO fellowship) at the lab of Frank Speleman.
In 2017 I did a 6 months internship at the lab of David Langenau, Harvard medical school, Boston.
- Cell of origin dictates aggression and stem cell number in acute lymphoblastic leukemia. Leukemia, 2018 (PMID: 29749398)