Stien De Coninck

ORCID: 0000-0003-0777-8205
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About
Contact & Profiles
Research Areas
  • Epigenetics and DNA Methylation
  • Acute Myeloid Leukemia Research
  • CAR-T cell therapy research
  • Acute Lymphoblastic Leukemia research
  • Cancer-related gene regulation
  • RNA modifications and cancer
  • Chronic Myeloid Leukemia Treatments
  • Immune cells in cancer
  • Lymphoma Diagnosis and Treatment
  • Chronic Lymphocytic Leukemia Research
  • Peptidase Inhibition and Analysis
  • Immune Cell Function and Interaction
  • Biochemical and Molecular Research

Ghent University
2019-2024

Cancer Research Institute Ghent
2019-2024

Ghent University Hospital
2020-2024

Molecular Research Institute
2022

Cancer cells display DNA hypermethylation at specific CpG islands in comparison to their normal healthy counterparts, but the mechanism that drives this so-called island methylator phenotype (CIMP) remains poorly understood. Here, we show methylation human T-cell acute lymphoblastic leukemia (T-ALL) mainly occurs promoters of Polycomb Repressor Complex 2 (PRC2) target genes are not expressed or malignant T-cells and which a reciprocal association with H3K27me3 binding. In addition, revealed...

10.1158/2643-3230.bcd-20-0059 article EN Blood Cancer Discovery 2020-09-23

T-cell lymphoblastic lymphoma (T-LBL) is a rare and aggressive lymphatic cancer, often diagnosed at young age. Patients are treated with intensive chemotherapy, potentially followed by hematopoietic stem cell transplantation. Although prognosis of T-LBL has improved intensified treatment protocols, they associated side effects 10-20% patients still die from relapsed or refractory disease. Given this, the search toward less toxic anti-lymphoma therapies ongoing. Here, we targeted recently...

10.3390/cancers15030647 article EN Cancers 2023-01-20

T cell acute lymphoblastic leukemia (T-ALL) and lymphoma (T-LBL) are rare aggressive hematological malignancies. Current treatment consists of intensive chemotherapy, leading to 80% overall survival but associated with severe toxic side effects. Furthermore, 10-20% patients still die from relapsed or refractory disease providing a strong rationale for more specific, targeted therapeutic strategies less toxicities. Here, we report novel MYH9::PDGFRB fusion in T-LBL patient demonstrate that...

10.3324/haematol.2023.283981 article EN cc-by-nc Haematologica 2023-11-09

TET2-mediated DNA demethylation plays a pivotal role in regulating pre-leukemic clonal expansion acute myeloid leukemia (AML), where TET2 mutations are also linked to AML progression. However, its function other types of leukemias, including T-cell lymphoblastic (T-ALL), remains unclear. Here, we used two different T-ALL mouse models study the possible tumor suppressor Tet2 T-ALL. Overexpression resulted mild but significant increase latency immature CD2-Lmo2tg model, no effect on survival...

10.1182/bloodadvances.2023011970 article EN cc-by-nc-nd Blood Advances 2024-05-29

<div>Abstract<p>Cancer cells display DNA hypermethylation at specific CpG islands in comparison with their normal healthy counterparts, but the mechanism that drives this so-called island methylator phenotype (CIMP) remains poorly understood. Here, we show methylation human T-cell acute lymphoblastic leukemia (T-ALL) mainly occurs promoters of Polycomb Repressor Complex 2 (<i>PRC2</i>) target genes are not expressed or malignant T and a reciprocal association H3K27me3...

10.1158/2643-3230.c.6550039 preprint EN 2023-04-04

<div>Abstract<p>Cancer cells display DNA hypermethylation at specific CpG islands in comparison with their normal healthy counterparts, but the mechanism that drives this so-called island methylator phenotype (CIMP) remains poorly understood. Here, we show methylation human T-cell acute lymphoblastic leukemia (T-ALL) mainly occurs promoters of Polycomb Repressor Complex 2 (<i>PRC2</i>) target genes are not expressed or malignant T and a reciprocal association H3K27me3...

10.1158/2643-3230.c.6550039.v1 preprint EN 2023-04-04
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