Stien De Coninck
- 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...
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...
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...
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...
<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...
<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...
<p>Supplementary Figure 1</p>
<p>Supplementary Figure 8</p>
<p>Supplementary Figure 10</p>
<p>Supplementary Figure 4</p>
<p>Supplementary Figure 15</p>
<p>Supplementary Figure 14</p>
<p>Supplementary Figure 16</p>
<p>Supplementary Figure 11</p>
<p>Supplementary Figure 6</p>
<p>Supplementary Figure 5</p>
<p>Supplementary Figure 12</p>
<p>Supplementary Figure 13</p>
<p>Supplementary Figure 9</p>
<p>Supplementary Figure 7</p>
<p>Supplementary Figure 2</p>
<p>Supplementary Figure 3</p>