A5036508870- Cytokine Signaling Pathways and Interactions
- Lymphoma Diagnosis and Treatment
- Acute Lymphoblastic Leukemia research
- T-cell and Retrovirus Studies
- Chronic Myeloid Leukemia Treatments
- Cancer-related gene regulation
- CAR-T cell therapy research
- Cancer Immunotherapy and Biomarkers
- Acute Myeloid Leukemia Research
- Single-cell and spatial transcriptomics
- Immune cells in cancer
- Myeloproliferative Neoplasms: Diagnosis and Treatment
- Immune Cell Function and Interaction
- CRISPR and Genetic Engineering
- RNA and protein synthesis mechanisms
- Reproductive System and Pregnancy
- Advanced biosensing and bioanalysis techniques
- Ubiquitin and proteasome pathways
- Lung Cancer Treatments and Mutations
- Histone Deacetylase Inhibitors Research
- Cancer Genomics and Diagnostics
- Epigenetics and DNA Methylation
- RNA modifications and cancer
- Eosinophilic Disorders and Syndromes
- Immunotherapy and Immune Responses
KU Leuven
2014-2024
VIB-KU Leuven Center for Cancer Biology
2017-2024
Universitair Ziekenhuis Leuven
2022
Wellcome Sanger Institute
2019
Cancer Genetics (United States)
2019
Wellcome/MRC Cambridge Stem Cell Institute
2019
VIB-KU Leuven Center for Microbiology
2014
Abstract Leukemia is caused by the accumulation of multiple genomic lesions in hematopoietic precursor cells. However, how these events cooperate during oncogenic transformation remains poorly understood. We studied cooperation between activated JAK3/STAT5 signaling and HOXA9 overexpression, two identified as significantly co-occurring T-cell acute lymphoblastic leukemia. Expression mutant JAK3 led to a rapid development leukemia originating from multipotent or lymphoid-committed...
A bstract The stromal compartment of the tumour microenvironment consists a heterogeneous set tissue-resident and tumour-infiltrating cells, which are profoundly moulded by cancer cells. An outstanding question is to what extent this heterogeneity similar between cancers affecting different organs. Here, we profile 233,591 single cells from patients with lung, colorectal, ovary breast (n=36) construct pan-cancer blueprint cell using single-cell RNA protein-based technologies. We identify 68...
Peripheral T-cell lymphoma (PTCL) is a heterogeneous group of non-Hodgkin lymphomas with poor prognosis. Up to 30% PTCL lack distinctive features and are classified as PTCL, not otherwise specified (PTCL-NOS). To further improve our understanding the genetic landscape biology PTCL-NOS, we perform RNA-sequencing 18 cases validate results in an independent cohort 37 cases. We identify FYN-TRAF3IP2, KHDRBS1-LCK SIN3A-FOXO1 new in-frame fusion transcripts, FYN-TRAF3IP2 recurrent detected 8 55...
Anaplastic lymphoma kinase (ALK)-positive anaplastic large cell is characterized by 2p23/ALK aberrations, including the classic t(2;5)(p23;q35)/NPM1-ALK rearrangement present in ~80% of cases and several variant t(2p23/ALK) occurring remaining cases. The ALK fusion partners play a key role constitutive activation chimeric protein its subcellular localization. Using various molecular technologies, we have fusions eight recently diagnosed with cytoplasmic-only expression. identified partner...
Peripheral T-cell lymphoma (PTCL) is a heterogeneous group of hematological cancers arising from the malignant transformation mature T cells. In cohort 28 PTCL cases, we identified recurrent overexpression MYCN, member MYC family oncogenic transcription factors. Approximately half all cases was characterized by expression signature. Inducible MYCN in lymphoid cells mouse model caused that recapitulated human with an Integration and data EZH2 as key downstream target MYCN. Remarkably, found...
Abstract The methyltransferase EZH2 functions as the enzymatic component of PRC2 complex, which deposits methyl groups on H3K27, leading to chromatin condensation and gene repression. Recent studies have shown that can also act a transcriptional modulator outside complex thus, independent its activity. In this study, we first aimed investigate effects inhibition versus protein degradation in hematological malignancies. We demonstrate is more effective blocking cellular proliferation compared...
Abstract Peripheral T cell lymphoma (PTCL) is a heterogeneous group of hematological cancers arising from the malignant transformation mature cells. In cohort 28 PTCL cases, we identified recurrent overexpression MYCN, member MYC family oncogenic transcription factors. Approximately half all cases was characterized by expression signature. Inducible MYCN in lymphoid cells mouse model caused that recapitulated human with Integration and data EZH2 as key downstream target MYCN. Remarkably,...
<p>Supplemental tables and figures</p>
<p>Supplemental tables and figures</p>
<div>Abstract<p>Leukemia is caused by the accumulation of multiple genomic lesions in hematopoietic precursor cells. However, how these events cooperate during oncogenic transformation remains poorly understood. We studied cooperation between activated JAK3/STAT5 signaling and HOXA9 overexpression, two identified as significantly co-occurring T-cell acute lymphoblastic leukemia. Expression mutant JAK3 led to a rapid development leukemia originating from multipotent or...
<div>Abstract<p>Leukemia is caused by the accumulation of multiple genomic lesions in hematopoietic precursor cells. However, how these events cooperate during oncogenic transformation remains poorly understood. We studied cooperation between activated JAK3/STAT5 signaling and HOXA9 overexpression, two identified as significantly co-occurring T-cell acute lymphoblastic leukemia. Expression mutant JAK3 led to a rapid development leukemia originating from multipotent or...
Background: The PRC2 complex, with core components EZH2, SUZ12 and EED, is responsible for writing the H3K27me3 histone mark that associated gene repression. Sequence data analysis of 419 T‐cell acute lymphoblastic leukemia (T‐ALL) cases demonstrated 14.3% harbored mutations in EZH2 (7.2%), (6.2%) and/or EED (3.8%). A significant positive association was found between loss‐of function JAK3 activating mutations. Aims: goals our study were to assess whether inactivation cooperates driving...