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View article: Xq24/ <i>IL13RA1</i> aberrations as key drivers of female bias in primary mediastinal large B‐cell lymphoma
Xq24/ <i>IL13RA1</i> aberrations as key drivers of female bias in primary mediastinal large B‐cell lymphoma Open
Female‐biased incidence in primary mediastinal large B‐cell lymphoma (PMBCL) is enigmatic and points to a potential contribution of the X chromosome in this disease. To elucidate the postulated involvement of X‐linked factor(s), we profile…
View article: Long-read single-cell genome, transcriptome and open chromatin profiling links genotype to phenotypes. v1
Long-read single-cell genome, transcriptome and open chromatin profiling links genotype to phenotypes. v1 Open
The 10X Multiome ATAC + Gene Expression assay permits capture of both RNA expression and epigenomic profiles from the same nuclei for a deeper understanding of cell type or state gene regulation. Here we present a modified version of the p…
View article: Single‐cell DNA and surface protein characterization of high hyperdiploid acute lymphoblastic leukemia at diagnosis and during treatment
Single‐cell DNA and surface protein characterization of high hyperdiploid acute lymphoblastic leukemia at diagnosis and during treatment Open
High hyperdiploid (HeH) B‐cell acute lymphoblastic leukemia (B‐ALL) is the most prevalent subtype of childhood ALL. This leukemia is characterized by trisomies and tetrasomies of specific chromosomes and additional point mutations. Here, w…
View article: TLE4 is a repressor of the oncogenic activity of TLX3 in T-cell acute lymphoblastic leukemia
TLE4 is a repressor of the oncogenic activity of TLX3 in T-cell acute lymphoblastic leukemia Open
View article: Selective targeting of malignant T cells
Selective targeting of malignant T cells Open
View article: Single-cell CRISPR screening characterizes transcriptional deregulation in T-cell acute lymphoblastic leukemia
Single-cell CRISPR screening characterizes transcriptional deregulation in T-cell acute lymphoblastic leukemia Open
T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive type of leukemia caused by accumulation of multiple genetic alterations in T-cell progenitors. However, for many genes it remains unknown how their mutations contribute to diseas…
View article: Dual targeting of EZH2 and Histone Deacetylases in hematological malignancies promotes transcriptional and metabolic deregulation leading to ferroptosis
Dual targeting of EZH2 and Histone Deacetylases in hematological malignancies promotes transcriptional and metabolic deregulation leading to ferroptosis Open
The methyltransferase EZH2 functions as the enzymatic component of the PRC2 complex, which deposits methyl groups on H3K27, leading to chromatin condensation and gene repression. Recent studies have shown that EZH2 can also act as a transc…
View article: Resistance to PSEN1-selective γ-secretase inhibitors in T-cell acute lymphoblastic leukemia
Resistance to PSEN1-selective γ-secretase inhibitors in T-cell acute lymphoblastic leukemia Open
PSEN1-selective gamma-secretase inhibitors (GSI), such as MRK-560, are a potential option for the treatment of T-cell acute lymphoblastic leukemia (T-ALL) with NOTCH1 activating mutations, as these show less toxicity compared to broad-spec…
View article: The unexpected and unresolved roles of <i>PDGFRA</i> and <i>PDGFRB</i> in T-cell acute lymphoblastic leukemia
The unexpected and unresolved roles of <i>PDGFRA</i> and <i>PDGFRB</i> in T-cell acute lymphoblastic leukemia Open
Not available.
View article: Single cell RNA sequencing reveals endothelial cell killing and resolution pathways in experimental malaria-associated acute respiratory distress syndrome
Single cell RNA sequencing reveals endothelial cell killing and resolution pathways in experimental malaria-associated acute respiratory distress syndrome Open
Plasmodium parasites cause malaria, a global health disease that is responsible for more than 200 million clinical cases and 600 000 deaths each year. Most deaths are caused by various complications, including malaria-associated acute resp…
View article: Single-cell CRISPR screening characterizes transcriptional deregulation in T-cell acute lymphoblastic leukemia
Single-cell CRISPR screening characterizes transcriptional deregulation in T-cell acute lymphoblastic leukemia Open
T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive type of leukemia caused by accumulation of multiple genetic alterations in T-cell progenitors. However, for many genes it remains unknown how their mutation contributes to diseas…
View article: CRISPR screening in hematology research: from bulk to single-cell level
CRISPR screening in hematology research: from bulk to single-cell level Open
The CRISPR genome editing technology has revolutionized the way gene function is studied. Genome editing can be achieved in single genes or for thousands of genes simultaneously in sensitive genetic screens. While conventional genetic scre…
View article: Data from HOXA9 Cooperates with Activated JAK/STAT Signaling to Drive Leukemia Development
Data from HOXA9 Cooperates with Activated JAK/STAT Signaling to Drive Leukemia Development Open
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 the cooperation between activate…
View article: Supplemental tables and figures from HOXA9 Cooperates with Activated JAK/STAT Signaling to Drive Leukemia Development
Supplemental tables and figures from HOXA9 Cooperates with Activated JAK/STAT Signaling to Drive Leukemia Development Open
Supplemental tables and figures
View article: supplementary table S2 from HOXA9 Cooperates with Activated JAK/STAT Signaling to Drive Leukemia Development
supplementary table S2 from HOXA9 Cooperates with Activated JAK/STAT Signaling to Drive Leukemia Development Open
supplementary table (excel)
View article: supplementary table S2 from HOXA9 Cooperates with Activated JAK/STAT Signaling to Drive Leukemia Development
supplementary table S2 from HOXA9 Cooperates with Activated JAK/STAT Signaling to Drive Leukemia Development Open
supplementary table (excel)
View article: supplementary table S3 from HOXA9 Cooperates with Activated JAK/STAT Signaling to Drive Leukemia Development
supplementary table S3 from HOXA9 Cooperates with Activated JAK/STAT Signaling to Drive Leukemia Development Open
supplementary table (excel)
View article: supplementary table S3 from HOXA9 Cooperates with Activated JAK/STAT Signaling to Drive Leukemia Development
supplementary table S3 from HOXA9 Cooperates with Activated JAK/STAT Signaling to Drive Leukemia Development Open
supplementary table (excel)
View article: Supplemental tables and figures from HOXA9 Cooperates with Activated JAK/STAT Signaling to Drive Leukemia Development
Supplemental tables and figures from HOXA9 Cooperates with Activated JAK/STAT Signaling to Drive Leukemia Development Open
Supplemental tables and figures
View article: Data from HOXA9 Cooperates with Activated JAK/STAT Signaling to Drive Leukemia Development
Data from HOXA9 Cooperates with Activated JAK/STAT Signaling to Drive Leukemia Development Open
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 the cooperation between activate…
View article: Supplemental Data 10 from Upregulation of MAPK Negative Feedback Regulators and RET in Mutant ALK Neuroblastoma: Implications for Targeted Treatment
Supplemental Data 10 from Upregulation of MAPK Negative Feedback Regulators and RET in Mutant ALK Neuroblastoma: Implications for Targeted Treatment Open
Supplemental data 10: Results of gene ontology analysis performed on the 77 ALK signature genes
View article: Supplementary Fig. S5 from Potentiation of antileukemic therapies by Smac mimetic, LBW242: effects on mutant FLT3-expressing cells
Supplementary Fig. S5 from Potentiation of antileukemic therapies by Smac mimetic, LBW242: effects on mutant FLT3-expressing cells Open
Supplementary Fig. S5 from Potentiation of antileukemic therapies by Smac mimetic, LBW242: effects on mutant FLT3-expressing cells
View article: Movie S1 from The Second-Generation Exportin-1 Inhibitor KPT-8602 Demonstrates Potent Activity against Acute Lymphoblastic Leukemia
Movie S1 from The Second-Generation Exportin-1 Inhibitor KPT-8602 Demonstrates Potent Activity against Acute Lymphoblastic Leukemia Open
Movie S1
View article: Supplementary Figure Legends from Potentiation of antileukemic therapies by Smac mimetic, LBW242: effects on mutant FLT3-expressing cells
Supplementary Figure Legends from Potentiation of antileukemic therapies by Smac mimetic, LBW242: effects on mutant FLT3-expressing cells Open
Supplementary Figure Legends from Potentiation of antileukemic therapies by Smac mimetic, LBW242: effects on mutant FLT3-expressing cells
View article: Supplementary Table 2 from Meta-analysis of Neuroblastomas Reveals a Skewed <i>ALK</i> Mutation Spectrum in Tumors with <i>MYCN</i> Amplification
Supplementary Table 2 from Meta-analysis of Neuroblastomas Reveals a Skewed <i>ALK</i> Mutation Spectrum in Tumors with <i>MYCN</i> Amplification Open
PDF file - 42K
View article: Data from Potentiation of antileukemic therapies by Smac mimetic, LBW242: effects on mutant FLT3-expressing cells
Data from Potentiation of antileukemic therapies by Smac mimetic, LBW242: effects on mutant FLT3-expressing cells Open
Members of the inhibitor of apoptosis protein (IAP) family play a role in mediating apoptosis. Studies suggest that these proteins may be a viable target in leukemia because they have been found to be variably expressed in acute leukemias …
View article: Supplemental Data 5 from Upregulation of MAPK Negative Feedback Regulators and RET in Mutant ALK Neuroblastoma: Implications for Targeted Treatment
Supplemental Data 5 from Upregulation of MAPK Negative Feedback Regulators and RET in Mutant ALK Neuroblastoma: Implications for Targeted Treatment Open
Supplemental data 5: Differential expression analysis upon ALK inhibition
View article: Supplementary Table 2 from Meta-analysis of Neuroblastomas Reveals a Skewed <i>ALK</i> Mutation Spectrum in Tumors with <i>MYCN</i> Amplification
Supplementary Table 2 from Meta-analysis of Neuroblastomas Reveals a Skewed <i>ALK</i> Mutation Spectrum in Tumors with <i>MYCN</i> Amplification Open
PDF file - 42K
View article: Supplementary Fig. S2 from Potentiation of antileukemic therapies by Smac mimetic, LBW242: effects on mutant FLT3-expressing cells
Supplementary Fig. S2 from Potentiation of antileukemic therapies by Smac mimetic, LBW242: effects on mutant FLT3-expressing cells Open
Supplementary Fig. S2 from Potentiation of antileukemic therapies by Smac mimetic, LBW242: effects on mutant FLT3-expressing cells
View article: Movie S2 from The Second-Generation Exportin-1 Inhibitor KPT-8602 Demonstrates Potent Activity against Acute Lymphoblastic Leukemia
Movie S2 from The Second-Generation Exportin-1 Inhibitor KPT-8602 Demonstrates Potent Activity against Acute Lymphoblastic Leukemia Open
Movie S2