Binje Vick
YOU?
Author Swipe
Human iPSC-derived bone marrow organoids for AML engraftment and immunotherapy testing Open
Acute myeloid leukemia (AML) is associated with complex treatment challenges and persistently poor outcomes. Leukemic stem cells are supported by the bone marrow niche microenvironment that may support disease progression and therapy resis…
View article: A platform of robust patient-derived leukemia models covering subgroups for which no cell lines exist
A platform of robust patient-derived leukemia models covering subgroups for which no cell lines exist Open
Preclinical cancer research requires robust model systems, especially for poor prognosis entities like acute myeloid leukemia (AML), a highly aggressive blood cancer. Here, primary tumor cells from 137 AML patients of all age groups were t…
View article: Figure 2 from Enhancer Hijacking Discovery in Acute Myeloid Leukemia by Pyjacker Identifies MNX1 Activation via Deletion 7q
Figure 2 from Enhancer Hijacking Discovery in Acute Myeloid Leukemia by Pyjacker Identifies MNX1 Activation via Deletion 7q Open
Activation of MECOM and its homolog PRDM16 by a GATA2 enhancer. A, Expression of MECOM in all samples in TPM, ranked by expression of MECOM, in which samples 15PB19457 and 15KM20146 with breakpoints near MECOM are highlighted in green. B, …
View article: Figure 3 from Enhancer Hijacking Discovery in Acute Myeloid Leukemia by Pyjacker Identifies MNX1 Activation via Deletion 7q
Figure 3 from Enhancer Hijacking Discovery in Acute Myeloid Leukemia by Pyjacker Identifies MNX1 Activation via Deletion 7q Open
Aberrant EPO expression might cooperate with EPOR amplification in AEL. A,EPO expression in all samples in TPM, with sample 15KM18875 with EPO overexpression highlighted in green. B, Proportion of samples with nonzero EPO expression in thr…
View article: Figure 4 from Enhancer Hijacking Discovery in Acute Myeloid Leukemia by Pyjacker Identifies MNX1 Activation via Deletion 7q
Figure 4 from Enhancer Hijacking Discovery in Acute Myeloid Leukemia by Pyjacker Identifies MNX1 Activation via Deletion 7q Open
The homeobox genes GSX2 and MNX1 can be activated by atypical mechanisms. A,GSX2 expression in all samples in TPM, with sample 16PB5693 with GSX2 expression highlighted in green. B,MNX1 expression in all samples in TPM, with sample 15PB870…
View article: Figure 7 from Enhancer Hijacking Discovery in Acute Myeloid Leukemia by Pyjacker Identifies MNX1 Activation via Deletion 7q
Figure 7 from Enhancer Hijacking Discovery in Acute Myeloid Leukemia by Pyjacker Identifies MNX1 Activation via Deletion 7q Open
Knockdown of MNX1 reduces tumor load of AML PDX cells in vivo. A, Scheme depicting the experimental setup of the in vivo constitutive experiment. AML-661 PDX cells expressing the cassettes for both CRE-ERT2 and the shRNA addressing MNX1 or…
View article: CAR-T cells targeting CCR9 and CD1a for the treatment of T cell acute lymphoblastic leukemia
CAR-T cells targeting CCR9 and CD1a for the treatment of T cell acute lymphoblastic leukemia Open
T cell acute lymphoblastic leukemia (T-ALL) is an aggressive malignancy characterized by high rates of induction failure and relapse, and effective targeted immunotherapies are lacking. Despite promising clinical progress with genome-edite…
View article: Supplementary Figures from Enhancer Hijacking Discovery in Acute Myeloid Leukemia by Pyjacker Identifies MNX1 Activation via Deletion 7q
Supplementary Figures from Enhancer Hijacking Discovery in Acute Myeloid Leukemia by Pyjacker Identifies MNX1 Activation via Deletion 7q Open
Supplementary Figure 1. Summary of the somatic alterations in the 39 ckAML samples. Supplementary Figure 2. Proportion of samples expressing the top pyjacker hits, for several AML cohorts profiled with RNA-seq. Supplementary Figure 3. Exam…
View article: Figure 1 from Enhancer Hijacking Discovery in Acute Myeloid Leukemia by Pyjacker Identifies MNX1 Activation via Deletion 7q
Figure 1 from Enhancer Hijacking Discovery in Acute Myeloid Leukemia by Pyjacker Identifies MNX1 Activation via Deletion 7q Open
Detection of enhancer hijacking in 39 ckAML samples. A, Schematic representation of the main sources of information used by Pyjacker: breakpoints, overexpression, monoallelic expression, and enhancers. B, Scatter plot of genes identified b…
View article: Data from Enhancer Hijacking Discovery in Acute Myeloid Leukemia by Pyjacker Identifies MNX1 Activation via Deletion 7q
Data from Enhancer Hijacking Discovery in Acute Myeloid Leukemia by Pyjacker Identifies MNX1 Activation via Deletion 7q Open
Acute myeloid leukemia (AML) with complex karyotype is characterized by high genomic complexity, including frequent TP53 mutations and chromothripsis. Genomic rearrangements can reposition active enhancers near proto-oncogenes, leading to …
View article: Figure 6 from Enhancer Hijacking Discovery in Acute Myeloid Leukemia by Pyjacker Identifies MNX1 Activation via Deletion 7q
Figure 6 from Enhancer Hijacking Discovery in Acute Myeloid Leukemia by Pyjacker Identifies MNX1 Activation via Deletion 7q Open
Putative enhancers in the CDK6 region interact with MNX1 in del(7q) AML. A, Chromatin interaction detected with 4C in the region around CDK6 using MNX1 as viewpoint, for three different del(7)(q22q36) samples and one control sample (GDM-1 …
View article: Supplementary Tables from Enhancer Hijacking Discovery in Acute Myeloid Leukemia by Pyjacker Identifies MNX1 Activation via Deletion 7q
Supplementary Tables from Enhancer Hijacking Discovery in Acute Myeloid Leukemia by Pyjacker Identifies MNX1 Activation via Deletion 7q Open
ST1 Methods for enhancer hijacking detection ST2 Ranked and scored hematopoietic enhancers (based on ChIP-seq data for H3K27ac and P300 from K562, MOLM1 and Kasumi1) ST3 Pyjacker results for the 10 AML cell lines ST4 Pyjacker results for t…
View article: Figure 5 from Enhancer Hijacking Discovery in Acute Myeloid Leukemia by Pyjacker Identifies MNX1 Activation via Deletion 7q
Figure 5 from Enhancer Hijacking Discovery in Acute Myeloid Leukemia by Pyjacker Identifies MNX1 Activation via Deletion 7q Open
MNX1 is expressed in 1.4% of all AML cases, often with del(7)(q22q36). A, qRT-PCR screen for MNX1 expression in three AML cohorts (Rotterdam, Ulm, and Jena). B, Fifteen MNX1-expressing samples with del(7)(q22q36) profiled with WGS, with a …
View article: Posttranscriptional depletion of ribosome biogenesis factors engenders therapeutic vulnerabilities in <i>NPM1</i>-mutant AML
Posttranscriptional depletion of ribosome biogenesis factors engenders therapeutic vulnerabilities in <i>NPM1</i>-mutant AML Open
NPM1 is a multifunctional phosphoprotein with key roles in ribosome biogenesis among its many functions. NPM1 gene mutations drive 30% of acute myeloid leukemia (AML) cases. The mutations disrupt a nucleolar localization signal and create …
Perturbing LSD1 and WNT rewires transcription to synergistically induce AML differentiation Open
Impaired differentiation is a hallmark of myeloid malignancies 1,2 . Therapies that enable cells to circumvent the differentiation block, such as all- trans retinoic acid (ATRA) and arsenic trioxide (ATO), are by and large curative in acut…
View article: Enhancer Hijacking Discovery in Acute Myeloid Leukemia by Pyjacker Identifies MNX1 Activation via Deletion 7q
Enhancer Hijacking Discovery in Acute Myeloid Leukemia by Pyjacker Identifies MNX1 Activation via Deletion 7q Open
Acute myeloid leukemia (AML) with complex karyotype is characterized by high genomic complexity, including frequent TP53 mutations and chromothripsis. Genomic rearrangements can reposition active enhancers near proto-oncogenes, leading to …
Effective eradication of acute myeloid leukemia stem cells with FLT3-directed antibody-drug conjugates Open
Refractory disease and relapse are major challenges in acute myeloid leukemia (AML) therapy attributed to survival of leukemic stem cells (LSC). To target LSCs, antibody-drug conjugates (ADCs) provide an elegant solution, combining the spe…
View article: Potent Activity of Duocarmyin- and Mmaf-Conjugated FLT3-Directed Antibody-Drug Conjugates Towards Acute Myeloid Leukemia Stem Cells <i>in Vitro</i> and <i>In Vivo</i>
Potent Activity of Duocarmyin- and Mmaf-Conjugated FLT3-Directed Antibody-Drug Conjugates Towards Acute Myeloid Leukemia Stem Cells <i>in Vitro</i> and <i>In Vivo</i> Open
Acute myeloid leukemia (AML) therapy failure due to relapse or refractory disease is likely attributed to the persistence of resting leukemic stem cells (LSCs) in the patient's bone marrow. As those cells do not divide, they have a decreas…
View article: Serially Transplantable, Genetically Modified Patient Derived Xenograft Models of Acute Myeloid Leukemia Represent Primary Patients' Cells and Enable Reliable and Reproducible Preclinical Therapy Trials
Serially Transplantable, Genetically Modified Patient Derived Xenograft Models of Acute Myeloid Leukemia Represent Primary Patients' Cells and Enable Reliable and Reproducible Preclinical Therapy Trials Open
Background: Acute myeloid leukemia (AML) is a heterogenous malignancy and efficient treatment strategies for high-risk patients are still lacking. To facilitate preclinical and translational leukemia research, e.g. to test novel therapeuti…
View article: Pyjacker identifies enhancer hijacking events in acute myeloid leukemia including<i>MNX1</i>activation via deletion 7q
Pyjacker identifies enhancer hijacking events in acute myeloid leukemia including<i>MNX1</i>activation via deletion 7q Open
Acute myeloid leukemia with complex karyotype (ckAML) is characterized by high genomic complexity, including frequent TP53 mutations and chromothripsis. We hypothesized that the numerous genomic rearrangements could reposition active enhan…
View article: CAR-T cells targeting CCR9 and CD1a for the treatment of T cell acute lymphoblastic leukemia
CAR-T cells targeting CCR9 and CD1a for the treatment of T cell acute lymphoblastic leukemia Open
T cell acute lymphoblastic leukemia (T-ALL) is an aggressive malignancy characterized by high rates of induction failure and relapse, and effective targeted immunotherapies are lacking. Despite promising clinical progress with genome-edite…
View article: Correction: Translatome proteomics identifies autophagy as a resistance mechanism to on-target FLT3 inhibitors in acute myeloid leukemia
Correction: Translatome proteomics identifies autophagy as a resistance mechanism to on-target FLT3 inhibitors in acute myeloid leukemia Open
Due to a technical problem, Figures 2, 3 and 6 were not displayed correctly in the original article. The original article has been corrected.
Targeting FLT3 with a new-generation antibody-drug conjugate in combination with kinase inhibitors for treatment of AML Open
Fms-like tyrosine kinase 3 (FLT3) is often overexpressed or constitutively activated by internal tandem duplication (ITD) and tyrosine kinase domain (TKD) mutations in acute myeloid leukemia (AML). Despite the use of receptor tyrosine kina…
T-cell exhaustion induced by continuous bispecific molecule exposure is ameliorated by treatment-free intervals Open
T-cell–recruiting bispecific molecule therapy has yielded promising results in patients with hematologic malignancies; however, resistance and subsequent relapse remains a major challenge. T-cell exhaustion induced by persistent antigen st…
View article: Venetoclax synergizes with gilteritinib in FLT3 wild-type high-risk acute myeloid leukemia by suppressing MCL-1
Venetoclax synergizes with gilteritinib in FLT3 wild-type high-risk acute myeloid leukemia by suppressing MCL-1 Open
BCL-2 inhibition has been shown to be effective in acute myeloid leukemia (AML) in combination with hypomethylating agents or low-dose cytarabine. However, resistance and relapse represent major clinical challenges. Therefore, there is an …
View article: P454: VENETOCLAX AND GILTERITINIB SYNERGIZE IN FLT3 WILDTYPE ACUTE MYELOID LEUKEMIA BY SUPPRESSION OF MCL-1 VIA COMBINED AXL AND FLT3 TARGETING
P454: VENETOCLAX AND GILTERITINIB SYNERGIZE IN FLT3 WILDTYPE ACUTE MYELOID LEUKEMIA BY SUPPRESSION OF MCL-1 VIA COMBINED AXL AND FLT3 TARGETING Open
Background: BCL-2 inhibition has been shown to be effective in older patients with acute myeloid leukemia (AML) in combination with hypomethylating agents or low-dose cytarabine. However, treatment resistance and relapse represent major cl…
A Novel Anti-CD73 Antibody That Selectively Inhibits Membrane CD73 Shows Antitumor Activity and Induces Tumor Immune Escape Open
CD73 catalyzes the conversion of ATP to adenosine, which is involved in various physiological and pathological processes, including tumor immune escape. Because CD73 expression and activity are particularly high on cancer cells and contrib…