A5081489511- Acute Myeloid Leukemia Research
- Phagocytosis and Immune Regulation
- Autophagy in Disease and Therapy
- Immune Cell Function and Interaction
- COVID-19 Clinical Research Studies
- Acute Lymphoblastic Leukemia research
- CAR-T cell therapy research
- Histone Deacetylase Inhibitors Research
- Hematopoietic Stem Cell Transplantation
- Myeloproliferative Neoplasms: Diagnosis and Treatment
- Signaling Pathways in Disease
- Cancer Genomics and Diagnostics
- Mesenchymal stem cell research
- Immune cells in cancer
- Chronic Myeloid Leukemia Treatments
- T-cell and Retrovirus Studies
- Peptidase Inhibition and Analysis
- Chronic Lymphocytic Leukemia Research
- Bone and Joint Diseases
- CRISPR and Genetic Engineering
- PI3K/AKT/mTOR signaling in cancer
- Multiple Myeloma Research and Treatments
- Pluripotent Stem Cells Research
- Biochemical and Molecular Research
- Bone and Dental Protein Studies
Georg Speyer Haus
2014-2024
German Cancer Research Center
2012-2024
Heidelberg University
2012-2024
Johannes Gutenberg University Mainz
2024
Frankfurt Cancer Institute
2020-2023
Goethe University Frankfurt
2020-2023
Deutschen Konsortium für Translationale Krebsforschung
2014-2023
Institut Curie
2006-2021
Université Paris-Saclay
2020-2021
Centre National de la Recherche Scientifique
2006-2021
T cell acute lymphoblastic leukemia (T-ALL) is an aggressive cancer of immature cells that often shows aberrant activation Notch1 and PI3K–Akt pathways. Although mutations activate signaling have previously been identified, the relative contribution growth factor-dependent unclear. We show here pharmacologic inhibition or genetic deletion insulin-like factor 1 receptor (IGF1R) blocks viability T-ALL cells, whereas moderate diminution IGF1R compromises leukemia-initiating (LIC) activity as...
Recently, a transcriptome-based consensus molecular subtype (CMS) classification of colorectal cancer (CRC) has been established, which may ultimately help to individualize CRC therapy. However, the lack animal models that faithfully recapitulate different subtypes impedes adequate preclinical testing stratified therapeutic concepts. Here, we demonstrate constitutive AKT activation in intestinal epithelial cells markedly enhances tumor invasion and metastasis Trp53ΔIEC mice...
Acute leukemias are systemic malignancies associated with a dire outcome. Because of low immunogenicity, display remarkable ability to evade immune control and often resistant checkpoint blockade. Here, we discover that leukemia cells actively establish suppressive environment prevent attacks by co-opting signaling axis skews macrophages toward tumor-promoting tissue repair phenotype, namely the GAS6/AXL axis. Using aggressive models, demonstrate ablation AXL receptor specifically in...
An altered lipidome in tumors may affect not only tumor cells themselves but also their microenvironment. In this study, a lipidomics screen reveals increased amounts of phosphatidylserine (PS), particularly ether-PS (ePS), murine mammary compared with normal tissue. PS was produced by synthase 1 (PTDSS1), and depletion Ptdss1 from mice reduced ePS levels accompanied stunted growth decreased tumor-associated macrophage (TAM) abundance. Ptdss1-deficient exposed less during apoptosis, which...
A network of lineage-specific transcription factors and microRNAs tightly regulates differentiation hematopoietic stem cells along the distinct lineages. Deregulation this regulatory contributes to impaired lineage fidelity leukemogenesis. We found that master regulator RUNX1 controls expression certain microRNAs, importance during erythroid/megakaryocytic differentiation. In particular, we show erythorid miR144/451 cluster is epigenetically repressed by megakaryopoiesis. Furthermore,...
Epigenetic changes can contribute to development of acute myeloid leukemia (AML), a malignant disease the bone marrow. A single-nucleotide polymorphism transcription factor growth independence 1 (GFI1) generates protein with an asparagine at position 36 (GFI1(36N)) instead serine (GFI1(36S)), which is associated de novo AML in humans. However, how GFI1(36N) predisposes poorly understood. To explore mechanism, we used knock-in mouse strains expressing or GFI1(36S). Presence shortened latency...