A5048000779- Glioma Diagnosis and Treatment
- Cancer, Hypoxia, and Metabolism
- Computational Drug Discovery Methods
- Cell Image Analysis Techniques
- Metabolomics and Mass Spectrometry Studies
- Acute Lymphoblastic Leukemia research
- Cancer Genomics and Diagnostics
- Drug Transport and Resistance Mechanisms
- Bioinformatics and Genomic Networks
- Mathematical Biology Tumor Growth
- Chronic Myeloid Leukemia Treatments
- Pharmacogenetics and Drug Metabolism
- Cancer, Lipids, and Metabolism
- Cancer Cells and Metastasis
- Ferroptosis and cancer prognosis
- Chemical Reactions and Isotopes
- CAR-T cell therapy research
- Immunodeficiency and Autoimmune Disorders
- Beetle Biology and Toxicology Studies
- 3D Printing in Biomedical Research
- thermodynamics and calorimetric analyses
- Microtubule and mitosis dynamics
- Nanoparticle-Based Drug Delivery
- Immune Cell Function and Interaction
- Caveolin-1 and cellular processes
Life & Brain (Germany)
2013-2023
University of Bonn
2009-2023
University Hospital Bonn
2022-2023
University of Southern California
2007-2015
University of Florida
2013
Hertie Foundation
2013
National Institute on Aging
2012
Cancer Research Institute
2012
The University of Texas Health Science Center at San Antonio
2012
National Institute of Dental and Craniofacial Research
2012
The tyrosine kinase c-Met promotes the formation and malignant progression of multiple cancers. It is well known that hyperactivation increases tumorigenicity tumor cell resistance to DNA damaging agents, properties associated with tumor-initiating stem cells. However, a link between signaling and/or maintenance neoplastic cells has not been previously identified. Here, we show activated functional in glioblastoma (GBM) neurospheres enriched for expression/function correlates marker...
Abstract Purpose: Glioblastoma is a highly malignant, invariably fatal brain tumor for which effective pharmacotherapy remains an unmet medical need. Experimental Design: Screening of compound library 160 synthetic and natural toxic substances identified the antihelmintic niclosamide as previously unrecognized candidate clinical development. Considering cellular interindividual heterogeneity glioblastoma, portfolio short-term expanded primary human glioblastoma cells (pGBM; n = 21), common...
Residual tumor cells remain beyond the margins of every glioblastoma (GBM) resection. Their resistance to postsurgical therapy is considered a major driving force mortality, but their biology remains largely uncharacterized. In this study, residual were derived via experimental biopsy resection margin after standard neurosurgery for direct comparison with samples from routinely resected tissue. vitro analysis proliferation, invasion, stem cell qualities, GBM-typical antigens, genotypes, and...
B cell lineage acute lymphoblastic leukemia (ALL) arises in virtually all cases from precursors that are arrested at pre–B receptor–dependent stages. The Philadelphia chromosome–positive (Ph+) subtype of ALL accounts for 25–30% adult ALL, has the most unfavorable clinical outcome among subtypes and is defined by oncogenic BCR-ABL1 kinase deletions IKAROS gene >80% cases. Here, we demonstrate receptor functions as a tumor suppressor upstream through induction cycle arrest Ph+ cells....
Investigation of clonal heterogeneity may be key to understanding mechanisms therapeutic failure in human cancer. However, little is known on the consequences intervention composition solid tumors.Here, we used 33 single cell-derived subclones generated from five clinical glioblastoma specimens for exploring intra- and interindividual spectra drug resistance profiles vitro In a personalized setting, explored whether differences pharmacologic sensitivity among could employed predict...
Cellular heterogeneity, for example, the intratumoral coexistence of cancer cells with and without stem cell characteristics, represents a potential root therapeutic resistance significant challenge modern drug development in glioblastoma (GBM). We propose here that activation innate immune system by stimulation receptors involved antiviral antitumor responses can similarly target different malignant populations glioma cells. used short-term expanded patient-specific primary human GBM to...
Musashi1 (Msi1) is an evolutionarily conserved RNA-binding protein (RBP) that has profound implications in cellular processes such as stem cell maintenance, nervous system development, and tumorigenesis. Msi1 highly expressed many cancers, including glioblastoma, whereas normal tissues, its expression restricted to cells. Unfortunately, the factors modulate trigger high levels tumors are largely unknown. The mRNA a long 3' untranslated region (UTR) containing several AU- U-rich sequences....
Abstract Background Ph-positive leukemias are caused by the aberrant fusion of BCR and ABL genes. Nilotinib is a selective Bcr/Abl tyrosine kinase inhibitor related to imatinib, which widely used treat chronic myelogenous leukemia. Because acute lymphoblastic leukemia only responds transiently imatinib therapy, we have mouse models test efficacy nilotinib against P190 form Bcr/Abl. Results After transplant 10,000 highly malignant leukemic cells into compatible recipients, untreated mice...
Abstract Purpose: Therapy resistance and fatal disease progression in glioblastoma are thought to result from the dynamics of intra-tumor heterogeneity. This study aimed at identifying molecularly targeting tumor cells that can survive, adapt, subclonally expand under primary therapy. Experimental Design: To identify candidate markers experimentally access subclonal glioblastoma, we established a discovery cohort paired vital cell samples obtained before after We further used two independent...
<p>Full-length blots presented in this study.</p>
<p>Niclosamide dose-response curves.</p>
<p>Patient data.</p>
<p>Supplementary legend</p>
<p>Niclosamide dose-response curves, supplementing data presented in Figure 2B.</p>
<p>Cell cycle analysis of pGBM #046 after niclosamide exposure.</p>
<p>List of pGBMs and their respective passage numbers used for the various experimental paradigms in this study.</p>
<p>Killer plate® compounds and screening data.</p>
<p>Legends for Supplementary Figs. S1-S8 and Tables</p>
<p>Maintenance of patient- and disease-specific genetic alterations ex vivo.</p>
<p>Control arms for Fig. 6 experiments AND Potential future approaches.</p>
<p>Confirmatory subclone selection experiments applying clinical sample BN046.</p>