Jan R. Dörr

ORCID: 0000-0002-4927-6548
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About
Contact & Profiles
Research Areas
  • CRISPR and Genetic Engineering
  • Genetics, Bioinformatics, and Biomedical Research
  • Epigenetics and DNA Methylation
  • CAR-T cell therapy research
  • Science, Research, and Medicine
  • Immune Cell Function and Interaction
  • Immunotherapy and Immune Responses
  • DNA Repair Mechanisms
  • Retinoids in leukemia and cellular processes
  • interferon and immune responses
  • RNA Interference and Gene Delivery
  • NF-κB Signaling Pathways
  • Cancer Genomics and Diagnostics
  • Histone Deacetylase Inhibitors Research
  • Immune cells in cancer
  • Computational Drug Discovery Methods
  • Single-cell and spatial transcriptomics
  • Acute Myeloid Leukemia Research
  • Cell death mechanisms and regulation
  • Telomeres, Telomerase, and Senescence
  • Cancer-related Molecular Pathways
  • Bioinformatics and Genomic Networks
  • Multiple Sclerosis Research Studies
  • Cytomegalovirus and herpesvirus research
  • Lymphoma Diagnosis and Treatment

Charité - Universitätsmedizin Berlin
2014-2025

Humboldt-Universität zu Berlin
2008-2025

Freie Universität Berlin
2025

Max Delbrück Center
2023-2025

German Cancer Research Center
2022-2024

Heidelberg University
2024

Berlin Institute of Health at Charité - Universitätsmedizin Berlin
2021-2024

Orthopädische Universitätsklinik
2022

Manpower Demonstration Research Corporation
2022

Ludwig-Maximilians-Universität München
2021

Statins, known as inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, exhibit numerous functions related to inflammation, such MHC class II down-regulation, interference with T cell adhesion, and induction apoptosis. Here we demonstrate that both subcutaneous oral administration atorvastatin inhibit the development actively induced chronic experimental autoimmune encephalomyelitis in SJL/J mice significantly reduce inflammatory infiltration into central nervous system...

10.1084/jem.20021425 article EN The Journal of Experimental Medicine 2003-03-10

Sleep disorders can cause tiredness. The relationship between sleep and fatigue in patients with multiple sclerosis (MS) has not yet been investigated systematically.To investigate the MS.Some 66 MS 20 to years old were studied by overnight polysomnography. Using a cut-off point of 45 Modified Fatigue Impact Scale (MFIS), entire cohort was stratified into fatigued subgroup (n=26) non-fatigued (n=40).Of patients, 96% (n=25) suffering from relevant disorder, along 60% (n=24) (p=0.001)....

10.1177/1352458510393772 article EN Multiple Sclerosis Journal 2011-01-28

BackgroundRecent data from animal models of multiple sclerosis (MS) and a pilot study indicated possible beneficial impact statins on MS.Methodology/Principal FindingsSafety, tolerability effects disease activity atorvastatin given alone or in combination with interferon-beta (IFN-β) were assessed phase II open-label baseline-to-treatment trial relapsing-remitting MS (RRMS). Patients at least one gadolinium-enhancing lesion (CEL) screening by magnetic resonance imaging (MRI) eligible for the...

10.1371/journal.pone.0001928 article EN cc-by PLoS ONE 2008-04-08

In malignancies, enhanced nuclear factor-κB (NF-κB) activity is largely viewed as an oncogenic property that also confers resistance to chemotherapy. Recently, NF-κB has been postulated participate in a senescence-associated and possibly senescence-reinforcing cytokine response, thereby suggesting tumor-restraining role for NF-κB. Using mouse lymphoma model analyzing transcriptome clinical data from patients, we show here therapy-induced senescence presents with depends on active signaling,...

10.1101/gad.17620611 article EN Genes & Development 2011-10-06

DNA amplifications in cancer do not only harbor oncogenes. We sought to determine whether passenger coamplifications could create collateral therapeutic vulnerabilities. Through an analysis of >3,000 genomes followed by the interrogation CRISPR-Cas9 loss-of-function screens across >700 cell lines, we determined that are accompanied distinct dependency profiles. In a proof-of-principle study, demonstrate coamplification bona fide gene DEAD-Box Helicase 1 (DDX1) creates increased on mTOR...

10.1158/2159-8290.cd-23-1189 article EN cc-by Cancer Discovery 2024-01-10

Apoptosis mediated by members of the tumor necrosis factor (TNF)-nerve growth superfamily plays a crucial role in interaction nervous and immune system.On one hand, it is involved defense mechanisms brain, privilege.On other induction glial-neuronal cell death neuroinflammatory diseases.Here, we show that contrast to known ligands, TNF-related apoptosis-inducing ligand (TRAIL) not constitutively expressed human whereas both apoptosis-mediating apoptosis-blocking TRAIL receptors are found on...

10.1523/jneurosci.22-04-j0001.2002 article EN Journal of Neuroscience 2002-02-15

Abstract Cellular senescence is a stress-inducible state switch relevant in aging, tumorigenesis and cancer therapy. Beyond lasting arrest, senescent cells are characterized by profound chromatin remodeling transcriptional reprogramming. We show here myeloid-skewed aberrant lineage plasticity its immunological ramifications therapy-induced (TIS) of primary human murine B-cell lymphoma. find myeloid transcription factor (TF) networks, specifically AP-1-, C/EBPβ- PU.1-governed programs,...

10.1038/s41467-025-57429-x article EN cc-by Nature Communications 2025-03-31

The CD20-targeting monoclonal antibody rituximab is an established component of immunochemotherapeutic regimens against B-cell lymphomas, where its coadministration with conventional anticancer agents has significantly improved long-term outcome. However, the cellular mechanisms by which exerts antilymphoma activity are only partially understood. We show here that induces typical features senescence, a growth arrest viable cells distinct biologic properties, in lymphoma cell lines as well...

10.1158/1535-7163.mct-15-0627 article EN Molecular Cancer Therapeutics 2016-02-16

Abstract Lesion-based targeting strategies underlie cancer precision medicine. However, biological principles – such as cellular senescence remain difficult to implement in molecularly informed treatment decisions. Functional analyses syngeneic mouse models and cross-species validation patient datasets might uncover clinically relevant genetics of response programs. Here, we show that chemotherapy-exposed primary Eµ- myc transgenic lymphomas with without defined genetic lesions recapitulate...

10.1038/s41467-020-17467-z article EN cc-by Nature Communications 2020-07-20

We measured the in vivo and vitro effects of interferon (IFN)beta glatiramer acetate (GA) on expression regulatory molecule, tumor necrosis factor related apoptosis inducing ligand (TRAIL), patients with multiple sclerosis (MS). confirmed prior observation that TRAIL is enhanced anti-CD3 activated T cells by addition IFNbeta. from IFNbeta-treated stimulated only, had higher levels than untreated patients, suggesting IFNbeta exposure has an effect association cell activation. In...

10.1191/1352458505ms1222oa article EN Multiple Sclerosis Journal 2005-10-29

ABSTRACT The chromosomal theory of inheritance has dominated human genetics, including cancer genetics. Genes on the same chromosome segregate together while genes different chromosomes assort independently, providing a fundamental tenet Mendelian inheritance. Extrachromosomal DNA (ecDNA) is frequent event in that drives oncogene amplification, dysregulated gene expression and intratumoral heterogeneity, through random segregation during cell division. Distinct ecDNA sequences, herein termed...

10.1101/2023.07.18.549597 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2023-07-19
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