Ulrike Harjes

ORCID: 0000-0003-0376-1262
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About
Contact & Profiles
Research Areas
  • Cancer, Hypoxia, and Metabolism
  • Cancer Genomics and Diagnostics
  • Cancer Immunotherapy and Biomarkers
  • Epigenetics and DNA Methylation
  • CAR-T cell therapy research
  • Cancer, Lipids, and Metabolism
  • BRCA gene mutations in cancer
  • Immune Cell Function and Interaction
  • RNA modifications and cancer
  • Peroxisome Proliferator-Activated Receptors
  • Immunotherapy and Immune Responses
  • Cancer Cells and Metastasis
  • Cancer, Stress, Anesthesia, and Immune Response
  • Immune cells in cancer
  • Cancer Research and Treatments
  • Metabolism, Diabetes, and Cancer
  • Genomic variations and chromosomal abnormalities
  • Hippo pathway signaling and YAP/TAZ
  • Pancreatic function and diabetes
  • RNA Research and Splicing
  • Liver Disease Diagnosis and Treatment
  • Cancer-related molecular mechanisms research
  • Endoplasmic Reticulum Stress and Disease
  • Angiogenesis and VEGF in Cancer
  • Mitochondrial Function and Pathology

KU Leuven
2015-2024

MRC Weatherall Institute of Molecular Medicine
2014-2020

University of Oxford
2014-2020

Cancer Research UK
2020

John Radcliffe Hospital
2012-2019

VIB-KU Leuven Center for Cancer Biology
2015-2018

Vlaams Instituut voor Biotechnologie
2016

Oxford Research Group
2016

Amsterdam UMC Location Vrije Universiteit Amsterdam
2010-2011

Cancer Center Amsterdam
2011

Fatty acid-binding protein 4 (FABP4) is an adipogenic and implicated in atherosclerosis, insulin resistance, cancer. In endothelial cells, FABP4 induced by VEGFA, inhibition of blocks most the VEGFA effects. We investigated DLL4-NOTCH-dependent regulation human umbilical vein cells gene/protein expression interaction analyses following inhibitor treatment RNA interference. found that directly NOTCH. Stimulation NOTCH signaling with recombinant DLL4 led to induction, independently VEGFA....

10.1074/jbc.m114.576512 article EN cc-by Journal of Biological Chemistry 2014-06-18

Fatty acid binding protein 4 (FABP4) is a fatty chaperone, which induced during adipocyte differentiation. Previously we have shown that FABP4 in endothelial cells by the NOTCH1 signalling pathway, latter of involved mechanisms resistance to antiangiogenic tumour therapy. Here, investigated role metabolism and angiogenesis. We analysed effect transient knockdown human umbilical vein on metabolism, viability Through therapeutic delivery siRNA targeting mouse FABP4, growth blood vessel...

10.1038/onc.2016.256 article EN cc-by Oncogene 2016-08-29

Abstract Background Epidemiological studies suggest that metformin may reduce the incidence of cancer in patients with diabetes and multiple late phase clinical trials assessing potential repurposing this drug are underway. Transcriptomic profiling tumour samples is an excellent tool to understand bioactivity, identify candidate biomarkers assess for mechanisms resistance therapy. Methods Thirty-six untreated primary breast were recruited a window study transcriptomic carried out before...

10.1038/s41416-019-0665-5 article EN cc-by British Journal of Cancer 2019-12-10

Abstract Angiogenesis, the formation of new blood vessels by endothelial cells, is a finely tuned process relying on balance between promoting and repressing signalling pathways. Among these, Notch critical in ensuring appropriate response cells to pro-angiogenic stimuli. However, downstream targets pathways effected Delta-like 4 (DLL4)/Notch their subsequent contribution angiogenesis are not fully understood. We found that Rho GTPase, RHOQ, induced DLL4 silencing RHOQ results abnormal...

10.1007/s10456-020-09726-w article EN cc-by Angiogenesis 2020-06-06

Genome-wide RNA expression profiling has yielded tumor subtypes with strong predictive or prognostic value for a wide variety of cancers. Recently, breast cancer two classifiers have been adopted by the World Health Organization (WHO) and approved Food Drug Administration (FDA). Also on basis DNA copy number profiles, different prognosis described, but not yet led to clinical implementation. The genomic revolution caused next generation sequencing samples presents additional mutation,...

10.1158/1078-0432.ccr-11-0462 article EN public-domain Clinical Cancer Research 2011-06-15
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