A5089366954- Cancer Cells and Metastasis
- Protein Tyrosine Phosphatases
- Cancer-related Molecular Pathways
- PI3K/AKT/mTOR signaling in cancer
- Cytokine Signaling Pathways and Interactions
- RNA modifications and cancer
- Cancer Mechanisms and Therapy
- Cancer Genomics and Diagnostics
- Galectins and Cancer Biology
- NF-κB Signaling Pathways
- Colorectal and Anal Carcinomas
- Plant Disease Resistance and Genetics
- Cancer Risks and Factors
- Epigenetics and DNA Methylation
- Pancreatic and Hepatic Oncology Research
- Monoclonal and Polyclonal Antibodies Research
- Immune Cell Function and Interaction
- Wnt/β-catenin signaling in development and cancer
- Peptidase Inhibition and Analysis
- HER2/EGFR in Cancer Research
- Cancer-related molecular mechanisms research
- Natural product bioactivities and synthesis
- Cell Adhesion Molecules Research
- Immune Response and Inflammation
- Breast Cancer Treatment Studies
University Hospital of Basel
2016-2024
University of Basel
2014-2024
Friedrich Miescher Institute
2013-2023
Novartis (Switzerland)
2011-2013
Novartis Institutes for BioMedical Research
2013
Princess Margaret Cancer Centre
2011
University of Toronto
2011
Pathways Behavioral Services
2011
University of California, Davis
2011
Ontario Institute for Cancer Research
2011
Abstract The SH2 domain-containing protein-tyrosine phosphatase PTPN11 (Shp2) is required for normal development and an essential component of signaling pathways initiated by growth factors, cytokines, extracellular matrix. In many these pathways, Shp2 acts upstream Ras. About 50% patients with Noonan syndrome have germ-line gain function mutations. Associations between increased risk some malignancies, notably leukemia neuroblastoma, been reported, recent data indicate that somatic...
The calcium-activated chloride channel anoctamin 1 ( ANO1 ) is located within the 11q13 amplicon, one of most frequently amplified chromosomal regions in human cancer, but its functional role tumorigenesis has remained unclear. region ∼15% breast cancers. Whether tumors, extent to which gene amplification contributes overexpression, and whether overexpression important for tumor maintenance have unknown. We found that highly expressed cancer cell lines primary tumors. Amplification...
Abstract An epithelial–mesenchymal transition (EMT) underlies malignant tumor progression and metastatic spread by enabling cancer cells to depart from the primary tumor, invade surrounding tissue, disseminate distant organs. EMT also enriches for stem (CSC) increases capacity of initiate propagate tumors upon transplantation into immune-deficient mice, a major hallmark CSCs. However, molecular mechanisms promoting tumorigenicity undergoing an CSCs have remained widely elusive. We here...
Abstract Tumor-specific T cells are frequently exhausted by chronic antigenic stimulation. We here report on a human antigen-specific ex vivo model to explore new therapeutic options for cell immunotherapies. generated with this resemble tumor-infiltrating phenotypic and transcriptional level. Using targeted pooled CRISPR-Cas9 screen individual gene knockout validation experiments, we uncover sorting nexin-9 (SNX9) as mediator of exhaustion. Upon TCR/CD28 stimulation, deletion SNX9 in CD8...
The protein-tyrosine phosphatase 1B (PTP1B; PTPN1) is an important regulator of mammalian metabolism and also helps control signaling by growth factors, cytokines, extracellular matrix. Gene knockout studies in mice established PTP1B as a key negative the insulin leptin receptors. Experiments using PTP1B(-/-) fibroblast lines, dominant-negative mutants, or small interfering RNAs indicate that contributes to dephosphorylation epidermal factor receptor platelet-derived receptors well. However,...
Copper chelators could help to reduce metastasis from breast tumors.
The phosphoinositide 3-kinase (PI3K) signaling cascade, a key mediator of cellular survival, growth, and metabolism, is frequently altered in human cancer. Activating mutations PIK3CA, which encodes the α-catalytic subunit PI3K, occur approximately 30% breast cancers. These result constitutive activity enzyme are oncogenic, but it not known whether they sufficient to induce mammary carcinomas mice. In present study, we show that expression mutant PIK3CA H1047R luminal epithelium evokes...