A5070676424- Cancer Cells and Metastasis
- Pancreatic function and diabetes
- Pancreatic and Hepatic Oncology Research
- Phagocytosis and Immune Regulation
- Oral and Maxillofacial Pathology
- Sarcoma Diagnosis and Treatment
- Immune cells in cancer
- Cancer Immunotherapy and Biomarkers
- Bone Tumor Diagnosis and Treatments
Queen Mary University of London
2022-2025
In pancreatic ductal adenocarcinoma (PDAC), differentiation of stellate cells (PSCs) into myofibroblast-like cancer-associated fibroblasts (CAFs) can both promote and suppress tumor progression. Here, we show that the Rho effector protein kinase N2 (PKN2) is critical for PSC myofibroblast differentiation. Loss PKN2 associated with reduced proliferation, contractility, alpha-smooth muscle actin (α-SMA) stress fibers. spheroid co-cultures PDAC cells, loss prevents invasion but,...
Abstract In solid tumours, malignant cells develop relationships with nonmalignant stromal to support tumour growth, tissue structure, and nutrient supply. a recent issue of this journal, Zheng Guo catalogue the cellular landscape in chordoma using combination single‐cell spatial transcriptomics. Despite mesenchymal nature chordoma, retain expression epithelial markers, addition mesenchymal, partial‐EMT, stem‐cell signatures. Cancer‐associated fibroblasts (CAFs) are among most abundant...
The penetrant PRKCA D463H mutation, a biomarker and potential driver in chordoid glioma, was found to provoke the development of chondrosarcomas heterozygous knock mice. This mutation entirely abrogates kinase activity, but strikingly no oncogenic phenotype is observed for related inactivating D463N indicating that lack activity not driver. In cells, mutant closely mirrored PKCa WT behaviours retained ATP binding, contrary mutant. Mechanistically, protein display quantitative alterations...
The extracellular matrix (ECM) is composed of complex fibrillar proteins, proteoglycans, and macromolecules, generated by stromal, immune, cancer cells. components organisation the evolves as tumours progress to invasive disease metastasis. In many solid tumours, dense fibrotic ECM has been hypothesised impede therapy response limiting drug immune cell access. Interventions target individual ECM, collectively termed matrisome, have, however, revealed tumour-suppressor, tumour-promoter,...