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Marrison, J.

Publications and source records attributed to Marrison, J..

2 recordsLinked to original sources

CellPhePy: a Python implementation of the CellPhe toolkit for automated cell phenotyping from microscopy time-lapse videos

We previously developed the CellPhe toolkit1, an open-source R package for automated cell phenotyping from ptychography time-lapse videos. To align with the growing adoption of python-based image analysis tools and to enhance interoperability with widely used software for cell segmentation and tracking, we developed a python implementation of CellPhe, named CellPhePy. CellPhePy preserves all of the core functionality of the original toolkit, including single-cell phenotypic feature extraction, time-series analysis, feature selection and cell type classification. In addition, CellPhePy introduces significant enhancements, such as an improved method for identifying features that differentiate cell populations and extended support for multiclass classification, broadening its analytical capabilities. Notably, the CellPhePy package supports CellPose segmentation and TrackMate tracking, meaning that a set of microscopy images are the only required input with segmentation, tracking and feature extraction fully automated for downstream analysis, without reliance on external applications. The workflows increased flexibility and modularity make it adaptable to different imaging modalities and fully customisable to address specific research questions. CellPhePy can be installed via PyPi or GitHub, and we also provide a CellPhePy GUI to aid user accessibility.

cell biology↗

TGF-beta promotes microtube formation in glioblastoma through Thrombospondin 1

Microtubes (MTs), cytoplasmic extensions of glioma cells, are important cell communication structures promoting invasion and treatment resistance through network formation. MTs are abundant in chemoresistant gliomas, in particular glioblastomas (GBMs), while they are uncommon in chemosensitive IDH-mutant and 1p/19q co-deleted oligodendrogliomas. To identify potential signaling pathways involved in MT formation we performed a bioinformatics analysis of TCGA data showing that the TGF-{beta} pathway is highly activated in GBMs compared to oligodendroglial tumors. In particular we observed that signaling pathways involved in extracellular matrix organization are differentially expressed between these tumor entities. Using patient-derived GBM stem cell lines, we demonstrated that TGF-{beta}1 stimulation promotes enhanced MT formation and communication via Calcium signaling. Inhibition of the TGF-{beta} pathway significantly reduced MT formation and its associated invasion in vitro and in vivo. Downstream of TGF-{beta}, we identified thrombospondin 1 (TSP1) as a potential mediator of MT formation in GBM through SMAD activation. TSP1 was upregulated upon TGF-{beta} stimulation and enhanced MT formation, which was inhibited by TSP1 shRNAs in vitro and in vivo. In conclusion, TGF-{beta} and its downstream mediator TSP1 are important mediators of the MT network in GBM and blocking this pathway could potentially help to break the complex MT driven invasion/ resistance network.

cancer biology↗