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CSF-1R inhibition alters macrophage polarization and blocks glioma progression
The results identify TAMs as a promising therapeutic target for proneural gliomas and establish the translational potential of CSF-1R inhibition for GBM.
Macrophage Ontogeny Underlies Differences in Tumor-Specific Education in Brain Malignancies.
Brain-Resident Microglia and Blood-Borne Macrophages Orchestrate Central Nervous System Inflammation in Neurodegenerative Disorders and Brain Cancer
- L. Sevenich
- BiologyFront. Immunol.
- 6 April 2018
In this review, recent developments in evaluating functions of brain-resident and recruited myeloid cells in neurodegenerative disorders and brain cancers will be discussed and unique or shared cellular traits of microglia and macrophages in different CNS disorders will be highlighted.
Analysis of tumor- and stroma-supplied proteolytic networks reveals a brain metastasis-promoting role for cathepsin S
Analysis of tumour–stroma interactions that modulate organ tropism of brain, bone and lung metastasis in xenograft models identified a number of potential modulators of site-specific metastasis, including cathepsin S as a regulator of breast-to-brain metastasis.
Pericellular proteolysis in cancer.
This review addresses how cancer cells, together with their surrounding microenvironment, regulate pericellular proteolysis and dissects the multitude of mechanisms by which perICEllular proteases contribute to cancer progression.
Synergistic antitumor effects of combined cathepsin B and cathepsin Z deficiencies on breast cancer progression and metastasis in mice
- L. Sevenich, U. Schurigt, T. Reinheckel
- Biology, MedicineProceedings of the National Academy of Sciences
- 21 January 2010
It is concluded that the double deficiency of Ctsb and Ctsz exerts significant synergistic anticancer effects, whereas the single deficiencies demonstrate at least partial reciprocal compensation.
Distinct functions of macrophage-derived and cancer cell-derived cathepsin Z combine to promote tumor malignancy via interactions with the extracellular matrix.
Examination of the roles of the cathepsin Z (CtsZ) protease in pancreatic neuroendocrine tumors in humans and mice found that tumor proliferation was exclusively regulated by cancer cell-intrinsic functions of CtsZ, whereas tumor invasion required contributions from both macrophages and cancer cells, indicating that cellular source can indeed impact molecular function.
Transgenic expression of human cathepsin B promotes progression and metastasis of polyoma-middle-T-induced breast cancer in mice
It is concluded that elevated proteolytic CTSB activity facilitates progression and metastasis of PymT-induced mammary carcinomas, and is associated with increased immune cell infiltration, enhanced VEGF levels and the promotion of tumor angiogenesis.
Cell type-dependent pathogenic functions of overexpressed human cathepsin B in murine breast cancer progression
It is concluded that CTSB overexpression in the PyMT mouse model promotes tumor progression not by a stromal effect, but by a direct, cancer cell-inherent mode of action: C TSB overexpressing renders thePyMT cancers more invasive by increasing proteolytic extracellular matrix protein degradation fostering collective cell invasion into adjacent tissue.
Reduced tumour cell proliferation and delayed development of high-grade mammary carcinomas in cathepsin B-deficient mice
An in vivo role for Ctsb is indicated in promoting cellular anaplasia in mammary cancers and proliferation in lung metastases and resistance to apoptosis induction by the lysosomotropic agent Leu-Leu-OMe.