PubMed · 13574437
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A H COONS. 1958. Fluorescent antibody methods.. https://pubmed.ncbi.nlm.nih.gov/13574437/
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In glioblastoma (GBM), the most frequent and lethal brain tumor, therapies suppressing recurrently altered signaling pathways failed to extend survival. However, in patient subsets, specific genetic lesions can confer sensitivity to targeted agents. By exploiting an integrated model based on patient-derived stem-like cells, faithfully recapitulating the original GBMs in vitro and in vivo, here, we identify a human GBM subset (∼9% of all GBMs) characterized by ERBB3 overexpression and nuclear accumulation. ERBB3 overexpression is driven by inheritable promoter methylation or post-transcriptional silencing of the oncosuppressor miR-205 and sustains the malignant phenotype. Overexpressed ERBB3 behaves as a specific signaling platform for fibroblast growth factor receptor (FGFR), driving PI3K/AKT/mTOR pathway hyperactivation, and overall metabolic upregulation. As a result, ERBB3 inhibition by specific antibodies is lethal for GBM stem-like cells and xenotransplants. These findings highlight a subset of patients eligible for ERBB3-targeted therapy.
A methodology for the quick and efficient study of phagocytosis has been developed. It uses the flow cytometer to exploit the change in size and granularity that occurs in cells upon the ingestion of particulate material. The numbers of cells that have phagocytosed particles can be calculated from the distinct shift in regions that occurs. The method also allows the factors governing phagocytosis to be studied in detail through the use of blocking agents or antibodies. Blood-derived monocytes were studied to investigate the role of complement in metal particle phagocytosis to further understand aseptic loosening. Factor C3b was found to be fundamental to the opsonization and phagocytosis of metal particles by monocytes.
BACKGROUND: beta3 integrins play a role in metastatic progression of prostate cancer by mediating adhesion of cancer cells to endothelium and migration through extracellular matrix (ECM). However, the role of beta3 integrins during transendothelial migration (TEM) of prostate tumor cells is poorly understood. We examined the role of beta3 integrins in TEM of PC3 human prostate cancer cells through a monolayer of human lung microvascular endothelial cells (HLMVECs). METHODS: PC3 cells were challenged with beta3 integrin antibodies or antisense nucleotides and their efficiency to migrate through monolayers of endothelial cells (ECs) was assessed using confocal microscopy. RESULTS: beta3 integrins in PC3 cells are not localized in focal contacts and their blockade significantly inhibited TEM by over 50% preferentially during late stages of migration. Formation of PC3 cell pseudopodia on matrigel was significantly reduced by beta3 integrin antisense oligonucleotides. CONCLUSIONS: beta3 integrins play important roles during TEM of PC3 cells while interacting with the matrix underneath the endothelium. These interactions are independent of the ability to cluster beta3 integrins into focal adhesions.