A5062740804- Cell Adhesion Molecules Research
- Immune cells in cancer
- Neuroinflammation and Neurodegeneration Mechanisms
- Glioma Diagnosis and Treatment
- Protease and Inhibitor Mechanisms
- Cellular Mechanics and Interactions
- Cancer Cells and Metastasis
- Extracellular vesicles in disease
- Immunotherapy and Immune Responses
- Signaling Pathways in Disease
- Chemokine receptors and signaling
- Neurogenesis and neuroplasticity mechanisms
- RNA Interference and Gene Delivery
- Cancer Immunotherapy and Biomarkers
- Cancer, Stress, Anesthesia, and Immune Response
- Peptidase Inhibition and Analysis
- Ferroptosis and cancer prognosis
- Single-cell and spatial transcriptomics
- CAR-T cell therapy research
- Nanoparticle-Based Drug Delivery
- Histone Deacetylase Inhibitors Research
- Hormonal Regulation and Hypertension
- Polyamine Metabolism and Applications
- Molecular Biology Techniques and Applications
- Electrolyte and hormonal disorders
Techno India University
2024
University of Calgary
2014-2023
Ontario Brain Institute
2018-2020
Allen Institute for Brain Science
2014-2016
Institute of Post Graduate Medical Education and Research
2004-2015
Bose (United States)
2004
Glioma cells in situ are surrounded by microglia, suggesting the potential of glioma–microglia interactions to produce various outcomes. As chemokines important mediators cell–cell communication, we sought first identify commonly expressed 16 human glioma lines. We found CCL2 (macrophage chemoattractant protein-1) messenger RNA be majority However, these lines did not express receptor, CCR2, which was on microglia. Next, overexpressed U87 line, has low basal level CCL2, investigate...
Remyelination failure in multiple sclerosis (MS) contributes to progression of disability. The deficient repair results from neuroinflammation and deposition inhibitors including chondroitin sulfate proteoglycans (CSPGs). Which CSPG member is repair-inhibitory or alters local inflammation exacerbate injury unknown. Here, we correlate high versican-V1 expression MS lesions with premyelinating oligodendrocytes, highlight its selective upregulation amongst members experimental autoimmune...
Abstract The capacity of glioma cells to invade extensively within the central nervous system is a major cause high morbidity rate primary malignant brain tumors. Glioma cell invasion involves attachment tumor extracellular matrix (ECM), degradation ECM components, and subsequent penetration into adjacent structures. These processes are accomplished in part by metalloproteinases (MMP) three-dimensional milieu parenchyma. As majority studies have used two-dimensional monolayer culture system,...
Microglia and macrophages are the largest component of inflammatory infiltrate in glioblastoma (GBM). However, whether there differences their representation activity prognostically-favorable isocitrate dehydrogenase (IDH)-mutated compared to -wild type GBMs is unknown. Studies on human specimens untreated IDH-mutant rare given they comprise 10% all often present at lower grades, receiving treatments prior dedifferentiation that can drastically alter microglia macrophage phenotypes. We were...
Oncogenic signaling by NOTCH is elevated in brain tumor-initiating cells (BTIC) malignant glioma, but the mechanism of its activation unknown. Here we provide evidence that tenascin-C (TNC), an extracellular matrix protein prominent increases activity BTIC to promote their growth. We demonstrate proximal localization TNC and human glioblastoma specimens orthotopic murine xenografts implanted intracranially. In tissue culture, was superior amongst several proteins enhancing sphere-forming...
Chemokines have been found to alter tumor growth and metastasis. We described previously that a particular chemokine receptor, CXCR4, was predominantly expressed on various glioma cell lines in resected glioblastoma specimens. Herein, we tested the ligand of stromal derived factor-1α (SDF-1α, CXCL12), response human cells. SDF-1α increased expression membrane type-2 matrix metalloproteinase (MT2-MMP), but not other MT-MMPs, MMP-2 or MMP-9. The enhanced MT2-MMP blocked by CXCR4 antagonist,...
BackgroundTenascin-C (TNC), an extracellular matrix protein overexpressed in malignant gliomas, stimulates invasion of conventional glioma cell lines (U251, U87). However, there is a dearth such information on stemlike cells. Here, we have addressed whether and how TNC may regulate the invasiveness brain tumor–initiating cells (BTICs) that give rise to progenies.
By rejuvenating the deficient activity of myeloid cells in glioblastoma, niacin improves treatment otherwise incurable brain tumors.
PD-1 on glioblastoma cells promotes brain tumor growth, and therapeutic antibodies cannot suppress its proliferative effects.
Abstract Glioblastomas (GBMs) are highly aggressive, recurrent, and lethal brain tumors that maintained via tumor‐initiating cells (BTICs). The aggressiveness of BTICs may be dependent on the extracellular matrix (ECM) molecules enriched within GBM microenvironment. Here, we investigated expression ECM in patients by mining transcriptomic databases also staining human specimens. RNA levels for fibronectin, brevican, versican, heparan sulfate proteoglycan 2 (HSPG2), several laminins were high...
Glioblastoma (GBM) is an aggressive brain cancer with a poor prognosis. The use of immune therapies to treat GBM has become promising avenue research. It was shown that amphotericin B (Amp B) can stimulate the innate system and suppress growth tumor initiating cells (BTICs). However, it not feasible histopathology determine activation in patients. We developed MRI technique rapidly detect therapeutic response animals treated drugs immunity. Ultra-small iron oxide nanoparticles (USPIOs) are...
The invasiveness of glioma cells, a major cause mortality in malignant brain tumors, is mediated part by the cellular microenvironment. We have reported that three-dimensional matrix type 1 collagen (3D-CL) gel, extracellular protein tenascin-C (TN) increased cells through downstream production metalloproteinase (MMP)-12. In present study, we investigated signaling mechanisms involved TN-stimulated invasiveness. found pan kinase C (PKC) inhibitor, bisindolylmaleimide I, decreased TN-enhanced...
array of tumor initiating cells and multiplex protein assay microglia conditioned media was performed.IL-8 MCP-1 were found to be potential factors for differentiation cells.
Abstract We reported previously that microglia decreased the growth of human brain tumor-initiating cells (BTICs). Through microarray analyses BTICs exposed in vitro to microglia, we found induction several genes ascribed have roles cell cycle arrest, reduced proliferation and differentiation. Herein, tested hypothesis one these genes, arrest specific 1 (Gas1), is a novel reduction factor induced by microglia. increased expression Gas1 transcript protein glioblastoma patient-derived BTIC...
Objective: Exogenous application of T11TS/SLFA3 in glioma model had shown the regression tumor load through immunopotentiation. The mechanistic module this interaction on immunological synapse formation and resulting effect is searched for delineating immunotherapeutic efficacy T11TS. Methods: After purification from sheep erythrocytes glycoprotein was characterized by SDS-PAGE analysis staining. modulatory T11TS animals were studied CD2 MHC class II expression peripheral lymphocytes, PMN,...
Brain tumor-initiating cells (BTICs) become less tumorigenic when co-cultured with microglia/macrophages (M/Ms) isolated from subjects not affected by glioma, but exposed to the M/Ms of glioma patients. Microglial and macrophages patients, however, can be reactivated non-toxic doses amphotericin B curb growth BTICs in vitro vivo.