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Title:
Microvesicles as mediators of intercellular communication in cancerāthe emerging science of cellular ādebrisā | Seminars in Immunopathology
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Cancer cells emit a heterogeneous mixture of vesicular, organelle-like structures (microvesicles, MVs) into their surroundings including blood and body fluids. MVs are generated via diverse biological mechanisms triggered by pathways involved in oncogenic transformation, microenvironmental stimulation, cellular activation, stress, or death. Vesiculation events occur either at the plasma membrane (ectosomes, shed vesicles) or within endosomal structures (exosomes). MVs are increasingly recognized as mediators of intercellular communication due to their capacity to merge with and transfer a repertoire of bioactive molecular content (cargo) to recipient cells. Such processes may occur both locally and systemically, contributing to the formation of microenvironmental fields and niches. The bioactive cargo of MVs may include growth factors and their receptors, proteases, adhesion molecules, signalling molecules, as well as DNA, mRNA, and microRNA (miRs) sequences. Tumour cells emit large quantities of MVs containing procoagulant, growth regulatory and oncogenic cargo (oncosomes), which can be transferred throughout the cancer cell population and to non-transformed stromal cells, endothelial cells and possibly to the inflammatory infiltrates (oncogenic field effect). These events likely impact tumour invasion, angiogenesis, metastasis, drug resistance, and cancer stem cell hierarchy. Ongoing studies explore the molecular mechanisms and mediators of MV-based intercellular communication (cancer vesiculome) with the hope of using this information as a possible source of therapeutic targets and disease biomarkers in cancer.
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Keywords {š}
google, scholar, pubmed, cas, cancer, cell, cells, microvesicles, microparticles, biol, res, exosomes, tumor, blood, membrane, transfer, factor, receptor, vesicles, article, communication, endothelial, intercellular, tissue, extracellular, thromb, angiogenesis, nat, mediators, lee, rak, growth, sci, human, release, progression, mol, exosome, pathway, shedding, information, oncogenic, stem, rev, protein, mechanism, natl, cellderived, secretion, derived,
Topics {āļø}
tissue-factor-bearing microvesicles arise p-selectin-mediated pathway host-derived tissue factor stimulate post-ischemic revascularization rab8-dependent exocytic pathway brian meehanĀ &Ā janusz rak acquired glycoprotein iib/iiia month download article/chapter carbonic anhydrase-positive particles elmo/dock180/rac module circulating tumour-derived microvesicles metalloprotease-dependent ectodomain shedding dendritic cell-derived exovesicles cell cycle-related mrnas tnf-alpha-mediated pathway blood-borne tissue factor oncogenic kinase signalling signalling molecules vesicle burst induced flow field-flow fractionation mv-based intercellular communication ongoing studies explore egf-erbb signalling gtpase-activating proteins tbc1d10a tsap6/steap3-null mice mt1-mmp proinvasive activity related subjects oncogene-driven tumor progression tumour derived microvesicles tissue factor activity anti-tumor progression effect impact tumour invasion tumor-shed vesicles depends fasl-bearing microvesicles p-glycoprotein cd40 ligand+ microparticles promote tumour growth colorectal cancer cells defective hematopoietic response hospital research institute cell-derived microparticles privacy choices/manage cookies cxcr4-null cells full article pdf epithelial cells induces activated human platelets cell-cell communication tumor-derived exosomes tumor-derived microvesicles tumor cell societies
Questions {ā}
- Diamant M, Tushuizen ME, Sturk A, Nieuwland R (2004) Cellular microparticles: new players in the field of vascular disease?
- Tesselaar ME, Romijn FP, van der Linden IK et al (2007) Microparticle-associated tissue factor activity: a link between cancer and thrombosis?
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headline:Microvesicles as mediators of intercellular communication in cancerāthe emerging science of cellular ādebrisā
description:Cancer cells emit a heterogeneous mixture of vesicular, organelle-like structures (microvesicles, MVs) into their surroundings including blood and body fluids. MVs are generated via diverse biological mechanisms triggered by pathways involved in oncogenic transformation, microenvironmental stimulation, cellular activation, stress, or death. Vesiculation events occur either at the plasma membrane (ectosomes, shed vesicles) or within endosomal structures (exosomes). MVs are increasingly recognized as mediators of intercellular communication due to their capacity to merge with and transfer a repertoire of bioactive molecular content (cargo) to recipient cells. Such processes may occur both locally and systemically, contributing to the formation of microenvironmental fields and niches. The bioactive cargo of MVs may include growth factors and their receptors, proteases, adhesion molecules, signalling molecules, as well as DNA, mRNA, and microRNA (miRs) sequences. Tumour cells emit large quantities of MVs containing procoagulant, growth regulatory and oncogenic cargo (oncosomes), which can be transferred throughout the cancer cell population and to non-transformed stromal cells, endothelial cells and possibly to the inflammatory infiltrates (oncogenic field effect). These events likely impact tumour invasion, angiogenesis, metastasis, drug resistance, and cancer stem cell hierarchy. Ongoing studies explore the molecular mechanisms and mediators of MV-based intercellular communication (cancer vesiculome) with the hope of using this information as a possible source of therapeutic targets and disease biomarkers in cancer.
datePublished:2011-02-12T00:00:00Z
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Angiogenesis
Biomarker
Cancer
Exosomes
Intercellular communication
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Oncogenes
Immunology
Internal Medicine
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headline:Microvesicles as mediators of intercellular communication in cancerāthe emerging science of cellular ādebrisā
description:Cancer cells emit a heterogeneous mixture of vesicular, organelle-like structures (microvesicles, MVs) into their surroundings including blood and body fluids. MVs are generated via diverse biological mechanisms triggered by pathways involved in oncogenic transformation, microenvironmental stimulation, cellular activation, stress, or death. Vesiculation events occur either at the plasma membrane (ectosomes, shed vesicles) or within endosomal structures (exosomes). MVs are increasingly recognized as mediators of intercellular communication due to their capacity to merge with and transfer a repertoire of bioactive molecular content (cargo) to recipient cells. Such processes may occur both locally and systemically, contributing to the formation of microenvironmental fields and niches. The bioactive cargo of MVs may include growth factors and their receptors, proteases, adhesion molecules, signalling molecules, as well as DNA, mRNA, and microRNA (miRs) sequences. Tumour cells emit large quantities of MVs containing procoagulant, growth regulatory and oncogenic cargo (oncosomes), which can be transferred throughout the cancer cell population and to non-transformed stromal cells, endothelial cells and possibly to the inflammatory infiltrates (oncogenic field effect). These events likely impact tumour invasion, angiogenesis, metastasis, drug resistance, and cancer stem cell hierarchy. Ongoing studies explore the molecular mechanisms and mediators of MV-based intercellular communication (cancer vesiculome) with the hope of using this information as a possible source of therapeutic targets and disease biomarkers in cancer.
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Biomarker
Cancer
Exosomes
Intercellular communication
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Oncogenes
Immunology
Internal Medicine
Pathology
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