2008
DOI: 10.1038/gt.2008.101
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Cancer gene therapy using mesenchymal stem cells expressing interferon-β in a mouse prostate cancer lung metastasis model

Abstract: Cell-based therapy for cancer is a promising new field. Among cell types that can be used for this purpose, mesenchymal stem cells (MSCs) appear to hold great advantage for reasons including easier propagation in culture, possible genetic modification to express therapeutic proteins and preferential homing to sites of cancer growth upon in vivo transfer. The present study evaluated the potential of genetically modified MSC, constitutively expressing interferon (

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Cited by 195 publications
(126 citation statements)
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“…Therapeutic proteins which raised great interest because of the possibility to be managed by MSCs are interferon (IFN ) [31,32] and (IFN ) [23,[31][32][33][34], interleukin (IL) 12 [35], cytokine IL2 [36] and chemokine CX3CL1 (fractalkine) [37]. There are a number of studies of effects of IFN and IFN incorporated into systems delivered by MSCs over tumor growth showing the inhibitory effect of IFN and its usefulness as adjuvant therapy for the elimination of micrometastasis in risk patients [38], while anticancer effect of IFN is determined as apoptosis-stimulation effect [39,40] and only toxicity observed after its systemic administration limits its clinical applications [41].…”
Section: Mscs Engineered As Anticancer Drug De-livery Systemsmentioning
confidence: 99%
“…Therapeutic proteins which raised great interest because of the possibility to be managed by MSCs are interferon (IFN ) [31,32] and (IFN ) [23,[31][32][33][34], interleukin (IL) 12 [35], cytokine IL2 [36] and chemokine CX3CL1 (fractalkine) [37]. There are a number of studies of effects of IFN and IFN incorporated into systems delivered by MSCs over tumor growth showing the inhibitory effect of IFN and its usefulness as adjuvant therapy for the elimination of micrometastasis in risk patients [38], while anticancer effect of IFN is determined as apoptosis-stimulation effect [39,40] and only toxicity observed after its systemic administration limits its clinical applications [41].…”
Section: Mscs Engineered As Anticancer Drug De-livery Systemsmentioning
confidence: 99%
“…In C26 colon and B16F10 melanoma mouse models, chemokine (C-X3-C-motif) ligand 1-expressing-MSCs reduced metastatic nodules and resulted in longer survival [51]. MSCs engineered to secrete interferon-β suppressed growth of breast, prostate, pancreatic and melanoma cancers in animal models [52][53][54][55], as did interleukin-12-expressing MSCs in renal cell cancer [56]. MSCs have also been transduced with interferon-γ [54], Tumour Necrosis Factor-Related Apoptosis-Inducing Ligand (TRAIL) [53,[57][58][59][60] and soluble decoy receptors such as type-I insulin-like growth factor receptor [61].…”
Section: The Promise Of Mscs In Cancer Therapymentioning
confidence: 99%
“…To be able to minimize toxicity and increase the local concentration of IFN-, M S C s w e r e s e l e c t e d a s d e l i v e r y v e h i c l e . M u r i n e M S C s w e r e engineered to release IFN-and injected via tail vein into immunocompetent mice with prostate cancer lung metastasis (Ren et al, 2008b). Following IFN--expressing MSC therapy, the mice showed a reduction of tumor volume in the lung, increased tumor cell apoptosis, decreased tumor cell proliferation and blood vessel counts, and an increase in the natural killer cell activity.…”
Section: Genes Delivered By Mscs Treated Tumor Referencementioning
confidence: 99%