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| 1 | Subcurative radiation significantly increases cell proliferation, invasion, and migration of primary glioblastoma multiforme in vivo显示文摘Tumor cell proliferation, infiltration, migration, and neovascularization are known causes of treatment resistance in glioblastoma multiforme(GBM). The purpose of this study was to determine the effect of radiation on the growth characteristics of primary human GBM developed in a nude rat. Primary GBM cells grown from explanted GBM tissues were implanted orthotopically in nude rats. Tumor growth was confirmed by magnetic resonance imaging on day 77(baseline) after implantation. The rats underwent irradiation to a dose of 50 Gy delivered subcuratively on day 84 postimplantation(n = 8), or underwent no radiation(n = 8). Brain tissues were obtained on day 112(nonirradiated) or day 133(irradiated). Immunohistochemistry was performed to determine tumor cell proliferation(Ki-67) and to assess the expression of infiltration marker(matrix metalloproteinase-2, MMP-2) and cell migration marker(CD44). Tumor neovascularization was assessed by microvessel density using von-Willebrand factor(vWF) staining. Magnetic resonance imaging showed well-developed, infiltrative tumors in 11 weeks postimplantation. The proportion of Ki-67-positive cells in tumors undergoing radiation was(71 ± 15)% compared with(25 ± 12)% in the nonirradiated group(P = 0.02). The number of MMP-2-positive areas and proportion of CD44-positive cells were also high in tumors receiving radiation, indicating great invasion and infiltration. Microvessel density analysis did not show a significant difference between nonirradiated and irradiated tumors. Taken together, we found that subcurative radiation significantly increased proliferation, invasion, and migration of primary GBM. Our study provides insights into possible mechanisms of treatment resistance following radiation therapy for GBM. | Adarsh Shankar Sanath Kumar Asm Iskander Nadimpalli RS Varma Branislava Janic Ana deCarvalho Tom Mikkelsen Joseph A Frank Meser M Ali Robert A Knight Stephen Brown Ali S Arbab | 2014 | Chinese Journal of Cancer2014，33，3： | 5 |
| 2 | Speciation of dimethylarsinic acid and monomethylarsonic acid by gas chromatography-mass spectrometry显示文摘 | Meser Z Vitanyi G Morabito R | 1999 | Chro- matogr A1999，832，18： | 1 |
| 3 | Patent pools: Licensing strategies in the absence of regulation 显示文摘 | Lampe R Meser P | 2012 | Advances in Strategic Manage- ment2012，29，： | 1 |
| 4 | Surface complexation of colloidal semiconductors strongly enhances interfacial electron-transfer rates显示文摘 | Meser J Punchihewa S Infelta P P | 1991 | Langmuir1991，7，12： | 1 |
| 5 | Nenral correlates of phonological and semantic-based anomia treatment in aphasia显示文摘 | Fridriksson J Meser D Bonilha L | 2007 | Neuropsyehologia2007，5，： | 1 |
| 6 | An indirect ELISA for the antibaodies against Porcine reproductive and respiratory syndrome virus using recombinant nucleocapsid protein as antigen显示文摘 | Helena Denal Christian Meser Jon Duri Tratschin | 1997 | J Virol Methods1997，65，2： | 1 |
| 7 | pH definition and measurement at high temperatures显示文摘 | Meser R E Holmes H F | 1992 | J Solution Chem1992，21，： | 1 |
| 8 | Acidity measurements at elevated temperatures显示文摘 | Meser R E Baes C F Sweeton F W | 1970 | J Phys Chem1970，74，： | 1 |
| 9 | 查看详情显示文摘 | Meser Z Vitanyi G Morabito R Fodor P | | 0，，： | 1 |
| 10 | Galculation of bottom hole pressure for deep, hot, sour gas wells 显示文摘 | MESER P H RAHGVANA R RAMEY JR H J | 1974 | JPT1974，26，1： | 1 |
| 11 | Induction of interleukin 6 by ionizing radiation in a human epithelial cell lime:control by corticosteroids显示文摘 | Beetz A Meser G Oppel T | 1997 | Int J Radiat Biol1997，，7： | 1 |
| 12 | Basal level of anti-Müllerian hormone is associated with oocyte quality in stimulated cycles显示文摘 | Ebner T Sommergruber M Meser M | 2006 | Hum Reprod2006，21，8： | 1 |
| 13 | Measurements and imaging of optical gain in optically pumped alkalbrare gas systems显示文摘 | K L Galbally-Kinney D L Meser W J Kessler | 2012 | ApplPhys Lett2012，100，04： | 1 |
| 14 | Role of low- molecular- weight heparin in invasive management of non - ST - elevation acute coronary syndromes 显示文摘 | Meser LR Kalus JS | 2004 | Ann Pharmacother2004，38，12： | 1 |
| 15 | Monitoring adenoviral based gene delivery in rat glioma by molecular imaging显示文摘AIM:To determine whether endothelial progenitor cells(EPCs)can be used as delivery vehicle for adenoviral vectors and imaging probes for gene therapy in glioblastoma.METHODS:To use cord blood derived EPCs as delivery vehicle for adenoviral vectors and imaging probes for glioma gene therapy,a rat model of human glioma was made by implanting U251 cells orthotopically.EPCs were transfected with an adenovirus(AD5/carrying hNIS gene)and labeled with iron oxide and inoculated them directly into the tumor 14 d following implantation of U251 cells.Magnetic resonance imaging(MRI)was used to in vivo track the migration of EPCs in the tumor.The expression of gene products was determined by in vivo Tc-99m single photon emission computed tomography(SPECT).The findings were validated with immunohistochemistry(IHC).RESULTS:EPCs were successfully transfected with the adenoviral vectors carrying hNIS which was proved by significantly(P<0.05)higher uptake of Tc-99m in transfected cells.Viability of EPCs following transfection and iron labeling was not altered.In vivo imaging showed the presence of iron positive cells and the expression of transgene(hNIS)product on MRI and SPECT,respectively,all over the tumors following administration of transfected and iron labeled EPCs in the tumors.IHC confirmed the distribution of EPC around the tumor away from the injection site and also showed transgene expression in the tumor.The results indicated the EPCs’ability to deliver adenoviral vectors into the glioma upon intratumor injection.CONCLUSION:EPCs can be used as vehicle to deliver adenoviral vector to glioma and also act as imaging probe at the same time. | Nadimpalli Ravi S Varma Kenneth N Barton Branislava Janic Adarsh Shankar ASM Iskander Meser M Ali Ali S Arbab | 2013 | World Journal of Clinical Oncology2013，4，4： | 0 |
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