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Results: 21 to 25 of 25

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Embryonic endothelial progenitor cells armed with a suicide gene target hypoxic lung metastases after intravenous delivery.
Wei J, Blum S, Unger M, Jarmy G, Lamparter M, Geishauser A, Vlastos GA, Chan G, Fischer KD, Rattat D, Debatin KM, Hatzopoulos AK, Beltinger C
(2004) Cancer Cell 5: 477-88
MeSH Terms: Animals, Bone Neoplasms, Bystander Effect, Carcinoma, Lewis Lung, Cell Hypoxia, Cytosine Deaminase, Embryonic and Fetal Development, Endothelium, Vascular, Fluorouracil, Gene Targeting, Genes, Transgenic, Suicide, Genetic Therapy, Genetic Vectors, Injections, Intravenous, Killer Cells, Natural, Lung Neoplasms, Male, Mice, Mice, Inbred C3H, Mice, Inbred C57BL, Neovascularization, Pathologic, Osteosarcoma, Pentosyltransferases, Prodrugs, Recombinant Fusion Proteins, Stem Cells, Survival Rate, Uracil, Vascular Endothelial Growth Factor A
Show Abstract · Added November 18, 2010
We show that mouse embryonic endothelial progenitor cells (eEPCs) home preferentially to hypoxic lung metastases when administered intravenously. This specificity is inversely related to the degree of perfusion and vascular density in the metastasis and directly related to local levels of hypoxia and VEGF. Ex vivo expanded eEPCs that were genetically modified with a suicide gene specifically and efficiently eradicated lung metastases with scant patent blood vessels. eEPCs do not express MHC I proteins, are resistant to natural killer cell-mediated cytolysis, and can contribute to tumor vessel formation also in nonsyngeneic mice. These results indicate that eEPCs can be used in an allogeneic setting to treat hypoxic metastases that are known to be resistant to conventional therapeutic regimes.
1 Communities
1 Members
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29 MeSH Terms
Broad spectrum receptor tyrosine kinase inhibitor, SU6668, sensitizes radiation via targeting survival pathway of vascular endothelium.
Lu B, Geng L, Musiek A, Tan J, Cao C, Donnelly E, McMahon G, Choy H, Hallahan DE
(2004) Int J Radiat Oncol Biol Phys 58: 844-50
MeSH Terms: Animals, Carcinoma, Lewis Lung, Cell Line, Tumor, Drug Evaluation, Preclinical, Endothelium, Vascular, Enzyme Activation, Humans, Indoles, Mice, Mice, Inbred C57BL, Phosphorylation, Protein-Serine-Threonine Kinases, Proto-Oncogene Proteins, Proto-Oncogene Proteins c-akt, Pyrroles, Receptor Protein-Tyrosine Kinases
Show Abstract · Added February 28, 2014
PURPOSE - Recent studies have demonstrated radiosensitization by inhibiting receptor tyrosine kinases (RTKs). Irradiation activates RTKs and their downstream prosurvival molecule, Akt. In this study, we investigated the mechanism by which SU6668, an inhibitor of RTKs involved in angiogenic pathways, enhances effects of irradiation.
METHODS AND MATERIALS - Western blots were used to determine Akt phosphorylation. Clonogenic assays were performed to determine endothelial survival after combination of SU6668 and irradiation. This combination therapy was also tested in mouse models with Lewis lung carcinoma or glioblastoma multiforme (GL261) for inhibition of tumor growth and tumor vasculature by examining tumor volume, tumor vascular window, and blood flow.
RESULTS - We found that SU6668 inhibited the Akt activation inducible by irradiation. Clonogenic survival of endothelial cells was decreased after the combined therapy compared with radiotherapy alone. In vivo studies demonstrated reduction of tumor vasculature and blood flow. In addition, 21 Gy in 7 fractions given concurrently with SU6668 resulted in tumor growth delay compared to either treatment alone.
CONCLUSION - These data suggest that the combination therapy was more effective in destroying tumor vasculature than either treatment alone. SU6668 augments tumor-suppressive effects of radiotherapy in Lewis lung carcinoma and GL261 xenographs, possibly through reducing the survival of tumor endothelium.
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16 MeSH Terms
SU11248 maintenance therapy prevents tumor regrowth after fractionated irradiation of murine tumor models.
Schueneman AJ, Himmelfarb E, Geng L, Tan J, Donnelly E, Mendel D, McMahon G, Hallahan DE
(2003) Cancer Res 63: 4009-16
MeSH Terms: Angiogenesis Inhibitors, Animals, Carcinoma, Lewis Lung, Combined Modality Therapy, Endothelium, Vascular, Glioblastoma, Humans, Indoles, Mice, Mice, Inbred C57BL, Neoplasm Recurrence, Local, Neoplasms, Experimental, Neovascularization, Pathologic, Pyrroles, Receptor Protein-Tyrosine Kinases, Sunitinib
Show Abstract · Added February 28, 2014
Receptor tyrosine kinase activation contributes to cell viability during cytotoxic therapy. The novel broad spectrum receptor tyrosine kinase inhibitor, SU11248, inhibits vascular endothelial growth factor receptor 2, platelet-derived growth factor receptor, c-kit, and fetal liver tyrosine kinase 3. In this study, we maintained SU11248 plasma levels beyond the completion of radiotherapy to determine whether tumor regrowth can be delayed. The antiangiogenic effects of SU11248 were demonstrated using human umbilical vein endothelial cells in vitro. Apoptosis increased and clonogenic survival decreased when SU11248 was used in combination with radiation from 0 to 6 Gy on endothelial cells. In vivo tumor growth delay was increased in C57B6J mice with Lewis lung carcinoma or glioblastoma multiform (GL261) hind limb tumors. Mice were treated with daily i.p. injections (40 mg/kg) of SU11248 during 7 days of radiation treatment (21 Gy). Combined treatment with SU11248 and radiation significantly reduced tumor volume as compared with either treatment alone. Concomitant reduction in vasculature was confirmed using the dorsal vascular window model. The vascular length established using images taken from a consistent quadrant in the window show the combination therapy was more effective in destroying tumor vasculature than either treatment alone. SU11248 maintenance administration beyond the completion of radiotherapy results in prolongation of tumor control. In summary, SU11248 enhances radiation-induced endothelial cytotoxicity, resulting in tumor vascular destruction and tumor control when combined with fractionated radiotherapy in murine tumor models. Moreover, inhibition of angiogenesis well beyond radiation therapy may be a promising treatment paradigm for refractory human neoplasms.
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1 Members
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16 MeSH Terms
Host cyclooxygenase-2 modulates carcinoma growth.
Williams CS, Tsujii M, Reese J, Dey SK, DuBois RN
(2000) J Clin Invest 105: 1589-94
MeSH Terms: Animals, Blotting, Western, Carcinoma, Lewis Lung, Cyclooxygenase 1, Cyclooxygenase 2, Endothelial Growth Factors, Isoenzymes, Lymphokines, Membrane Proteins, Mice, Mice, Inbred C57BL, Mice, Knockout, Neoplasms, Experimental, Neovascularization, Pathologic, Prostaglandin-Endoperoxide Synthases, Tumor Cells, Cultured, Vascular Endothelial Growth Factor A, Vascular Endothelial Growth Factors
Show Abstract · Added March 5, 2014
Cyclooxygenase-2 (COX-2; Ptgs2) acts as a tumor promoter in rodent models for colorectal cancer, but its precise role in carcinogenesis remains unclear. We evaluated the contribution of host-derived COX-1 and COX-2 in tumor growth using both genetic and pharmacological approaches. Lewis lung carcinoma (LLC) cells grow rapidly as solid tumors when implanted in C57BL/6 mice. We found that tumor growth was markedly attenuated in COX-2(-/-), but not COX-1(-/-) or wild-type mice. Treatment of wild-type C57BL/6 mice bearing LLC tumors with a selective COX-2 inhibitor also reduced tumor growth. A decrease in vascular density was observed in tumors grown in COX-2(-/-) mice when compared with those in wild-type mice. Because COX-2 is expressed in stromal fibroblasts of human and rodent colorectal carcinomas, we evaluated COX-2(-/-) mouse fibroblasts and found a 94% reduction in their ability to produce the proangiogenic factor, VEGF. Additionally, treatment of wild-type mouse fibroblasts with a selective COX-2 inhibitor reduced VEGF production by 92%.
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18 MeSH Terms
Oncolytic therapy using a mutant type-1 herpes simplex virus and the role of the immune system.
Lambright ES, Caparrelli DJ, Abbas AE, Toyoizumi T, Coukos G, Molnar-Kimber KL, Kaiser LR
(1999) Ann Thorac Surg 68: 1756-60; discussion 1761-2
MeSH Terms: Animals, Carcinoma, Lewis Lung, Disease Models, Animal, Genetic Therapy, Herpesvirus 1, Human, Mice, Mice, Inbred C57BL, Mice, SCID, Neoplasm Transplantation, Tumor Lysis Syndrome, Viruses
Show Abstract · Added March 5, 2014
BACKGROUND - Herpes simplex virus (HSV)-1716, a replication-restricted herpes simplex virus type 1, has shown efficacy as an oncolytic treatment for central nervous system tumors, breast cancer, ovarian cancer, and malignant mesothelioma. We evaluated the efficacy of HSV-1716 in a murine lung cancer model, Lewis lung carcinoma.
METHODS - Lewis lung carcinoma cells were infected with HSV-1716 and implanted in the flanks of mice at varying ratios of infected to uninfected cells. Tumor burden was assessed by measurement of the weight of the tumor nodule. The role of the immune system was examined by performing experiments in both immunocompetent and SCID mice. Tumors were implanted in the opposite flank to evaluate the vaccine effect.
RESULTS - In immunocompetent and SCID animals, ratio of 1:10 (infected-to-uninfected) cells completely prevented tumor formation and ratio of 1:100 suppressed tumor growth. Established tumors at a distant site in the groups receiving HSV-1716 infected cells showed no difference in size versus control, suggesting absence of a vaccine effect.
CONCLUSIONS - We conclude that HSV-1716 may provide a oncolytic therapy for lung cancer even in the absence of immune system induction and a "carrier" cell could potentially deliver this vector.
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11 MeSH Terms