The Experts below are selected from a list of 7035 Experts worldwide ranked by ideXlab platform
Ling Geng - One of the best experts on this subject based on the ideXlab platform.
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Hedgehog signaling in the murine melanoma microenvironment
Angiogenesis, 2007Co-Authors: Ling Geng, Kyle C. Cuneo, Michael K. Cooper, H. Wang, Konjeti R. Sekhar, Dennis E. HallahanAbstract:The Hedgehog intercellular signaling pathway regulates cell proliferation and differentiation. This pathway has been implicated to play a role in the pathogenesis of cancer and in embryonic blood vessel development. In the current study, Hedgehog signaling in Tumor related vasculature and microenvironment was examined using human umbilical vein endothelial cells and B16F0 (murine melanoma) Tumors models. Use of exogenous Sonic hedgehog (Shh) peptide significantly increased BrdU incorporation in endothelial cells in vitro by a factor of 2 (P < 0.001). The Hedgehog pathway antagonist cyclopamine effectively reduced Shh-induced proliferation to control levels. To study Hedgehog signaling in vivo a hind Limb Tumor model with the B16F0 cell line was used. Treatment with 25 mg/kg cyclopamine significantly attenuated BrdU incorporation in Tumor cells threefold (P < 0.001), in Tumor related endothelial cells threefold (P = 0.004), and delayed Tumor growth by 4 days. Immunohistochemistry revealed that the Hedgehog receptor Patched was localized to the Tumor stroma and that B16F0 cells expressed Shh peptide. Furthermore, mouse embryonic fibroblasts required the presence of B16F0 cells to express Patched in a co-culture assay system. These studies indicate that Shh peptide produced by melanoma cells induces Patched expression in fibroblasts. To study Tumor related angiogenesis a vascular window model was used to monitor Tumor vascularity. Treatment with cyclopamine significantly attenuated vascular formation by a factor of 2.5 (P < 0.001) and altered vascular morphology. Furthermore, cyclopamine reduced Tumor blood vessel permeability to FITC labeled dextran while having no effect on normal blood vessels. These studies suggest that Hedgehog signaling regulates melanoma related vascular formation and function.
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The receptor tyrosine kinase inhibitor SU11248 impedes endothelial cell migration, tubule formation, and blood vessel formation in vivo, but has little effect on existing Tumor vessels
Angiogenesis, 2004Co-Authors: Katherine L. Osusky, Dennis E. Hallahan, Yu Shyr, Ling GengAbstract:Antiangiogenic agents produce regression in few Tumors in clinical trials, but are effective in preventing recurrences. To determine whether the vascular endothelial growth factor (VEGF) receptor is a molecular target to prevent metastatic disease, we utilized a non-specific inhibitor of the VEGF receptor, SU11248. This receptor tyrosine kinase (RTK) inhibitor prevented migration of endothelial cells and markedly attenuated capillary-like tubule formation in endothelial cells in culture. Similarly, this agent prevented blood vessel formation in the Tumor vascular window model. VEGF RTK inhibition produced minimal effects on established blood vessels in the Tumor vascular window model and little effect on blood flow studied by power Doppler analysis. To determine whether these agents attenuate the development of metastases, Lewis lung carcinoma Tumors were resected from the dorsal skin and lung metastases were quantified with and without treatment with SU11248. The RTK inhibitor attenuated the formation of lung metastases following resection of the hind Limb Tumor. In contrast, these agents did not induce regression of primaries but slowed the progression of Tumor growth. These findings suggest that the greatest role for VEGF antagonists may be to prevent the formation of new blood vessels, during and after conventional therapy is given to existing neoplastic disease.
Dennis E. Hallahan - One of the best experts on this subject based on the ideXlab platform.
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Hedgehog signaling in the murine melanoma microenvironment
Angiogenesis, 2007Co-Authors: Ling Geng, Kyle C. Cuneo, Michael K. Cooper, H. Wang, Konjeti R. Sekhar, Dennis E. HallahanAbstract:The Hedgehog intercellular signaling pathway regulates cell proliferation and differentiation. This pathway has been implicated to play a role in the pathogenesis of cancer and in embryonic blood vessel development. In the current study, Hedgehog signaling in Tumor related vasculature and microenvironment was examined using human umbilical vein endothelial cells and B16F0 (murine melanoma) Tumors models. Use of exogenous Sonic hedgehog (Shh) peptide significantly increased BrdU incorporation in endothelial cells in vitro by a factor of 2 (P < 0.001). The Hedgehog pathway antagonist cyclopamine effectively reduced Shh-induced proliferation to control levels. To study Hedgehog signaling in vivo a hind Limb Tumor model with the B16F0 cell line was used. Treatment with 25 mg/kg cyclopamine significantly attenuated BrdU incorporation in Tumor cells threefold (P < 0.001), in Tumor related endothelial cells threefold (P = 0.004), and delayed Tumor growth by 4 days. Immunohistochemistry revealed that the Hedgehog receptor Patched was localized to the Tumor stroma and that B16F0 cells expressed Shh peptide. Furthermore, mouse embryonic fibroblasts required the presence of B16F0 cells to express Patched in a co-culture assay system. These studies indicate that Shh peptide produced by melanoma cells induces Patched expression in fibroblasts. To study Tumor related angiogenesis a vascular window model was used to monitor Tumor vascularity. Treatment with cyclopamine significantly attenuated vascular formation by a factor of 2.5 (P < 0.001) and altered vascular morphology. Furthermore, cyclopamine reduced Tumor blood vessel permeability to FITC labeled dextran while having no effect on normal blood vessels. These studies suggest that Hedgehog signaling regulates melanoma related vascular formation and function.
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The receptor tyrosine kinase inhibitor SU11248 impedes endothelial cell migration, tubule formation, and blood vessel formation in vivo, but has little effect on existing Tumor vessels
Angiogenesis, 2004Co-Authors: Katherine L. Osusky, Dennis E. Hallahan, Yu Shyr, Ling GengAbstract:Antiangiogenic agents produce regression in few Tumors in clinical trials, but are effective in preventing recurrences. To determine whether the vascular endothelial growth factor (VEGF) receptor is a molecular target to prevent metastatic disease, we utilized a non-specific inhibitor of the VEGF receptor, SU11248. This receptor tyrosine kinase (RTK) inhibitor prevented migration of endothelial cells and markedly attenuated capillary-like tubule formation in endothelial cells in culture. Similarly, this agent prevented blood vessel formation in the Tumor vascular window model. VEGF RTK inhibition produced minimal effects on established blood vessels in the Tumor vascular window model and little effect on blood flow studied by power Doppler analysis. To determine whether these agents attenuate the development of metastases, Lewis lung carcinoma Tumors were resected from the dorsal skin and lung metastases were quantified with and without treatment with SU11248. The RTK inhibitor attenuated the formation of lung metastases following resection of the hind Limb Tumor. In contrast, these agents did not induce regression of primaries but slowed the progression of Tumor growth. These findings suggest that the greatest role for VEGF antagonists may be to prevent the formation of new blood vessels, during and after conventional therapy is given to existing neoplastic disease.
Riad Salem - One of the best experts on this subject based on the ideXlab platform.
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Comparison of two different methods for inoculating VX2 Tumors in rabbit livers and hind Limbs.
Journal of vascular and interventional radiology : JVIR, 2008Co-Authors: Sumeet Virmani, Kathleen R. Harris, Barbara Szolc-kowalska, Tatjana Paunesku, Gayle E. Woloschak, Fred T. Lee, Robert J. Lewandowski, Kent T. Sato, Robert K. Ryu, Riad SalemAbstract:Purpose To compare two methods to ( a ) propagate VX2 cell strain in rabbit hind Limbs and ( b ) inoculate liver parenchymal Tumors in rabbits. Materials and Methods One hundred forty-two New Zealand white rabbits were used for this study (60 with hind Limb Tumor [donors] and 82 with liver Tumors [recipients]). In the donor group, nine rabbits received frozen VX2 cell suspension and 51 were injected with freshly prepared VX2 cell suspension. In the recipient group, 32 rabbits were injected with VX2 Tumor cells and 50 were implanted with a small Tumor fragment in the liver parenchyma. Success rates in terms of Tumor growth were compared by using χ 2 or Fisher exact tests, with alpha=.05. Results Hind Limb and liver Tumors were successfully grown in 48 of the 60 rabbits in the donor group (80%) and 57 of the 82 rabbits in the recipient group (70%). The success rate of growing hind Limb Tumors increased from 33% (three of nine rabbits) to 88% (45 of 51 rabbits) when fresh VX2 cells instead of frozen were injected percutaneously ( P P P Conclusions The authors recommend ( a ) the use of fresh VX2 cell suspension for percutaneous injection in the hind Limbs of rabbits to maintain the VX2 cell strain and ( b ) the surgical implantation of freshly harvested VX2 Tumor fragment into the liver parenchyma to establish liver Tumors.
Guy Fabry - One of the best experts on this subject based on the ideXlab platform.
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Ilizarov reconstruction after a failed upper Limb salvage procedure in oncology: a case report.
Journal of shoulder and elbow surgery, 2000Co-Authors: Ralph Sakkers, Johan Lammens, Peter Reynaert, Guy FabryAbstract:structive treatment after upper Limb Tumor excision, only a few focus on the management and final outcome in cases of failure. This report describes Ilizarov’s segmental bone transport technique as a salvage procedure in a patient with collapse of an infected osteoarticular allograft of the distal humerus and proximal ulna. Failure caused by collapse and especially infection is well documented in the literature, with an infection frequency between 6% and 14% and failure up to 57%.1,3,4,7-9 The treatment of infected grafts still remains a problem but can be done with excision of infected tissue and reconstruction with bone transport procedures.
Sumeet Virmani - One of the best experts on this subject based on the ideXlab platform.
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Comparison of two different methods for inoculating VX2 Tumors in rabbit livers and hind Limbs.
Journal of vascular and interventional radiology : JVIR, 2008Co-Authors: Sumeet Virmani, Kathleen R. Harris, Barbara Szolc-kowalska, Tatjana Paunesku, Gayle E. Woloschak, Fred T. Lee, Robert J. Lewandowski, Kent T. Sato, Robert K. Ryu, Riad SalemAbstract:Purpose To compare two methods to ( a ) propagate VX2 cell strain in rabbit hind Limbs and ( b ) inoculate liver parenchymal Tumors in rabbits. Materials and Methods One hundred forty-two New Zealand white rabbits were used for this study (60 with hind Limb Tumor [donors] and 82 with liver Tumors [recipients]). In the donor group, nine rabbits received frozen VX2 cell suspension and 51 were injected with freshly prepared VX2 cell suspension. In the recipient group, 32 rabbits were injected with VX2 Tumor cells and 50 were implanted with a small Tumor fragment in the liver parenchyma. Success rates in terms of Tumor growth were compared by using χ 2 or Fisher exact tests, with alpha=.05. Results Hind Limb and liver Tumors were successfully grown in 48 of the 60 rabbits in the donor group (80%) and 57 of the 82 rabbits in the recipient group (70%). The success rate of growing hind Limb Tumors increased from 33% (three of nine rabbits) to 88% (45 of 51 rabbits) when fresh VX2 cells instead of frozen were injected percutaneously ( P P P Conclusions The authors recommend ( a ) the use of fresh VX2 cell suspension for percutaneous injection in the hind Limbs of rabbits to maintain the VX2 cell strain and ( b ) the surgical implantation of freshly harvested VX2 Tumor fragment into the liver parenchyma to establish liver Tumors.