The Experts below are selected from a list of 9 Experts worldwide ranked by ideXlab platform
Dominic Fan - One of the best experts on this subject based on the ideXlab platform.
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Therapy of multidrug resistant human prostate tumors in the prostate of nude mice by simultaneous targeting of the epidermal growth factor receptor and vascular endothelial growth factor receptor on tumor-associated endothelial cells.
The Prostate, 2006Co-Authors: J. Erik Busby, Sun Jin Kim, Sertac Yazici, Toru Nakamura, Jang Seong Kim, Marva Maya, Xuemei Wang, Kim Anh, Dominic FanAbstract:BACKGROUND Inhibiting epidermal growth factor receptor (EGF-R) and vascular endothelial growth factor receptor (VEGF-R) activation with AEE788 can decrease prostate cancer (Cap) growth/progression. We determined whether tumor cells or tumor-associated endothelial cells were the primary target by treating multidrug-resistant (MDR) Cap growing in the prostate of nude mice. METHODS MDR human Cap cells with 30-fold increased taxane-resistance were implanted into nude mouse prostates. After 2 weeks, mice were randomized to control, paclitaxel, AEE788, and AEE788/paclitaxel for 10 weeks. Mice were necropsied and tumors stained. RESULTS AEE788 or AEE788 plus paclitaxel significantly reduced tumor incidence and tumor weight, and eradicated lymph node metastasis. Inhibiting VEGF-R and EGF-R phosphorylation induced apoptosis of tumor-associated endothelial cells causing a second apoptotic wave of surrounding tumor cells. CONCLUSION Inhibiting VEGF-R and EGF-R activation on tumor-associated endothelial cells with AEE788 combined with paclitaxel can Bypass Cap cell resistance and prevent lymph node metastasis. Prostate © 2006 Wiley-Liss, Inc.
J. Erik Busby - One of the best experts on this subject based on the ideXlab platform.
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Therapy of multidrug resistant human prostate tumors in the prostate of nude mice by simultaneous targeting of the epidermal growth factor receptor and vascular endothelial growth factor receptor on tumor-associated endothelial cells.
The Prostate, 2006Co-Authors: J. Erik Busby, Sun Jin Kim, Sertac Yazici, Toru Nakamura, Jang Seong Kim, Marva Maya, Xuemei Wang, Kim Anh, Dominic FanAbstract:BACKGROUND Inhibiting epidermal growth factor receptor (EGF-R) and vascular endothelial growth factor receptor (VEGF-R) activation with AEE788 can decrease prostate cancer (Cap) growth/progression. We determined whether tumor cells or tumor-associated endothelial cells were the primary target by treating multidrug-resistant (MDR) Cap growing in the prostate of nude mice. METHODS MDR human Cap cells with 30-fold increased taxane-resistance were implanted into nude mouse prostates. After 2 weeks, mice were randomized to control, paclitaxel, AEE788, and AEE788/paclitaxel for 10 weeks. Mice were necropsied and tumors stained. RESULTS AEE788 or AEE788 plus paclitaxel significantly reduced tumor incidence and tumor weight, and eradicated lymph node metastasis. Inhibiting VEGF-R and EGF-R phosphorylation induced apoptosis of tumor-associated endothelial cells causing a second apoptotic wave of surrounding tumor cells. CONCLUSION Inhibiting VEGF-R and EGF-R activation on tumor-associated endothelial cells with AEE788 combined with paclitaxel can Bypass Cap cell resistance and prevent lymph node metastasis. Prostate © 2006 Wiley-Liss, Inc.
Sun Jin Kim - One of the best experts on this subject based on the ideXlab platform.
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Therapy of multidrug resistant human prostate tumors in the prostate of nude mice by simultaneous targeting of the epidermal growth factor receptor and vascular endothelial growth factor receptor on tumor-associated endothelial cells.
The Prostate, 2006Co-Authors: J. Erik Busby, Sun Jin Kim, Sertac Yazici, Toru Nakamura, Jang Seong Kim, Marva Maya, Xuemei Wang, Kim Anh, Dominic FanAbstract:BACKGROUND Inhibiting epidermal growth factor receptor (EGF-R) and vascular endothelial growth factor receptor (VEGF-R) activation with AEE788 can decrease prostate cancer (Cap) growth/progression. We determined whether tumor cells or tumor-associated endothelial cells were the primary target by treating multidrug-resistant (MDR) Cap growing in the prostate of nude mice. METHODS MDR human Cap cells with 30-fold increased taxane-resistance were implanted into nude mouse prostates. After 2 weeks, mice were randomized to control, paclitaxel, AEE788, and AEE788/paclitaxel for 10 weeks. Mice were necropsied and tumors stained. RESULTS AEE788 or AEE788 plus paclitaxel significantly reduced tumor incidence and tumor weight, and eradicated lymph node metastasis. Inhibiting VEGF-R and EGF-R phosphorylation induced apoptosis of tumor-associated endothelial cells causing a second apoptotic wave of surrounding tumor cells. CONCLUSION Inhibiting VEGF-R and EGF-R activation on tumor-associated endothelial cells with AEE788 combined with paclitaxel can Bypass Cap cell resistance and prevent lymph node metastasis. Prostate © 2006 Wiley-Liss, Inc.
Sertac Yazici - One of the best experts on this subject based on the ideXlab platform.
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Therapy of multidrug resistant human prostate tumors in the prostate of nude mice by simultaneous targeting of the epidermal growth factor receptor and vascular endothelial growth factor receptor on tumor-associated endothelial cells.
The Prostate, 2006Co-Authors: J. Erik Busby, Sun Jin Kim, Sertac Yazici, Toru Nakamura, Jang Seong Kim, Marva Maya, Xuemei Wang, Kim Anh, Dominic FanAbstract:BACKGROUND Inhibiting epidermal growth factor receptor (EGF-R) and vascular endothelial growth factor receptor (VEGF-R) activation with AEE788 can decrease prostate cancer (Cap) growth/progression. We determined whether tumor cells or tumor-associated endothelial cells were the primary target by treating multidrug-resistant (MDR) Cap growing in the prostate of nude mice. METHODS MDR human Cap cells with 30-fold increased taxane-resistance were implanted into nude mouse prostates. After 2 weeks, mice were randomized to control, paclitaxel, AEE788, and AEE788/paclitaxel for 10 weeks. Mice were necropsied and tumors stained. RESULTS AEE788 or AEE788 plus paclitaxel significantly reduced tumor incidence and tumor weight, and eradicated lymph node metastasis. Inhibiting VEGF-R and EGF-R phosphorylation induced apoptosis of tumor-associated endothelial cells causing a second apoptotic wave of surrounding tumor cells. CONCLUSION Inhibiting VEGF-R and EGF-R activation on tumor-associated endothelial cells with AEE788 combined with paclitaxel can Bypass Cap cell resistance and prevent lymph node metastasis. Prostate © 2006 Wiley-Liss, Inc.
Toru Nakamura - One of the best experts on this subject based on the ideXlab platform.
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Therapy of multidrug resistant human prostate tumors in the prostate of nude mice by simultaneous targeting of the epidermal growth factor receptor and vascular endothelial growth factor receptor on tumor-associated endothelial cells.
The Prostate, 2006Co-Authors: J. Erik Busby, Sun Jin Kim, Sertac Yazici, Toru Nakamura, Jang Seong Kim, Marva Maya, Xuemei Wang, Kim Anh, Dominic FanAbstract:BACKGROUND Inhibiting epidermal growth factor receptor (EGF-R) and vascular endothelial growth factor receptor (VEGF-R) activation with AEE788 can decrease prostate cancer (Cap) growth/progression. We determined whether tumor cells or tumor-associated endothelial cells were the primary target by treating multidrug-resistant (MDR) Cap growing in the prostate of nude mice. METHODS MDR human Cap cells with 30-fold increased taxane-resistance were implanted into nude mouse prostates. After 2 weeks, mice were randomized to control, paclitaxel, AEE788, and AEE788/paclitaxel for 10 weeks. Mice were necropsied and tumors stained. RESULTS AEE788 or AEE788 plus paclitaxel significantly reduced tumor incidence and tumor weight, and eradicated lymph node metastasis. Inhibiting VEGF-R and EGF-R phosphorylation induced apoptosis of tumor-associated endothelial cells causing a second apoptotic wave of surrounding tumor cells. CONCLUSION Inhibiting VEGF-R and EGF-R activation on tumor-associated endothelial cells with AEE788 combined with paclitaxel can Bypass Cap cell resistance and prevent lymph node metastasis. Prostate © 2006 Wiley-Liss, Inc.
