Lani
06-17-2006, 03:06 PM
It attackes PDGF receptors, which breast cancer induced new blood vessels have as well I believe.
Food for thought--combining targetted therapies?
Just speculation for now--how about a clinical trial?
Imatinib Has Antiangiogenic Effects in Prostate Cancer Metastasis
NEW YORK (Reuters Health) Jun 16 - As a treatment for prostate cancer that has spread to bone, imatinib (Gleevec/Glivec) seems to target not the tumor cells themselves but tumor-related endothelial cells, thereby blocking tumor-induced angiogenesis, the results of an animal study indicate.
In animal studies as well as clinical trials, platelet-derived growth factor receptor (PDGFR) blockers, like imatinib, have proven to be effective against prostate cancer bone metastases. However, it was unclear if these agents were targeting tumor cells or their associated endothelial cells since both express activated PDGFR.
To investigate, Dr. Isaiah J. Fidler, from M. D. Anderson Cancer Center in Houston, and colleagues created a nude mouse model of human prostate cancer metastatic to bone. The animals were then treated with distilled water, imatinib, paclitaxel, or both agents for 10 weeks.
The researchers report in the Journal of the National Cancer Institute for June 7that imatinib, alone or in combination with paclitaxel, was significantly more effective than placebo in reducing bone metastases, median tumor weight, bone lysis, and lymph node metastases. In vitro, however, imatinib had little effect on the prostate cancer cells that were implanted into the mice.
Further analysis showed that while imatinib blocked PDGFR activation on both tumor cells and their related endothelial cells, the drug only increased apoptosis of the latter. Moreover, imatinib alone, and to a greater extent in combination with paclitaxel, decreased mean vessel density, which, in turn, promoted the death of tumor cells.
"Whether this approach can be useful for other tumor types is unknown," the team comments. "The heterogeneity of angiogenesis in human tumors" means that more work is needed before "optimal treatment regimens with targeted antivascular agents can be developed."
J Natl Cancer Inst 2006;98:783-793.
Food for thought--combining targetted therapies?
Just speculation for now--how about a clinical trial?
Imatinib Has Antiangiogenic Effects in Prostate Cancer Metastasis
NEW YORK (Reuters Health) Jun 16 - As a treatment for prostate cancer that has spread to bone, imatinib (Gleevec/Glivec) seems to target not the tumor cells themselves but tumor-related endothelial cells, thereby blocking tumor-induced angiogenesis, the results of an animal study indicate.
In animal studies as well as clinical trials, platelet-derived growth factor receptor (PDGFR) blockers, like imatinib, have proven to be effective against prostate cancer bone metastases. However, it was unclear if these agents were targeting tumor cells or their associated endothelial cells since both express activated PDGFR.
To investigate, Dr. Isaiah J. Fidler, from M. D. Anderson Cancer Center in Houston, and colleagues created a nude mouse model of human prostate cancer metastatic to bone. The animals were then treated with distilled water, imatinib, paclitaxel, or both agents for 10 weeks.
The researchers report in the Journal of the National Cancer Institute for June 7that imatinib, alone or in combination with paclitaxel, was significantly more effective than placebo in reducing bone metastases, median tumor weight, bone lysis, and lymph node metastases. In vitro, however, imatinib had little effect on the prostate cancer cells that were implanted into the mice.
Further analysis showed that while imatinib blocked PDGFR activation on both tumor cells and their related endothelial cells, the drug only increased apoptosis of the latter. Moreover, imatinib alone, and to a greater extent in combination with paclitaxel, decreased mean vessel density, which, in turn, promoted the death of tumor cells.
"Whether this approach can be useful for other tumor types is unknown," the team comments. "The heterogeneity of angiogenesis in human tumors" means that more work is needed before "optimal treatment regimens with targeted antivascular agents can be developed."
J Natl Cancer Inst 2006;98:783-793.