Major symposium examines new cancer treatments
“Because the need for new cancer treatments is so great, cancer is an extremely important research priority, so events like this Symposium provide an important opportunity to share knowledge and discuss new breakthroughs in the field of oncology.”
International experts will gather in Dubai this weekend for a major symposium on oncology, which will include sessions on breakthrough treatments for forms of cancer which previously had no viable remedies. via AME Info
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Since: Dec 05
#1 Jan 18, 2008
Sutent (sunitinib) is an inhibitor of multiple protein kinases, platelet-derived growth factor (PDGFR), vascular endothelial growth factor receptors (VEGFR), stem cell factor receptor (KIT), FMS-like tyrosine kinase (Flt3), colony stimulating factor (CSF-1R), and the neurotrophic factor receptor (RET). Because these proteins are involved in both tumor proliferation and angiogenesis, Sutent has both anti-tumor as well as anti-angiogenic properties. In addition, because Sutent inhibits multiple kinases, it possesses activity against multiple types of tumors.
The largest group of kinases are Protein kinases, which act on and modify the activity of specific proteins. So people will try and get some sort of gene-based test to measure the expression-mutation of these kinases. But something more elemental is going on. Does the drug even enter the cell? Once entered, does it immediately get metabolized or pumped out, or does it accumulate?
The new EGFRx Anti-Tyrosine Kinase Profile Assay measures the net effect of everthing which goes on (Functional Profiling). Are the cells ultimately killed, or arent they? In photomicrographs (two magnifications), it is fairly easy to see that some clones of tumor cells dont accumulate the drug. These cells won't get killed by it. Sutent is conveniently pigmented, brilliant yellow. It is easy to see which cells have taken it up. But you wouldnt pick this up with an assay which only measured the kinases themselves.
Normal chemotherapy kills both cancer cells and healthy normal cells (mainly rapidly-dividing cells). Oncologists try to minimize damage to normal cells and to enhance the cell-killing effect on cancer cells. Too often, this delicate balance is not achieved.
Targeted therapy drugs interfere with specific molecules (receptors and enzymes inside and outside a cancer cell). By focusing on these molecular and cellular changes, targeted cancer drugs go after the target in these cells, rather than just all cells. Because of this,targeted drugs may be more effective than current treatments, and may be less harmful to normal cells.
Functional profiling can discriminate between the activity of different targeted drugs and identify situations in which it is advantageous to combine the targeted drugs with other types of cancer drugs. Because these new smart drugs will work for some but not all cancer patients who receive them, whole cell profiling can accurately identify patients who would benefit from treatment with molecularly-targeted anti-cancer therapies.
Not only is this an important predictive test that is available, but it is also a unique tool that can help to identify newer and better drugs, evaluate promising drug combinations, and serve as a gold standard correlative model with which to develop new DNA, RNA, and protein-based tests that better predict for drug activity.
This kind of technique exists, and might be very valuable, especially when active chemoagents are limited in a particular disease; it makes more sense than ever to test the tumor first. Afterall, cutting-edge techniques can often provide superior results over tried-and-true methods that have been around for many years.
The EGFRx Anti-Tyrosine Kinase Profile Assay is the only assay that involves direct visualization of the cancer cells at endpoint. This allows for accurate assessment of drug activity, discriminates tumor from non-tumor cells, and provides a permanent archival record, which improves quality, serves as control, and assesses dose response in vitro.
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