[MOL] Signal transduction and ansomycins.... [00976] Medicine On Line


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[MOL] Signal transduction and ansomycins....



Signal Transduction and Ansomycins

Excerpt from Update: The Prevention and Treatment of Breast Cancer

Signal Transduction

There's a foundation, called the Breast Cancer Research Foundation that supports clinical trials and genetic studies in breast cancer. Every year they have a symposium in New York that's open to the public, where people can come every year to present their various findings.

The E1A is one of the targets that was discussed at that particular symposium. This isn't research that I was involved in directly, but it was part of the research that I'm involved in peripherally because of the activities of the Breast Cancer Research Foundation. It is one of the components of the signaling pathway in the cell that tells the cell to divide. It's a very complicated matrix of chemical reactions that tells the cell to divide.

A cell can be stimulated to start to divide because estrogen acts on the estrogen receptor or HER-2 is stimulated. That's a much more complicated story, or other signals start at the cell surface. But then there's a cascade of events that eventually leads to cell division. That's called signal transduction, where the signal is transduced to a number of events, and this is a component of that particular process. That's also a potential target for therapeutics, and there's a variety of different ways for approaching that particular target.


Ansomycins

The HER-2 molecule -- that thing on the surface of the cell -- like every other molecule in the body, has to be made, but it has to be folded in a certain way for it to be functional. The body just doesn't make the chemicals, it has to actually fold the chemicals and put them in the right configuration. The way this chemical folds is that there are a class of proteins in the cell called chaperone proteins, the function of which is to hold the molecule in the right position so it can fold properly. And there is a certain class of chaperone molecules that are called heat-shock proteins. Well, we have a drug that gets into the heat-shock protein, and prevents the HER-2 from getting there. So the HER-2 can't fold correctly, and when it doesn't fold correctly, the body, the cell, destroys it. These drugs, which are called ansomycins, actually make the cell destroy its own HER-2. So, not only can you attack HER-2 by interfering with the HER-2 itself, with some drug like Herceptin®, or interfere with the functioning or the reproduction of the HER-2 with targets, which is E1A, but you can also actually destroy the HER-2 in the cell by preventing the body, the cell, from folding it properly. These drugs are called ansomycins, and they're actually in clinical trial right now. There's one other drug called 17-AEG that we're studying that actually does that. It looks profoundly exciting and actually kills cancer cells beautifully in the laboratory, and now we're doing the clinical studies to see if it works.


 
 
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