I have a deep and abiding interest in the development of a cure for cancer, or better still, an absolutely effective method of prevention. This should be true of anyone who plans for longevity. Live long enough and you'll meet a fatal cancer with your name on it - unless something is done about that unfortunate fact in the intervening time.
Cancer researchers are hard at work on a number of very promising strategies for eliminating cancer with near-perfect targeting. If you couple that with a methodology of detection sensitive enough pick up the first few hundred cancer cells as they develop, and at a price point to run all the time, then that might make a good method of prevention - at least until we can engineer our aging biochemistry to stop generating cancers in the first place. But first things first.
I noticed a couple of items regarding the use of the immune system as a cancer therapy; targeting is still the name of the game, but the biotechnology that actually kills cancer cells is home grown rather than developed in a lab.
The new tumor targeting strategy [cleverly] harnesses one of the body's natural antibodies and immune responses. "The killing agent we chose is already in us," says UW-Madison chemistry professor Laura Kiessling, who led the work with postdoctoral researcher Coby Carlson. "It's just not usually directed toward tumor cells."
In a series of cell-based experiments, the researchers' system recognized and killed only those cells displaying high levels of receptors known as integrins. These molecules, which tend to bedeck the surfaces of cancer cells and tumor vasculature in large numbers, have become important targets in cancer research.
"What we've shown is that you don't need a receptor that's found solely on tumor cells," she says. "You just need one that's found in significantly higher numbers on cancerous cells than on normal ones."
Although stem cells hold incredible promise in the fight against certain diseases, in cancer they're anything but helpful. In fact, mounting evidence is showing that a tumor's growth and spread may depend on "cancer stem cells," which comprise only a very small subset of the tumor. Now, a new study by Rockefeller University scientists shows that immunity to cancer stem cells may help protect people with a precancerous condition from developing the full-blown disease, and that these cells could be an important target for cancer vaccines.
This immune response, which correlates so closely with clinical outcome, appears to be targeting the cancer stem cells rather than the bulk tumor cells in myeloma - something that gives researchers hope for a completely new approach. "In immunology for the longest time, we've tried to focus on targeting bulk tumors. But maybe we should be targeting stem cells," Dhodapkar says. "You need to target the roots to really kill the tree, but what we've been doing is trimming the branches and it hasn't worked."
If, ten or twenty years from now, as seems likely, we have access to robust cancer therapies and even more robust methods of detecting cancer early, will that be enough? Will that keep someone cancer free between 60 and 120, for example? It's an interesting question, given that the chances of contracting new cancers are an accelerating prospect with each passing year.
The risk of cancer in any tissue increases with age - and as for most failing machines, quite dramatically so in later life. This stems from underlying changes in biochemistry and the simple rules that determine failure rates in machinery based on gradual wear in component parts - possibly the shortening of your telomeres, possibly damage to stem cells, possibly something else, possibly all of the above. Is it good enough to have a good after-the-fact cure on hand when the risk of occurance is increasing enormously with each passing year? Is there a point past which a good therapy is just overloaded by sheer weight of new cancer bursting from your cells, and where does that point occur?
Food for thought.
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