Fight Aging!

A couple of recent items circulating through the popular science press illustrate the interesting relationship between cancerous cells and their mitochondria - a relationship that can be exploited to attack cancer. Most of the press has focused on the particular compounds used in the threads of research (dichloroacetate and capsaicin) rather than on the underlying mechanism, which is a pity, and rather indicative of the state of science journalism in general. The hammer is meaningless without the knowledge of how to use it - and a better understanding of the problem may lead one to a more effective tool for the job. Still, one or two articles are actually quite good in their focus on the science:

Cancer cells manage their energy production in a most peculiar way. A healthy cell relies on its mitochondria (descendants of bacteria that took up residence in the single-celled ancestors of animals and plants about 2 billion years ago) to oxidise sugar molecules and release useful energy. Most cancer cells, however, use a less efficient mechanism called glycolysis to power themselves. They thus cut their mitochondria out of the loop.

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Cancer cells seem to adjust so well to glycolysis that even if blood vessels do grow into a tumour and the oxygen thus returns, they stick with it. From the cancer's point of view that is a very good choice, as one of the other jobs of the mitochondria is to kill a cell if it goes bad - a process known as apoptosis.

The role of dichloroacetate is to re-activate the mitochondria by stimulating an enzyme that feeds pyruvate into their energy-generating cycle. (The drug is already tested and approved for the treatment of certain mitochondrial diseases.) It seems this reactivation also allows the mitochondria to stimulate apoptosis.

So it seems quite feasible to engineer one part of a cancerous cell to kill that cell in a form of biological judo. Some of the best potential therapies for a range of condition these days rely on the use of existing mechanisms, subverted to the task at hand. I imagine there are much more efficient ways of doing this ahead in the future - all part and parcel of the strategy of identifying a biochemical difference in cancer cells and then sending in a therapy that acts on that difference.

But on to the capsaicin and another illustration of the same mechanism, triggered a different way:

The tests on cultures of human lung and pancreatic cancers revealed that the family of molecules to which capsaicin belongs, the vanilloids, bind to proteins in the cancer cell mitochondria causing apoptosis (cell death) without harming surrounding healthy cells.

The Nottingham University breakthrough study raises hopes that the innate vulnerability of all cancers has been discovered and that drugs could now be developed to attack mitochondria in a similar way to capsaicin.

Lead researcher Dr Timothy Bates said that the mitochondria in cancer cells could be targeted by other compounds and that the investigation and development of anti-mitochondrial drugs for cancer chemotherapy was likely to be "extremely significant" in the fight against cancer.

All very interesting; the diversity of cancer research is continually a surprise - it is driving a great deal of new understanding in the functioning of our cells. We will have ever greater need of that knowledge in the years ahead, as scientists continue to work on ways to help us live longer, healthier lives.

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