Slanted Science

There is no greater prize in science. Keep your Albert Einstein World Award of Science. Pfft to your National Medal of Science. And spfff to your Arkansas State Fair Best Cow (Milkers Class). The one they’re all out there to win is The Nobel Prize. And this year’s winners in the field of medicine have just been announced: Elizabeth Blackburn, Carol Greider and Jack Szostak. Congrats to them all, and let’s have a look at what got them there.

Telomeres. That’s what these guys won this prestigious prize (and a fair bit of cash) for. What are they and why was their discovery worthy of a Nobel? Well, in the future you could go to the SlantedScience tutorial pages to find out. In the meantime, here’s a brief explanation. Just about every cell in an animal’s body (that means you too, you animal) contains all of the DNA required to make every single cell, and carry out every single process, needed by that animal. But rather than being in one long strand, this enormous amount of DNA is separated into several smaller strands (23, in the case of you and me. 39 for a dog. Don’t worry, you’ll get over it; more doesn’t always mean better, as my wife constantly reassures me).

Whenever a cell divides (during the time when an embryo is developing, for example. Or after a wedding, when the liver needs to replace the cells you slaughtered mercilessly the night before), these strands of DNA must be accurately reproduced, so that each of the new cells receives the same DNA as was present in their mother cell.

However, the enzymes which carry out this task have a problem: they can’t quite reach the end of each strand, or chromosome. These scientists, years ago (that’s how the Nobel prize works; the work has to show its validity and importance over a fair few years) wondered this: if a chromosome can’t be copied to its very ends each time, then surely each cell division has an inherent loss of information. Therefore, after a few cell divisions, some important information will be lost and the whole lot will be useless.

The answer, they found, was telomeres: small, otherwise uselss little units of DNA which sit on the ends of chromosomes and act as fall guys each time a cell divides and can’t quite copy to the chromosome ends. Telomeres are gradually shortened with each cell division, and this is suspected to play a role in aging.

And cancer.

This discovery rapidly attracted the attention of cancer researchers, and it was soon discovered that cancer, the naughty little fella, has subverted this natural mechanism to its own malevolent purpose. Cells naturally have an enzyme called telomerase, which has the ability to increase the telomeres in any individual cell. The result, of course, is to increase a cell’s lifespan. What cancer does, it turns out, is to inappropriately turn on telomerase, which means that a cancer cell is constantly having its telomeres reinvigorated and can thus undergo a lot more cell divisions than it was originally supposed to. If you imagine the process of forming a tumor as being a marathon, then a normal cell would be running the race with no water breaks, and run out of breath at about 10 miles. A cancer cell, on the other hand, would be receiving isotonic fluids (telomere extensions) every few hundred yards (courtesy of telomerase), and so would be able to run for much longer.

And that represents the importance of these guys’ discovery, and what won them the Nobel: the impact on aging and cancer, two of the most important (read “lucrative”, you cynics) research areas in science today.

Congratulations to all three of them, and may they spend the prize money wisely (my PayPal account details are available on request).