08 April 2009

Interview w/Professor Blackburn

"Interview with Elizabeth Blackburn: Aging & Disease" & "Dealing with Cancer" Frontline (India)

Prof. Elizabeth H. Blackburn (physiology, biology, UC Berkeley) researches the ends of eukaryotic chromosomesW T, or telomeresW. I became aware of her entirely as a result of reading the interview in Frontline of India.

Blackburn's research became interesting to the broader public as a result of discoveries that there was a very strong link between telomeres and health conditions associated with aging.
Yes. We are looking at that. There are these successfully treated AIDS patients who have been on high activity antiretroviral therapy [HAART] for some years. Their lives have been saved, and they have been kept going for years on these drugs. The virus is kept [at a] very low [level] although it is never completely contained. And do you know what’s happening? It’s sort of an epidemic. These [successfully treated HAART] individuals are now developing diseases that look like the diseases of the aged. For their age group, these people are getting more cardiovascular diseases, more dementia, more osteoarthritis, more renal disease and a whole spectrum of diseases that are [making them] look as if they are really old.
Telomeres are regulated and restored through an unusual combination protein-enzyme known (naturally) as "telomerase." As cells divide, the telomeres at the end of each chromosome are subdivided until they are either restored or depleted. If the telomere is depleted, the cell cannot subdivide and therefore dies. In some cases, the body supplies cells with telomerase to enable continuing subdivision and growth. In other cases, cells "develop" the ability to supply their own telomerase; their growth ceases to be regulated by the body, and they can become cancerous.

Prof. Blackburn and her assistant, Carol Greider, discovered telomerase in the 1970's. The implications of telomerase in the lives of cells was extremely far-reaching: it affected research into cancer, AIDS, aging, and organ regeneration.

The interview is pretty basic, and mostly geared to readers like myself who have never heard of telomerase. However, it veers towards speculation towards the end:
FLO: Though we know that diseases are caused by a whole lot of factors, do you see a kind of paradigm developing that would ultimately, perhaps in the distant future, lead to a unidirectional telomerase-based approach for attacking disease?

EHB: You know part of me wants to say yes. That would be terrific, but you risk hubris when you say something like that because you are then immediately proved wrong. But, as I said, because so much evidence has come in a consistent fashion, this seems like a pretty good attack on the problem. We see [that] these environmental factors like chronic stress are obviously acting on telomerase and telomere lengths through the immune system. We also see [that] when people are dealing with their stress well, it is correlating with having higher [levels of] telomerase and better telomere lengths. We put two and two together and say what if people could be helped to deal with their stresses.

Now you can’t change life. You can’t change the fact that somebody had a chronically ill childhood or the father has dementia. But, maybe, you can give people these tools, or things they can do that will help them cope. Would that modulate their telomerase up? I love it because it is very, very cheap.
I can imagine this would lead to a massive boom in the biochip industry as therapy becomes dominated by direct polymerase sampling and chain reactions. A web search turned up this recent patent for a biochip that directly captures and analyzes circulating tumor cells (CTC).

Sources & Additional Reading:
SuperscriptW links to relevant Wikipedia article; superscriptC to Cells Alive article; superscriptT to Library/Thinkquest article. Errors in the summary below are my fault, and not the fault of the linked authors.

The reference to HAART involves some explanation: HIV, the virus that causes AIDS, is known as a retrovirusW C it attacks the actual DNA of the patient via the enzyme for DNA replication (i.e., RNA), and thereby integrates itself into the patient's DNA. As a consequence, antiretroviral therapy (ART) mainly consists of chemical inhibitors. Usually ART is administered with several inhibitors (sometimes referred to as a "cocktail"), in which case it is known as "high activity" ART, or HAART. See "Recommended HIV Treatment Regimens" and "Approved Medications to Treat HIV Infection" , US Department of Health and Human Services (Dec 2008).

Put another way, therapies for AIDS target the process of cell reproduction at the polymerase level—at the point in which DNA strands are replicated through interaction with the enzyme RNAW. This naturally has deleterious side-effects, since some desirable polymerase activity is also suppressed. The overall effect is similar to regular aging: as organisms get older, their body fails to reproduce moribund cells.

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