Health & Medicine / Cancer

Photo courtesy of Elisabeth Fall

Imagine that this scientist kept a to-do list: On it would be a cure for cancer and, further down, understanding the diseases associated with aging. Elizabeth Blackburn is the 59-year-old Tasmanian-born scientist responsible for launching one of the hottest fields in the life sciences, the study of telomeres. These tiny strips of DNA cap the ends of chromosomes, and her research promises to yield potent therapeutics for many of the scourges that plague humanity.

The Cambridge-educated biochemist’s work has been honored with just about every major award in science—the Lasker, the Gruber, and the Gairdner prizes—and she recently made the list of Time magazine’s 100 most influential people. Telomeres drew her attention because of their crucial role in preventing the tips of chromosomes from fraying when a cell divides. Usually, when a cell makes a copy of itself, the telomeres shorten, which may explain why cells age and die. In the mid-1980s, Blackburn and her graduate student, Carol Greider, discovered telomerase, an enzyme she has likened to Dr. Jekyll and Mr. Hyde. Sometimes telomerase is a good guy because it helps produce immune cells and stops telomeres from shortening, but it can also make cells immortal, which prompts them to turn malignant. Because of the enzyme’s properties, it may eventually be the basis for therapies to combat cancer, heart disease, and diabetes—perhaps even halt the ravages of age.

Despite her accolades, Blackburn is warm and accessible, with traces of the shy science nerd who would serenade creatures as a child. In her comfortably cluttered office at the University of California at San Francisco, she talked with DISCOVER about how she became beguiled by bits of DNA.

You grew up in Launceston, a small city on the island of Tasmania. Did you feel cut off from the world?
It felt very remote, but Melbourne was an hour’s flight away, and I felt there was a big world out there.

Both your parents were physicians. Did that influence your career choice?
I just liked science. I liked animals. No one ever said “be a doctor.” But because so many members of my extended family—aunts, uncles—were doctors, there was this expectation that I’d probably be a physician. It never occurred to me that as a woman I wouldn’t have gone into science. I’m sure that’s just the example of having a mother who was doing some kind of career.

You left Australia in 1971 to get your Ph.D. at Cambridge in England. At that time, molecular biology was undergoing tremendous intellectual ferment. Did that attract you to the field?
The way I got into the field was very straightforward. I decided I wanted to go to Cambridge, and then I got introduced to Fred Sanger. I was very conscientious, and I asked him when I first got there if I should start reading up on things. But he said, “No, I think you can just start these experiments,” so I plunged right in.

Sanger was already a Nobel Prize winner for his work in sequencing insulin. Was working in his lab daunting?
At Cambridge, there was a completely unintimidating culture, and there were no class divisions among the students. I remember I referred to him as “Dr. Sanger” to the man who was in charge of the lab supply storeroom. And he said, “Who? We all call him Fred.” Sanger was on the cusp of devising methods for DNA sequencing [for which he won a second(pdf) Nobel]. But what he had gotten working was sequencing RNA by using the same essential principle as he’d used for sequencing insulin. He had little blocks of overlapping pieces of the puzzle, and basically, he fit the pieces together. And that just struck me as being really interesting.

John Sedat, another graduate student, who later became my husband, had studied bacteriophages [viruses that infect bacteria] that had a little single strand of DNA. John suggested to Fred that he use the phage as the training wheels for learning how to sequence DNA. It was only one strand. How simple could you get? So Fred and a number of people in the lab, including me, were all using different methods to try and sequence it.

Fred is the one who actually invented the methodology to sequence DNA. But we were all trying different ways, and the ones I learned turned out to be totally appropriate for telomeres.

You began telomere research in 1975 as a postdoctoral student at Yale. You’ve said, “Telomeres just grabbed me and kept leading me on.” Why were you so intrigued?
Studying organisms at a molecular level was totally compelling because it was moving from being a naturalist, which was the 19th-century kind of science, to being very focused and really getting to the heart of these molecules.

We knew they carried genetic material and that the ends of chromosomes were protected in special ways. But what did that mean? You have no clue. It was like you were trying to look at something from 400,000 miles up. You could see a speck on Earth, but you had no idea that if you homed in on it, it was a cat.

I discovered what telomeric DNA consisted of and that it was a special form of DNA. It looked different from anything anybody had seen because of the way it was structured, and analyzing it allowed us to see things that were new. Molecularly speaking, this was uncharted territory. What beguiled me was the excitement of figuring out what it means.

What led you to the discovery of telomerase enzyme?
Scientists in the Netherlands observed that the telomeric DNA fragment would get longer and longer. This was in 1983. So I suspected there must be an enzyme. When I got tenure at the University of California at Berkeley in 1983, I got brave and started thinking about entering a whole new era of research, and so began the hunt for that enzyme activity.

Experiments confirmed that there was an enzyme, which we called telomerase, and that it is actually doing something inside cells that matters. We tracked the enzyme over time and saw it going up and down at the right time, and the pattern was right, so we know the enzyme was influencing telomere production.