Nobel Prize in Medicine Awarded for Cracking DNA Puzzle
for National Geographic News
|October 5, 2009|
The Nobel Prize in medicine or physiology has been awarded to three scientists at American universities who are unraveling how the body protects chromosomes—the carrier of the genetic code for life, the Nobel Prize assembly announced today in Stockholm.
The Nobel Prize of $1.4 million U.S. dollars (10 million Swedish kronor) will be split equally between Australian-born Elizabeth Blackburn at the University of California, San Francisco; American Carole Greider at Johns Hopkins University; and British-born Jack Szostak at Harvard University.
It's the first time that the Nobel Prize in medicine has been awarded to two women at the same time.
(Related: "Nobel Prize for Medicine Goes to HIV, HPV Discoverers" .)
"We spoke to them all this morning and they were a bit sleepy when they got the call, but they were all very happy and are looking forward to coming to Stockholm to receive their prize," said Göran Hansson, Nobel Prize committee secretary.
DNA Mystery Solved by Nobel Prize Laureates
The winning scientists' work has revealed how the ends of chromosomes can be copied, which has implications for understanding human aging, cancer, and several inherited diseases.
"They have solved a fundamental mystery and opened up a whole new field of research," said Shankar Balasubramanian, a telomere expert at the University of Cambridge in the U.K.
Telomeres are the caps on the end of chromosomes, which carry the genetic code that's written in our DNA.
(Behind the Nobel Prize science: quick guide to chromosomes and human genetics.)
When cells divide and replicate, the DNA molecules must be copied. However, during division, the ends of the strands of DNA can degrade.
In theory, telomeres—and therefore the chromosome as a whole—should become significantly shorter every time a cell divides, but in some cases they don't—an enigma that had perplexed scientists for decades.
But in 1982 Blackburn and Szostak discovered that a unique DNA sequence in the telomeres protects the chromosomes from degrading.
Later, in 1984, Greider and Blackburn identified telomerase, the enzyme that makes telomere DNA and prevents chromosomes from shortening and becoming unstable.
As telomeres shorten each time a cell divides, the process contributes to cell aging.
But when the telomerase enzyme is very active, the telomere length is maintained—giving the cell eternal youth. This process allows cancer cells to grow and divide without aging.
Inhibiting or interfering with telomerase in cancer cells may kill the cell and someday cure cancer, scientists say.
Several promising clinical trials are under way in this area, making the unique enzyme's discovery "major scientific progress," said Nobel Prize committee member Jan Andersson of the Karolinska Institute.
Likewise some age-related illnesses, such as Alzheimer's disease, may be linked to a lack of telomerase activity, causing the cell to degrade quicker.
Boosting telomerase activity could help to slow down aging and stabilize some of these illnesses, scientists say.
Furthermore a number of inherited diseases are caused by telomerase defects, including congenital aplastic anemia, which occurs when cells don't divide sufficiently inside bone marrow.
Nobel Prize Winners "Asked the Right Questions"
"It was always clear that nature was doing something unusual to maintain telomeres, but it took a lot of intuition to ask the right questions and understand what was going on," Cambridge's Balasubramanian said.
"Blackburn, Greider, and Szostak did that, and by doing so opened up a very significant new area of biology, linked to several important human conditions," he added.
The Nobel Prize has been awarded since 1901, as directed in the will of chemist, engineer, and dynamite inventor Alfred Nobel.
This year's prizes in physics, chemistry, literature, peace, and economics will be announced over the next two weeks.
The awards are officially handed out each year at a ceremony on December 10, the anniversary of Nobel's death.
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