PARIS: Discoveries into the molecular mechanics of the cell, which were rewarded with the Nobel Prize for Medicine on Monday, have opened up a new front in the fight against cancer.
The three laureates, Leland Hartwell of the US and Paul Nurse and Tim Hunt of Britain were awarded the prize for work in the 1970s and 1980s on how cells reproduce.
Cancer researchers said the trio had set down a theoretical basis and laid bare a string of potential clues for explaining how malignant cells can reproduce wildly.
Hartwell, working on baker’s yeast, identified a gene that launches the cell cycle process, something he aptly called the “start” gene. He also made a landmark conceptual contribution — the “checkpoint” theory, under which the cycle is arrested in order to repair any damage to the DNA’s cell.
Nurse, working on a distant cousin to baker’s yeast, found a gene called CDK1 (cyclin dependent kinase 1), which produces a protein that regulates the different phases of the cycle. That protein, Hunt discovered, carries out its work through helper molecules called cyclins. “CDK and cyclin together drive the cell from one cell phase to the next,” the Nobel Prize committee said on Monday.
“The CDK molecules can be compared with an engine and the cyclins with a gearbox, controlling whether the engine will run in the idling state or drive the cell forward in the cell cycle.”
Many intriguing questions, as well as hopes for cures, arise from the research. The area which has excited the keenest interest is what causes the “checkpoint” mechanism to fail, letting parts of the DNA code get lost or rearranged, thus creating a flawed daughter cell.
And why is the failure so catastrophic in cancer, in which mutated cells replicate so easily? Scientists are already making use of the new knowledge, focusing on the molecular cascade of replication.
One of the key players is a gene called p53, likened to a “cellular policeman.” If a cell is defective or damaged, p53 stops cell division until the damage is repaired. If the damage cannot be repaired, p53 unleashes protein mechanisms to destroy the cell. In about half of all human cancers, the p53 is inactivated, which enables malignant cells to reproduce uncontrollably. —AFP
