PARIS -- Programmed cell death, the research area honored by the 2002 Nobel Prize for medicine, is the Achilles' heel of cancer and a potential key for fighting other life-threatening diseases.

The work focuses on the way cells reproduce themselves by dividing. Every day, billions of cells die and in their place billions are created to sustain the body's organs and functions.

A molecular taskforce stands by to ensure that the new clones are healthy duplicates, and many of these watchdogs have now been identified thanks to new laureates, Sydney Brenner and John Sulston of Britain and Robert Horvitz of the United States.

The guardians in question are proteins in the cell nucleus that vigilantly check each stage of the complex duplication cycle.

If conditions are OK, the proteins send a signal to certain genes which produce another batch of proteins that carry out the next stage in division.

But if the conditions are wrong -- if for instance the cell's DNA is damaged -- the monitors send out a message to the so-called death genes, whose job is to ensure that a potentially sick cell does not reproduce.

If the cell cannot fix the problem, the death genes order the cell to commit suicide.

This process, called apoptosis or programmed cell death, is therefore an essential part of a healthy life.

And when it goes badly wrong, life-threatening disease can result.

One such example is cancer, which in around half of all diagnosed cases has been pinned to a death gene called the P53 tumor suppressor.

If the P53 itself is flawed, it allows a cell to continue to divide, even if the cell's DNA is pitted with mutations.

Those mutations can lead to other mutations and disruptions in the cell's machinery; the cell thus proliferates out of control, eventually becoming a tumor.

In some families, there is a history of members with a flawed P53, and thus someone who carries this version of the gene may be at risk of cancer. In other cases, the P53 may be disrupted by an outside factor, such as a virus.

Cancer is an example of where apoptosis fails to work and there is insufficient cell death.

But the situation also exists in reverse, in diseases such as AIDS, brain disease, stroke and heart attacks, where healthy cells are somehow destroyed by excessive apoptosis.

Understanding how the genetic mechanism works is the first stage -- although in a long road -- towards drugs that prevent or reverse the problem.

None of it could have been possible without the trio's pioneering work on genes using a tiny, one-millimeter earthworm, caenorhabditis elegans.

Brenner laid the foundation in the 1960s by establishing C.

Elegans as a laboratory model for genetic research.

Small -- with just 959 cells in its one-millimeter length -- and plentiful, with relatively few genes and a short life-span, it was an ideal candidate for the laboratory.

Sulston took this further in the 1970s by uncovering the steps of the cell death process and becoming the first to identify the role of genetic flaws in triggering it.

In the 1980s, Horvitz identified the first death genes and demonstrated that corresponding genes exist in humans.

"We now know that most genes that are involved in controlling cell death in C. elegans have counterparts in humans," AFP quoted the Karolinska Institute as saying in its citation.