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TUMOUR cells many enhance their lethal powers by eating their neighbours and
using their DNA. This could explain why tumours are so successful at developing
drug resistance.

Cells become cancerous when they build up a set of mutations in their DNA
that give them their deadly abilities. These include rapid growth, formation of
tumours, and the freedom to detach from their tissue of origin and spread
throughout the body. The accepted theory is that each cancer cell has to develop
these mutations on its own, or inherit them from its parent.

But now, Lars Holmgren of the cancer centre at the Karolinska Hospital in
Sweden has found another way that cancer cells can acquire new genetic
mutations鈥攗sing ingested DNA. 鈥淭his is the sort of thing bacteria do all
the time,鈥� says Holmgren.

The genetic abnormalities in tumour cells cause large numbers of them to
commit suicide in a process called apoptosis, where the cell shrinks, breaks
into pieces and starts shredding its chromosomes. Other mutated cells then eat
up the pieces.

To discover what happened to the ingested DNA, Holmgren and his colleagues
took rat cells that contained two cancer-causing genetic mutations and forced
them to undergo apoptosis. The team then allowed mouse cells to dine on the
debris. They found that healthy mouse cells were not affected by the meal. But
cells that had defective copies of the gene for a protein called p53
acquired the ability to form tumour-like clumps in lab experiments, and formed
tumours when injected into mice.

The result is intriguing because the p53 gene stops cells from
replicating when they have DNA damage. More than half of human tumours contain
defects in the p53 pathway.

This could explain how certain tumours become resistant to treatment. Loss of
p53 would allow them to exchange drug-resistance genes in the same way
bacteria do, acquiring defences more rapidly then they could independently.

Ironically, most cancer therapies may encourage this genetic exchange because
they increase the amount of apoptosis in a tumour. But the researchers stress
that the best treatment strategy is still to try to kill as many cells as
possible, even if some eventually learn to fight back.

鈥淭hey鈥檝e uncovered what may be a dramatic piece of biology,鈥� says Gerard
Evan, a cancer biologist at the University of California, San Francisco. But he
says it will be important to see if this exchange can take place in a tumour in
the body as well as in a test tube. Holmgren鈥檚 team has already started these
experiments.

While exchanging DNA in order to live might seem community-minded, Holmgren
sees his work as confirmation of cancer cells鈥� capacity for selfish replication.
鈥淚f you are willing to eat your neighbours and use their stuff to survive, I
wouldn鈥檛 call that cooperative,鈥� he says.