Jack Roth and his colleagues at the M. D. Anderson Cancer Center in Houston,
Texas, succeeded in shrinking tumours or halting their growth by giving lung
cancer patients with a defective or missing p53 gene—one of a
family of tumour suppressor genes—a normal copy. The work is important
because more than half of all cancer patients are believed to have mutated or
missing p53 genes. At present, more than 85 per cent of lung cancer
patients die within five years of diagnosis.

Using a genetically engineered virus as a cellular transport vehicle, Roth’s
group injected p53 genes directly into the tumours of nine relapsed
lung cancer patients, all of whom had one mutated and one missing copy of their
p53 genes. In three patients, the treated tumours stopped growing, and
in three others they visibly shrank. “Our goal has been to, in some way, change
the inner workings or the genetics of a cancer cell,” says Roth. “I think this
is an indication that it can be done.”

But the researchers warn against undue optimism. Because of other untreated
tumours, all the patients in the study eventually died—some only a month
after receiving the new treatment. “They are injecting [the gene] into one
lesion of many,” says Bert Vogelstein at the Johns Hopkins Oncology Center in
Baltimore, Maryland. “It is one step in a very long stairway.”