The discovery that the HIV drug nelfinavir has the potential to slow cancer growth gives hope that drugs designed to battle one killer disease may also help fight another.
Phillip Dennis and his colleagues at the US National Cancer Institute in Bethesda, Maryland, decided to test the impact of HIV drugs on cancer cells after they noticed that the toxic effects of the virus on cells were similar to the changes seen in cancerous cells.
The researchers used six approved HIV drugs in their experiments. They found that three of the drugs significantly slowed the growth of the tumour cells, and increased cell death.
Nelfinavir was found to be the most effective of the three drugs. Known for its ability to impede the activity of protein-degrading enzymes in the cell, the drug blocked tumour growth in mice injected with cancer cells.
Ian Hampson from the University of Manchester, who has previously shown that a different HIV drug called Iopinavir has potential for stopping cervical cancer, says that the new finding is not particularly surprising.
"Cancers have many parallels to viral infection," Nature magazine quoted him as saying. He says that just as viruses like HIV defend themselves against the immune system by switching on the host cell's garbage disposal unit called the proteasome, cancer-causing mutations can also activate the proteasome. Therefore, he says, drugs that block protein breakdown, such as nelfinavir, can theoretically halt both diseases.
Nelfinavir is now in preliminary clinical trials, which should reveal the dose that can be tolerated by patients with cancer, and how it affects solid tumours in the body.
The idea of moving drugs between branches of medicine is gaining ground. While HIV drugs are being tested against the SARS virus, the anti-malarial drug chloroquine is being explored as a potential cancer therapy.
Dennis says that "the concept of screening all drugs for anti-cancer properties has potential", and he hopes that a plan to test every drug approved by the US Food and Drug Administration on tumour cells will go ahead.
The new findings have been published in the journal Clinical Cancer Research.