Oncology and genetics
Grabbing cancer by the short and curlies
A new technique for analysing tumours promises better understanding and more effective treatment
Sep 24th 2011 | SAN FRANCISCO | from the print edition
ONE of the great hopes nurtured by the Human Genome Project was that it would crack cancer open. Knowing which genes were going wrong would, the theory went, allow specifically tailored drugs to be developed. And this is, indeed, happening. Only last month America’s Food and Drug Administration approved a medicine called Xalkori (generically, crizotinib) for patients who have a particular type of non-small-cell lung cancer, the most common form of that disease. Xalkori blocks the growth of tumours caused by a mutant form of the gene which encodes a signalling molecule known as anaplastic lymphoma kinase. This mutation occurs in 3-5% of lung-cancer patients, and in trials Xalkori caused a dramatic shrinkage of the tumour in around half of those treated.
The catch is that the respite does not last. Typically, someone will respond for about a year, but after that his tumour starts growing again and the disease continues on its course. This is a pattern seen again and again with the new generation of drugs that genomics has helped to create. They slow the disease, but only for a few months. The presumption is that further mutations are arising in a tumour all the time, and that eventually one of them makes a molecular change that nullifies the effect of the drug. Researchers would dearly like to find a way to deal with this.