Heidi Ledford in Nature:
Two compendiums of data unite genetic profiling with drug testing to create the most complete picture yet of how mutations can shape a cancer’s response to therapy. The results, published today in Nature1,2, suggest that the effectiveness of most anticancer agents depends on the genetic make-up of the cancer against which they are used. One study found a link between drug sensitivity and at least one mutation in a cancer-related gene for 90% of the compounds tested. Lab-grown cancer cells are a mainstay of research into the disease. The two projects catalogue the genetic features of hundreds of such cell lines, including mutations in cancer-associated genes and patterns of gene activation. They then match these features with how the cells respond to approved and potential drugs. “This is a very powerful finding,” says Tom Hudson, president of the Ontario Institute for Cancer Research in Toronto, Canada, who was not affiliated with the work. “It could provide valuable information for designing clinical trials, and lead to more focused and less expensive approaches to drug development.”
Cancer treatments are increasingly being tailored to target particular genetic variants of the disease. Even so, drug companies still struggle to work out which patients are most likely to benefit from a drug in advance of clinical trials, says Levi Garraway, a cancer researcher at the Dana-Farber Cancer Institute in Boston, Massachusetts, and a co-author on the study. Aiming to smooth the path to rational drug deployment, Garraway and his team compiled the Cancer Cell Line Encyclopedia, an assembly of genomic information for 947 cell lines, drug sensitivity for 479 of those lines, and 24 anticancer agents1. Another team, led by Mathew Garnett of the Wellcome Trust Sanger Institute in Hinxton, UK, has created a similar profile using 639 tumour cell lines and 130 drugs2.