Normally found genes in specific cancers seem to play a important role in disease progression.
The findings attain significance as they may offer new drug targets for blitzing tumours.
The research teams—led by Stephen Elledge of Brigham and Women's Hospital in Boston, Massachusetts, and Greg Hannon of Cold Spring Harbor Laboratory in New York—say that their findings provide an alternative approach to the traditional search for oncogenes, rogue genes that can turn normal cells into tumours.
The researchers call their approach "non-oncogene addiction" idea, which suggests that a tumour relies heavily on certain normal cell pathways, and that drugs disabling gene products in those pathways could be deadly to cancer. The two teams have even designed a method to knock down thousands of genes relatively cheaply and quickly.
According to the researchers, the method uses 'short hairpin RNAs' (shRNAs), pieces of RNA that can be designed to target and shut off specific genes, to target normal genes into colon cancer cells, breast cancer cells and healthy breast cells.
They have revealed that the shRNAs slow or stop the cancer cells from growing without impairing the healthy cells, something that point the way to new cancer drug targets. "It will take time and money to sort out which of these are the best drug targets, but the important thing is that we are finding them," Elledge says.
Even though drugs against oncogene products—like Novartis' Gleevec (imatinib) and Genentech's Tarceva (erlotinib)—have been a welcome advance for patients with cancer, patients often develop resistance to them, says Gary Schwartz of New York's Memorial Sloan-Kettering Cancer Center.
"Everyone's looking for the next Gleevec, but even though these targeted drugs have been exciting, they have not had the overwhelming impact we would have hoped for," says Schwartz, who is trying to find funding for a clinical trial of a drug that inhibits a normal cell-cycle pathway.
Schwartz says that early clinical trials with the drug have indicated that it may operate best in a 'therapeutic window' in which it is more harmful to cancer cells than to healthy cells.
Elledge and Hannon say that their work will complement two large projects aiming to spur development of more drugs like Gleevec and Tarceva, which target mutations involved in certain blood and lung cancers. Both projects involve sequencing the genomes of cancer cells to find more oncogenes and help scientists understand the biology of cancer.
One — the The Cancer Genome Atlas — began in December 2005, and is expected to cost 1.35 billion dollars over 9 years. The other is led by scientists at the Wellcome Trust Sanger Institute in Cambridge, UK.