The technique developed by Rockefeller University's Laboratory of Mammalian Cell Biology and Development can eliminate the random bystander genes and identify the ones that are critical for cancer, researchers said.
Applying the technique to head and neck cancers, scientists found seven new tumour-suppressor genes whose role in cancer was previously unknown.
The new technique, which the lab recently applied to a screen for skin tumour genes, is particularly useful because it takes a fraction of the resources and much less time than the traditional method for determining gene function - breeding genetically modified animals to study the impact of missing genes.
"Using knockout mice, which are model organisms bred to have a particular gene missing, is not feasible when there are 800 potential head and neck cancer genes to sort through," said Daniel Schramek, a postdoctoral fellow in the lab.
"It can take about two years per gene. Our method can assess about 300 genes in a single mouse, in as little as five weeks," Schramek.
The researchers made use of Ribonucleic acid (RNA) interference, a natural process whereby RNA molecules inhibit gene expression.
They took short pieces of RNA which are able to turn off the function of specific genes, attached them to highly concentrated viruses, and then, using ultrasound to guide the needle without damaging surrounding tissue, they injected the viruses into the sacs of mouse embryos.
When the mice grew, the researchers determined which genes, when turned off, were promoting tumour growth, and what they found was surprising.
"Among the seven novel tumour suppressor genes we found, our strongest hit was Myh9, which codes for the protein myosin IIa, a motor protein with well-known function in cell structure and cell migration," said Schramek.
"Through further functional studies we found that myosin IIa is also required for activation of the main guardian of the genome - a tumour suppressor protein called p53," said Schramek.
The lab showed that when the myosin IIa gene was mutated, p53 was not able to build up in the cell nucleus, and chaos ensued: genes responsible for repairing damaged cells and killing off tumour cells were not activated, and invasive carcinomas spread within three months.
The researchers devised a strategy to reactivate p53 in these cells, and showed in vitro that tumour suppression was restored.