But the ultimate goal of pharmacogenomics is to find tests and treatments based on a snapshot of a person's entire genetic makeup. “We want to go from looking at a few genes to looking at all the genes and SNPs in a cell,” says Nicholas Dracopoli, vice president of clinical discovery at Bristol-Myers Squibb in Princeton, NJ.

Cancer is one of the diseases that researchers believe will eventually yield to pharmacogenomics. Since most cancers are the result of multiple genetic missteps, scientists want to create multi-faceted therapies, similar to the anti-viral cocktails used against HIV. “If we can hit the tumor with combo therapy, it will be far more effective than managing the disease one stage at a time,” says Dracopoli.

Cheaper and faster DNA sequencing and the availability of the HapMap -- a detailed map of small genetic variations in humans, a first draft of which was completed in October -- will be crucial for identifying drug targets or disease markers. “With the HapMap, we now have a tool to interrogate genetic changes relatively inexpensively across the entire genome,” Dracopoli says.

Another key to speeding the transition to pharmacogenomics, says Dracopoli, will be to look for genetic markers that predict response to a drug at the same time that the drug is being developed. The FDA recommended such an approach in a set of guidelines for pharmacogenomics released in March. For most of the currently available targeted drugs, the specific mutation that makes a person respond well to a drug was identified in academic labs after the drug had been approved. But earlier integration is the key to bringing diagnostic tests and targeted therapies to the clinic faster, says Dracopoli.

According to Brian Spear, director for genomic and proteomic technologies at Abbott Laboratories in North Chicago, IL, many companies already collect genetic information in early clinical trials, in order to analyze differences in the way a drug is metabolized.

But incorporating testing into later stages of clinical testing will prove more difficult, he says. Scientists would first need to identify the group of people in a trial who respond well to a drug, then figure out which genetic variations were linked to that response. They would then need to confirm those markers in additional clinical trials, which drug companies fear could be a lengthy and expensive process.