As with any much-hyped medical discovery, however, the caveats here are almost as important as the headlines. These findings aren’t going to be translated into new diagnostic tests, much less treatments, any time soon. That’s largely because no one has yet figured out why these particular genetic changes should affect a woman’s cancer risk. And that, in part, stems from the fact that these variations aren’t mutations in identifiable genes, just alterations in stretches of DNA — regions sometimes unkindly called “junk DNA” — whose function is unknown.

In fact, these findings are purely statistical conclusions drawn from analyses of large groups of people and their genomes. While it seems unlikely that they’re simply spurious correlations — among other things, the number of research teams confirming each others’ findings argues against that — odder things have happened on the frontiers of science. Nick Wade of the NYT has more.

Dire straits for diabetes drug – A little more than a week ago, the New England Journal of Medicine published cardiologist Steve Nissen’s analysis suggesting that the heavily prescribed diabetes drug Avandia may boost the risk of heart attacks by roughy 40 percent. Nissen himself acknowledged that his paper — a “meta-analysis” that drew conclusions by pooling data from several dozen different clinical trials, a frequently used but often controversial technique — wasn’t conclusive, and a variety of his critics ranging from Avandia’s maker, GlaxoSmithKline, former FDA official Scott Gottlieb and the editors of the U.K. medical journal the Lancet (PDF) have argued that the medical community should wait for the results of a large clinical trial that won’t produce data for another year or two.

Since then, however, Republican Sen. Charles Grassley has accused the FDA of reaching the same conclusion internally but without taking any action; GSK warned that the large Avandia trial everyone is waiting for may be jeopardized because patients concerned about the drug’s safety are bailing out; and early indications suggest that ordinary patients may be doing likewise. It’s a huge disaster for what had been a $3 billion-a-year drug, and one that could have been mitigated if GSK and the FDA had been more open about potential safety problems early on. Because there’s no question that an important cost-benefit question — that is, whether diabetics benefit more from the blood-sugar control Avandia makes possible than they put at risk with the potential higher risk of heart attacks — has been lost in the furor.

Chinese drug official sentenced to death – Think FDA officials have it tough these days? Yesterday, the Chinese government sentenced its former top food and drug official, Zheng Xiaoyu, to death for taking $850,000 in drug-company bribes to overlook fake or defective medicines and food products.

Man Bites Dog Watch: Biotech CEO says drug prices are too high – Elan Pharmaceuticals CEO Kelly Martin appears to have broken one of the industry’s taboos by arguing that the common practice of charging all the market will bear for new biotech drugs — the very reasoning that has led to drugs for rare genetic diseases that cost $200,000 a year — is “unsustainable.” While there’s not enough detail in this interview snippet from the Financial Times (via Forbes) to know exactly what Martin means by this, it certainly sounds as if Elan might be edging toward some kind of slightly more rational pricing policy — or at least acknowledging that Medicare and private insurers aren’t likely to continue paying through the nose forever. Too bad some people seem to think that Elan might make a tasty takeover target for Big Pharma, whose own addiction to high prices hasn’t shown much evidence of waning.

Amgen’s woes continue to mount – From bad to worse to… even worse, I guess. Last week, experts at the European Union’s drug regulator recommended against approval of Amgen‘s colon-cancer drug Vectibix, saying its benefits didn’t outweigh its disadvantages. Vectibix has hit a number of snags recently, including a halted clinical trial in which a combination of Vectibix and Genentech‘s Avastin appeared to worsen patients’ odds of survival. The London-based European Medicines Agency was also concerned that evidence suggesting that Vectibix slows the progression of cancer was weak.

Separately, the EU gave preliminary approval to Roche’s Mircera, a potential competitor to Amgen’s best-selling anemia drugs Epogen and Aranesp. Mircera’s U.S. approval has been delayed and Amgen has sued Roche for patent infringement in any case, but seeing a competitor edge closer to the starting line can’t be good news for the beleaguered biotech. The LAT has more; so does Pharmalot.

Odds and ends from around the Web – A collection of quick takes on interesting items that might warrant a deeper look down the line:

• Ten years after Bill Clinton launched a drive to find an AIDS vaccine within a decade, the goal is nowhere in sight (Scientific American)
• Dendreon, still reeling from the FDA’s decision to postpone approval of its prostate-cancer vaccine, cuts staff by 18 percent (AP via Forbes)
• Medicare announced it won’t reimburse for artificial disks used as alternatives to spinal fusion, at least in patients 60 and older, dashing the hopes of medical-device makers (NYT)
• A California doctor’s group has begun posting its prices for straightforward procedures in an attempt to ward off competition from inexpensive walk-in medical clinics (LAT via the Merc)
• Medical researchers have teamed up with hedge-fund managers to offer a $1 million prize for the best new ideas in cancer research (Reuters)

Researchers have been looking for genes related to particular disorders for more than 30 years, and have been frustrated in that hunt for almost as long. With the exception of a few conditions caused by a single malfunctioning gene — most notably, perhaps, cystic fibrosis and Huntingdon’s disease — most disease appears to result from a complex interplay of multiple genetic effects and environmental factors. Even worse, until recently most studies that tried to untangle the genetic side of the equation operated by laborious trial-and-error — researchers would study families or other groups of people with a particular disease, then apply various biochemical and mathematical tools to try to identify which portions of the genome they shared, in the hopes that they’d eventually narrow the search down to a particular gene. The process produced so many unproven — and largely inaccurate — “candidate” genes that biologists began to joke about “gene of the week” discoveries.

One of the major changes in recent years has been the advent of a new way of sifting through genetic data. Instead of sequencing entire genomes — or even chunks of genomes — researchers have started restricting their searches to the specific ways in which one individual’s genes differ from those of other people. Think of it this way: Sequencing a human genome involves reading all three billion nucleotide “letters” of it, the overwhelming majority of which are the same from person to person. But if you set two — or eight, or 500 — genomes next to one another, the places where individual “letters” vary will jump out. Researchers have now mapped 10 million or so of these genetic variations, which are technically known as single-nucleotide polymorphisms, or SNPs (pronounced “snips”), and compiled them into a database known as the HapMap. (One private biotech, Perlegen Sciences, donated at least 2.1 million SNPs it had discovered to the project.)

In other words, sorting through SNPs is a lot faster than trolling through entire genomes, which in turn makes it possible to scan genetic information from much larger groups of people with a particular disease. In practice, these techniques may finally be turning disease-association studies into more of a science than an art.

Unfortunately, that doesn’t mean that medical breakthroughs are likely to flow immediately from the resulting gene-disease links. The latest diabetes findings raise the number of genes that contribute to the disease to ten — but those ten genes only account for two to 20 percent of overall diabetes risk. What’s more, it’s not entirely clear what these gene variants do differently that might contribute to the disease, much less how modern medicine might go about preventing or repairing the damage. So there’s plenty of slogging yet to be done.

The NYT’s Nicolas Wade has more.