There are two fundamental ways that a healthy normal cell can traverse the pathway to becoming a cancer cell: 

• Activation of an oncogene.
• Inactivation of a tumor suppressor gene.

It is easy to comprehend how inhibiting an overly active oncogene would throttle back cancer growth. In fact, it’s being done already with drugs like gleevec and rituxan.

Harder to conceive is how to restore the function of a missing tumor suppressor gene. Despite hearty and hale efforts, this hasn’t been accomplished in any practical way.

So rather than beating your head against the wall of an intractable problem, why not approach it from a different angle? To wit, don’t try to resurrect a missing gene function, but instead take advantage of the fact that it is missing. This concept is embodied in a newish idea called synthetic lethality.

Two genes are synthetically lethal if the absence of one alone isn’t problematic, but the absence of both leads a cell to expire. Not only is this a devilishly clever idea, it’s been put to the test in a recent publication.

Writing in The New England Journal of Medicine,  Fong et al. report on a clinical trial with a small molecule called olaparib (published online, 24 June 2009). The patients in the study inherited a loss of function in one of the two copies of either BRCA1 or BRCA2. Both are tumor suppressor genes that assist in preventing errors during DNA replication, and the tumors formed because the second copy became mutated.

Olaparib inhibits another enzyme independently involved in DNA proofreading. Patients getting the drug are spared the most common toxic consequences of cancer chemotherapy because normal cells have an intact BRCA system.

This may seem complicated, but the trial is a terrific success story in advancing cancer treatment. Don’t be too optimistic, though: no drug exists that is completely lacking in toxic repercussions, and no drug exists that securely avoids the challenge of drug resistance. But we’ll take any progress we can get!

The following is surely one of the funnier exchanges in movies of the last few decades:

Arthur:  Hobson, do you know what the worst thing is about being me?

Hobson:  I should imagine your breath, sir.

(Dudley Moore and Sir John Gielguid in Arthur)

But what foul chemistry lies behind bad breath?

The villainous reaction is perpetrated by Gram negative bacteria, which break proteins down to amino acids. The sulfur-containing ones can then form stinky chemicals called volatile sulfide compounds (VSCs to the aficionado).

Recent work from Tel Aviv University adds a new twist. Sterer et al. show that prior to breakdown, oral proteins have to be denuded of their sugars by an enzyme called beta-galactosidase. This activity is produced mainly by Gram positive organisms, so it takes a flourishing microbial ecology to lead to the dreaded halitosis (Journal of Breath Research 3:1 [March 2009] doi: 10.1088/1752-7155/3/1/016006 ).

And based on this work there’s new hope for dragon-breath sufferers. The researchers have applied for a patent for a new device that measures both kinds of bacteria. It’s small, cheap, and turns blue if you’re in danger. Best of all is its name: OkayToKiss.

The mainstream media regularly barrages us with the fact that citizens of developed countries tend to being overweight, even obese. So we diet, we exercise, we pop pills, and sometimes we even resort to surgery to shed the unwanted poundage.

All this obsession on weight loss appears to be high on the futility list. The World Health Organization reports that about 400 million of us are obese, with another 1.2 billion way overweight.

So if behavior modification doesn’t yield good results, could science rescue us from fatness? Possibly, at least according to a new study from UCLA.

Anyone who ever studied biochemistry at least dimly recalls the Krebs cycle, which is involved in the metabolism of sugars and fats. The glyoxylate shunt is a less-remembered feature of the famous cycle, most likely because it is only found in microorganisms and plants, not in humans.

The lure of the shunt pathway is that it enables fat to be made into sugar, not just the reverse. And it’s the biosynthesis of fat from sugar-rich diets that bedevils so many otherwise healthy folks. Accordingly, Dean et al. engineered the two key enzymes from the glyoxylate shunt into mouse livers (Cell Metabolism, [3 June 2009], 525–536).

The results of the experiment are striking: mice with the new enzymes are resistant to diet-induced obesity. For reasons unknown, females appear to benefit even more than their male counterparts in resisting the portly consequences of a high-fat diet.

Don’t start eating lots of dessert just yet though. Effective and safe gene therapy in humans is still in the future, so for now we’ll have to stick to the old-fashioned but virtuous routine of diet and exercise to control our urge toward corpulence.

Most of us give little thought to the countless batteries we encounter every day. They power cell phones, iPods, cameras, computers, watches, and myriad other electronic devices, without which life would be ever so less pleasant.

Chemistry, of course, is the driver of battery technology. From lithium-ion to zinc-carbon to lead-acid, chemical energy is the underlying force that produces electrical energy. But battery technology has not kept pace with other innovations in modern life, and power output, weight, cost, and longevity remain major challenges for those hoping to score big with a battery breakthrough.

So to score big, think small. At least that’s the approach taken by a collaborative project between MIT and the Korea Advanced Institute for Science and Technology (Science 324 [22 May 2009], 1051–1055).

These investigators used a tiny bacterial virus (M13) modified to bind both carbon nanotubes and amorphous iron phosphate, and thus to align charges along a conducting electrode. Doing so allowed creation of a bioengineered Li-ion battery that is small, dense, and high performing.

Alas, it’s not a practical product yet, but does offer new meaning to the much-used term “going viral.”