I’ve snuck into a quiet little room with big comfortable chairs and more than one sleeping microbiologist. (With ‘sunrise sessions’ starting at 6.30 AM, who can blame them!) So, as I listen to the gentle snoring of one of my companions, here are a few highlights from a press conference on the human microbiome.

As a loyal NatureNews reader, you’ve heard plenty about the microbiome (for instance here or here). Basically it’s the sum of all the bacteria living in the human body. A frequently trotted out statistic: there are ten times more bacterial cells in the human body than human cells. It’s incredibly complex. Many of your bacteria are different from my bacteria. And the population of bacteria on your forearm is very different from the population in the crease of your elbow, said NYU’s Martin Blaser. David Relman of Stanford noted that our microbiomes might one day be used as a biometric, like a fingerprint, except that the microbes might reveal a bit more: where you’ve been, what you ate while you were there, etc. He also pointed out that microbiomics (my word, not his) began in 1683 when van Leeuwenhoek scraped one of his teeth and compared the results under a microscope to samples taken from his colleagues.

The panelists agreed that since we don’t understand everything that our microbes are doing for us, we also don’t understand the long-term ramifications of taking antibiotics. Blaser speculated that there could be cumulative effects from disrupting your microbiome that we don’t yet appreciate. Claire Fraser-Liggett said her friends call her a ‘thereapeutic nihilist’ because she avoids taking antibiotics whenever possible.

Blaser made another interesting comment: that our current focus on finding genetic variations linked to disease may one day give way to a realization that differences in our bacteria are just as important.

Richard Henkel of the Centers for Disease Control gave a talk yesterday about biosafety in the lab. It was primarily a nitty-gritty run-down of which forms to fill out if there’s a theft, loss, or release of potentially harmful microbes or toxins that are on the US ‘select agent’ list. In case you’re wondering, you may need to file a ‘Form 3’ in that event. And he gave a few interesting statistics on how many Form 3’s have been filed over the years:

2003: 4

2004: 19

2005: 19

2006: 24

2007: 60 (plus one case in which an institution failed to report an illness contracted from on-the-job exposure)

2008 (through April): 32

(Henkel attributes the dramatic increase to higher awareness of proper reporting.)

Between the talks and the poster presentations, researchers here have been studying microbes in just about every environment you can imagine. Here’s a quick run down of what microbes call home: the crook of your elbow, 26,500 year old Antarctic algal mats, the space shuttle assembly platform, a tar pond, hospital room drains, stored space shuttle food waste, the guts of the medicinal leech Hirudo verbana, ready-to-use fresh salad in Vienna, infant formula production facilities, Chihuahua cheese, uranium contaminated groundwater, sea turtle tumours, the ‘dead zone’ off the coast of Oregon, and of course the usual deep sea thermal vents and acid mine drainage pools.

Where they do not call home: the Atacama Desert.

Two researchers from the University of Colorado in Denver, Munira Albuthi and Timberley Roane, are proposing an unusual use for an unusual bacterium: detoxifying Native American artifacts.

The bacterium is Cupriavidus metallidurans CH34 (the bacterium formerly known as Ralstonia metallidurans CH34, for those of you keeping track). C. metallidurans has an unusual ability to flourish around heavy metals at concentrations that would normally be lethal. (The critter was first isolated from the sludge of a Belgium zinc decantation tank, according to the Joint Genomes Institute.)

Now, Albuthi and Roane hope to use the bacterium to decontaminate Native American artifacts. The artifacts were once collected by museums, but have since been returned to Native American tribes. Unfortunately, before they were returned, the artifacts were treated with a mercury-containing pesticide for preservation. The mercury poses a health hazard, and Albuthi and Roane hope to spray down the artifacts with C. metallidurans, which is able to detoxify the mercury. So far, they’re just in preliminary stages of testing, but the bacterium was able to remove 60% of the mercury from a mercury-soaked piece of paper.

Here’s one of the more creative uses of viruses that I’ve come across: harnessing viruses that attack bacteria to kill off a bug commonly associated with particularly nasty pimples.

The bacterium in the crosshairs is Propionibacterium acnes, and has been linked to the more serious pimples of the most common form of acne: “acne vulgaris”. Michael Davis of Central Connecticut State University has been swabbing the foreheads, noses, and backs of students to build a collection nearly 400 P. acnes isolates. He and his team of graduate and undergraduate students then tested several dozen viruses against the P. acnes cultures. They’ve found a few that can kill specific strains of P. acnes, and now they’re exposing their viruses to UV light to create viral mutants that, they hope, will be active against a wide variety of P. acnes strains. Davis along with his team (undergrads Margaret Zurowski and Brandon Albright, and grad student Kathryn Neely) presented their work as a poster this morning.

Hello and welcome to the American Society for Microbiology’s annual microbial extravaganza! This year’s shindig is in Boston, and the Boston Convention and Exhibition Center has literally laid out a red carpet to welcome the glitterati of the microbiology world. (I was amused to see that they’ve also placed the pressroom right next to the children’s daycare center. A subtle comment on our maturity level? Perhaps.)

Judging from this morning’s poster session, this looks to be a fun meeting. It’s a busy one, too – with over 3000 presentations, it can be hard to pick out which ones to attend. If any of you out there have suggestions to help me weed through the 300+ page program, please let me know: you can contact me by posting a comment here or via email: h.ledford at boston dot nature dot com.

In cancer, it’s typically not the primary tumour that kills – it’s the metastases. Little wonder, then, that a major topic at the meeting was developing drugs not to shrink the primary tumour, but to stop it from spreading.

Danny Welch from the University of Alabama at Birmingham presented data on an interesting protein called KISS1. (Welch claims the protein is so named because he lived near Hershey, Pennsylvania at the time of its discovery. For you international readers, Hershey, Pennsylvania is the home of Hershey’s, the chocolate company that makes ‘Hershey’s kisses”.)

Anyway, KISS1 inhibits metastasis, but the fascinating thing is that it does so without preventing the spread of tumour cells. Instead, it keeps the metastasized cells from flourishing in their new environment. In other words, if you inject KISS1-expressing tumour cells into mice, they’ll form a primary tumour and cells from the primary tumour will migrate to the lungs. And then they’ll just sit there, lost and lonely.

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In 1889 Stephen Paget came up with the ‘seed to soil’ theory to explain why some cancers seem to spread to specific organs, rather than just invading the body at random. He said that perhaps there were features of the soil (the organ) that determined whether the seed (the cancer) took root there. Some soils simply aren’t hospitable to some seeds (having gardened in the heavy red clay of North Carolina, I can attest to that…)

Quite a few speakers evoked the seed to soil theory in talks about metastasis. One such speaker, Sara Sukumar of Johns Hopkins University, mentioned it while talking about her rapid autopsy program. The program is meant to test the assumption that the characteristics of the original ‘primary’ tumour will be shared by its metastatic offspring. There is some evidence to support this: gene expression patterns in some breast cancer tumours have been shown to resemble gene expression in their distant metastases, for example. But Sukumar says our understanding of this relationship is hindered by a lack of tissue to study because researchers often have only a single biopsy from each patient.

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NCI director John Niederhuber was around today to answer questions from conference attendees. First, though, he gave everyone the hard truth about the budget.

The data:

Number of years that funding for NCI has remained flat: 4

Rate of biomedical research inflation (apparently slightly higher than the overall rate of inflation in the United States): 3.8% per year

Percent decrease in purchasing power at the NCI since 2004: 15%

Niederhuber said that for the first few years of flat funding, NCI tried to cope with its shrinking budget by trimming the size of their grants rather than decreasing the number of awards. Those days are over, he said today, and this year NCI will offer fewer of their competing research project grants. Niederhuber also said that he was not optimistic about the possibility of any future budget increases, “no matter which party takes over the White House”.

Today’s plenary session on ‘late-breaking clinical trials’ offered up a few new promising phase III trial results for the prevention of colorectal cancer.

The first was an update on a kind of cox-2 inhibitor called celecoxib (marketed as Celebrex). You may remember the cox-2 inhibitors — they’re a class of anti-inflammatory drugs that were the center of a scandal a few years ago when it turned out they carried increased risk of cardiovascular side effects, such as heart attacks or stroke. Most of the scandal (and accusations of suppressed negative data) revolved around rofecoxib, better known as “Vioxx”, which was subsequently pulled from the market. Celecoxib is still available but carries the dreaded black-boxwarning. (The black box is the FDA’s strongest warning, and is the last stop before yanking a drug off the market entirely.)

But celecoxib had shown promise for preventing colorectal cancer in those at high risk for the disease, and I’ve heard it said on several occasions that the negative press about the drugs’ possible cardiovascular harm unfairly restricted use of what could have been a valuable cancer preventative. Today, Monica Bertagnolli of Brigham and Women’s Hospital in Boston reported that the protective effects of celecoxib have persisted in patients that stopped taking the drug 1.5 years ago, when the study was halted due to the realization that celecoxib posed a cardiovascular risk.

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