In the 1950s and ’60s, several villages in the Oceanic country of Papua New Guinea began to see an odd disease. Villagers of the Fore people in the Eastern Highlands - predominantly women and children - would show an array of frightening symptoms that rapidly worsened over about six months: muscle tremors, uncontrollable laughter, slurring of speech and finally an inability to move and swallow. In the 1960’s, European scientists began to study people with the disease, called kuru for the Fore word for “shiver,” and made two astonishing discoveries. First, that kuru represented a new kind of infectious disease that caused the brain and nervous system to degenerate. Second, that kuru probably resulted from people eating their dead relatives.

Yeah, that’s not a typo. Before the Fore people of Papua New Guinea were known for kuru, they were known for “mortuary feasts,” where villagers would mark the death of a family member by consuming him or her. And not just a nibble here or there - according to a 1979 book by anthropologist Shirley Lindenbaum, “meat, viscera, and brain were all eaten.” That’s a good way to spread a disease caused by prions - the mechanism for kuru eventually discovered by Daniel Carleton Gajdusek in research that won him the 1976 Nobel Prize in Physiology or Medicine. Now, kuru continues to fascinate the scientific community, as a new medical paper presents how the savage disease caused rapid natural selection in Papua New Guinea, selecting for a gene variant that may offer clues to how to treat prion diseases with no known cure.

Prions are also the culprit behind bovine spongiform encephalopathy, better known as Mad Cow Disease, which is thought to have broken out in Britain due to cannibalistic feeding practices in cattle. In short, prion diseases are caused by misshaped proteins that are a bad influence on native prion proteins present in all species, causing them to change shape, clump together, and eventually kill the cell. So when a prion disease enters a person’s nervous system - by, say, eating a person with a prion disease - it tends to wreak havoc in the brain, producing the odd symptoms of kuru or BSE.

At the height of kuru, 1 out of 50 people in some Fore villages succumbed to the untreatable, fatal disease. Women and children tended to die more often from kuru, likely because they usually were given the brains to eat while the men got the good, meaty parts. But what about those who participated in the mortuary feasts, but never contracted the disease? Was there something genetically different about them that made them resistant? Sounds like a case for…evolution!

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4:15 p.m. - Of Mice and Mammoths

The last talk of the day (for me, as I had to leave before the final, final talk) made for a great reminder of how far the field of evolutionary biology, wrapped in a relatively simple story told engagingly by Hopi Hoekstra of Harvard. Hoekstra described her research quest as “the hunt for genes that make a difference,” and she uses a really nice model system - the oldfield mice of the southern United States. These mice typically are brown in color, but they have migrated in the recent (meaning thousands) of years to the gulf and atlantic coasts and taken up residence, like a retired couple, on the beach. But a brown mouse on a beach is a target, and their predators, which include birds and coyotes, find it all to easy to locate their brown fur on white sand and make a beachside snack out of them.

Cue natural selection - soon you have brown oldfield mice inland, and predominantly white oldfield mice that live on the beach. Hoekstra tested whether the fur color really does construe an evolutionary advantage with a simple experiment - make a bunch of clay mice colored brown or white, and leave them out on the beach. Sure enough, the brown clay mice quickly showed divots and bitemarks left by attacks from (presumably very frustrated) predators.

That would have been a fine experiment for the 1959 conference, but Hoekstra’s next step was pure 2009 - she took examples of brown and white mice back to the lab, bred them, and searched for the genes that determined fur color. Her laboratory narrowed the gene candidates down to three genes, and in one of them - a receptor called Mc1r - the substitution of a single amino acid flipped the switch from brown fur to white fur. Amazingly, when another group of scientists sequenced the genome of extinct mammoths in 2006, they found the same amino-acid substitution in the same gene, implying that mammoths, like the oldfield mice, came in different color varieties.

After so much high theory and methodological complexity, Hoekstra’s experiment sent all of us (or at least me) home with a warm feeling - not only was her experiments a beautiful example of evolutionary biology that would have been impossible in 1959, it was a great example of teachable science, the kind of story that a 3rd-grader could wrap their head around and begin to see the truth of evolution. The cloud hanging over Darwin/Chicago 2009 was the uneasy feeling that all this scientific progress was still losing out in the arena of public opinion, but Hoekstra’s work and charismatic speaking style (on the heels of similar ambassador figures Neil Shubin and Michael Shue) chased away some of the pessimism, and left me confident that the more examples we find of Darwin’s elegant theory at work in nature, the easier it will be to convince the world that it is true.

And with that, we’re finished. Happy Halloween to those of you who have followed me this far, and thanks very much for reading and perhaps linking to the posts. I’ll be back Monday with a digest post to help navigate the coverage of the last few days, and Jeremy Manier will be here Tuesday with his own thoughts on the conference.

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5:00 p.m. - Biomedicine and Bracketology

Here’s the final report from today’s session, join us again tomorrow for a full Halloween day of evolutionary science and philosophy! Also, continue to follow PZ Myers of Pharyngula and Skip Evans of Wisconsin Citizens for Science for their reports on the conference.

Both talks in the final session of the day focused on how the incredible advances in gathering genetic information over the last decade have done much to shake up the worlds of genetics and evolutionary biology. As we’ve written about previously, the 1959 conference helped solidify what’s known as the modern synthesis of evolution that incorporated the then-new information about DNA, genes and molecular mechanisms of inheritance, an arrangement that forever married the two fields. Well, could the participants in that conference have predicted that 50 years later we would have a reasonably complete genome for humans, not to mention 43 other vertebrate species? And did they know how much trouble it would cause?

Eric Lander, who was one of the leaders of the Human Genome Project, said he felt slightly out of place at a conference about Darwin, but the modern synthesis marriage sometimes makes strange bedfellows! Regardless, Lander’s talk was a great primer on how the dogma of genetics has been forever altered by what we learned from the HGP and the genomes of other animals: that we have far fewer genes than we thought (~20,000 vs. previous estimates of 100,000), that much of what is handed down between generations is “non-coding” DNA that doesn’t make proteins, that those “non-coding” sections may create important regulatory elements that help organisms develop. Lander, who described himself as a biomedical scientist, said much of what has been found since the explosion of genetic data has been bad news for medical geneticists - many disease-associated alleles have been found, but most have very marginal effects on the probability of a person developing that disease. But Lander said it was a glass half-full/half-empty situation:

“Those people who want to do personal genomics - take your DNA and tell you your risk of diabetes - they’re in trouble. This is not going to be the best way to do that,” Lander said. “But if I want to understand what diabetes is about…I start to get clues to the pathways that matter to diabetes.”

The final talk of the day covered how genetics has caused a similar reshuffling in the field of phylogeny - the science of organizing life into “trees” that show the evolution and relationships of species. Philip Ward, from UC-Davis, talked about the durability of the “Tree of Life” simile, which Darwin readily used in Origin of Species - the only figure in the book is an early phylogenic tree. Modern phylogeny produces beautifully complex trees that look like 10,000-team basketball tournaments run in reverse, with the winner being life’s common ancestor. But as biologists have turned to genetics to build these trees, they’ve found that they lead to completely different trees than the ones built from morphology, the physical characteristics of organisms.

One reason for this is a tricky effect called convergence - two species that are not closely related and live continents apart could form a resemblance because they evolved in similar environments. Ward studies a type of ant that is found in both Asia and America, and morphology would suggest that they are closely related species despite being so far apart geographically. However, genetic data showed the ants were more distantly related than previously could have been estimated from their looks, suggesting they evolved to look similar due to their similar environments, without a recent common ancestor.

But the Tree of Life remains a strong structural model, Ward said. So strong, in fact, that it has been adopted by creationists, who describe an “orchard of life” of animals that evolved after Noah’s flood. As with most mentions of creation “science” at the meeting, Ward’s slides about these theories drew mostly giggles from an audience decidedly on the side of Darwin, even as genetics reveals a world more complex than he ever could have imagined.

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We’re only a few hours away from the start of Darwin/Chicago 2009, 2+ days of the world’s leading evolutionary biologists discussing the past and future of the field. Come back to this space tonight at 6:00 pm Central time for live-blog coverage of the opening event at Rockefeller Chapel, and keep coming back all day Friday and Saturday for frequent updates from the conference.

Before things get into full swing, I wanted to play armchair Linnaeus and organize the conference’s 30-some talks into a few major themes. So much is packed into Friday and Saturday, with two simultaneous programs covering “biological sciences” and “history and philosophy,” I won’t be able to see everything, but the list also contains what I’m hoping to prioritize in order to get at least a representative sample of the event.

Evolution Goes to Church

Rockefeller Memorial Chapel, the looming gothic structure on the southeast side of campus where convocations and communion services are held, has been the site of Darwin discussion before - as mentioned yesterday, Sir Julian Huxley gave a speech predicting the end of religion at the 1959 conference. Thursday night’s trio of speakers both follows that agnostic tradition and nicely previews the main threads of the more tightly-packed Friday and Saturday schedules.

Addressing the renewed vigor of the evolution vs. religion debate, Ronald Numbers of the University of Wisconsin will recap the historic path of these conflicts, emphasizing that the “young earth” element of today’s creationists is a relatively new development. Harvard’s Marc Hauser, meanwhile, will pull the rug out from under one of the main creationist arguments - that morality could not have developed under natural selection and must have been given to humans by a supernatural power. But lest you think evolutionary biologists are too distracted by the external debate to do the hard work in their own field, legendary geneticist Richard Lewontin will open the night’s proceedings talking about the challenges of directly determining how genes contribute to an organism’s fitness.

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There has certainly been no shortage of attention on Charles Darwin this year. With the dual landmarks of Darwin’s 200th birthday and the 150th anniversary of The Origin of Species, virtually every scientific publication, museum, conference and institution has taken the opportunity to pay tribute to the life and work of the man who gave us the theory of evolution. But now that the celebrations are (mostly) over, it’s time for the field of evolutionary biology to move forward, capitalizing on new technologies and discoveries that were only a dream when Darwin drew upon decades of observation and thought to craft his revolutionary book.

That same challenge faced evolutionary biologists in 1959, when they gathered at the University of Chicago to observe the 150th and 100th birthdays of Darwin and his book. Brought together were many of the 20th century’s greatest thinkers on the subject of evolution, including legendary biologists Julian Huxley, Theodosius Dobzhansky, and Ernst Mayr, Darwin’s grandson Charles Galton Darwin, and John Scopes of Scopes Monkey Trial fame. And according to Robert Richards, professor of the history of science and medicine at the University of Chicago, the discussions that took place at that conference helped solidify what we now think of as the “modern synthesis” of evolutionary theory, the merging of Darwin’s ideas about the gradual effects of natural selection with the then-new field of genetics.

Darwin/Chicago 2009, which begins Thursday night at the University of Chicago, will try to recapture that spirit and make a similar impact upon the path of evolutionary biology. Once again bringing the field’s brightest lights to Hyde Park for an exchange of ideas, Richards and the conference’s other organizers hope that the event will do more than merely acknowledge a triple anniversary, but will instead re-evaluate evolution science in light of a world much different from the 19th century environment that shaped Darwin’s thoughts. Here, with Richards’ assistance, are three reasons why now is a great time to talk about Charles Darwin and evolution.

1) New technologies

The 1959 conference took place only six years after James D. Watson and Francis Crick published their landmark paper on the double-helix structure of DNA. And it wasn’t until 1957 that the “central dogma” of biology - that DNA encodes for RNA which encodes for proteins - was enunciated by Crick. So the ‘59 conference took place at the dawning of the genetic age, when the biological substrate that Darwin’s natural selection acts upon was finally understood.

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Studies of human disease often work from the patient backwards - doctors and scientists take the common symptoms of a particular disorder and use them as clues to figure out what first went awry to spur the disease. For neurological diseases like Parkinson’s or amytrophic lateral sclerosis (aka Lou Gehrig’s Disease), symptoms and brain images have pointed the research at particular parts of the brain, which are then studied in animal models and on the genetic or cellular level. But disease research can also work from the other direction, where a particular cellular process is identified as a potential culprit in the disorder before a patient with that defect is even found.

That’s the case with a paper published this month by a team of University of Chicago researchers studying the cellular mechanisms that underlie diabetes. There are many types of diabetes mellitus, but all can be traced back to the hormone insulin - the body’s signal that cells should soak up sugar from the blood. Most cases of juvenile, or Type 1, diabetes result from the immune system erroneously attacking and killing the Beta-cells of the pancreas, which release insulin. Type 2 diabetes, which often develops in adulthood, results from a reduced sensitivity to insulin and/or a decreased release of the hormone.

But diabetes can also have a genetic origin, in some rare cases, when one of the genes involved in the secretion of insulin is disrupted. Previously on the blog, we’ve talked about the story of Lilly Jaffe, whose diabetes was found to be caused by a rare genetic mutation in a protein called a potassium channel, critical for the release of insulin. The mutated potassium channel seen in Lilly’s case interferes with the trigger of insulin release, causing lower amounts of the hormone to circulate through her blood. Thus, Lilly was treated by daily injections of insulin, until doctors at the University of Chicago detected the mutation and prescribed her a drug that directly targeted the potassium channel.

Now researchers at the University of Chicago have found another ion channel that must function properly for the right amount of insulin to be released. Only problem: there’s no patient.

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And so Neuroscience 2009 comes to an end, and it’s time to put away my badge, rest my weary feet and note-taking hand and think about biology below the neck again. Here’s the final installment of our live coverage, but come back tomorrow for a roundup of the conference with highlights, loose observations and links to other people’s thoughts on the conference. Thanks for reading!

2:30 PM - The Final Talk

The schedule may say that Neuroscience 2009 runs through the end of the day today, but judging by how many suitcase-toting scientists were jumping in airport cabs this afternoon, a small portion of the 30,000+ attendance makes it to the very end. Indeed, even the main stage ends its conference early, shutting down after a talk by Mt. Sinai School of Medicine’s Eric Nestler, an expert in the field of molecular psychiatry.

Nestler’s research focuses on the gritty details of how drugs of abuse change the expression of a person’s genes - yes, it was another addiction talk, and the former addiction researcher that I am, it was great to see the topic getting so much attention this year. In the addiction press conference I attended yesterday, Nestler hinted at a bombshell idea - frequent users of addictive drugs such as cocaine, heroin or alcohol may change the mechanics of their genes so permanently, the modifications could be passed on to their children. This “inheritable addiction” has already been observed in lab rats, Nestler said, mirroring similar results seen with the offspring of obese rats (which I talked about on Monday).

But that data must be too fresh for mass consumption, despite Nestler telling a roomful of reporters about it the day before. His talk today focused on the steps leading up to that discovery, carefully examining how repeated cocaine increases or decreases the activity of hundreds of genes in the reward pathway of the brain. Those long-lasting changes, which can cause cells of the reward pathway to actually grow and change shape, help explain why addiction is such a difficult condition to treat - it may require a complete re-re-structuring of the brain.

Much of the addiction research I’ve talked about this week has taken place in animals, but before Nestler’s talk, I came across a rare experiment that looks at the behavioral effects of a commonly-used drug in humans. It might seem strange that we know a ton about the specific genes that are up or down-regulated by cocaine, but not so much about its effects upon humans, but that’s due to procedural reasons - it’s quite hard to get approval for a study that gives illegal drugs to humans.

Michael Ballard, from the University of Chicago laboratory of Harriet DeWit, was trying to fill in at least one of those gaps in the research by testing the effects of THC (the active ingredient in marijuana) to presumably eager volunteers. Ballard then tested the subjects’ ability to judge facial expressions and determine the emotional content of pictures and personality trait words while they were under the influence of the drug. Interestingly, higher doses of THC caused the subjects to misjudge the facial expressions they were shown, suggesting an effect of the drug on social perception. The other tests were normal during the drug effect, but when brought back to the laboratory a week later, the subjects showed a decreased ability to remember neutral and negative personality traits, possibly indicating that their memories of the drug effect were biased toward happier stimuli. Ballard hopes to continue that research into other drug types - he’s currently testing amphetamine - to give the field of addiction research much-needed, laboratory-controlled human data to make sense of the flood of animal experiments.

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As described on Monday and hinted at all week, this weekend marks the start of Neuroscience 2009, the annual mega-conference of more than 30,000 neuroscientists. After years of staging the meeting in areas with distractingly nice climates such as New Orleans, Orlando and San Diego, this year should be all business with the rainy chill of Chicago keeping people indoors. But there’s still a lot of fun to be had, with big-time speakers, immersive poster sessions, the never-ending hunt for the best vendor knick-knack giveaway and the night-time socials. Because of Neuroscience’s massive size, there are a million different ways to navigate a path through the science, but here’s a quick extremely long guide to what I’m looking forward to experiencing. Remember to tune in to ScienceLife all weekend (and through Wednesday) for coverage.

Saturday: Magicians Were the First Neuroscientists

Each year one of the most interesting lectures falls under the sober heading of “Dialogues Between Neuroscience and Society,” which basically means “we invited someone from outside of neuroscience to talk about neuroscience.” At previous meetings I’ve attended, that meant hearing public figures such as the Dalai Lama and Frank Gehry offering their own perspective on the brain, the mind and thinking - necessary reminders that the microscopic neurons those 30,000 scientists are concentrated on actually add up to some pretty amazing things in practice. 

This year’s Dialogues speakers are neuroscientists of a different sort: magicians Apollo Robbins and Eric Mead. Even though I saw a local version of this talk earlier this year with Robbins and neuroscientist Susana Martinez-Conde (which I wrote about it for the Tribune), I’m excited to see it again, because it really is a neat demonstration of how magicians have used the brain’s limitations to produce convincing illusions. Robbins, whose act is centered on his considerable abilities as a pickpocket, is a master of using diversion to direct a person’s attention one direction while he slips off their watch from another angle. As Robbins and Martinez-Conde explained back in January, this deceptively simple trick actually says a lot about how the brain shifts attention from stimulus to stimulus, and how a normal brain is “tricked” may help us learn about the neurobiological process that underlie an attentional disorder like ADHD. You can watch a video of a similar symposium organized by Martinez-Conde back in 2007 called “The Magic of Consciousness” - which includes Teller of Penn & Teller in a rare speaking role.

Also Saturday: We’re only two weeks away from the University of Chicago’s big Darwin conference, but I still will probably take in at least part of the symposium on Evolution of Brain and Behavior. Harvard’s Elizabeth Spelke caps off the day with a lecture on how the brain processes math - thankfully, it’s scheduled early in the conference, before my own brain will surely grow too tired to handle such a heavy topic.

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Because of limitations in funding and expertise, most laboratories choose to become skilled in one particular technique, be it behavior, molecular biology or electrophysiology – the practice of recording electrical activity in neurons. But as neuroscientists get closer to resolving some of the most complex mysteries of the brain, some researchers find themselves increasingly reaching the limits of those chosen methods. A behavioral researcher might wonder what cellular processes mediate the performance of an animal on a learning task, while a scientist studying neurons in isolation can only speculate about what those microscopic observations mean in an intact organism.

“Really the major problem in neuroscience right now is defining what is the underlying cause,” said Daniel McGehee, associate professor of anesthesia and critical care (and, full disclosure, my former thesis advisor).

The solution to that problem is collaboration, said McGehee and Xiaoxi Zhuang, associate professor of neurobiology, and a recent publication by the two researchers is a vivid example. Published late last month in the Journal of Neuroscience, their study of how an intracellular signal expressed in only one region of the brain mediates certain types of learning could only have been done by combining the strengths of their two laboratories.

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(photo courtesy of Nature)

Bruce Lahn knew that his 2005 papers on the recent evolution of brain genes might stir up some controversy. In the journal Science, the University of Chicago professor of human genetics and his colleagues studied two genes involved in regulation of brain size during development. Intriguingly, they found variants of these genes that are favored by natural selection and are more prevalent in some geographic groups than others. Despite caveats about the complex, multi-dimensional nature of genetic differences, Lahn expected that people on the fringe might twist his research to justify racist beliefs. But he was  surprised at the degree of controversy, particularly the negative reaction from other scientists who distorted his conclusions to make straw-man arguments and even questioned the worth of doing such research in the first place.

That experience, Lahn says now, made him wiser about the way that human genetics research is interpreted by the public and even his scientific peers. But rather than shy away from the type of research that provoked such hubbub, Lahn decided that scientists needed a new moral framework to deal with rapidly growing information about how genes differ between individuals and groups. In an opinion piece published in the journal Nature today, Lahn and co-author Lanny Ebenstein argue that scientists and society at large must embrace the idea of genetic diversity, rather than persist in the more palatable assumption, increasingly disproven by science, that there are no meaningful genetic differences between geographic and ethnic human groups.

“I think the danger really is in the moral attitudes of the people themselves,” Lahn said when we discussed his essay earlier this week. “Instead of trying to suppress the science we should try to build a moral consensus that is constructive to the overall well-being of the species. I think that’s what’s important.”

“The truth about human diversity cannot be changed, but attitudes can change,” he continued. “I think it’s better to change attitudes than to hide factual truths.”

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The Nobel Prize Medal (from nobelprize.org)

The University hasn’t directly won any of the first two Nobel Prizes awarded this week, but one of today’s winners has a UChicago connection: George E. Smith, one of three scientists who will share the $1.4 million prize in physics, received his doctorate at the University of Chicago 50 years ago in 1959. And Monday’s prize has a much more tenuous connection to the proprietor of this very blog, which I’ll explain below.

First, today’s prize rewarded innovations that power technology integral to our daily lives: digital cameras and the Internet. Smith and Willard S. Boyle received the award for the invention of charge-coupled devices, CCDs, the technology put to work in the millions of digital cameras now in use. Charles K. Kao, the third recipient of today’s award, was responsible for improving the use of fiber optic cables, changing the material used in those cables to dramatically extend the distance that light can travel within. Thanks to Dr. Kao, I can quickly research this blog post and you can quickly read it, downloading the information through fiber optic cables that he helped create.

Monday, the award was given to three scientists who made crucial advances in the study of chromosomes, cancer and aging. No, it wasn’t Janet Rowley, but her friend Elizabeth Blackburn was one of the awardees alongside Jack Szostak and Carol Greider. The trio were honored for the discovery of telomeres, repeated sequences at the ends of DNA that prevent genetic material from being damaged and degraded every time a cell is replicated. There really is no better metaphor to explain the function of telomeres than the one used by the Associated Press all day yesterday: “It’s been compared to the way plastic tips on the ends of shoelaces keep the laces from fraying.”

In honor of their award, Scientific American republished an excellent article by Greider and Blackburn that explains why telomeres (and their enzyme partner telomerase, which preserves telomere length) are significant to the study of aging and cancer. As people and their cells age, telomerase works less efficiently, and telomeres and chromosomes shrink, making the cell replication process less accurate. The inability to create new cells could lead to conditions associated with old age, such as artherosclerosis and a weakened immune system. In cancer cells, on the other hand, telomerase is a bad thing, allowing tumor cells to replicate rapidly, grow, and spread around the body. Researchers have thus turned to telomerase inhibitors as a potential cancer treatment.

It is with tongue firmly in cheek that I note my nanoscale contribution to the field of telomere research, from my time at the National Institute of Child Health and Human Development in 2002. I worked in the laboratory of Jeffrey Baron, who studied mechanisms of bone growth in children. As humans grow, a strip of cartilage in the bones of arms and legs called the growth plate produces new cells that lengthen those bones; some time after puberty, those growth plates disappear. With Ben Nwosu and Ola Nilsson, we studied whether the telomeres in those growth plates grow shorter with age - I mostly helped by doing dissections on our chosen animal model, the rabbit, as we bantered about World Cup results. Somewhat unfortunately, we found that the telomere length does not change as a rabbit grows older, suggesting that telomeres are not responsible for the closing of the growth plate after puberty. But disproving a hypothesis is just as important sometimes as proving one, and we were able to publish the results in the journal Hormone Research.

So on behalf of telomere researchers the world over, I’d like to thank the Nobel Committee for their award. But I’ll happily defer the prize money to Blackburn, Grieder and Szostak.

For information about the grants that the University of Chicago received as part of the ARRA package, click here.

If the scientists you know have an extra spring in their step today, here’s why: over $5 billion in National Institutes of Health funding was announced this week, the scientific portion of the federal stimulus package passed in the spring. In his January inaugural address, President Barack Obama made researchers’ neck hair stand up when he promised to “restore science to its rightful place,” and this was the first installment of that pledge - a much-needed boost of cash after five years of flat NIH budgets put many laboratories in jeopardy.

“We’re announcing that we’ve awarded $5 billion — that’s with a b — in grants, through the Recovery Act, to conduct cutting-edge research all across America, to unlock treatments to diseases that have long plagued humanity, to save and enrich the lives of people all over the world,” Obama said Wednesday at an NIH event announcing the grants.

A $42 million slice of that $5 billion pie was awarded to the University of Chicago, and I’ve spent the day talking to some of the researchers who snagged the biggest awards. They are all, as you might guess, thrilled to have an infusion of money to help finally launch projects that have languished unfunded or undermanned. In all, more than 100 UChicago researchers shared in the $42 million pot, with grants ranging from $10,000 to $5.6 million. After the jump is some information on the day’s big winners and the projects their new grants will fund.

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Dr. Funmi Olopade and Dr. Mary Ann Malloy at the Harold Washington Public Library in Chicago, September 22, 2009 (photo by Rob Mitchum)

On Monday we previewed Dr. Funmi Olopade’s public lecture at the Harold Washington Public Library in Chicago titled “Nature, Nurture and Breast Cancer.” For that post, I talked about some recent work from Olopade’s research group that compared the types of breast tumors found in West African women with the tumors seen most often in black and white American women. That research indicated that there likely is a genetic difference between women of African origin and Caucasian, North American women that leads to fewer breast cancer cases but a  higher rate of aggressive, harder-to-treat tumors in black women here and abroad. But the patients from Senegal and Nigeria which Olopade’s group studied also showed different proportions of tumors when compared to African-American women, suggesting a strong role for environmental factors in causing breast cancer as well.

In her library appearance Tuesday evening with NBC reporter Dr. Mary Ann Malloy, Olopade expanded upon those mysterious “environmental factors” that likely contribute to the higher breast cancer numbers in North America. To a rapt audience, Olopade listed off the most well-known and common risk factors for breast cancer: age, family history and “the most important risk factor,” being a woman.

(Chicago Public Radio’s Chicago Amplified is supposed to post audio from Tuesday night’s event, but it’s not up yet. I’ll add a link when it’s available.)

But even to a crowd that, judging from their questions, was very well informed about breast cancer medicine and science, Olopade inspired gasps of surprise by rattling off some less-publicized environmental factors: breastfeeding, age at childbirth, even height. Many of these factors, in combination with more mundane things like lack of moderation in diet, exercise and alcohol intake, are behaviors more commonly seen in rich countries where women have achieved a more equal status in their work and private lives.

“I think what we’re still struggling with is, as we get more affluent and as people live the good life, then you see the rising incidence of breast cancer,” Olopade said. “We want people to have the good life, but what is it about the good life that is predisposing us to breast cancer?”

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Dr. Funmi Olopade

A fact often lost in the charity walks and commercials that have dramatically raised awareness of breast cancer over the past two decades is that beneath the diagnostic umbrella of  “breast cancer” are numerous types of tumors. Other than the fact that all of these tumors are found in breast tissue, different forms of breast cancer grow at different rates, will express different types of hormone receptors or genes that can act as drug targets, and are more or less likely to become “invasive,” spreading throughout the body. To complicate matters further, not every population experiences these different types of breast cancer in equal proportions - black women in the United States have a poorer survival rate for breast cancer than white women, and women in Africa  have an equal breast cancer mortality rate to North American women despite four times as many diagnoses of the disease in the U.S., Canada and Mexico.

University of Chicago Medical Center researcher Olufunmilayo Olopade (Funmi, for short) has dedicated her career to the study of these discrepancies since moving to Chicago from her home country of Nigeria in the 1980’s. Olopade, a professor of medicine and human genetics, has received several accolades for her work, including the prestigious MacArthur fellowship (known sometimes as the “genius grant”) in 2005. On Tuesday evening, she’ll give a lecture at the Harold Washington Library Center in Chicago titled “Nature, Nurture and Breast Cancer” that will explain what we know about the genetic and environmental factors that cause the disease in more than 200,000 American women each year.

In a recent Journal of Clinical Oncology paper, Olopade and colleagues from Chicago, Senegal and Nigeria looked for physiological reasons to explain the differences in breast cancer rates and outcomes between American and African populations. Learning more about these differences could help direct women into the most effective treatments for their particular type of breast cancer, Olopade said, as well as offer clues as to how genes versus the environment cause breast tumors to arise.

“Breast cancer doesn’t affect all individuals the same way,” Olopade said this past weekend, as she prepared for Tuesday’s lecture. “What we found is that the types of cancer that people get in different populations differ, that’s why when we talk about personalized medicine at an individual level we also have to talk about it on a population level.”

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The shortened "Philadelphia chromosome" seen in certain leukemias (picture from nature.com)

The big science news of the day was the announcement of the Lasker Awards, informally thought of as the American version of the Nobel Prize for physiology and medicine. This year’s clinical medical research award went to a trio of researchers from Oregon Health & Science University, Sloan-Kettering Cancer Center and drug company Novartis, but you could just as easily say it was awarded to a drug: the cancer treatment Gleevec. And Gleevec’s roots stretch back to the campus of the University of Chicago and a very familiar face on this blog: Janet Rowley.

This year, Rowley has already received the Presidential Medal of Freedom, the Gruber Genetics Prize and stood at President Obama’s shoulder as he repealed federal limitations on stem cell research. Oh, and she’s already won the Lasker Award herself, in 1998. So it’s okay that she’s not mentioned among today’s winners.

As with most stories of scientific discovery moving from the laboratory bench to the pharmacy, it’s simplistic to pin the achievement on one, three, or even ten people. The path to Gleevec’s discovery go back beyond Rowley to the 1950’s when Peter Nowell and David Hungerford - working at the University of Pennsylvania in Philadelphia - found an odd, shortened chromosome in patients with a form of cancer called chronic myelogenous leukemia (CML). They called that stubby piece of DNA, appropriately enough, the Philadelphia chromosome.

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