Editor’s note: I will be on vacation next week, and so will the blog. A tanner ScienceLife will return on July 6th.

People often worry that the latest ubiquitous technology is changing or harming them, and the link between cell phones and cancer is a treasured old superstition at this point. But chalk up another strike against the invisible deadly waves of mobile phones, as a British Medical Journal study found no link between pregnant women living near phone towers and the incidence of childhood cancers. “We found no pattern to suggest that the children of mums living near a base station during pregnancy had a greater risk of developing cancer than those who lived elsewhere,” the adorably British senior author Paul Elliott told the Guardian. The story is also fodder for another fascinating use of the new Guardian story tracker, which aggregates web commentary on major science stories.

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The genome-sequencing service 23andme hasn’t had the best press this month, after a mix-up of the DNA test results for 96 people renewed concerns about the utility and harm of such tests. But yesterday the 23andme team scored some points with the publication online of the first research study to come from their pool of data (customers who consented to having their genetic information used for this purpose). It’s a curious paper, a genome-wide association study concerned not with cancer or disease but characteristics such as earlobe shape, sneezing reflexes, and curly hair. Also this week, Wired published a great story about the role that can be played by personal genomics companies in the hunt for new information about conditions such as Parkinson’s disease.
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Was Michaelangelo a secret neuroscientist?

The World Cup in South Africa has rightly given the people of the continent reason to celebrate and show off their ability to host an international party. But there remain severe political, economic, and health problems in Africa that a month-long soccer tournament can do little to repair. A primary concern is the epidemic of HIV/AIDS that has swept across African countries, reducing average life expectancy by as much as 20 years in some countries.

The face of this tragedy is often the millions of AIDS orphans left behind when their parents succumb to the disease. But depleting an entire generation of people has ripple effects in both directions, a recent study by University of Chicago and Stanford University researchers finds. Since the disease, unlike most, kills largely young and middle-age people, the other demographic left behind are the elderly. As Tim Kautz, an economics graduate student at the University of Chicago, and his colleagues found, the older generation is left with greater responsibility and less support.

The study, published last week in the British Medical Journal, used huge demographic surveys of 22 countries in sub-Saharan Africa to analyze the effects of the AIDS epidemic on the elderly. Despite the huge dip in the middle age groups, the elderly population of Africa is growing - expected to rise 55 percent between now and 2025, according to a United Nations report. In countries where it remains traditional for adult offspring to take care of their ancestors, it’s a real problem when those offspring are disappearing. Kautz observed that family structure firsthand while leading AIDS education courses in Tanzania one summer during his undergraduate years.

“What I observed while I was there living with a host family, made me realize family how the living arrangments are so different from the United States,” Kautz said. “I saw how elderly people lived with adult children…and how important informal networks and family were in caregiving. ”

As an undergraduate at Stanford, Kautz worked with the Center for Health Policy to study the effect of the AIDS epidemic on the elderly population of Africa. Analyzing the surveys, the researchers determined that the number of unattended elderly people (defined here as 60 or older) has already begun to spike, moving from 23.5 percent in 1993 to 26.1 percent in 2004. Extrapolating to the future, that rise is expected to continue; according to their calculation, every one percent increase in AIDS mortality rate leads to a 1.53 percent increase in older people living by themselves. Some more math, and an estimated 582,000 to 917,000 newly unattended elderly people were created in 2006 alone.

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Attaining a healthy weight is often billed as an individual pursuit, with television commercials eagerly encouraging customers to take hold of their habits. But for all the calorie-counting and exercise schedules you can give a person, their struggle with weight doesn’t occur in isolation. Family members and friends can negatively influence your diet, whether it’s meals at home or dining out, and your activity levels - encouraging a night at the bar instead of an hour on the treadmill.

But those external influences can also be harnessed for good, as a front page article by Julie Deardorff in the Chicago Tribune showed yesterday. Deardorff focused on the Maudsley Approach, a family-based treatment for anorexia and bulimia that involves the parents or other relatives in encouraging the patient to eat. That strategy is a shift from the traditional treatment for eating disorders, which usually involves a one-on-one inpatient program designed to convince the patient to regain healthy eating habits. But the Maudsley Approach, designed in part by University of Chicago psychiatrist Daniel Le Grange, has evidence on its side: trials, such as this one, that showed better outcomes with family-based treatment compared to traditional psychotherapy.

I spoke to Le Grange about the Maudsley Approach and other research trends for our Dr. FAQ video series in March; here’s the video that most directly focuses on family-based treatment.

While family appears to be a useful tool for positively changing the diet of someone with an eating disorder, there is also a dark side to the familial influence on food habits. Study after study has found that obesity runs in families, through an as-yet-undetermined interaction of genetics and environmental factors. Even in families where one member undergoes a surgical procedure for their obesity such as gastric bypass, the ripple effects through their family remain.

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The Kv1.2 channel (image courtesy Fatemeh Khalili-Araghi/Theoretical and Computational Biophysics Group at UIUC)

Inside the human body are millions of miniature machines, the gatekeepers of the electrical impulses that keep our hearts beating and our minds thinking. They’re called ion channels; portals that allow small ions such as sodium, potassium, calcium, and chloride, to pass in or out of cells. A simple responsibility, with a complex and crucial outcome, as the flow of ions allows muscles to contract and action potentials to fire along the length of neurons.

While the job of an ion channel may seem straightforward, their design is anything but. Because the channels are awfully tiny, scientists have been forced to determine their workings through indirect experiments. A handful of pictures of the channels have also been taken, via the method of X-ray crystallography, but the photos can only capture an ion channel at rest - imagine trying to figure out how a car engine works from a single photograph.

But what if you could take the volumes of indirect information about an ion channel and instruct a computer to fill in the blanks? That was the approach taken recently by a team of scientists from the University of Illinois and the University of Chicago to tackle a target at the top of the list for ion channel researchers: the potassium channel voltage sensor.

“A potassium channel is a switch that opens and lets ions flow,” said Benoît Roux, professor of biochemistry and molecular biophysics at the University of Chicago and an author of the paper. “And that voltage dependence switch is necessary to understand how the nerve impulse works.”

Think of the ion channel as a garage door, and the voltage sensor as the control box. The channel only opens at a particular voltage, so it needs a way of both detecting voltage changes and powering the transition from closed to open states. It does so with the voltage sensor, a group of positively-charged amino-acids that can be pushed a small distance inward or outward by changes in voltage.

Scientists have a fuzzy idea of how that voltage sensor works from electrophysiological experiments, but the fine points of the mechanism are still unclear. As with any unknown territory in science, competing theories with colorful names like the paddle model, the helical-screw model and the transporter model attempt to fill the void. But Roux and his colleagues decided to test the movement of the voltage sensor with a complex computer simulation of one particular potassium channel, called Kv1.2, found in the heart and brain.

“This is not something you can do on a desktop computer,” Roux said. “Other people have had access to big computers, but it’s the strategy to compute that quantity that has never been done. This shows that it’s possible to address this kind of question at the most quantitative level with an atomistic model, and that has never been shown before.”

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Forty years ago, Bangladesh was facing a health crisis. Contamination of water sources throughout the country were causing an incredibly high rate of child mortality, with more than a quarter-million children dying each year from waterborne infectious diseases. As a solution, international charity organizations launched a massive humanitarian effort to bring cleaner water to the Bangladeshis, installing roughly 10 million hand-pumped wells that brought up water from deep underground.

It wasn’t until more than 20 years later that scientists discovered how that well-intentioned plan had backfired. Though the underground water was free from the bacterial contamination of surface sources, it was tainted instead with arsenic, the toxic chemical that can cause skin abrasions, cancer, and other diseases. A survey by the World Health Organization found that as many as 77 million people - half the population of Bangladesh - were drinking water with levels of arsenic higher than the recommended safe limit of 10 µg/L. Unflinchingly, the WHO characterized the situation as “the largest mass poisoning of a population in history.”

There’s no dispute that arsenic is bad for you, as indicated by its notorious and frequent role as a poison in mystery plots. But at lower, chronic doses, it has been hard to characterize just how dangerous arsenic can be to a person. Epidemiological studies of its toxicity have been able to retrospectively correlate increased rates of disease with the average amount of arsenic exposure in a particular area or group, but such studies lack specificity and can be distorted by various factors. In bleak fashion, the tragedy in Bangladesh offered a perfect setting for determining more precisely how decades of arsenic exposure can increase the risk of disease and death.

Such a study was launched in 2000 by Habibul Ahsan, director of the Center for Cancer Epidemiology and Prevention at the University of Chicago Medical Center. With a project called the Health Effects of Arsenic Longitudinal Study, or HEALS, Ahsan’s group laid out an ambitious plan to measure the arsenic levels in thousands of wells and people, who could then be followed to assess the health effects of their exposure. Beginning in late 2000, hundreds of staff members fanned out across Bangladesh, traveling by car, foot, or (during the rainy season) boat to remote villages where blood and urine samples were gathered and well water was sampled. After 18 months, nearly 12,000 subjects in a Bangladeshi region called Araihazar were recruited, nearly all of whom provided follow-up urine samples roughly every 2 years thereafter.

All that legwork gave the HEALS researchers a baseline from which to track the mortality of individuals with different levels of arsenic exposure. Over 9 years of monitoring (so far), more than 400 of their subjects died for various reasons. By indexing those deaths with whether the person’s urine samples showed high, moderate, or low level arsenic exposure and controlling for other factors such as age, sex, smoking and body mass, the researchers could make firmer conclusions about arsenic’s toll.

The results, published this weekend in The Lancet, were staggering. For the quarter of the subject pool drinking water with the highest levels of arsenic (an average of 27 times the safe level), the risk of dying from a chronic disease was nearly 70 percent higher compared to those below the safe level. Those drinking a more moderate dose of arsenic in their water - from just above the safe limit of 10 µg/L to 15 times the limit - also showed an increased risk of mortality of roughly 20-30 percent. The latter result is relevant to people around the world, including parts of the United States where arsenic levels in groundwater remain dangerously high.

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Personalized Medicine: The Brake vs. The Accelerator

A recurring theme on the blog - and presumably on every other medicine and science blog - has been the push toward personalized medicine, the utopian future where every patient receives individualized care for a disease or even the genetic risk of disease. But the road to that future world of health care has been slower than some experts anticipated, with disappointing clinical trials, scientific setbacks and regulatory hurdles all acting as speed bumps. Those obstacles are partially why National Institutes of Health director Francis Collins was dinged this week in a New York Times article for promising “a complete transformation in therapeutic medicine” within a decade or two of the Human Genome Project’s completion…ten years ago.

So it was interesting to see Collins’ revised opinion on the timeline for personalized medicine this week in the New England Journal of Medicine, in an editorial co-written with FDA Commissioner Margaret Hamburg. It’s a strange partnership in some ways: the country’s top scientist and the country’s top regulator. The editorial reads accordingly, with a first half marked by the go-go optimism of Collins followed by the “woah, let’s slow down” realism of Hamburg.

Still, there are some interesting initiatives within. Collins gives the glass-half-full version of the New York Times’ Human Genome Project assessment, stating that hundreds of disease-related gene variants have been characterized and are now promising drug targets. The issue, Collins claims is the lack of financial incentives for companies to pursue those targets, something he hopes to fix by allowing the NIH to step in and do the preclinical “Valley of Death” work that scares off pharmaceutical companies. Collins also promises an expanded effort to establish tissue banks and genetic databases from clinical trials and epidemiological studies such as the Framingham Heart Study, to enable better research into biomarkers that predict disease or response to treatment.

On the flipside, Hamburg argues that extreme caution should be employed in approving tests for those very biomarkers. Her argument - that most current tests are inaccurate or misleading - is backed up by the FDA’s recent move to more aggressively regulate test marketed for at-home use. While the editorial offers a table of three tests approved to predict a patient’s response to a cancer drug such as Gleevec or cetuximab, Hamburg writes that some 2,000 genetic tests are currently used by clinical laboratories - some FDA-approved, some not. The editorial promises a genetic testing registry that will offer consumers and physicians information about the tests, but promises that the agency will keep a close eye on tests that “are broadly marketed to laboratories or the public.”

If that sounds all a bit good cop/bad cop, it’s true. The key will be in the balance between the forces pushing personalized medicine forward and those entrusted with testing its validity. As Collins and Hamburg put it, “When the federal government created the national highway system, it did not tell people where to drive - it built the roads and set the standards for safety…We are now building a national highway system for personalized medicine.”

More World Cup Science

When I wrote my World Cup science piece last week, I didn’t realize that several scientists were holding back their timely soccer-science articles until the tournament was in full swing. But sure enough, a flood of new research has crossed the wires in the past week, about everything from the controversial vuvuzela horns to the age-old debate of “soccer” vs. “football.”

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With all the talk of tomorrow’s better cancer treatments, it’s important occasionally to remember that millions of people have been treated with successfully with today’s - and yesterday’s - medicine. For someone newly diagnosed with cancer, it’s inspiring to hear the stories of those who have fought the disease and survived, a helpful dose of optimism in a trying time. Two weeks ago, a ballroom at the Westin Hotel in Chicago was filled with such stories, from people who have survived as long as 43 years after the diagnosis of cancer.

The 20th annual Cancer Survivors Day brought together over 100 patients and their families for a day of food and fun. Speakers included Leslie Wallene Yang, a gastroenterologist at the University of Chicago Medical Center who is herself a cancer survivor, and Marcia Wallace, the voice of Bart’s teacher Edna Krabappel on The Simpsons. And the bawdy blues tunes of Lynne Jordan & the Shivers proved that cancer survivors can get down like the rest of them (seriously, check out the disco moves on the woman at 4:35!). Here’s our video of the event, shot by John Easton and edited by yours truly.

Photos by Cheryl Reed

How do you turn a massive health crisis like the Haiti earthquake into a medical journal article? The chaos following the 7.2 earthquake that killed more than 200,000, injured 300,000, and left hundreds of thousands more homeless was certainly not conducive to orderly collection of data. But the often-improvised responses of non-governmental organizations, health care centers and military operations to the earthquake hold important lessons for future emergency medicine efforts, wherever they may be needed.

That’s the message a team of physicians and scientists trumpet in an article published last week in the journal Disaster Medicine and Public Health Preparedness on the Chicago Medical Response. A collaboration between 6 Chicago medical centers quickly forged in the days following the Haiti quake, the group united global health programs and volunteer efforts that were only loosely connected before the disaster. The resulting Voltron of medical/humanitarian response was able to respond more effectively to the Haitian crisis, argue the authors - which include Christine Babcock and Christian Theodosis, the point people for the University of Chicago’s Haiti team.

“Pooling common resources and drawing upon each institution’s natural strengths allow for a more seamless, sustainable, and comprehensive response to emergencies,” the authors write.

Putting such an effort together was not without its hiccups. While each medical center experienced a flood of volunteers as the immense toll of the earthquake became apparent, mobilizing that outpouring of support was not simply a matter of putting everyone on a plane and hoping for the best. Volunteers needed to be vetted for their language skills, experience with disaster medicine, and their specialty - especially important as the need on the ground shifted from trauma surgery to rehabilitation and physical therapy. For every physician, nurse or therapist that went to Haiti, someone back at home had to be found to cover their shifts. Costs associated with travel, supplies, and diverted attention at work also had to be addressed - the article estimates that over 1500 hours of staff and faculty time was dedicated to human resources alone, not counting any of the time on the ground in Haiti.

By banding together, the various hospitals could share some of that burden while pooling their connections. The University of Chicago, Northwestern University Feinberg School of Medicine, and the University of Illinois at Chicago each had their own distinct global health initiatives in place, including unique partnerships with international NGOs. The wide menu of collaborators allowed the Chicago Medical Response to pour resources into several sites in Haiti, including the Love A Child orphanage and hospitals in Port-au-Prince. Sharing the load also expanded the volunteer pool, allowing more physicians or nurses from needed specialties or with helpful language skills to be located without straining the hospital schedules too badly.

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In the first part of his “The Genome at 10″ series on Sunday, Nicholas Wade of the New York Times wrote about frustration in the wake of the Human Genome Project. Despite optimistic promises at its unveiling in 2000, scientists haven’t found as many of the answers to disease in DNA as was initially hoped. Instead, our knowledge of the genome has created even more questions and complexity in the search for the genetic sources of disease.

As a result, more and more attention has been paid in recent years to epigenetics, the non-genetic control of gene expression. Through processes such as DNA methylation and histone acetylation, biology has developed ways of controlling the volume of protein production - silencing or activating a particular gene when its protein is needed.

“Picture the reading of DNA (gene transcription) as the opening of a zipper,” described Stephen Archer, chair of cardiology at the University of Chicago Medical Center. “Transcription factors must run along this DNA zipper to allow the DNA to open so the gene can be read. Methylation blocks this reading, much like having a thread stuck in the zipper prevents its opening. This way, methylation silences a perfectly normal gene.”

For a disease such as pulmonary arterial hypertension (PAH), which Archer studies, the search for a straight genetic cause has been unsatisfactory. PAH is marked by blockage of blood vessels to the lungs, and is known to run in families. 10 years ago, when a PAH-linked genetic mutation was found in a gene called BMPR2, researchers hoped that aberrant genetics were to blame for the disease. But at most, only a quarter of people with that mutation developed PAH, and not all people with PAH carried that mutation, Archer said. That led PAH researchers  to look elsewhere for answers, including at a mitochondrial protein called superoxide dismutase 2 (SOD2), which is known to be lower in PAH patients.

But when researchers looked at the SOD2 gene in people with PAH, they found no mutation. That suggested epigenetics may be to blame, Archer said.

“The question was why is SOD2 downregulated?,” Archer said. “So we began looking at the possibility it might be present but functionally inhibited.”

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Everyone gets angry from time to time. But there’s angry, and there’s angry - wall-punching, object-throwing, call-the-police angry. The latter type of tantrum, if it’s a recurrent problem, could be a symptom of a psychiatric condition currently known as intermittent explosive disorder, or IED. Though it has appeared in every edition of the Diagnostic and Statistical Manual of Mental Disorders (albeit under different names), IED remains a hazy sort of diagnosis to many both inside and outside psychiatry. But over the last 20 years, Emil F. Coccaro, M.D., Chair and the E.C. Manning Professor of Psychiatry and Behavioral Neuroscience at the University of Chicago Medical Center, has built up a diverse body of research defining the causes, consequences, and best available treatments for IED.

Coccaro’s research group is currently in the midst of a flurry of publications that break down IED from a number of angles: its familial nature, its association with other negative health outcomes, its correlation with brain activity. So I sat down with him to talk about what is currently known about the disorder, what distinguishes a person from IED from a person with “a temper,” and how it is currently treated by psychiatrists. Coccaro was blunt about the history of the disorder, saying that some of the mystery surrounding the disease is due to early difficulties defining it.

“There have been controversies about it because people have wondered how much of it is out there and does it really exist,” Coccaro said. “The criteria in DSM-3 and DSM-4 were never that good.”

The problem, he said, was in the dynamics of the disorder. While it was clear that patients with IED had recurring, out-of-proportion episodes of aggression, the original criteria stated that the patient would be relatively “even-keeled” between. But Cocaro said that psychiatrists have come to understand that IED - which may appear in between 4 and 7 percent of the United States population - is more likely to reflect quieter impulsive aggressive “rumblings” between the big “blow-ups”.

“People who have this explosive problem are not like Bruce Banner where they get angry and become this monster and then come back to baseline,” Coccaro said. “They’ll have big explosions, but at baseline they are a bit irritable, still, and are at high risk for blowing up when somebody frustrates or angers them.”

More specific criteria have not only helped psychiatrists diagnose the disorder, it has also allowed for more thorough research. A breakthrough finding by Coccaro in 1989 was that the function of the serotonin system - a neurotransmitter also known to be involved in depression - correlated with aggressive behavior. People with lower serotonin function were, on average, more aggressive and impulsive, a relationship that only strengthened as diagnoses of IED became more accurate.

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For the next month, the world’s attention (and mine) will be focused on South Africa for the 2010 World Cup. Though it’s just starting to break through the public consciousness in the States, the World Cup is such a massive cultural force in the rest of the world that its tremors are felt even in scientific circles. A recent psychology study on how to take the best penalty kick got a lot of media play this week, and at least two different economists developed models to predict the winner via a country’s GDP and other factors (both picked Brazil).

I jumped into PubMed to see what other World Cup-related research could be found, and it turned out the water there was very deep. Since the last World Cup in 1996, dozens of scientific and medical articles have been published, ranging from editorials advising fans about potential diseases they need to be immunized against in South Africa to surveys of injuries suffered by referees during the tournament. But one topic appeared to drive much of the World Cup-related scientific debate, and it explains just how seriously the competition is taken around the world: does watching important World Cup games cause heart attacks?

The controversy started with a 2008 New England Journal of Medicine article called “Cardiovascular Events During World Cup Soccer.” A team of German researchers looked at emergency medicine records from June 9 to July 9, 2006, when the last World Cup was taking place in Germany, and compared the period to two control months free from international tournaments. According to the authors, “six of the seven games in which the German team participated were associated with an increase in the number of cardiac emergencies,” averaging out to a 2.5-fold increase in heart attacks. People with a history of coronary artery disease had an even higher health risk of watching their countrymen on the pitch: a four times increase in events. Blog founding father Jeremy Manier wrote about the study for the Chicago Tribune, and related it to local stress about the Cubs and Bears.

But wait - a counter-attack was sprung this year by an Italian team of researchers, who focused upon their own population during not only the 2006 World Cup, but the 2002 event as well as the 2004 European Championships. Studying more than 25,000 hospital admissions, the authors failed to find any uptick in heart-related events, even when Italy’s national team defeated France in a tense penalty shootout to win the ‘06 Cup (there was, however, at least one Italian with a chest injury that day). The Italian authors claim that their negative results are more in line with previous literature, including an English study that found only a small (but significant) increase in heart attacks and strokes during club soccer matches.

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As the weather warms in the Chicago area, it might seem like a strange time to be talking about cold hands. But for some people, uncomfortably cold hands is not just an artifact of the long Midwestern winter, but a medical syndrome that may require treatment. Defined by its primary symptom rather than a single cause, Cold Hands Syndrome is marked by, well, cold hands, as well as pain, numbness and occasionally discoloration or even tissue damage. The source of these symptoms is a loss of circulation to the hands and fingers, but the cause of that decreased blood flow can range from Raynaud’s Disease to blood clots to arteriosclerosis to lupus to scleroderma. As Ginard Henry, assistant professor of surgery at the University of Chicago Medical Center, describes it, Cold Hands Syndrome is “a range of different diseases” that cause similar symptoms in one’s extremities.

“Your hands are almost like a lawn at the end of a street, and you are giving the lawn water to grow,” Henry said. “If anything disrupts that flow of water then the lawn doesn’t grow and you have a problem.”

Henry and colleagues Lawrence Zachary, associate professor of surgery, and Nadera Sweiss, assistant professor of medicine, have launched the Cold Hands Clinic at the Medical Center, uniting expert physicians from a number of disciplines to focus on this unusual problem. I sat down with Henry to ask him about Cold Hands Syndrome: what it is, how it’s diagnosed, and how it is treated. Befitting the diverse causes of the disorder, there are a number of different treatments, including measures as simple as moisturizing and the use of drugs such as Viagra and Botox for, shall we say, purposes other than their primary use.

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Almost all cases of Type I diabetes are currently treated with the same method: insulin. Because of an immune response that attacks the insulin-producing cells of the pancreas, diabetics must replace the endogenous hormone from external sources to process sugar and maintain safe blood glucose levels. Except for a tiny minority of cases where a genetic mutation is found to explain their disease, insulin injections become an unpleasant daily ritual for Type I diabetics that they will need for their entire lives.

But scientists and clinicians hope to someday offer diabetics more permanent ways of managing, or even erasing their disease. Transplantation of pancreatic islets - which contain beta cells, the insulin factories of the pancreas - have achieved very limited success, offering the recipient temporary glucose control. But finding compatible donors is difficult, the patient must continuously take immunosuppressive drugs, and even with therapy, 90 percent of those transplants fail within five years.

In 2003, an even better solution was proposed: what if a diabetic could simply regenerate their own damaged pancreatic beta cells? A team from Massachusetts General Hospital announced that mice were capable of pancreatic cell regeneration when the overactive immune response was controlled alongside an injection of spleen cells. Several groups, including one from the University of Chicago, recreated the study, and while they failed to replicate the effectiveness of spleen cells, a promising degree of beta-cell regeneration was observed.

“I think it was a little bit controversial for a long time. Most people felt that when you lost the beta cells, they were pretty much gone. But recently it became clear that, at least in mice, there is a pretty substantial regeneration by some groups,” said Anita Chong, professor of surgery at the University of Chicago Medical Center.  “If the observation in mouse could be translated into humans, this would be very significant.”

So Chong’s group continued to study regeneration, looking for specific treatments or protocols that would maximize the recovery of beta cells. Yet the studies were laborious, with time-intensive data collection requiring 20-30 hours of microscope work for each mouse in a given study.

“We realized that the standard way of looking at beta cell regeneration was extremely tedious and subjective,” Chong said.

A workaround for that laboratory annoyance was inspired by an unlikely source: the firefly. The laboratory of Graeme Bell, professor of medicine and human genetics, developed a transgenic mouse with the enzyme luciferase (responsible for the firefly’s distinctive glow) attached to the insulin promoter. So cells that produce insulin will also produce luciferase, and when an activating luciferin salt is injected, they glow. While imperceptible to the naked eye, the mouse can be placed in a photon-counting detector that allows researchers to quickly assess the amount of pancreatic beta cells present.

Those mice were then used for a regeneration study published earlier this year in the journal PLoS One. The hypothesis, according to first author and surgical resident Eric Grossman, was to test whether merely controlling glucose levels in a mouse model of diabetes would help pancreatic beta cells to regenerate. Half the mice received an islet cell transplant, while the other half were simply treated with insulin via an implantable pellet.

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Most scientific conferences contain two very different approaches to storytelling. On the exhibit floor, pharmaceutical companies, laboratory suppliers, publishers and chambers of commerce compete for attendee’s attention with ever more grandiose booths that resemble small palaces. But in the many, many rooms surrounding that circus, scientific data is presented (usually) in decidedly unflashy fashion, thanks to the understated personalities of most scientists and a sense of research presentation propriety. 

The American Society of Clinical Oncology meeting illustrated that divide more vividly than any other scientific conference I’ve attended. Just last month, I was impressed by the exhibit booth architecture display at the BIO meeting, but the exhibitor showcase at ASCO made other conferences’ huts look like a miniature golf course. With Jumbotron-sized video monitors, 3D animations, futuristic chairs, and more sales reps per square foot than anywhere else in the world, it’s an overstimulating experience to walk through.

But the research presentations of ASCO are the polar opposite - quick-fire 15-minute “just the data” talks light on drama even as exciting new treatments are described. The structure for presenting clinical trial results is apparently very codified for cancer researcher: provide rationale for trial, describe study design, show effect of treatment (or lack thereof), compare side effects to other treatments, suggest future directions. Context for the data is later provided by a discussant, who is at more liberty to deliver a judgement on whether the findings have immediate clinical relevance. Whether that’s down to ethics or merely tradition, it’s a much more formal experience than other conferences I’ve seen.

The overwhelming size of the conference makes it hard to deliver a 30,000-foot overview of the proceedings; one must merely pick a particular cancer track and hope for the best. On Monday, following the University of Chicago trail led me to a series of presentations on head and neck cancer, a particular specialty of the Medical Center and our current CEO, Everett Vokes. Like all cancer types, the head and neck variety can be broken down into several sub-types, including thyroid cancer, which can be further broken down into its own sub-types. One disease on the smaller end of this Russian nesting doll hierarchy is medullary thyroid cancer (MTC), diagnosed in only 1,400 Americans a year but essentially untreatable.

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In the New Yorker last month, Malcolm Gladwell wrote elegantly about the euphoria and frustration of cancer drug discovery. Tracing in parallel the path of a modern biotechnology company and a team of doctors in the 1950’s, Gladwell illustrated the unexpected twists and turns that mark every new drug’s journey from laboratory to clinic, in a game where the stakes are literally life and death. The dramatic scene that Gladwell chose to open his piece? The American Society of Clinical Oncology meeting, a huge gathering of cancer researchers where the highly-anticipated results of clinical trials for the next wave of promising anti-cancer agents are presented in a flourish of success or a sigh of failure.

The ASCO meeting this year is being held in Chicago, whose McCormick Place is one of the few convention centers gargantuan enough to hold tens of thousands of researchers from around the world. Throughout the Escher-like hallways of that building, echoes of Gladwell’s opening scene were taking place, with Kaplan-Meier curves - the graph that shows differences between the drug-treated group of patients and the control group - delivering their positive and negative verdicts. Over the weekend, two success stories featured University of Chicago involvement; both were exciting small steps in the battle of science against different types of cancer.

One of the most difficult to treat cancers is also one of the most common: lung cancer, which is newly diagnosed in more than 200,000 people a year in the United States. Lung cancer researchers, including Ravi Salgia of the University of Chicago Medical Center, have been looking for proteins that are behaving badly inside lung cancer cells and that may represent promising targets for cancer therapy. One such target, the enzyme anaplastic lymphoma kinase or ALK, is overactive in a small percentage of lung cancer patients due to a chromosomal translocation - a break in the DNA that produces a dangerous Frankenstein protein called EML4-ALK.

While only 4 percent of patients with lung cancer are positive for EML4-ALK, the mechanism suggests that an inhibitor of the protein may be effective in attacking cancer in that population. Sunday, researchers (including Salgia) presented evidence of that strategy working - an inhibitor of ALK called crizotinib successfully controlled lung cancer in 90 percent of patients enrolled in a small trial. In 57 percent of the patients, tumors actually shrank - an incredible advance in a cancer that is nearly always untreatable. The authors said that a larger, Phase 3 trial is already underway to verify the findings in a larger population.

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