Robin Tricoles

Esophageal lesions meet their match

Field Willingham, MD, MPH

Once esophageal tumors establish themselves, a patient’s prognosis is grim and morbidity vast. But when lesions are caught early and removed, especially in the premalignant stage, the odds of survival markedly improve.

When a case calls for it, Emory gastroenterologist Field F. Willingham, MD, MPH, uses a hybrid approach to ousting superficial esophageal lesions. Superficial esophageal lesions are commonly caused by acid reflux disease, or GERD. GERD occurs when stomach acid flows into the esophagus and can lead to a condition known as Barrett’s esophagus, where the cells in the lower esophagus become damaged. This in turn can lead to dysplasia, or pre-cancerous cells.

But for superficial cancers, it is now possible to remove a portion of the lining layer of the GI tract, containing the tumor, with an endoscope.  This can help carefully selected patients avoid a major surgery. The technique, known as an EMR, allows the removal of superficial esophageal tumors and pre-cancer with an endoscope, a slender tube-like instrument.

Detecting and removing esophageal tumors early is essential for a favorable outcome. Once tumors firmly establish themselves in esophageal tissue, the prognosis is grim and morbidity vast. In the past, a diagnosis of an esophageal tumor meant the removal of the esophagus and often the stomach. But now EMR can be used in tandem with radio frequency ablation.

In surgical situations in which radio frequency ablation is not feasible, Willingham and his colleagues are beginning to use an alternate technique, known as cryotherpay, in tandem with EMR. Cryotherapy involves freezing superficial cells to rid the esophagus of suspect cells.

“So, if the end of the esophagus is twisted, or if we can’t touch it with this balloon device, then we can use cryotherapy,” says Willingham. “We’re trying to kill the lining layer with the tumor cells without killing the deeper layer.”

Willingham and his colleagues are seeing evidence that using these very three very different, technologies in tandem or alone will provide patients with a better way to rid them of esophageal lesions while preserving their quality of life.

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Genetic alteration opens door to targeted treatment of rare tumor

A cross section of an epithelioid hemangioendothelioma

Emory pathologist Sharon Weiss, MD, was the first to describe an extraordinarily rare tumor known as an epithelioid hemangioendothelioma (EHE). Thirty years later, researchers have identified a genetic alteration linked to this odd vascular tumor.

It’s hoped this newfound information will lead to a better understanding of the mechanisms underlying the development of this tumor and hence development of a targeted treatment. None yet is available. However, these findings already have been used to develop a new diagnostic test for this blood vessel disease.

The research, published in a recent issue of Science Translational Medicine, was done in collaboration with Cleveland Clinic’s Taussig Cancer Institute and led by Brian Rubin, MD, PhD, of Cleveland Clinic’s Pathology and Laboratory Medicine Institute and Lerner Research Institute.

The genetic alteration formerly in question involves a translocation between chromosomes 1 and 3, where chromosomes 1 and 3 exchange DNA fragments that are transposed onto opposite chromosomes. The result: the swapped DNA encodes a unique, fused gene that contains components from each chromosome. Because genes are translated into proteins, the result of this unique gene is a correspondingly unique protein, one thought to cause cancer.

Epithelioid hemangioendotheliomas comprise less than one percent of all cancers. Roughly 100 new cases are diagnosed in the United State each year. EHE are eccentric in their epidemiology, structure and aggressiveness. Slow to metastasize, they tend to occur in both young men and women when soft tissue is involved but occur mostly in women when the liver and lungs are affected.

However, it’s their peculiar structure that has so far made targeted treatment problematic, especially in the liver and lungs. “Instead of being one mass as you might expect with liver cancer, the patient with EHE often presents with little nodules throughout the liver,” says Weiss.

“The reason this occurs is that the growth starts in the liver’s portal vein, grows along its length, and then tracks out through the vessels. The growths blister out from the vessel creating these little nodules. Epithelioid hemangioendothelioma don’t possess the classic features of vascular tumors. In fact, EHE may have so many sites of involvement that the cancer can’t be cured, short of transplantation.”

Using EHE tissue samples gleaned from Weiss’s vast library, Rubin developed a genetic probe to detect the distinct chromosomal translocations in the tumor. The probe now serves as a powerful diagnostic tool of EHE and opens the door to understanding these tumors’ mechanisms.

“Once you understand the mechanism behind it, you can start trying to target those pathways in a therapeutic way,” says Weiss.

Posted on by Robin Tricoles in Cancer 1 Comment

Fertility: a new frontier in treating those with HIV

HIV

Not long ago, physicians who treated those with HIV focused only on helping their patients stay well. Today some physicians are also beginning to focus on helping those patients conceive.

“Most of the patients who are now diagnosed with HIV are in their reproductive years, and as many as a third express a desire to have children,” says Emory reproductive endocrinologist Vitaly Kushnir, MD.

This emerging area of treatment has been made possible thanks to the growing effectiveness of a combination of drugs known as Highly Active Antiretroviral Therapy, or HAART, used for years to treat retroviruses, including HIV.

“Now that people with HIV are living longer, fertility and HIV is an emerging area of interest,” says Kushnir. “Several studies have indicated that HIV drugs if given early in the course of the disease can reduce the risk of transmission from an HIV-positive person to an HIV-negative person.”

But researchers and physicians know very little yet about how treatments for HIV, the virus itself, and the comorbidities associated with HIV affect fertility. So, Kushnir and his colleague, Emory pathologist William Lewis, MD, decided it was time to explore existing data on how HIV and its treatment affect fertility, especially in women. Their review paper on the subject appears in the August 2011 issue of Fertility and Sterility.

Because there are safety concerns and legal restrictions on fertility treatments in couples in which one partner is HIV positive and the other is not, treatment options often are limited.

“This is becoming more and more of an issue,” says Kushnir. “It’s probably time for us to have a more open discussion about the access these patients have to fertility treatment. I think the current system probably discourages these patients from pursuing treatments that are a lot safer than trying to get pregnant on their own.”

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How the fetal environment affects long-term health

David Barker, MD, PhD

Why do some people, given the same apparent set of risk factors, develop certain diseases and others do not? British scientist David Baker, MD, PhD, is examining this question from a unique perspective.

Barker, a professor of clinical epidemiology at the University of Southampton in the United Kingdom, is a pioneer in a field known as fetal programming. Fetal programming is the process in which environmental influences during prenatal development alter the body’s structures—for life.

He and other experts spoke on the fundamentals of the subject recently at the first Predicting Lifespan Health Conference at Emory University. “What we’re really looking for is just a few core mechanisms, which are linked to early human development and lead to a plethora of disorders,” says Barker.

Emerging evidence suggests that chronic diseases of adult life, including cardiovascular disease, type 2 diabetes and certain cancers, have their origin through fetal programming, explains Michelle Lampl, associate director of the Emory/Georgia Tech Predictive Health Institute. “These diseases and others are initiated by adverse influences before birth,” says Lampl.

Speakers addressed fetal programming and the placenta, long-term cardiovascular disease and kidney function in low birth-weight babies, epigenetics and immunity, as well as postnatal influences from infant diet and growth patterns.

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What’s left when it comes to research?

Cesare Lombroso

In an editorial appearing in a recent issue of The Lancet, Emory Rollins School of Public Health professor Dr. Howard Kushner contends that the connection between left-handedness and a raft of mental and physical disorders has gained currency since the 1980s and ‘90s.

Although Kushner acknowledges a long history of suspicion surrounding left-handedness, he spotlights one Cesare Lombroso, a Turin physician who spent a great deal of time in and around the 19th century pointing a negative finger at left-handedness. Lombroso’s contemporaries mistakenly considered his studies, albeit mere observations, to be cutting-edge science.

Although scientific standards have changed since Lombroso’s time and today’s studies do not portray left-handedness with such profound negativity, Kushner says, “general claims about the pathology of left-handedness persist.” This despite studies showing left-handers displaying exceptional intellectual and creative talents.

So, what are we to conclude about the connection between left-handedness and health? Kushner doesn’t say. Instead, he asks us to consider that despite all the advanced scientific tools we have at our disposal, researchers should keep in mind that these very tools may not enable us to conclusively explain the mystery behind left-handedness and its meaning. Yet, we should not stop trying. After all, he says, today’s researchers are making solid contributions to such research–while raising provocative questions along the way.

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The science behind the Mediterranean diet

The diet calls for lots of fruits and vegetables.

Researchers, physicians, and health care providers from across the United States and Italy met recently at the Rollins School of Public Health for the first Emory Conference on Mediterranean Diet and Health. Participants focused on the diet’s relation to cardiovascular disease, cancer, neuropsychiatric disorders, and vascular health.

The Mediterranean diet is characterized by a high consumption of fruits, vegetables, legumes, complex carbohydrates, and nuts; moderate consumption of fish and red wine; low consumption of cheese and red meat; and olive oil as the chief source of fat, explains Viola Vaccarino, MD, PhD, one of the conference chairs.

When topped with exercise, the Mediterranean diet—really a pattern of eating habits traditionally followed by people in the Mediterranean regions in the early 1960s—has proven beneficial for many throughout the years. But why this is so isn’t clear.
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Global climate change and health risks

Public health experts, including researchers, practitioners and policy makers from Emory, CARE, the Centers for Disease Control and Prevention (CDC), and other public and private organizations met at Emory recently for a symposium focusing on the health risks associated with global climate change.

Climate change is affecting the growth of crops, access to water, floods, malnutrition, and the prevalence of disease.

The goal was to form an agenda to develop the tools, policies, and approaches needed to address climate health risks and incorporate climate change adaptation into global health and development work.

And for good reason: right now climate change is contributing to the destruction of livelihoods and the aggravation of social inequalities, said speaker Jean-Michel Vigreux. Vigreux, CARE’s senior vice president of program quality and impact, said climate change is affecting the growth of crops, access to water, floods, malnutrition, and the prevalence of disease–especially climate sensitive disease. All this, he says, disproportionately affects the poor and other vulnerable populations.

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Scientists still searching for HIV’s lethal ways

Guido Silvestri, MD

It’s a knotty, complex question, and one that’s nearly 30 years old: how does HIV cause AIDS? That is, how does the virus slowly destroy the immune system?

Emory immunologist and Georgia Research Alliance Eminent Scholar Guido Silvestri, MD, and his colleagues are using a method called comparative AIDS research to try and answer that question. In other words, the scientists compare humans infected with HIV who develop AIDS and nonhuman primates from Africa who are infected with SIV, or simian immunodeficiency virus.

Silvestri is chief of the Division of Microbiology and Immunology at Yerkes National Primate Research Center.

Although SIV is very similar to HIV in terms of genetic and molecular structure, once infected with this virus, the Old World Monkey, the sooty mangabey, does not get sick.

“It’s a major mystery in AIDS research because these animals have virus replication that remains active in their body as long as they’re alive,” says Silvestri. “So, it’s not just the infection and the virus replicating that kills people. There’s something more that happens.”

Silvestri describes this research in Emory University’s Sound Science.

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Cholera in the time of disaster

Alex Larsen couldn’t make it to the 2010 International Association of National Public Health Institutes (IANPHI) annual meeting. That’s because Larsen, Haiti’s minister of health, was attending to an outbreak of cholera in this impoverished republic.

Vibrio cholerae bacteria

Larsen was scheduled to speak on NPHIs’ role in disaster preparedness and response. Instead, Scott Dowell, director of the CDC’s division of global disease detection and emergency response, updated attendees about goings-on in Haiti since the massive January 12 earthquake and the recent outbreak of cholera.

The first two weeks after the tremblor and its immediate aftershocks, human and monetary resources were spent on search and rescue, including emergency trauma care, orthopedic surgery and amputations, says Dowell.

The number killed now stands at 200,000. The number displaced: 1.3 million. In addition to an initial lack of safe drinking water, hunger and poor sanitation, anecdotal accounts of diphtheria and tetanus outbreaks circulated. The headquarters housing the ministry of public health was itself devastated when it collapsed, killing most of the minister’s staff who had remained inside.

Since the earthquake, Dowell says the water supply has slowly improved with long-term sources coming on line. Efforts to better separate sewage and water are coming to fruition, too.

As far as the cholera outbreak is concerned, this chapter of Haiti’s public health challenges is just beginning thanks in part to Haiti having never before experienced a known cholera epidemic, says Dowell. That is, its population is most likely immunologically naïve to cholera, making people vulnerable to the bacteria’s devastating ways: severe diarrhea, vomiting, and abdominal pain culminating in overwhelming dehydration and even death.

Despite its troubles, Dowell says there’s long-term hope for Haiti. As found in other countries affected by cholera, an aggressive program to provide clean water and keep sewage and water separate, can eventually squelch the bacteria’s rampage—and in the meantime prevent other diseases from taking hold.

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Shedding light on the vitamin D-Parkinson’s connection

Vitamin D may be called a vitamin, but it’s not. That’s because we can make it by exposing our skin to sunshine. So, technically that makes vitamin D a hormone–a steroid hormone to be exact. In fact, we get most of our exposure to vitamin D directly from sunshine and some from foods such as milk, fortified orange juice and oily fishes like salmon.

But no matter what you call it or where you get it, vitamin D is vital to growth, development and maintenance of our cells. Doctors have known for decades that vitamin D promotes calcium uptake and bone formation, but evidence is accumulating that it regulates the immune system and the development of the nervous system. Growing evidence suggests a link between low vitamin D levels and Parkinson’s disease, but whether this is a cause-and-effect relationship is unknown.

Marian Evatt, MD

That’s why Emory neurologist Marian Evatt, MD, and her colleagues are conducting a clinical trial exploring the effects of vitamin D supplementation on patients with Parkinson’s disease who have low vitamin D levels. The study also includes further epidemiological studies of vitamin D in Parkinson’s disease.

Parkinson’s disease affects nerve cells in several parts of the brain, particularly those that use the chemical messenger dopamine to control movement. The most common symptoms of Parkinson’s disease are tremor, stiffness and slowness of movement.

“Vitamin D has become associated with many chronic diseases: diabetes, hypertension, cardiovascular disease, and some of the autoimmune diseases, including multiple sclerosis,” says Evatt. “But we haven’t yet determined the specific effect of vitamin D in specific conditions because it has such broad effects.”

To hear Evatt talk about what vitamin D is, what it does, and why we need it, please go to Emory’s latest Sound Science podcast.

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