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Hereditary Prostate Cancer Risk
Thursday, January 12, 2012

After a 20-year quest to find a genetic driver for prostate cancer that strikes men at younger ages and runs in families, researchers have identified a rare, inherited mutation linked to a significantly higher risk of the disease.

A report on the discovery was published in the January 12, 2012 issue of the New England Journal of Medicine. UNC-Chapel Hill scientist Ethan Lange, PhD, was part of the team of investigators at the Johns Hopkins University School of Medicine, the University of Michigan Health System, Wake Forest University and the Translational Genomics Research Institute.  

Lange is associate professor of genetics and biostatistics and a member of UNC Lineberger Comprehensive Cancer Center. The research team found that men with prostate cancer were 20 times more likely to carry this mutation than screened men without prostate cancer.

Lange explains, “For the first time we have identified an inherited high-risk mutation for prostate cancer. The mutation is significantly more common in men with a family history of prostate cancer that strikes at an earlier age, compared to older patients with no family history. Our findings suggest it could be a valuable early screening tool for men, particularly those with a family history of early-onset disease. The benefit to this population of men could be similar to the benefit of current screening strategies employed for BRCA1 and BRCA2 mutations in women with family history of early-onset breast cancer.

“There is still work to be done regarding understanding the biological function of the mutation and the precise level of absolute risk for carriers of this mutation - a process that took years for the BRCA1 and BRCA2 genes. Still, our results strongly suggest this is the most clinically important mutation identified for prostate cancer to date.”

While accounting for only a small fraction of all prostate cancer cases, the discovery may provide important clues about how this common cancer develops and help to identify a subset of men who might benefit from additional or earlier screening. This year, an estimated 240,000 men in the United States will be diagnosed with prostate cancer.

James P. Evans, MD, PhD, Bryson Distinguished Professor of Genetics in the UNC School of Medicine, leads UNC Lineberger’s clinical genetics program and is an internationally recognized expert in clinical cancer genetics. He was not involved in the study, but observes, “The genetics of prostate cancer have proven surprisingly difficult to unravel and this work represents significant and welcome progress. While fewer than one percent of Caucasian men carry the described mutation in this particular gene, for those men who do carry it, the increased risk for developing prostate cancer is likely greater than for any previous mutation found to date. Larger follow-up studies will be necessary to understand the importance of this finding for prostate cancer, and it remains to be seen whether this mutation is associated with other cancers.”

Lange and Kathleen Cooney, MD, one of two study senior authors, were the first to identify the human chromosome region of interest where the mutation, called HOXB13, was ultimately found. Lange, who has been a collaborator on Dr. Cooney’s University of Michigan Prostate Cancer Genetics Project for 17 years, led the statistical analyses and was actively involved in designing the study and interpreting the findings for the current study.

This particular mutation was found in families of European descent, while two different mutations on the HOXB13 gene were identified in families of African descent. Since only seven of the 94 families studied were of African descent, more research will be required before the significance of those mutations is known. African-American men are more likely to be diagnosed with prostate cancer at younger ages and have a more aggressive form of the disease.

Lange concludes, “Over the past couple years, genetic sequence analysis - the ability to evaluate nearly every base of the DNA code over large genomic regions as opposed to a relatively small number of preselected bases - has become possible for large research studies. The National Institutes of Health and private research companies have invested hundreds of millions of dollars into developing this technology, and our results represent one of the first successes demonstrating its use in identifying a strong but uncommon genetic risk factor for a common disease. This new technology should, in the near future, lead to many exciting discoveries of genes important to a wide range of common, complex human diseases.”


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Source: UNC Chapel Hill
Time Stamp: 1/12/2012 at 6:52:33 PM UTC

New Method to Prevent Heart Attacks

Wednesday, March 17, 2010

Cardiovascular disease is by far the absolute most common national disease in Sweden and a little more than 26,000 people are treated every year at hospitals due to acute cardiac infarction, according to the Heart and Lung Foundation. KTH researcher Matilda Larsson at the School of technology and health at KTH has recently defended her thesis and her research aims at developing methods which can as early as possible assess the risk of cardiovascular disease.

The earlier the risk of cardiovascular disease can be identified, the easier it will be to avoid acute cardiac infarction which will save lives. But even if research and health care has been improved considerably over the past few years, cardiovascular disease even in the future will be one of the most common reasons for sickness and mortality in Sweden. That is why Matilda Larsson’s research is, to say the least, of vital importance.

One of the problems that we face today is that the methods used for risk assessment are new, and they need to be fine-tuned. The people that use the technology that is available must have considerable experience in being able to interpret the data they receive,” says Matilda Larsson.

To rectify this problem, Matilda Larsson has developed the existing ultrasound technology so that the information is more easily accessible.

By visualising the data, the doctor will find it easier to interpret the results,” says Matilda Larsson.

The usual method is that the doctor measures the heart’s blood flow and how the cardiac valves operate. With the Speckle tracking method, Matilda Larsson and her colleagues study how the ultrasound image’s greyscale pattern changes, and she can also measure the movement patterns and deformation of the heart and the vascular tissue.

The long-term objective is to have access to a sensitive method which can predict myocardial infarction at an early stage,” says Matilda Larsson.
Her thesis is called “Quantification and visualisation of cardiovascular function using ultrasound” and she has applied for a patent for a method used within this area.

Matilda Larsson originally comes from Östervåla between Gävle and Uppsala, but she will not be returning there for quite some time.

Now I will continue as a post doctoral student at the university in Leuven, Belgium, where I conducted some of my thesis work. We will study movements and deformation of the carotis,” says Matilda.

Image Caption: Matilda Larsson, in the background you can see her research in the form of a state of the heart diagram. This method provides a picture as to how the heart works during an entire cardiac cycle.
Image Credit: KTH Royal Institute of Technology
Source: KTH
Time Stamp: 3/17/2010 at 3:12:23 PM UTC

Researchers Identify Gene that May Play Role in Atherosclerosis

Monday, March 15, 2010

To understand the role of inflammation in cardiovascular and other diseases, it is essential to identify and characterize genes that induce an inflammatory response in the body -- and the genes that regulate them.

A study published online this week in the journal Proceedings of the National Academy of Sciences suggests that a gene called Hu antigen R (HuR) plays a critical role in inducing and mediating an inflammatory response in cells experiencing mechanical and chemical stresses. The study was supported by the National Institutes of Health.

The findings may open up new possibilities for developing treatments of metabolic diseases associated with inflammation, such as atherosclerosis. Atherosclerosis typically occurs in branched or curved regions of arteries where plaques form because of cholesterol build-up. Inflammation can alter the structure of plaques so that they become more likely to rupture, causing a blood vessel blockage and leading to heart attack or stroke.

This is the first systematic study showing that HuR not only responds to external stimuli as a stress-sensitive gene, but it also regulates other stress-sensitive genes,” said senior author Gang Bao, the Robert A. Milton Chair in Biomedical Engineering in the Wallace H. Coulter Department of Biomedical Engineering at Georgia Tech and Emory University.

The study results show that HuR promotes the expression of genes that support atherosclerosis and inhibits the expression of genes that combat atherosclerosis.

We found that suppressing expression of HuR inhibited the inflammatory response of cells, which shows that designing drugs that block HuR function may reduce the risk of plaques rupturing,” explained Bao.

Bao guided Won Jong Rhee, a former postdoctoral fellow in his laboratory, to conduct a series of experiments investigating the biology, behavior and pathways of HuR.

The researchers first studied how the HuR gene responds to different flow environments and chemical treatments. They exposed human umbilical vein endothelial cells to disturbed flow -- which occurs in artery regions where plaques form -- and found that the cells expressed higher levels of HuR than when they experienced a static or laminar flow environment. This finding was validated in tissue experiments with results showing increased amounts of HuR in regions of a mouse aorta that were exposed to disturbed flow.

Then the researchers treated endothelial cells with statins, medications used to treat atherosclerosis by reducing the number of cholesterol-containing low-density lipoprotein (LDL) molecules in the blood and inhibiting inflammation. The results indicated a decreased level of HuR with statin treatment.

After establishing HuR as a stress-sensitive gene regulated by external stimuli, including flow and statin treatment, the researchers conducted experiments to determine whether HuR regulates the expression of other stress-sensitive genes. They found that reducing the level of HuR in cells increased the levels of two genes that combat atherosclerosis -- Kruppel-like factor 2 (Klf2) and endothelial nitric oxide synthase (eNOS). The reduction in HuR also decreased the expression of bone morphogenic protein-4 (BMP-4), a gene that supports atherosclerosis.

Reducing the level of HuR in cells also significantly inhibited many inflammatory responses of the endothelial cells, including the expression of two potential atherosclerosis drug targets: inter-cellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1).

Though this study showed that HuR plays a critical role in inducing and mediating an inflammatory response in cells subjected to a stressful environment, the underlying mechanism for this regulation is still not known.

HuR protein often binds to messenger RNAs to increase their stability and translation, but we found that regulation of other stress-sensitive genes by HuR was not due to changes in mRNA stability by direct protein binding,” explained Bao.

To uncover the pathways that lead to HuR’s stress sensitivity, the researchers conducted a series of studies to reveal that HuR functions by adding a phosphate group to the transcriptional factor nuclear factor kappa B (NFkB) and its inhibitor IkBa. Additional research is underway to reveal what mRNAs HuR binds to and the mechanisms used to respond to mechanical and chemical stresses. Identifying the triggers for inflammation and unraveling the details of inflammatory pathways may eventually furnish new therapeutic targets.

Hanjoong Jo, the Coulter Department’s Ada Lee and Pete Correll Professor in Biomedical Engineering, Kyunghwa Chang, graduate student Chih-Wen Ni and research scientist Zhilan Zheng also contributed to this research.

Image Caption: Images showing reduced levels of HuR (red) in the thoracic aorta and an area with greater curvature, compared to a region with less curvature, which is prone to atherosclerosis because endothelial cells (blue) are exposed to disturbed flow there.
Image Credit: Georgia Tech/Gang Bao
Source: Georgia Institute of Technology
Time Stamp: 3/15/2010 at 7:23:49 PM UTC

Under Embargo Till: 21:00 UTC March 09, 2010
Posted: 21:00 UTC 03/09/2010

Research Finds Shortcomings in Comparative Effectiveness Drug Research

Tuesday, March 9, 2010

An analysis by researchers at the Keck School of Medicine of the University of Southern California (USC) has found that only 32 percent of medication studies published in top medical journals compare the effectiveness of existing treatments. These studies, known as comparative effectiveness studies, help doctors know which therapies work best and under what circumstances they are most effective.

More government funding, and other changes, are needed to promote comparative effectiveness studies and improve their quality, according to the study’s co-authors, Michael Hochman, M.D., assistant professor of clinical medicine at the Keck School, and Danny McCormick, M.D., M.P.H, assistant professor of medicine at Harvard Medical School.

The study, “Characteristics of Published Comparative Effectiveness Studies of Medications,” published in the March 10 edition of the Journal of the American Medical Association (JAMA), provides the first formal analysis of comparative effectiveness research, which is a priority issue for the Obama Administration. Last year, Congress appropriated $1.1 billion in funding for comparative effectiveness studies as part of the American Recovery and Reinvestment Act.

“Research on new therapies is, of course, critical for scientific advancement, but we also need research that examines how to use existing therapies appropriately,” said Hochman, lead author of the study. “For example, which of the more than 30 blood pressure medications on the market works best and in whom? Are certain diets and exercise regimens as good as medications for controlling cholesterol? Is it safe to aim for normal blood sugar levels when treating patients with diabetes? These are questions that comparative effectiveness studies should address.”

Hochman and McCormick analyzed 328 medication studies published between June 1, 2008 and Sept. 30, 2009 in six leading medical journals, of which 104 (32 percent) were comparative effectiveness studies, as defined by Hochman and McCormick’s analysis. The rest either compared medications against an inactive control group (such as a placebo) or involved unapproved therapies not currently available to doctors.

The study also showed that just 11 percent of the comparative effectiveness studies compared medications with non-pharmacologic therapies (such as lifestyle changes or surgery), and fewer than a third compared different medication strategies (such as the optimal blood sugar target in patients with diabetes). The rest compared medications with each other. In addition, just 19 percent of the comparative effectiveness studies focused on safety and only 2 percent included cost-effectiveness analyses.

“Most of the comparative effectiveness studies we reviewed simply tested whether medication ‘x’ is better than medication ‘y,’ rather than addressing fundamental questions such as ‘How can we use this medication more effectively? When is this medication better than surgery? Which among two effective approaches is the safest?’” said McCormick, the study’s senior author.

The research also showed that 87 percent of the comparative effectiveness studies received at least some funding from non-commercial organizations, such as non-profit foundations or government institutions.

“Despite the widespread belief that the pharmaceutical industry conducts most clinical research involving medications, our study shows a critical need for non-commercial funding for comparative effectiveness research,” Hochman said.

Hochman and McCormick believe their results highlight the need for more government funding for comparative effectiveness research. In addition, Hochman and McCormick recommend that the U.S. Food and Drug Administration require pharmaceutical companies to compare medications with other existing treatments whenever alternative therapies for a particular condition exist. Currently, companies often win approval for their products simply by showing that they are better than a placebo.

“Many of our nation’s research priorities are driven by the pharmaceutical industry,” Hochman said. “The pharmaceutical industry, not surprisingly, focuses on the development of new and marketable products. But once these products win approval, we need funding for research that examines how to use these therapies in an effective, safe, and rational manner.”

Source: University of Southern California
Time Stamp: 3/9/2010 at 21:00:00 UTC

Under Embargo Till: 21:00 UTC March 09, 2010
Posted: 21:00 UTC 03/09/2010

Kidney Donors Suffer Few Ill-Effects from Life-Giving Act

Tuesday, March 9, 2010

In a landmark study of more than 80,000 live kidney donors from across the United States, Johns Hopkins researchers have found the procedure carries very little medical risk and that, in the long term, people who donate one of their kidneys are likely to live just as long as those who have two healthy ones.

The findings, published in the March 10 issue of the Journal of the American Medical Association, confirm what doctors have long believed: Kidney donation, which saves the life of the recipient, poses little risk to the donor.

Donating a kidney is safe,” says transplant surgeon Dorry L. Segev, M.D., Ph.D., associate professor of surgery at the Johns Hopkins University School of Medicine. “Live donors start healthy and it’s the highest priority of the surgeon and the entire transplant community to make sure they stay healthy. This study says we have succeeded. While there are never any guarantees with surgery, donating a kidney is safer than undergoing almost any other operation.”

Segev and his colleagues looked at data from a national registry of 80,347 live kidney donors in the United States from April 1, 1994 to March 31, 2009. There were 25 deaths in the first 90 days after donation surgery over the course of those 15 years, putting the risk of surgical mortality at 3.1 per 10,000 cases. The risk was slightly higher for some subgroups that typically have higher risk from surgery — namely, men (5.1 deaths per 10,000 cases) and African-Americans (7.6 deaths per 10,000 cases) — but the risk in those groups was still very small.

By contrast, Segev says, the risk of surgical mortality from gallbladder removal is roughly six times higher (18 per 10,000 cases), while the risk from non-donor nephrectomy — removing a kidney because of cancer or another medical reason — is approximately 260 per 10,000 cases, 100 times the risk of donating a kidney.

In the analysis, the research team found the risk to kidney donors remained low even as the number of live donor kidney transplants in the United States nearly doubled over the past 15 years from 3,009 in 1994 to 5,968 in 2008. Patients with kidney failure have been relying more and more on live kidney donors who offer to give one of their kidneys to a friend or family member in need because there is a profound organ shortage in the United States, and live donor transplants tend to survive longer than those from cadavers. Thousands of people die each year while awaiting kidneys from deceased donors. The 15-year period covered by the study included a transition from mostly open-abdomen kidney removal to minimally invasive, laparoscopic kidney donation, a technique with tiny scars and shorter recovery times. At The Johns Hopkins Hospital, where the laparoscopic procedure for kidney donation was pioneered, researchers say it has made kidney donation much less onerous.

Previous studies of live donors have been done at single-transplant centers with homogenous populations. Segev’s study is the first to use national data.

Whatever happens when people donate kidneys, on average, it doesn’t affect the rest of their lives — and that has never been shown before in a study of this size and scope,” he says.

Other Johns Hopkins researchers on the study include Abimereki D. Muzaale, M.D., M.P.H.; Brian S. Caffo, Ph.D., Shruti H. Mehta, Ph.D.; Andrew L. Singer, M.D., Ph.D.; and Robert A. Montgomery, M.D., Ph.D.

Source: Johns Hopkins Medicine
Time Stamp: 3/9/2010 at 21:00:00 UTC

Umbilical Stem Cells May Help Recover Lost Vision for Those With Corneal Disease

Tuesday, December 8, 2009

New research from the University of Cincinnati may help in the recovery of lost vision for patients with corneal scarring.

Winston Whei-Yang Kao, PhD, professor of ophthalmology, along with other researchers in UC’s ophthalmology department found that transplanting human umbilical mesenchymal stem cells into mouse models that lack the protein lumican restored the transparency of cloudy and thin corneas.

Mesenchymal stem cells are “multi-potent” stem cells that can differentiate into a variety of cell types.

These findings are being presented Dec. 8 in San Diego at the 49th Annual Meeting of the American Society of Cell Biology.

Corneal transplantation is currently the only true cure for restoration of eyesight that may have been lost due to corneal scarring caused by infection, mechanical and chemical wounds and congenital defects of genetic mutations,” Kao says. “However, the number of donated corneas suitable for transplantation is decreasing as the number of individuals receiving refractive surgeries, like LASIK, increases.”

Worldwide, there is a shortage of suitable corneas for transplantation, and at the present time, there is no effective alternative procedure besides corneal transplantation to treat corneal blindness,” he continues. “There is a large need to develop alternative treatment regimens, one of which may be the transplantation of mesenchymal stem cells.”

Researchers used mouse models that did not have the lumican gene, also known as lumican knock-out models. Lumican is a protein that controls the formation and maintenance of transparent corneas.

Lumican knock-out models manifested thin and cloudy corneas,” he says. “Transplantation of the umbilical stem cells significantly improved transparency and increased corneal stromal thickness in these mice.”

In addition, Kao says, the umbilical mesenchymal stem cells survived in the mouse stroma (connective tissue) for more than three months with minimal or no rejection and became corneal cells, repairing lost functions caused by mutations.

Our results suggest a potential treatment regimen for congenital and/or acquired corneal diseases,” he says, adding that the availability of human umbilical stem cells is almost unlimited. “These stem cells are easy to isolate and can be recovered quickly from storage when treating patients.

These findings have the potential to create new and better treatments—and an improved quality of life—for patients with vision loss due to corneal injury.”

This study was funded by grants from the National Eye Institute, Research to Prevent Blindness and the Ohio Lions Eye Research Foundation.

Image Caption: Winston Whei-Yang Kao, PhD
Image Credit: University of Cincinnati
Source: University of Cincinnati
Time Stamp: 12/8/2009 at 6:36:47 PM UTC

Under Embargo Till: 21:00 UTC December 07, 2009
Posted: 21:00 UTC 12/07/2009

HIV-Related Memory Loss Linked to Alzheimer's Protein

Monday, December 7, 2009

More than half of HIV patients experience memory problems and other cognitive impairments as they age, and doctors know little about the underlying causes. New research from Washington University School of Medicine in St. Louis suggests HIV-related cognitive deficits share a common link with Alzheimer's-related dementia: low levels of the protein amyloid beta in the spinal fluid.

However, by analyzing biomarkers in the fluid surrounding the brain and spinal cord, the researchers report Dec. 8 in the journal Neurology, they could distinguish patients with HIV-related cognitive impairments from patients with mild Alzheimer's disease. This is important because as patients with HIV age, some will develop cognitive deficits related to HIV and others to Alzheimer's. New treatments in the pipeline to improve memory and thinking may not work for both conditions.

"HIV patients with cognitive dysfunction don't have early Alzheimer's - although some of the symptoms may be similar," says lead author David Clifford, M.D., an authority on the neurological complications of HIV and director of Washington University's AIDS Clinical Trials Unit. "The underlying biology of both conditions may be related to amyloid, and we think this clue can help us find the cause of cognitive impairment in HIV patients.

Cognitive dysfunction is a major problem among the estimated 1 million Americans living with HIV. The impairments are often mild but can affect a person's daily life, relationships and ability to hold a job. They include difficulties with memory, processing complex information and making decisions. These problems are expected to worsen as HIV patients live longer, due to potent drug cocktails that keep the virus in check.

In the new research, the scientists looked at the spinal fluid of 49 HIV patients with cognitive impairments, 21 HIV patients with normal cognitive function, 68 patients with mild Alzheimer's and 50 normal, healthy "controls." The Alzheimer's patients were older (average age 74) than the controls (average age 50), impaired HIV patients (average age 48) and cognitively normal HIV patients (average age 43).

They tested the spinal fluid for the presence of amyloid beta - the protein that folds and accumulates in the brains of Alzheimer's patients and is thought to play a key role in driving the brain damage that characterizes the disease. They also looked at other biomarkers associated with Alzheimer's, including tau, a protein found in tangled nerve fibers in Alzheimer's patients.

When amyloid beta accumulates in the brains of Alzheimer's patients, levels decrease in the spinal fluid, and Clifford and his colleagues expected to find low levels of the protein in samples of the Alzheimer's patients they studied.

But they were surprised to find the same low levels in the spinal fluid of HIV patients with cognitive dysfunction. Both groups of patients had significantly lower amyloid beta levels than HIV patients without cognitive impairments and the normal controls. The lower levels are an indicator that amyloid beta in the brain alters the normal turnover of the protein in the body.

Although Australian and European researchers had uncovered a link between HIV-related cognitive deficits and amyloid beta in 2005 in a smaller study, Clifford thought that finding was an artifact and embarked on the current study largely to disprove it.

"I really did not expect the biology of HIV cognitive dysfunction to be related to Alzheimer's," Clifford says. "If you look at the brains of HIV patients with cognitive impairments, they don't look like Alzheimer's brains - they don't have the same atrophy or a plethora of plaques and tangles characteristic of Alzheimer's."

But low amyloid beta is where the similarity to Alzheimer's disease ends. The researchers found that patients with mild Alzheimer's had significantly higher levels of tau than either group of HIV patients or normal controls - a finding that strongly suggests Alzheimer's and HIV cognitive dysfunction are not one and the same, Clifford says.

He suspects the HIV-related cognitive impairment may be due to low levels of the virus that hide out in the brain, beyond the reach of drugs that can't easily cross the blood-brain barrier. Another cause may be low-grade inflammation in the brain that is driven by the virus.

Almost all HIV patients in the study were taking anti-retroviral therapy. "I am almost certain the dementia in AIDS patients is linked to HIV and not to anti-retroviral drugs - we see it even in patients who haven't received HIV therapy," Clifford says. "However, the more subtle impairment may be in some way associated with a change in the way the body processes amyloid beta. This will certainly be an important area of future research."

The research is funded by grants from the National Institutes of Health.

Clifford DB, Fagan AM, Holtzman DM, Morris JC, Teshome M, Shah AR, Kauwe JSK. CSF biomarkers of Alzheimer disease in HIV-associated neurologic disease. Neurology. Dec. 8, 2009.

Source: Washington University in St. Louis
Time Stamp: 12/7/2009 at 21:00:00 UTC

Isolation, Stress May Contribute to Breast Cancer Risk

Monday, December 7, 2009

Social isolation and related stress could contribute to human breast cancer susceptibility, research from a rat model designed at the University of Chicago to identify environmental mechanisms contributing to cancer risk shows.

The researchers found that isolation and stress result in a 3.3-fold increase in the risk of developing cancer among rats with naturally occurring mammary tumors.

The research establishes, for the first time, that isolation and stress could be a factor in human breast cancer risk, said Martha McClintock, a psychologist at the University of Chicago and an author of a paper in current issue of the Proceedings of the National Academy of Sciences. Researchers at the University have been studying social isolation in the context of breast cancer development after having found that that many women living in high-crime neighborhoods must deal with a variety of stressors, including social isolation. In particular, African American women have been noted to have an earlier onset of breast cancer, although total incidence is similar to women from other ancestries.

We need to use these findings to identify potential targets for intervention to reduce cancer and other and its psychological and social risk factors,” said McClintock, the David Lee Shillinglaw Distinguished Service Professor in Psychology and Comparative Human Development at the University. “In order to do that, we need to look at the problem from a variety of perspectives, including examining the sources of stress in neighborhoods as well as the biological aspects of cancer development.”

The results of the study are published in a PNAS paper titled, “Social Isolation Dysregulates Endocrine and Behavioral Stress While Increasing Malignant Burden of Spontaneous Mammary Tumors.” Gretchen Hermes, a former researcher at the University and now a resident in psychiatry at the Yale University School of Medicine, is lead author of the study.

The paper is part of a series of publications by University of Chicago researchers exploring the connection between social isolation and breast cancer biology, and part of an ongoing research program at Chicago where work is being done on cancer by researchers from a wide number of disciplines. That work was enabled by the University’s Biopsychological Sciences Building, designed for such interdisciplinary research on behavior and biology and enhanced when the University received a $10 million grant from the National Institutes of Health to finance its Center for Interdisciplinary Health Disparities Research and is supported by the University of Chicago Cancer Research Center.

The study published in PNAS found that isolation led to a higher production of a stress hormone, corticosterone, among rats that were kept alone and subjected to the disturbances of colony life as well as stressful situations, such as the smell of a predator or being briefly constrained. Additionally, the isolated rats took longer to recover from a stressful situation than rats that lived together in small groups.

The study also suggests a causal relationship between social interaction and disease by showing that living alone first causes rats to have higher stress hormones, beginning in young adulthood, become fearful, anxious and vigilant and then prone to malignancy in late-middle age. The study further showed that the stress hormone receptor entered the nucleus of mammary tumor cells in isolated rats, where gene regulation occurs, something that happened less often in the cells of the non-isolated rats.

The researchers further found that rats living in isolation experienced a 135 percent increase in the number of tumors and a more than 8,000 percent increase in their size. The impact of isolation was much larger than the impact another environmental source of tumor formation—the unlimited availability of high-energy food.

In natural situations, estrogen and progesterone produced from ovaries play a role in the majority of naturally occurring mammary and breast cancers tumors. In the rat study, tumors naturally developed in late middle age, while ovaries were no longer fully functioning, further suggesting the role of isolation and stress hormones in cancer development.

Joining McClintock and Hermes in preparing the PNAS paper were Bertha Delgado, researcher at Ben Gurion University, Israel; Maria Tretikova, Resident in Pathology at the University of Chicago Medical Center; Sonia Cavigelli, Assistant Professor of Biobehavioral Health at Penn State University; Thomas Krausz, Director of Anatomic Pathology at the University; and Suzanne Conzen, Associate Professor of Medicine at the University. The National Institute of Environmental Health Sciences/National Cancer Institute, the U.S. Department of Defense, and the State of Connecticut Department of Mental Health and Addictive Services supported the research.

The paper is part of a series published by McClintock and her colleagues using animal models to study the onset of cancer.

Rats provide an excellent model for studying human health. They are gregarious animals that are constantly interacting, with complex social relationships and shared care for their young. Additionally, isolation is a natural part of their social order, as a rat stands sentry at each colony and needs to be extremely vigilant to danger on behalf of the rest of the group.

A paper published by University researcher Jason Yee and colleagues showed that rats that developed reciprocal supportive relationships during stress, in which they both asked for help and gave assistance to others, were likely to live longer. That research was reported in “Reciprocal Affiliation Among Adolescent Rats During a Mild Group Stressor Predicts Mammary Tumors and Lifespan,” in the journal Psychosomatic Medicine.

Hermes was lead researcher in a paper published in Developmental Psychobiology that isolation disrupts the development of puberty in rats by accelerating maturation of ovarian function while simultaneously delaying mammary tissue development. As a result, the rats are more likely to development mammary tumors. The work was in a paper, “Isolation and the Timing of Mammary Gland Development, Gonadarche and Ovarian Senescence: Implications for Mammary Tumor Burden.”

In a paper in the American Journal of Physiology, Hermes and McClintock reported that isolation caused a more pronounced inflammatory disease response in females than in males. That work was published in the paper “Social isolation and the inflammatory response: Sex differences in the enduring effects of a stressor.”

More recently, in a paper published in Cancer Prevention Research, Conzen and McClintock reported that social isolation of a genetic mouse model of human breast cancer resulted in larger mammary tumor growth. In a paper titled “A model of gene-environment interaction reveals altered mammary gland gene expression and increased tumor growth following social isolation,” Conzen and McClintock showed that social isolation was associated with the increased expression of specific sets of genes involved in metabolism and inflammation.

Source: University of Chicago
Time Stamp: 12/7/2009 at 8:15:38 PM UTC

H1N1 More Risky than Seasonal Flu in Children with Sickle Cell Disease

Monday, December 7, 2009

Infection with the H1N1 virus, or swine flu, causes more life-threatening complications than seasonal flu in children with sickle cell disease, according to research from Johns Hopkins Children’s Center. The findings, to be presented on Dec. 7 at the annual meeting of the American Society of Hematology, warn parents and caregivers that such children are more likely to need emergency treatment and stays in an intensive-care unit.

The researchers analyzed the records of 118 children with sickle cell disease treated for any kind of flu at Hopkins Children’s between September of 1993 and November of 2009. Of them, 28 were infected with the H1N1 virus, a new strain that emerged for the first time in April of 2009.

While both the seasonal flu and the H1N1 virus caused similar general symptoms like fever, cough and a runny nose in most of the children, sickle cell patients infected with H1N1 were three times more likely to develop acute chest syndrome, a leading cause of death among these patients, marked by inflammation of the lungs, reduced oxygen capacity and shortness of breath. H1N1-infected children were five times more likely to end up in the intensive-care unit, and were overall more likely to end up on a ventilator and more likely to need a blood transfusion than those with seasonal flu.

Another Hopkins Children’s study, released earlier this year, found that children with sickle cell disease are hospitalized with seasonal flu nearly 80 times more often than other children.

The researchers say their findings point to the need to include children with sickle cell disease in the list of those who must be immunized against all flu strains, which already includes children with asthma, diabetes, heart disease and other chronic conditions.

“Children with sickle cell disease are hospitalized about once a year for pain crises and other complications, so we should do everything we can to prevent hospitalization from the flu by using safe and effective vaccines,” says lead investigator John J. Strouse, M.D. Ph.D., a pediatric hematologist at Hopkins Children’s.

Named for the unusually sickle-shaped red blood cells caused by a genetic abnormality, sickle cell anemia affects nearly 100,000 Americans. The cells’ abnormal structure reduces their oxygen delivery to vital organs and causes them to get stuck in the blood vessels, leading to severe pain and so-called “sickling crises,” which require hospitalization.

The CDC recommends that all children over 6 months of age get seasonal and H1N1 flu shots, except those who are allergic to eggs or have had a severe reaction to a flu vaccine in the past.

Co-investigators include Martha Amoako, B.S.; Megan Reller, M.D., M.P.H.; and James Casella, M.D. The research was funded by the National Heart Lung and Blood Institute and the Doris Duke Charitable Foundation.

Source: Johns Hopkins Medicine
Time Stamp: 12/7/2009 at 6:02:10 PM UTC

Random DNA Mix-Ups Not So Random in Cancer Development

Thursday, December 3, 2009

Researchers at the UC San Diego School of Medicine have pinpointed a mechanism that may help explain how chromosomal translocations – the supposedly random shuffling of large chunks of DNA that frequently lead to cancer – aren’t so random after all. They have developed a model of such chromosomal mix-ups in prostate cancer which indicates that the male sex hormone (androgen) receptor unexpectedly plays a key role in driving specific translocations in the development of cancer.

A better understanding of the origin and behavior of such translocations may ultimately lead to ways to both predict and perhaps interfere with their formation, and in turn, cancer development.

Chunru (Ruth) Lin, Liuqing (Luke) Yang and Michael G. Rosenfeld, MD, Howard Hughes Medical Institute investigator and Professor of Medicine at the UC San Diego School of Medicine, headed the basic research study, to be published on line December 3, 2009 in advance of publication in the journal Cell.

A series of studies showed that, under certain conditions involving some sort of genetic “stress” – such as cigarette smoke, a toxic chemical exposure or radiation – the androgen receptor can act in concert with several key enzymes and pathways induced by genotoxic stress to unexpectedly direct specific translocations leading to cancer.

In the future, one goal would be to find tumor-causing translocations in breast and other cancers and develop a chemical library screen to find compounds that might inhibit these events in cancer formation/behavior,” said Rosenfeld.

According to Rosenfeld, chromosome mix-ups are a hallmark of leukemias and lymphomas and, increasingly, other cancers such as more aggressive forms of prostate cancer. Scientists have known that various types of genetic stress can lead to random breaks in DNA and rearrangements in chromosomes, resulting in excessive cell growth and cancer, but the exact mechanisms have been poorly understood.

Evidence from other research teams pointed to the important role of the androgen receptor in the development of translocations in more aggressive forms of prostate cancer. The UC San Diego research team created a tumor translocation model in prostate cancer and found that instead of random DNA breaks, the breaks were in specific chromosomal areas bound by the androgen receptor which directed the pattern of cancer-causing translocations.

Rosenfeld’s group identified several mechanisms, some involving specific enzymatic pathways that worked together with the androgen receptor to form specific translocations.

“Our findings suggest that sex steroid receptors – androgen and estrogen receptors – can cause mutations when in the presence of genotoxic stress, and form site-specific chromosomal translocations,” Rosenfeld said.

He noted that understanding the molecular mechanisms that underlie tumor translocations and the specific strategies used by normal cells to protect against such rearrangements could provide insights into cancer development and eventually help in the development of new therapeutic approaches.

Additional contributors include co-first authors Chunru Lin and Liuqing Yang, Bogdan Tanasa, Kenny Ohgi and Jie Zhang of the Howard Hughes Medical Institute (HHMI); Bong-gun Ju, HHMI and Sogang University, Seoul; Kasey Hutt, UCSD Bioinformatics Graduate Program; Dave Rose, UCSD Department of Medicine, Division of Endocrinology and Metabolism; and Xiang-Dong Fu and Christopher K. Glass, UCSD Department of Cellular and Molecular Medicine.

This study was funded in part by grants from The National Institutes of Health/National Cancer Institute, the Department of Defense and the Prostate Cancer Foundation.

Source: University of California, San Diego Health Sciences
Time Stamp: 12/3/2009 at 5:33:33 PM UTC

Death from childhood stroke

Tuesday, December 1, 2009

Stroke is an important cause of childhood morbidity and is in the top ten causes of childhood death.  For the first time, new research has looked at trends in death from childhood stroke in England and Wales, from 1921 to 2000.

In the study, ‘Mortality from childhood stroke in England and Wales, 1921-2000’, academics in the Division of Child Health at Bristol University investigated how death rates varied according to age, gender, stroke subtype, period of death and birth cohort. 

The study, funded by The Stroke Association (UK) and published by Archives of Disease in Childhood found:

· Most deaths from childhood stroke occur due to hemorrhagic stroke, ruptured blood vessels leaking blood into the brain;

· Children less than one year old and males have the highest stroke death rate;

· Mortality rates from childhood stroke steadily declined during the 1960s and 1970s but plateaued in the 1980s and 1990s;

· Birth cohort mortality rates fell for each successive generation since the 1950s suggesting the influence of prenatal or perinatal factors.

Dr Finbar O’Callaghan, Consultant Senior Lecturer in Pediatric Neurology in the Division of Child Health at Bristol University and senior author on the paper, said: “The decline in birth cohort mortality since the 1950s is striking and points to changes in causal factors that are operating early in life and affecting successive generations of children.”

Dr Andrew Mallick, Pediatric Neurology Research Associate in the Division of Child Health at Bristol University and co-author of the study, added: “Despite the potential limitations of using mortality data, this study has provided some compelling insights into childhood stroke in England and Wales.”

Joanne Murphy, Research Liaison Officer for The Stroke Association said: “It’s a common myth that stroke only happens to older people when it is actually one of the top ten causes of deaths in children and can be devastating for families. Because people don’t think that children can have a stroke, it can take longer to be diagnosed.  As with stroke in adults, a quick diagnosis and rapid treatment is essential to save lives and reduce disability.

Childhood stroke is under researched which is why we are funding the team at the University of Bristol to find out more about how many children have strokes and what their outcomes may be. It is imperative that we raise awareness of this issue so more children get the chance to make a good recovery.”

From the data evaluated, the researchers found 6,029 deaths from childhood stroke between 1921-2000. Analysis by period of death showed that rates declined in the 1960s and 1970s but then plateaued.

At all time points males had a higher mortality rate than females.  Infants had a relatively high mortality rate (24.5 per million person years) but rates fell steeply in early childhood (2.5 per million person years at age five to nine years) before rising again in late adolescence (7.5 per million person years at age 15-19 years).  An increased rate was found for males at all ages but was greatest in infancy.

Hemorrhagic stroke accounted for 71 per cent of stroke deaths.  Birth cohort analysis showed a trend of declining mortality with each successive generation since the 1950s.

There has been one previous study by Dr Heather Fullerton that analyzed stroke deaths in US children. The study, confined to the years 1979 to 1998, did not analyses mortality by birth cohort. However, there are some striking similarities to the two studies. 

Both studies have shown a similar decline in mortality rates analyzed by period of death in the latter part of the twentieth century together with higher risk for males and for infants.  It has previously been assumed that the high mortality rate in infancy was due to very high rates in the very youngest children (younger than one month).  The study in the USA was not able to analyses this assertion but this paper has found that this assumption was incorrect.

Source: University of Bristol
Time Stamp: 12/1/2009 at 4:43:16 PM UTC

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