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Intercampus initiative works to increase participation in clinical trials; first phase of study to focus on cancer

Sept. 13, 2007

NEW YORK — Before a new treatment becomes available, researchers must recruit hundreds or thousands of patients to participate in clinical research trials. But finding these patients is often difficult. Many potential candidates are unaware of the studies or unable to participate due do logistical hurdles. As a result, patients miss out on opportunities for novel treatment approaches — and beneficial new therapies take longer to reach the public.

In a new initiative, researchers at Weill Cornell Medical College (WCMC) and Cornell’s College of Agriculture and Life Sciences (CALS) have teamed up to develop strategies to better understand and enhance patient participation in clinical trials. The project, called Improving Methods for Patient Accrual to Clinical Trials (IMPACT), is one of several recent efforts at WCMC to foster clinical research programs across the medical spectrum.

“Low patient accrual in clinical trials poses a serious problem for the advancement of medical science,” said John Leonard, professor of medicine at WCMC, attending physician at NewYork-Presbyterian Hospital/Weill Cornell Medical Center and co-leader of the study.

The time required to conduct clinical trials is widely recognized as a limiting step in moving novel treatments forward, Leonard said. For example, less than 2 percent of patients choose to participate in clinical trials for cancer therapies across the United States. Even a modest increase of 2 to 3 percentage points would make a major impact, meaning the difference between completing a study in two years instead of three years — and potentially resulting in thousands of lives saved if the standard of care is improved more rapidly.

“Hundreds of studies have sought to identify and overcome barriers to enrollment. This project is the first to assess the problem from a socio-psychological perspective using the specialized methods of risk communication,” said Katherine McComas, principal leader of IMPACT and assistant professor of communication at Cornell. “We will be using two proven approaches — the model of Risk Information Seeking and Processing, and Theory of Planned Behavior. These will allow us to examine specific factors that influence how patients inform themselves about a clinical trial and decide whether to participate.”

IMPACT investigators will collaborate with The Leukemia and Lymphoma Society, which has helped finance the first phase of the project, including a national survey on attitudes toward participation in clinical trials. The funding will also support a doctoral student in the Department of Communication.

“Our aim is to provide data-supported recommendations for strategies to improve the accrual of patients in clinical trials,” said Andrew Dannenberg, also a co-leader of the IMPACT project, professor of medicine at WCMC and attending physician at NewYork-Presbyterian Hospital/Weill Cornell Medical Center.

Future phases of the study will develop specific tools to better educate patients about clinical trials and break down common barriers to participation, Dannenberg added, “so that new therapies for many disorders can be more rapidly designed and evaluated in order to deliver their maximal benefit.”

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September 17, 2007 Posted by | Cancer, Clinical Trials, Cornell University, Global Health Vision, Global News, News | 2 Comments

Research links genetic mutations to lupus

WINSTON-SALEM, N.C. – A gene discovered by scientists at Wake Forest University School of Medicine has been linked to lupus and related autoimmune diseases. The finding, reported in the current issue of Nature Genetics, is the latest in a series of revelations that shed new light on what goes wrong in human cells to cause the diseases.

“This research is a huge leap toward understanding the cause of lupus and related autoimmune diseases,” said Fred Perrino, Ph.D., a co-author on the paper and a professor of biochemistry at Wake Forest. “There had been few clues before now.”

Perrino, who discovered the gene in 1998, said he suspected it was involved in human disease, but it took a group of researchers from around the world collaborating to put the puzzle together.

“We’ve known that lupus was a complex disease, but now we have a specific protein and a particular cellular process that appears to be one of the causes,” said Perrino. “We’re connecting the dots to understand the biology of what’s going on with the disease.”

In Nature Genetics, lead author Min Ae Lee-Kirsch, M.D., from the Technische Universität Dresden in Dresden, Germany, and colleagues report finding variations of the TREX1 gene discovered by Perrino in patients with systemic lupus erythematosus. The study involved 417 lupus patients from the United Kingdom and Germany. Mutations were found in nine patients with lupus and were absent in 1,712 people without lupus.

“Our data identify a stronger risk for developing lupus in patients that carry variants of the gene,” said Lee-Kirsch.

In recent years, the gene was also linked to Aicardi-Goutieres syndrome, a rare neurological disease that causes death in infants, and to chilblain lupus, an inherited disease associated with painful bluish-red skin lesions that occur during cold weather and usually improve in summer. The current research also links it to Sjogren’s syndrome, a form of lupus.

The diseases are all autoimmuine diseases, which means that the body makes antibodies against itself. In lupus, these antibodies cause pain and inflammation in various parts of the body, including the skin, joints, heart, lungs, blood, kidneys and brain. The disease is characterized by pain, heat, redness, swelling and loss of function.

Perrino began studying the protein made by the gene more than 14 years ago.

“We basically cracked open cells to locate the protein and find the gene,” said Perrino. “In the 14 years since, we’ve learned a lot about the protein and how it functions.”

The gene manufactures a protein, also known as TREX1, whose function is to “disassemble” or “unravel” DNA, the strand of genetic material that controls processes within cells. The “unraveling” occurs during the natural process of cells dying and being replaced by new cells. If a cell’s DNA isn’t degraded or unraveled during cell death, the body develops antibodies against it.

“If the TREX1 protein isn’t working to disassemble the DNA, you make antibodies to your own DNA and can end up with a disease like lupus,” said Perrino.

Perrino and colleagues at Wake Forest have been studying the gene and its protein since 1993. Thomas Hollis, Ph.D., an assistant professor of biochemistry at Wake Forest, is credited with solving the structure of both TREX1 and a similar protein, TREX2. Perrino has also developed a way to measure the function of the proteins.

In a study reported in April in the Journal of Biological Chemistry, Hollis and Perrino found that three variations of the gene reduced the activity of the protein by four- to 35,000-fold.

“Now that we have the structure, we can understand how it disassembles DNA and how mutations in the gene may affect that process,” said Hollis.

The researchers hope that understanding more about the gene’s mutations and the structure of the protein may lead to drug treatments to help ensure that mutant copies of the gene are inactive.

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Media Contacts: Karen Richardson, krchrdsn@wfubmc.edu; Shannon Koontz, shkoontz@wfubmc.edu; at 336-716-4587.

Wake Forest University Baptist Medical Center is an academic health system comprised of North Carolina Baptist Hospital and Wake Forest University Health Sciences, which operates the university’s School of Medicine. U.S. News & World Report ranks Wake Forest University School of Medicine 18th in primary care and 44th in research among the nation’s medical schools. It ranks 35th in research funding by the National Institutes of Health. Almost 150 members of the medical school faculty are listed in Best Doctors in America.

Contact: Karen Richardson
krchrdsn@wfubmc.edu
336-716-4453
Wake Forest University Baptist Medical Center

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July 29, 2007 Posted by | Alberta, Baltimore, Barcelona, Bethesda, Biological Sciences, Calgary, Canada, Clinical Trials, France, Genes, Genetic, Genetic Link, Genetic Marker C allele of rs10505477, Genetics, Genome, Genomic, Global, Global Health Vision, Global News, Health Canada, Human Genome, Italy, Japan, Lupus, Nature Genetics, Newfoundland, News, News Australia, News Canada, News Israel, News Italy, News Jerusalem, News Switzerland, News UK, News US, News USA, NIH, Nova Scotia, Nunavut, Osaka, Ottawa, Prince Edward Island, Public Health, Quebec, Research, RSS, RSS Feed, Slovakia, Spain, Toronto, UK, US, Virginia, Wake Forest University Baptist Medical Center, WASHINGTON, Washington DC, Washington DC City Feed, World Health Organisation, World News | 1 Comment

Loss of cell’s ‘antenna’ linked to cancer’s development

Contact: Karen Mallet
Karen.Mallet@fccc.edu
215-728-2700
Fox Chase Cancer Center

Fox Chase Cancer Center researchers described dismantling proteins in journal Cell

Submarines have periscopes. Insects have antennae. And increasingly, biologists are finding that most normal vertebrate cells have cilia, small hair-like structures that protrude like antennae into the surrounding environment to detect signals that control cell growth. In a new study published in the June 29 issue of Cell, Fox Chase Cancer Center researchers describe the strong link between ciliary signaling and cancer and identify the rogue engineers responsible for dismantling the cell’s antenna.

Cilia-based sensing has important roles in sight, smell and motion detection and in helping an embryo develop into a normal baby. Defects in cilia can produce a range of disorders, including kidney cysts, infertility, respiratory problems, reversal of organs (for example, heart on the right) and a predisposition to obesity, diabetes and high blood pressure. In each case, cells fail to appropriately detect growth-controlling signals and develop abnormally. Now, researchers are adding cancer to this list.

“Many cancers arise from defects in cellular signaling systems, and we think we have just identified a really exciting signaling connection,” Fox Chase Cancer Center molecular biologist Erica A. Golemis, Ph.D., points out. In the new study, Golemis and her Fox Chase colleagues found that two proteins with important roles in cancer progression and metastasis, HEF1 and Aurora A, have an unexpected role in controlling the temporary disappearance of cilia during normal cell division, by turning on a third protein, HDAC6. This action causes the “antenna” to be dismantled in an untimely way.

Why cilia come and go on normal cells is not entirely understood, but scientists increasingly suspect that it may play a role in timing the cell division process. Commonly, cancer cells have entirely lost their cilia, and this absence may help explain why tumors fail to respond properly to environmental cues that cause normal cells to stop growing. Hence, the discovery that too much HEF1 and Aurora A cause cilia to disassemble provides important hints into what may be happening in cancers.

Defects in cilia have already been identified in one disease that represents a significant public health burden. Polycystic kidney disease, or PKD, arises from genetic mutations that cause flawed kidney-cell ciliary signaling. PKD is the most common serious hereditary disease, affecting more than 600,000 Americans and 12.5 million people worldwide.

In this incurable syndrome, patients develop numerous, fluid-filled cysts on the kidneys. For many patients, chronic pain is a common problem. PKD leads to kidney failure in about half of cases, requiring kidney dialysis or a kidney transplant.

The proteins involved in dismantling the cilia are no strangers to Golemis and her team. Golemis has been studying HEF1 for over a decade, since she first identified the gene. She first discovered that HEF1 has a role in controlling normal cell movement and tumor cell invasion. Golemis’ laboratory has also shown that Aurora A and HEF1 interact to initiate mitosis (chromosome separation) during cell division.

Suggestively, many cancers produce too much of the Aurora A protein, including breast and colorectal cancers and leukemia. In 2006, excessive production of HEF1 (also known as NEDD9) was found to drive metastasis in over a third of human melanomas, while HEF1 signaling also contributes to the aggressiveness of some brain cancers (glioblastomas).

“Now there’s a new activity for these proteins at cilia,” said co-author Elizabeth P. Henske, M.D., a medical oncologist and genetics researcher who studies the genetic basis of kidney tumors. This complex HEF1 and Aurora A function may mean the increased levels of these proteins in cancer affect cellular response to multiple signaling pathways, rather like a chain reaction highway accident.

Clinical Application

The research has significant implications for the understanding and treatment of cancer. The experiments leading to the new paper showed that “small-molecule inhibitors of Aurora A and HDAC6 selectively stabilize cilia,” the authors concluded, “suggesting a novel mode of action for these clinical agents.” Clinical trials of such inhibitors have already begun, so learning more about the mechanisms of their targets is important in understanding how these agents work and who might benefit from them.

“It is also tantalizing to consider that closer connections exist between dysplastic disorders leading to cysts and cancer than have previously been appreciated,” the authors wrote. “Overall, deregulated Aurora A/HEF1/HDAC6 signaling may have broad implications for studies of human development and disease.”

The authors are now investigating possible roles for HEF1 and Aurora A in PKD. They are intrigued by the fact that a study published last year showed that important gene, PKHD1, commonly mutated in PKD has also been found as a target of mutation in colorectal cancer.

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In addition to Golemis and Henske, co-authors include Elena N. Pugacheva, Ph.D., Tiffiney Hartman, Ph.D., and Sandra A. Jablonski, Ph.D., all of Fox Chase Cancer Center. Grants from the National Institutes of Health, Department of Defense, Pennsylvania Tobacco Settlement Funds and the Susan B. Komen Foundation supported this research, along with the Cancer Center support grant from NIH and an appropriation from the Commonwealth of Pennsylvania to Fox Chase Cancer Center.

Fox Chase Cancer Center was founded in 1904 in Philadelphia as the nation’s first cancer hospital. In 1974, Fox Chase became one of the first institutions designated as a National Cancer Institute Comprehensive Cancer Center. Fox Chase conducts basic, clinical, population and translational research; programs of cancer prevention, detection and treatment of cancer; and community outreach. For more information about Fox Chase activities, visit the Center’s web site at http://www.fccc.edu or call 1-888-FOX CHASE.

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June 29, 2007 Posted by | Alberta, Baltimore, Calgary, Cancer, Chemotherapy, Clinical Trials, Fox Chase Cancer Center, Global, Global Health Vision, Global News, Leukemia, Medical Journals, News, News Australia, News Canada, News Israel, News Jerusalem, News UK, News US, Osaka, Research, Spain, Virginia, WASHINGTON, Washington DC, World News | 1 Comment

New genetic test developed at Emory advances detection and diagnosis of muscular dystrophy

Contact: Holly Korschun
hkorsch@emory.edu
404-727-3990
Emory University

A new genetic test targeting the most common types of muscular dystrophy–those caused by mutations in the dystrophin gene–is far quicker with greater accuracy and sensitivity than existing tests. It can be used to confirm clinical diagnoses, to test female family members who may be carriers, and to perform prenatal testing.

The test was developed by Michael Zwick, PhD, and Madhuri Hegde, PhD, assistant professors in the Department of Human Genetics and the Emory Genetics Laboratory in the Emory University School of Medicine.

Muscular dystrophy includes more than 30 genetic diseases characterized by progressive weakness and degeneration of the skeletal muscles that control movement. Some forms are seen in infancy or childhood, while others may not appear until middle age or later. Duchenne muscular dystrophy (DMD) is the most common form of muscular dystrophy and primarily affects boys. It is caused by absence of dystrophin, an important muscle protein involved in maintaining the strength of muscle fibers.

According to the National Institute of Neurodegenerative Diseases and Stroke (NINDS), DMD onset is between 3 and 5 years, with rapid progression. Most boys are unable to walk by age 12 and later need a respirator to breathe. Girls in these families have a 50 percent chance of inheriting and passing the defective gene to their children. Becker muscular dystrophy, which is similar to Duchenne but less severe, results from faulty or not enough dystrophin.

As currently implemented the new test, called EmArray Dystrophin, detects 99 percent of mutations in the dystrophin gene including deletions, duplications and point mutations.

The EmArray Dystrophin test uses a new kind of microarray technology that contains the entire sequence of the dystrophin gene, the largest known gene in humans, on a chip the size of a microscope slide. The test initially detects deletions and duplications, then microarray-based resequencing is used to rapidly identify subtle genetic variations that may cause muscular dystrophy.

The EmArray Dystrophin test confirms clinical diagnosis of Duchenne and Becker muscular dystrophy in a male and characterizes the type and size of the mutation. Women with a family history of Duchenne or Becker who are at risk to be carriers can be tested, then, if found to be carriers, can have prenatal testing.

“Previously, access to prenatal testing was limited for some women when the affected male relative was not available for testing. The EmArray Dystrophin test greatly improves access to prenatal and carrier testing for women without the need to test a male relative, in a rapid timeframe,” according to Vanessa Rangel Miller, MS. In addition to improved testing, the Emory Genetics Laboratory, Parent Project Muscular Dystrophy, leading researchers and clinicians are working together to develop a database for mutations and clinical data.

“Our new genetic test, along with new therapies currently in clinical trials, is a very positive development for muscular dystrophy patients and their families,” says Dr. Hegde.

In the last five years DMD research has accelerated, resulting in more knowledge about the role of the dystrophin gene and an increased understanding about what happens to a muscle cell lacking the dystrophin protein. Researchers around the world are investigating a number of different treatment strategies, all with the goal of slowing or stopping muscle degeneration. Several clinical trials are underway and many others are in development, including testing of an oral medication intended to circumvent mutations in the dystrophin gene and increase normal gene expression.

According to Dr. Hegde, about 13 percent of mutations in the dystrophin gene are nonsense mutations–point mutations in a sequence of DNA that can result in mistakes in gene expression and nonfunctional proteins. New data published online in the current edition of the journal Nature show that PTC124, an investigational new drug designed to bypass dystrophin nonsense mutations and restore a functional protein, was effective in a preclinical (animal) model of Duchenne muscular dystrophy (DMD). (www.clinicaltrials.gov).

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Other treatment for symptoms associated with muscular dystrophy may include physical therapy, respiratory therapy, speech therapy, orthopedic appliances and corrective orthopedic surgery. Drug therapy may include corticosteroids, anticonvulsants, immunosuppressants and antibiotics.

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June 27, 2007 Posted by | Clinical Trials, Emory Genetics Laboratory, Emory University, Genes, Genetic, Genetics, Genome, Genomic, Global, Global Health Vision, Global News, Human Genome, Muscular Dystrophy, News, News Australia, News Canada, News Israel, News Jerusalem, News UK, News US, Research, Virginia, WASHINGTON, Washington DC, World News | 2 Comments

Multifunctional nanoparticle platforms for targeting and imaging cancer cells

Dead on Target

There has been much recent interest in how nanotechnology will impact the field of medicine. Unfortunately, a number of promising nanostructured systems have turned out to be extremely toxic to humans, thus precluding their use in clinical applications and dashing hopes of an early success for the interdisciplinary field of nanobiotechnology. Now a group of researchers at the University of Michigan Nanotechnology Institute for Medicine and Biological Sciences have devised a multifunctional nanoparticle platform comprising nanoparticles synthesized within dendrimers equipped with targeting molecules and dyes. These dendrimer nanoparticle systems are able to seek out and specifically bind to cancer cells.

Xiangyang Shi, Suhe Wang, James R. Baker Jr., and their colleagues have designed dendrimer nanoparticle systems that are stable, water soluble, and biocompatible. The researchers start out by synthesizing gold nanoparticles within amine-terminated dendrimers. Next, dye molecules and a targeting molecule, folic acid, are attached to the ends of the dendrimers. Finally, the remaining amine groups are acetylated to ensure that the complex particles do not bear any surface charges. This last step is especially important to ensure the biocompatibility of these systems and to prevent the nonspecific adhesion of other materials. Molecular dynamics simulations indicate that the folic acid attachments project out into the solvent and are readily available for binding to cells, whereas the dye molecules stay far removed from the metal nanoparticles and thus retain their bright fluorescence.

Many cancer cells, including those implicated in cancers of the ovary, kidney, uterus, testis, brain, colon, and lungs, tend to overexpress folic acid receptors. Owing to the folic acid attachments grafted onto the dendrimer nanoparticles, the dendrimer nanoparticles are seen to latch onto the cancer cells via these folic acid receptors. Since the dendrimer nanoparticles are also equipped with dye molecules, the high concentrations of nanoparticles accumulated in the cancer cells can be imaged by confocal microscopy, and indeed diseased cells can be easily told apart from healthy cells. Further verification comes from electron microscopy experiments. The high contrast provided by the gold nanoparticles allows the determination of the specific sites in the cell machinery where the nanoparticles are attached. Shi pointed out that it should be possible to design dendrimer nanoparticles with other biological ligands such as proteins and antibodies to image and target various biological systems.

“Beyond imaging, it may also be possible to specifically target and destroy cancer cells that internalize the nanoparticles by applying laser heat that intensifies in the presence of gold nanoparticles”, said Wang. “Another possibility is the attachment of drug molecules to these dendrimer nanoparticle systems”, added Baker, “since this will allow the direct delivery of drugs to the target cells”. The researchers are currently conducting further in vivo experiments to evaluate the suitability of this system for clinical applications.

Contact: Xiangyang Shi, University of Michigan, Ann Arbor (USA)

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June 22, 2007 Posted by | Biological Sciences, Cancer, Clinical Applications, Clinical Trials, Global, Global Health Vision, Global News, Nanobiotechnology, News, News Australia, News Canada, News Israel, News Jerusalem, News UK, News US, Research, University of Michigan, Virginia, Washington DC, World News | Leave a comment

Nursing Home Placement Associated with Accelerated Cognitive Decline in Alzheimer’s Disease

Study by Rush Alzheimer’s Disease Center finds adult day care may help the transition

(CHICAGO) – People with Alzheimer’s disease experience an acceleration in the rate of cognitive decline after being placed in a nursing home according to a new study by the Rush Alzheimer’s Disease Center. The study, published in the June issue of the American Journal of Psychiatry, finds that prior experience in adult day care may lessen this association.

The observational study involved 432 older persons with Alzheimer’s disease who were recruited from health care settings in the Chicago area. At baseline, they lived in the community and 196 participants were using day care services from 2 to 6 days a week for an overall mean of 1.7 days a week. At six month intervals for up to four years, they completed nine cognitive tests from which a composite measure of global cognition was derived.

On average, cognition declined at a gradually increasing rate for all participants. During the study period, 155 persons were placed in a nursing home, and placement was associated with a lower level of cognition and more rapid cognitive decline.

Study participants who had previous adult day care experience fared better. As level of day care use at study onset increased, the association of nursing home placement with accelerated cognitive decline substantially decreased. Thus, people using day care 3 to 4 days a week at the beginning of the study showed no increase in cognitive decline upon nursing home placement.

“The findings suggest that experience in day care may help individuals with Alzheimer’s disease make the transition from the community to institutional residence,” said study author Robert S. Wilson, Ph.D., a neuropsychologist at the Rush Alzheimer’s Disease Center.

The study also found that a higher level of education was associated with accelerated cognitive decline upon nursing home placement. Yet, day care use markedly reduced the association of education with accelerated cognitive decline in the nursing home; further evidence that there is a robust association between day care experience and cognition during the transition to a nursing home.

The authors considered the possibility that nursing home placement is simply a sign of increased severity of Alzheimer’s disease. Yet, the nursing-home-related increase in cognitive decline was observed even after simultaneous control for cognitive and noncognitive indicators of dementia severity at the time of nursing home entry.

Alternatively, the increased cognitive decline upon placement may reflect difficulty adapting to an unfamiliar environment, consistent with clinical reports of increased confusion and behavior problems in those with dementia during acute hospitalization or trips away from home. Patients who had prior adult day care services may have been better able to adjust to the unfamiliar environment.

“The findings suggest that the transition from the community to a nursing home is particularly difficult for people with Alzheimer’s disease and that those planning for their care should consider the possibility that experience in adult day care programs may help prepare affected persons for institutional living,” said Wilson.

The research was supported by grants from the National Institutes on Aging, which leads the federal effort supporting and conducting research on aging and the medical, social and behavioral issues of older people, including Alzheimer’s disease and age-related cognitive decline.

The Rush Alzheimer’s Disease Center is one of approximately 30 NIA-supported Alzheimer’s Disease Centers across the U.S. which conduct basic science, clinical, and social and behavioral research on dementia and AD. General information on aging and aging research can be viewed at the NIA’s home website, http://www.nia.nih.gov.

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June 1, 2007 Posted by | Alberta, Alzheimers, Baltimore, Calgary, Clinical Trials, Global, Global Health Vision, Global News, Irvine, News, News Australia, News Canada, News UK, News US, Research, Rush Alzheimer’s Disease Center, Virginia, Washington DC, World News | Leave a comment

Chronic Multisymptom Illnesses, one battle on many fronts.

My good friend Jeanne Hambleton, a journalist and advicate from the UK, has asked me to contribute an article for her upcoming book, Pain 24/7 – To publish a self help FMS book 12/05/2007

Jeanne’s book is being written to raise severly needed research funds into Fibromyalgia, Chronic Fatigue Stndrome, M.E. and is a vital part of moving forward with research into these illnesses.

Please if you can, contribute to the book project by visiting this link: http://www.jeannehambleton.chipin.com/signup
as your donation no matter what size it is, will help bring this vitally important book into existance, hopefully on schedule.The need is urgent and the time to act is now.

Jeanne asked me write an article called three illnesses, one battle, but I did take the liberty with her permission to include “Chronic Multisympton Illnesses” in general, and how this is several illnesses being fought on many fronts.

Chronic Multisymptom illnesses (CMI) come in a number of forms, ranging from “Fibromyalgia”, “Chronic Fatigue Syndrome, M.E.”, and “Gulf War Syndrome.”, simply to name the more common and widely recognized ones.

Each of these illnesses faces one common challenge in the medical community. A severe lack of research funding. In spite of the lack of funding we have begun to learn a great deal about some of these illnesses, however the funding is scant at best when it comes to developing these discoveries into usable treatments.

One area we severly need improvement on is in Physician Education. Many Physicians, and these are good Doctors, simply have not taken the time to read the latest clinical research results. They were trained at a time when these illnesses were thought to be some form of somataform illness or psychiatric disorder and unfortunately so many of them are still under the beliefe that this is the case. To quote a favorite phrase used in psychotherapy, “denial is not a river.”

We severly need all Medical Professionals to be on the same page when it comes to understanding these illnesses. It is the simple way out to to deny these illnesses are legitimate in nature and dismiss them as such when the current medical facts are far from that common misconception. It creates a situation where many learned medical professionals appear as if they simply do not understand these mechanisms, nor do they want to, and it is creating a situation where many suffer needlessly as a result.

I strongly urge the medical community to look at the facts. If one is not part of the solution, one becomes part of the problem. One of the main area’s where a lack of Physician Education has taken it’s toll is in Canada. Most Canadian Physicians simply don’t know how to diagnose or treat these illnesses. As a result the Statistics Canada data on these illnnesses is severly flawed. This fatal flaw affects research funding in a very negative way.

I am calling for the Medical Community to come together and formulate a plan to make Physician Education into these illnesses a major priority.
I will do my part to help make this happen and work with as many Clinical Researchers as I can to help develop this vital information.

The time to create change is now so that we can move forward and find viable treatments that can restore the sufferer’s of these illnesses to some kind of reasonable quality of life. The refusal to do so or denial of these illnesses is neglegent, and neglegence is not in anyones best interest, it does not serve the best interest of the patient, neither does it serve the best interest of the Physician. The evidence is there and we must act upon it. The Physicians oath to “do no harm” is poorly served by dismissing these illnesses based on information that is decades outdated.

I plan to work with many of the top Clinical Reachers in these fields to improve Physician Understanding and Awareness in the coming months and cannot understate the importance of the work that lies ahead of us all.

Each of us has a responsability to learn as much as we can to bring these illnesses into a managable modality that will improve the quality of life for these patients.

Sincerely,

Richard L. Usher

Editor

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References:

1.) http://fmsglobalnews.wordpress.com/2007/02/01/interview-with-dr-daniel-j-clauw-university-of-michigan-health-system-professor-department-of-internal-medicine-rheumatology/
2.) http://fmsglobalnews.wordpress.com/2007/02/14/fibromyalgia-the-silent-epidemic/

http://fmsglobalnews.wordpress.com/2007/05/13/chronic-multisymptom-illnesses-one-battle-on-many-fronts/
http://www.free-press-release.com/news/200705/1179079690.html

May 13, 2007 Posted by | Chronic Multisymptom Illnesses, Clinical Trials, Global, Global Health Vision, Global News, News, University of Michigan | Leave a comment

Researchers Create Model of Cancer-Preventing Enzyme, Study How It Works

May 11 2007

Contact: Katherine Kostiuk
Sr. Information Specialist
573-882-3346
KostiukK@missouri.edu

Proline dehydrogenase is important because it plays a role in apoptosis, the process of cell death, by enabling the creation of superoxide, a highly reactive electron-rich oxygen species. Superoxide is involved in the destruction of damaged cells and therefore is important in preventing the development and spread of cancer. The protein proline dehydrogenase “opens up to allow oxygen to ‘steal’ electrons” and create a superoxide, said Tommi A. White, an MU doctoral student in biochemistry.

White worked with John J. Tanner, professor of chemistry and biochemistry in MU’s College of Arts and Science, and Navasona Krishnan, a doctoral student at the Unviersity of Nebraska-Lincoln, and Donald F. Becker, an associate professor at the University of Nebraska-Lincoln, to create the first model of proline dehydrogenase. Because the human form of this enzyme is difficult to work with, the team studied proline dehydrogenase from the bacteria Thermus thermophilus. They used bioinformatics and biochemical studies to show that this enzyme is functionally similar to the human version, so their results can be generalized to the human version, as well as the bacterial version.

Using X-ray crystallography and biochemical analysis, the team created a model of proline dehydrogenase that can tell scientists more about the molecule’s structure and functions.

“The three-dimensional model tells us a lot about the structure of the molecules and helps us understand how they work,” Tanner said. “This protein is important in cancer prevention because it enables the creation of superoxide, which aid in cell death. Cells aren’t meant to live forever, and at some point, they need to die and be destroyed. Cells that are damaged or diseased are usually destroyed in this process. Our structure tells us how oxygen gets access to electrons stored in the enzyme. We think we’ve identified a gate that opens to let oxygen into the enzyme where the electrons are stored.”

In this way, proline dehydrogenase is important in preventing cancer. White said it’s unusual for proline dehydrogenase to be involved in such a process because the usual job of this type of enzyme is to transfer electrons to the mitochondrial membrane, not allow them to be attached to oxygen to create highly reactive superoxides.

Tanner and White said they hope to continue to study proline dehydrogenase and the molecules that can inactivate it. They also plan to examine another protein they suspect works in collaboration with proline dehydrogenase to understand how that protein affects the cancer-preventing abilities of proline dehydrogenase.
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May 11, 2007 Posted by | Cancer, Clinical Trials, DNA, Enzymes, Genetics, Global, Global Health Vision, Global News, Human Genome, News, Uncategorized, University of Missouri, Washington DC | Leave a comment

Dealing deadly cancers a knockout punch

Contact: Cathy Ward
cathy.ward@oncolyticsbiotech.ca
403-670-7370
Oncolytics Biotech Inc.

New scientific evidence is helping to build a compelling case for oncolytic viruses as a first-line and adjunctive treatment for many cancers.

Reovirus, a non-pathogenic virus under development at Calgary, Alberta-based Oncolytics Biotech, has shown powerful anti-cancer activity against cultured tumor cells, in animal models, and in human clinical trials. Oncolytics’ proprietary reovirus formulation, Reolysin®, is active against numerous cancers, including intractable sarcomas and melanomas.

Recent studies also indicate that Reolysin works synergistically with standard anti-cancer drugs, providing significantly stronger responses than either agent alone.

In addition, other studies completed in the past year have shown Reolysin has the ability to prime patients’ immune systems against their particular cancer, leading to additional cancer cell killing. It is through this second “inflammatory” mechanism that researchers hope Reolysin will bring about long-term remissions of once-untreatable cancers.

At the Fourth International Conference on Oncolytic Viruses as Cancer Therapeutics in March 2007 in Scottsdale, Arizona, several presentations focused on reovirus efficacy alone or in combination with standard chemotherapies.

In one study, investigators examined the tumor-killing ability of reovirus plus cisplatin, a standard chemotherapy agent, in a mouse melanoma model that included both cultured cells and live animals. The results of the preclinical study showed that the combination of reovirus and cisplatin was significantly more effective than cisplatin or reovirus alone at killing melanoma cancer cells in a mouse model. The investigators intend to explore the mechanism of this promising synergistic action in further detail in future preclinical work.

Another presentation at the Arizona conference reported on the use of Reolysin plus the cancer drug cyclophosphamide in an animal model of melanoma. When treated with both agents, test animals experienced enhanced tumor regression compared with either agent alone, and without additional toxicity. Oncolytics has permission from the U.K. regulatory authorities to test Reolysin in three separate human trials in combination with the cancer drugs gemcitabine, paclitaxel/carboplatin and docetaxel.

Perhaps the most exciting findings of Reolysin combination therapy were reported at the American Association for Cancer Research Annual Meeting in April, 2007. In mice transplanted with a human colon cancer, Reolysin plus gemcitabine completely eradicated the tumors in four of five test animals. It is rare to see the virtual elimination of tumours as well as the long-lasting therapeutic effect that was observed in this study.

“Combination therapy results for reovirus in animals are particularly encouraging because they suggest that Reolysin can improve the anti-tumor activity of standard chemotherapy agents in advanced cancer patients without causing additional toxicity,” said Dr. Karl Mettinger, Chief Medical Officer of Oncolytics.

Physicians often prefer to treat cancer with multiple agents, but toxicity limits these approaches. Since reovirus typically is not pathogenic in humans nor associated with severe toxicity in clinical studies, its co-administration is not expected to increase a treatment’s overall toxicity.

Dual Mechanism

Reovirus works by entering and replicating within cancer cells containing an activated ras pathway, a mutation present in about two-thirds of all human cancers. Reovirus enters a cancer cell, makes thousands of copies of itself, and then causes the cell to burst, which releases viruses that infect and kill adjacent cancer cells. Normal cells are not harmed.

In addition to killing cancer cells directly, reovirus is believed to activate an anti-tumor immune response through the body’s natural killer cells and T cells. Through this mechanism, which persists for weeks or months, the body continues to fight off cancer long after the virus clears from the body.

Future directions

On April 11, 2007, Oncolytics announced it had initiated a Phase II trial to evaluate intravenous administration of Reolysin in patients with sarcomas that have metastasized to the lung. For patients with deadly soft tissue sarcoma, the lungs are the most common site of metastatic disease. To date, surgery has been the only effective therapy for metastatic sarcoma.

The multi-center, Phase II study follows successful completion of systemic administration trials with Reolysin in the U.K. and the U.S. This will be the second of several Phase II trials Oncolytics plans for 2007. The Company also has a collaborative agreement with the U.S. National Cancer Institute to conduct multiple clinical trials with Reolysin which are expected to begin in 2007, including a Phase II melanoma trial and a Phase I/II ovarian cancer trial.

“It is hoped that the trials will clearly show that Reolysin alone or in combination with either radiation or chemotherapy can stop or reverse the growth of advanced cancers without adding harmful side effects,” said Dr. Mettinger.

Global Health Vision

May 10, 2007 Posted by | Alberta, Calgary, Cancer, Clinical Trials, Global, Global Health Vision, Global News, Oncology, Viruses | Leave a comment