Awareness, Detection And Treatment Programs Required To Improve Breast Health Care In Pakistan

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Main Category: Breast Cancer
Article Date: 03 Aug 2012 - 1:00 PDT
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Awareness, Detection And Treatment Programs Required To Improve Breast Health Care In Pakistan

Among most women in Pakistan, there is limited awareness of breast cancer occurrence, detection, and screening practices, or the importance of self-breast exams and clinical breast exams, according to a study in the August issue of the Journal of the American College of Radiology. In Pakistan, breast cancer is the most common cancer affecting women and the incidence is rising. It is usually diagnosed in later stages and often at a younger age compared with populations in the West.

"Breast cancer care in limited-resource countries generally suffers because of multiple obstacles, including a lack of recognition of breast health as a public health priority, a shortage of trained health care workers and social or cultural barriers. An improved understanding of existing obstacles in breast cancer care is critical to identify those factors that may be correctable and thereby devise effective interventions for improving early breast cancer detection and treatment in disadvantaged countries," said Sughra Raza, MD, co-author of the study.

Questionnaires were developed to address demographics, financial and educational levels, knowledge regarding breast cancer occurrence and treatment, and religious and cultural beliefs that may affect seeking care for breast disease. Using the questionnaires, one-on-one surveys were administered by community health workers in Karachi to 200 women and 100 general practitioners.

Survey results showed that women's knowledge of breast cancer incidence, diagnosis and treatment was proportionate to educational level, while willingness to address breast health issues and interest in early detection were high regardless of education level. Very few women had ever undergone clinical breast examinations or mammography. Among general practitioners, most understood major risk factors and importance of early detection. However, 20 percent did not believe breast cancer occurs in Pakistan, and 30 percent believed that it is a fatal disease. Female general practitioners were more likely to perform clinical breast examinations than male general practitioners.

"Although there is limited awareness regarding breast cancer occurrence, detection, and screening practices, as well as the importance of self-breast exams and clinical breast exams, the majority of women are very keen to learn more, to participate in their own care and to lower their risk," said Raza.

"Awareness and educational activities, including training female clinical health workers to perform clinical breast exams, will be beneficial, as we begin instituting awareness, detection and treatment programs in the face of a rapidly rising incidence and late-stage detection of breast cancer in Pakistan," said Raza.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
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'Antisense' Compound Rids Muscle Cells Of Toxic RNA: A Promising Step Toward Muscular Dystrophy Treatment

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Main Category: Muscular Dystrophy / ALS
Also Included In: Genetics
Article Date: 03 Aug 2012 - 0:00 PDT Current ratings for:
'Antisense' Compound Rids Muscle Cells Of Toxic RNA: A Promising Step Toward Muscular Dystrophy Treatment

Scientists have reversed symptoms of myotonic muscular dystrophy in mice by eliminating a buildup of toxic RNA in muscle cells. The work, carried out by scientists at the University of Rochester Medical Center, Isis Pharmaceuticals Inc. and Genzyme, is published in Nature.

After experimental antisense compounds were administered to mice twice a week for four weeks, symptoms of the disease were reduced for up to one year - a significant portion of a mouse's lifespan.

The investigators say that while the work is an encouraging step forward against myotonic dystrophy, one of the most common forms of muscular dystrophy, it's too soon to know whether the approach will work in patients. But they are cautiously optimistic, noting that the compound is extremely effective at reversing the disease - whose genetic underpinnings make it particularly vulnerable to an antisense approach - in a mouse model.

"These results give us strong encouragement about the possibility of developing a treatment that could fundamentally alter the disease. It's an important step on a long path," said senior author Charles Thornton, M.D., a neurologist at the University of Rochester Medical Center who has been pursuing new treatments for the disease for more than two decades.

"But, it's too early to know if this treatment will work as well in people as it did in the laboratory. Unfortunately, in biomedical research there are previous examples of compounds that worked in mice but not in people," added Thornton, the Saunders Family Distinguished Professor in Neuromuscular Research.

About 35,000 Americans have myotonic dystrophy, an inherited disorder that is marked by progressive muscle weakness and stiffness; eventually many patients have difficulty walking, swallowing, and breathing. The disease can also affect the eyes, the heart, and the brain. While there are medications to treat some of the disease symptoms, there is no drug to stop its progression.

The recent progress comes about a decade after several scientists, including Thornton, discovered that the genetic defect that causes the disease works quite differently than most other inherited diseases. In many diseases, a genetic flaw means that an important protein is not made correctly, or not made at all.

But in myotonic dystrophy, the defect results in the creation of an abnormal messenger RNA, which accumulates in the nucleus, getting in the way and stopping other proteins from doing their jobs. One of those proteins is MBNL1, which helps create chloride channels that are important for electrical control of muscles. When that process is thwarted, muscles send errant electrical signals, causing symptoms.

The approach outlined in the Nature paper exploits the roots of the defect, harnessing an enzyme whose usual job is to cut RNA into pieces. Working closely with the Rochester and Genzyme teams, scientists at Isis created synthetic compounds - short snippets of chemically modified DNA - that bind to the toxic RNA, modifying it in such a way that it was targeted for destruction by one of the body's own enzymes, RNase H.

With the team's most effective compounds, symptoms in the mice were reversed. The level of toxic RNA was reduced by more than 80 percent; stiffness in muscles eased dramatically; the microscopic structure of muscle was improved; and electrical signaling in muscles returned to normal.

The possibility of targeting "toxic RNA" - a buildup of abnormal RNA causing cellular processes to go awry - makes myotonic dystrophy an excellent target for antisense drugs, said Thornton.

The compounds are called "antisense" because their genetic code is the mirror image of the target RNA strand, known in scientific parlance as the "sense" molecule. The antisense compound will only stick to the precise RNA that is part of the myotonic dystrophy gene, leaving thousands of other vitally important RNAs alone.

While antisense technology has been in development for a couple of decades, it has not been effective at eliminating RNA in muscle cells until now. Results like those in the Nature paper are creating enthusiasm particularly among scientists who study neurodegenerative diseases, Thornton says. He points to promising work by a team from the University of California at San Diego on Huntington's disease, as well as research out of Cold Spring Harbor Laboratory on spinal muscular atrophy.

"For 20 years we studied myotonic dystrophy, hoping that someday we would learn enough to spot its Achilles heel," said Thornton. "This work comes close to doing that.

"I know it is unscientific for me to think so, but I can't help but see a little glimmer of 'medical justice' in this approach. For the same reason that the toxic RNA makes people sick, by hanging around too long in the nucleus and gumming up the works, it also becomes more susceptible to antisense drugs, because these drugs seem to work extraordinarily well against RNA in the nucleus," he added.

"Based upon these exciting preclinical data, we have initiated a drug discovery project for myotonic dystrophy with Dr. Thornton's team to identify an antisense drug to begin clinical testing," said C. Frank Bennett Ph.D., Senior Vice President, Research at Isis Pharmaceutical, Inc. "Myotonic dystrophy represents an ideal opportunity for an antisense drug as the disease-causing gene produces a toxic RNA that is not easily targeted with other therapeutic approaches. In just a few years, we have been able to expand our severe and rare disease franchise and maintain a broad research program, in which we are evaluating many different diseases that could be treated with an antisense drug."

Thornton was inspired to create a robust research effort to address the disease largely because of his experience treating patients. He is co-director of the Medical Center's Wellstone Muscular Dystrophy Cooperative Research Center, one of the world's top centers for the treatment of muscular dystrophy. He is also a scientist in the Center for Neural Development and Disease, where he runs a laboratory looking at the roots of the disease and exploring new treatments. On any given day, he is both seeing patients coping with conditions like myotonic dystrophy, as well as running laboratory experiments aimed at stopping the disease altogether.

As the research progressed, Thornton struck up a collaboration with Isis Pharmaceuticals Inc., the creator of the only antisense medication on the market, and Genzyme, a company with experience treating muscle diseases. Earlier this summer Isis announced an agreement with Biogen Idec Inc. to explore antisense treatments for myotonic dystrophy - an effort closely linked to Thornton's work.

Now scientists at Isis and the University of Rochester are working to improve their lead compound further, developing antisense compounds with stronger activity against the toxic RNA, but with minimal effects on the rest of the body. An unknown factor at this point, Thornton says, is whether the compounds will also improve the muscle-wasting aspect of the disease. That symptom, which causes great difficulty for patients, has been hard for scientists to create in mice, and so it's difficult to predict how it might respond to antisense knockdown technology.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our muscular dystrophy / als section for the latest news on this subject. The first author of the paper is Thurman Wheeler, M.D., assistant professor of Neurology at the University of Rochester Medical Center, who conducted many of the experiments. Other authors include Masayuki Nakamori, now at the University of Osaka in Japan; Sanjay Pandey, A. Robert MacLeod, and C. Frank Bennett of Isis Pharmaceuticals; and Andrew Leger, Seng Cheng, and Bruce Wentworth of Genzyme.
The work was funded by the National Institute of Neurological Disorders and Stroke, the National Institute of Arthritis and Musculoskeletal and Skin Diseases, the Saunders Family Neuromuscular Research Fund, Run America, the Muscular Dystrophy Association, and the Uehara Memorial Foundation.
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''Antisense' Compound Rids Muscle Cells Of Toxic RNA: A Promising Step Toward Muscular Dystrophy Treatment'

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Potential Treatment For Macular Degeneration And Retinitis Pigmentosa Uses Nanoparticles To Deliver Steroids To Retina

Main Category: Eye Health / Blindness
Also Included In: Seniors / Aging
Article Date: 15 Dec 2011 - 0:00 PST

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Hitching a ride into the retina on nanoparticles called dendrimers offers a new way to treat age-related macular degeneration and retinitis pigmentosa. A collaborative research study among investigators at Wayne State University, the Mayo Clinic and Johns Hopkins Medicine shows that steroids attached to the dendrimers targeted the damage-causing cells associated with neuroinflammation, leaving the rest of the eye unaffected and preserving vision.

The principal authors of the study, Raymond Iezzi, M.D. (Mayo Clinic ophthalmologist) and Rangaramanujam Kannan, Ph.D. (faculty of ophthalmology at The Wilmer Eye Institute of Johns Hopkins) have developed a clinically relevant, targeted, sustained-release drug delivery system using a simple nanodevice construct. The experimental work in rat models was initiated and substantially conducted at Wayne State University, and showed that one intravitreal administration of the nanodevice in microgram quantities could offer neuroprotection at least for a month, and appears in the journal, Biomaterials (33(3), 979-988).

Both dry age-related macular degeneration and retinitis pigmentosa are caused by neuroinflammation, which progressively damages the retina and can lead to blindness. Macular degeneration is the primary cause of vision loss in older Americans, affecting more than 7 million people, according to the National Institutes of Health (NIH). Retinitis pigmentosa encompasses many genetic conditions affecting the retina and impacts 1 in 4,000 Americans, the NIH estimates.

"There is no cure for these diseases, said Iezzi. "An effective treatment could offer hope to hundreds of millions of patients worldwide. We tested the dendrimer delivery system in rats that develop neuroinflammation leading to retinal degeneration. The target was activated microglial cells, the immune cells in charge of cleaning up dead and dying material in the eye. When activated, these cells cause damage via neuroinflammation - a hallmark of each disease."

"Dendrimers are tree-like, non-cytotoxic polymeric drug delivery vehicles (~ 4 nm). Surprisingly, the activated microglia in the degenerating retina appeared to eat the dendrimer selectively and retain them for at least a month. The drug is released from the dendrimer in a sustained fashion inside these cells, offering targeted neuroprotection to the retina," said Kannan.

The treatment reduced neuroinflammation in the rat model and protected vision by preventing injury to photoreceptors in the retina. Although the steroid offers only temporary protection, the treatment as a whole provides sustained relief from neuroinflammation, the study found. The researchers believe that this patent-pending technology with significant translational potential will be advanced further, through this multi-university collaboration among Johns Hopkins, Mayo Clinic and Wayne State.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our eye health / blindness section for the latest news on this subject. The study was funded by grants from the Ligon Research Center of Vision at Wayne State University, the Ralph C. Wilson Medical Research Foundation, Office of the Vice President for Research at Wayne State University, and Research to Prevent Blindness.
The researchers declare no conflict of interest.
Co-authors include Bharath Raja Guru, Ph.D., Case Western Reserve University; Inna Glybina and Alexander Kennedy, Wayne State University; and Manoj Mishra, Ph.D., The Wilmer Eye Institute of Johns Hopkins.
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Wayne State University - Office of the Vice Presid. (2011, December 15). "Potential Treatment For Macular Degeneration And Retinitis Pigmentosa Uses Nanoparticles To Deliver Steroids To Retina." Medical News Today. Retrieved from
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Cognitive Problems Still Evident Several Years After Breast Cancer Treatment

Main Category: Breast Cancer
Also Included In: Neurology / Neuroscience
Article Date: 13 Dec 2011 - 3:00 PST

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A new analysis has found that breast cancer survivors may experience problems with certain mental abilities several years after treatment, regardless of whether they were treated with chemotherapy plus radiation or radiation only. Published early online inCANCER, a peer-reviewed journal of the American Cancer Society, the study indicates that there may be common and treatment-specific ways that cancer therapies negatively affect cancer survivors' mental abilities.

Previous research suggests that chemotherapy can cause problems with memory and concentration in breast cancer survivors. To compare the effects of different types of cancer treatment on such mental abilities, Paul Jacobsen, PhD, of the Moffitt Cancer Center and Research Institute in Tampa, and his colleagues examined 62 breast cancer patients treated with chemotherapy plus radiation, 67 patients treated with radiation only, and 184 women with no history of cancer. Study participants completed neuropsychological assessments six months after completing treatment and again 36 months later, which is further out from the end of treatment than most previous studies of this type.

The study confirmed that chemotherapy can cause cognitive problems in breast cancer survivors that persist for three years after they finish treatment. In addition, the investigators found that breast cancer survivors who had been treated with radiation (and not chemotherapy) often experienced problems similar to those in breast cancer survivors treated with both chemotherapy and radiation. They did not find that hormonal therapy (such as tamoxifen) caused cognitive difficulties.

"These findings suggest that the problems some breast cancer survivors have with their mental abilities are not due just to the administration of chemotherapy," said Dr. Jacobsen. "Our findings also provide a more complete picture of the impact of cancer treatment on mental abilities than studies that did not follow patients as long or look at mental abilities in breast cancer survivors who had not been treated with chemotherapy," he added.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our breast cancer section for the latest news on this subject. Article: "Cognitive functioning after cancer treatment: A three-year longitudinal comparison of breast cancer survivors treated with chemotherapy or radiation and non-cancer controls." Kristin M. Phillips, Heather S. Jim, Brent J. Small, Christine Laronga, Michael A. Andrykowski, and Paul B. Jacobsen. CANCER; Published Online: December 12, 2011 (DOI: 10.1002/cncr.26432).
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Side Effects Of Breast Cancer Drugs Can Be So Bad Women End Treatment And Risk Return Of Cancer

Main Category: Breast Cancer
Also Included In: Compliance;  Pain / Anesthetics
Article Date: 12 Dec 2011 - 1:00 PST

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Why do so many postmenopausal women who are treated for estrogen-sensitive breast cancer quit using drugs that help prevent the disease from recurring?

The first study to actually ask the women themselves -- as well as the largest, most scientifically rigorous study to examine the question -- reports 36 percent of women quit early because of the medications' side effects, which are more severe and widespread than previously known. The Northwestern Medicine research also reveals a big gap between what women tell their doctors about side effects and what they actually experience.

"Clinicians consistently underestimate the side effects associated with treatment," said lead investigator Lynne Wagner, an associate professor in medical social sciences at Northwestern University Feinberg School of Medicine and a clinical psychologist at Robert H. Lurie Comprehensive Cancer Center of Northwestern University. "They give patients a drug they hope will help them, so they have a motivation to underrate the negative effects. Patients don't want to be complainers and don't want their doctor to discontinue treatment. So no one knew how bad it really was for patients."

The symptom most likely to cause women to stop using the drugs was joint pain. Other side effects women reported as compromising their quality of life were hot flashes, decreased libido, weight gain, feeling bloated, breast sensitivity, mood swings, irritability and nausea.

Wagner's research was presented at the 34th Annual San Antonio Breast Cancer Symposium.

The drugs, aromatase inhibitors, stop the production of estrogen in postmenopausal women, whose breast cancer cells are stimulated by estrogen. About two-thirds of breast cancers are estrogen sensitive, and aromatase inhibitors reduce the recurrence of cancer in postmenopausal women.

The women at highest risk for quitting the medications before the recommended five years are those who still are experiencing residual side effects from recent chemotherapy or radiation therapy when they start the aromatase therapy, according to the study. Women who had surgery for breast cancer but not chemotherapy or radiation therapy, or who weren't taking many other medications, were more likely to keep taking the aromatase medication.

"The more miserable they were before they started, the more likely they were to quit," Wagner said. "By the time they get through chemotherapy or radiation, they have to face five more years of another medication that will make them feel lousy. They feel like they already lost enough time to cancer and have reached their threshold for feeling bad."

"This is a wake-up call to physicians that says if your patient is feeling really beaten up by treatment, the risk of her quitting early is high," Wagner said. "We need to be better at managing the symptoms of our patients to improve their quality of life."

The new research exposes the disparity between clinicians' reporting of side effects and women's actual experiences. In a previous study, clinicians reported 5 percent of their patients experienced moderate to severe symptoms as a result of taking aromatase inhibitors. The new Northwestern study surveyed 686 women with a detailed questionnaire about their symptoms before treatment and at three, six, 12 and 24 months after starting treatment. The researchers found after three months of treatment that 33 to 35 percent of women had severe joint pain, 28 to 29 percent had hot flashes, 24 percent had decreased libido, 15 to 24 percent had fatigue, 16 to 17 percent had night sweats and 14 to 17 percent had anxiety. These numbers increased as women were on treatment longer.

Earlier studies also asked women to recall their symptoms after treatment ended, which is less accurate than reporting them at regular intervals while taking the drugs.

As a result of the side effects, 36 percent of women ended treatment before an average of 4.1 years. After two years, 10 percent had quit; the remainder quit between 25 months and the 4.1 years.

"These findings can help us identify women at risk for quitting the therapy, counsel them about the importance of staying on it and provide treatment for troubling side effects," Wagner noted.

Weight gain can be addressed with nutritional counseling, while mood swings and irritability can be treated with cognitive behavioral therapy or mind-body techniques, Wagner said. Joint pain can be tempered with nonsteroidal anti-inflammatory drugs, or women may be switched to a different hormonal medication. Nausea can be reduced with medication.

For the study, patients who had postmenopausal breast cancer filled out a 46-question survey rating their quality of life and symptoms associated with breast cancer and endocrine treatment. The survey included an item asking how much they were bothered by side effects of treatment from zero (not bothered) to four (severely bothered). For each additional one-point increase on this item, the patient's risk of quitting treatment early rose 29 percent. The patients were randomized to take one of two hormonal treatments (anastrozole or exemestane) daily for five years.

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Personalized Treatment For Crohn's Disease A Step Closer Following Gene Mapping

Main Category: Crohn's / IBD
Also Included In: Genetics
Article Date: 12 Dec 2011 - 0:00 PST

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Three new locations for Crohn's Disease genes have been uncovered by scientists at UCL using a novel gene mapping approach.

The complex genetic and environmental causes of Crohn's Disease (CD) have long been difficult to untangle. CD, a type of Inflammatory Bowel Disease that affects about 100 to 150 people per 100,000 in Europe, is characterised by inflammation in the gastrointestinal tract. Even though twin and family studies suggest a high heritability for CD of 50-60%, so far the locations of much of the genetic information implicated in this chronic disease have remained elusive.

Now, three newly identified gene regions on chromosome 16 have filled in some of the missing gaps, as well as showing that different patients carry different sets of faulty genes. Published today in the American Journal of Human Genetics, the findings could pave the way for personalised treatment and also lead to improved understanding of how complex diseases are inherited.

Dr Nikolas Maniatis, senior author from the UCL Research Department of Genetics, Evolution and Environment, said: "This paper shows how personalised medicine could work and also help to separate out patients. For example, just as there are many different types of cancer with different underlying genes, it seems that there are also mutations in different genes for different types of Crohn's Disease."

The research team used UK data provided by the Wellcome Trust Case Control Consortium (WTCCC), which includes genetic information of 1698 CD patients. The team's results were also replicated using independent US data provided by the American National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), which contains genetic information of 813 patients with CD.

Instead of comparing lots of genomic sites, one at a time, across the entire genome, the team instead looked at segments of DNA, each of which contains many variable sites. They used a mapping technique based on refined genetic maps that have the ability to show how stretches of DNA have been passed down together through the generations. By taking this into account when analysing genetic information from patients with CD the team were able to localise the faulty genes.

Dr Maniatis said: "This project essentially maps the most likely location of faulty sites for Crohn's Disease in the genome. By combining several pieces of information together, our technique lets us increase the power of our analysis."

Applying their technique on chromosome 16, which has long been known to harbour NOD2, an important gene for CD, the team indentified three novel genes, called CYLD, IRF8 and CDH1/CDH3, associated with CD and involved with inflammation and immune dysregulation in the body. Although these genes have different functions, all three are implicated in pathways involved in CD.

Dr Maniatis said: "These are very exciting times, as we can use these genetic maps to pinpoint where the causal sites of Crohn's Disease are located. Although it has been shown in the past that a proportion of patients suffering from Crohn's Disease do not carry the NOD2 mutations, up until now no other genes on chromosome 16 have been published in genome-wide analyses."

Professor Dallas Swallow, collaborator and co-author, also from the UCL Research Department of Genetics, Evolution & Environment, said: "This research will complement the work of those examining cellular and molecular changes, and ultimately lead to more personalised strategies for treatment. The next step is to search the rest of the genome.

"Importantly the work also shows that this method will allow more information to be derived from the valuable datasets collected by organisations such as the Wellcome Trust. This method can also be used to analyse other complex disorders, allowing us to make similar progress on other diseases, such as diabetes and Parkinson's disease."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our crohn's / ibd section for the latest news on this subject. 'Dissecting the Genetics of Complex Inheritance: Linkage Disequilibrium Mapping Provides Insight into Crohn's Disease' is published in the American Journal of Human Genetics.

University College London

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Breaking Oncogene's Hold On Cancer Cell Provides New Treatment Direction

Main Category: Cancer / Oncology
Article Date: 12 Dec 2011 - 0:00 PST

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Just as people's bodies and minds can become addicted to substances such as drugs, caffeine, alcohol, their cancers can become addicted to certain genes that insure their continued growth and dominance.

Researchers at Baylor College of Medicine and Harvard Medical School have developed ways to exploit the addictions of cancers to kill them without harming normal tissues. A report on their work appears online in the journal Science.

Many cancers are driven by the overexpression of oncogenes. These oncogenes are two-faced. On one hand, they promote processes that allow the cells to become immortal and to grow unchecked. On the other hand, the expression of these oncogenes creates additional anti-growth cellular stresses, conflicts that the cancer cell must subvert in order to survive. One classical example of an oncogene that creates such a delicate balance is c-myc. In patients, hyper-activation of c-myc is associated with the most aggressive cancer types, with 20-40 percent of all cancers having an activated myc gene.

"For 30 years, scientists have tried to attack the oncogene myc," said Dr. Thomas Westbrook, assistant professor of molecular and human genetics and biochemistry and molecular biology at BCM and a senior author of the report. "However, it has not been amenable to the drugs we have. Now we have to take advantage of the stresses the oncogene puts on the cancer cell and determine if we can ramp those up to kill the tumor."

"Tumor cells experience considerable mitotic stress," said Westbrook. Regular chemotherapy take advantage of this, but the drugs kill dividing cancer and normal cells. Experts think that special programs within the cancer cell allow it to cope with the stress as it grows and divides (mitosis).

"The fundamental question we asked was how are the stresses in cancer cells different from those in normal cells?" said Westbrook. "We want to exploit that idea and see if we can exacerbate that stress.

To identify genes involved in coping with this stress, Westbrook and his colleague Dr. Stephen Elledge of Harvard Medical School used a special RNA interference screen to disrupt the function of each gene in the genome and identify the genes required to allow the cancer cell to tolerate the stress of the myc oncogene.

One of the core biochemical processes they uncovered was SUMOylation, a three-step process. Westbrook, Elledge, and colleagues showed that SUMO-activating enzyme, the first step in the process, is required for myc-driven cancers to go through cell division. Thus, inhibiting SAE could be a therapeutic strategy for myc-cancers.

To test this, they turned off the SAE enzyme in a form of myc-driven breast cancer.

"The tumors stopped growing and many of them melted away," said Westbrook. Today, many of the mice are still alive and healthy. If they did not turn off production of the enzyme, the tumors grew and eventually killed the animals.

"If you inhibit this enzyme in a non-myc driven breast cancer, nothing happens," said Westbrook. "If you inhibit it in normal cells of many kinds, nothing happens."

That means that turning off SAE2 exacerbates the stress on cancer cells but not normal cells and thus be a great way to kill cancers without many of the side effects of traditional chemotherapies.

The findings in this report have particular importance for an aggressive form of breast cancer called triple negative breast cancer (TNBC). This subtype is often driven by myc, and there are currently no effective treatments for these patients.

"This may provide that target," said Westbrook. The therapeutic value is that a drug targeting SAE will cause the cancer cell to no longer tolerate myc but will not be detrimental to normal cells.

In addition, myc drives many others kinds of cancers and he anticipates that inhibiting this enzyme in these tumors may have the same effect.

Others who took part in this work include Jessica D. Kessler, Tingting Sun, Kristen L. Meerbrey, Earlene M. Schmitt, Samuel O. Skinner, Mitchell Rao, Peng Yu, Rocio Dominguez-Vidana, Ronald J. Bernardi, Tiffany Hsu, Ido Golding, C. Kent Osborne, Chad J. Creighton, Susan G. Hilsenbeck, Rachel Schiff, Chad A. Shaw, all of BCM; ,Kristopher T. Kahle, Michael R. Schlabach, Qikai Xu, Mamie Z. Li, Anthony C. Liang and Nicole L. Solimini, all of Harvard and Brigham and Women's Hospital; Bing Yu and Ji Luo, both of the National Cancer Institute and Zachary C. Hartman of the University of Texas MD Anderson Cancer Center.

Funding for this work came from the National Institutes of Health, the U.S. Department of Defense, the Human Frontier Science Program, the Welch Foundation, the National Science Foundation, the Susan G. Komen for the Cure, the National Cancer Institute, the U.S. Army Innovator Award, the Howard Hughes Medical Institute, the V Foundation for Cancer Research and the Mary Kay Ash Foundation for Cancer Research.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
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Study Challenges Decades-Old Treatment Guidelines For Anorexia

Main Category: Anxiety / Stress
Article Date: 10 Dec 2011 - 1:00 PST

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Adolescents hospitalized with anorexia nervosa who receive treatment based on current recommendations for refeeding fail to gain significant weight during their first week in the hospital, according to a new study by UCSF researchers.

The findings, published in the January issue of the Journal of Adolescent Health with an accompanying editorial, challenge the current conservative approach to feeding adolescents with anorexia nervosa during hospitalization for malnutrition.

The American Psychiatric Association, American Dietetic Association and others recommend starting with about 1,200 calories per day and advancing slowly by 200 calories every other day. This "start low and go slow" approach is intended to avoid refeeding syndrome a potentially fatal condition resulting from rapid electrolyte shifts, a well-known risk when starting nutrition therapy in a starving patient.

The UCSF study is the first to test these recommendations, which have been in place since 2000. "Our findings show that the current recommendations are just not effective", said Andrea Garber, PhD, RD, associate professor of pediatrics in the Division of Adolescent Medicine at UCSF, who led the research with colleagues in the UCSF Adolescent Eating Disorders Program.

Study participants were hospitalized due to signs of malnutrition, including low body temperature, blood pressure, heart rate and body mass index. The vast majority of the 35 primarily white, female adolescent patients received low calorie diets based on the current recommendations. Patients were fed six small meals per day, and when they refused food, they were given high calorie liquid supplements as a replacement. The patients' vital signs were monitored closely, with their heart rates measured continuously and electrolytes checked twice a day.

While the low calorie diets did prevent refeeding syndrome for those patients, about 83 percent of them also experienced significant initial weight loss and no overall weight gain until their eighth day in the hospital. This finding represents "a missed opportunity," according to Garber.

"Studies show that weight gain during hospitalization is crucial for patients' long-term recovery," she said, "we have to make the most out of their short time in the hospital."

Although 94 percent of patients in the study started on fewer than 1,400 calories a day, it included a range of diets from 800 to 2,200 calories. This range allowed the researchers to examine the effect of increasing calories. According to Garber, two important findings emerged:

The calorie level of the starting diet predicted the amount of weight that would be lost in the hospital. In other words, those on lower calorie diets lost significantly more weight.

Higher calorie diets led to less time in the hospital. In fact, Garber said, "we showed that for every 100 calories higher, the hospital stay was almost one day shorter."

While the study finds that current recommendations are too cautious, it raises other questions, according to the research team. For example, while a shorter hospital stay may reduce insurance costs, patients may not be ready to go home yet.

"Shorter is not necessarily better" said Garber. "We have to consider the potential implications down the line, both psychological and emotional."

Another unanswered question relates to refeeding syndrome, which remains "a very real fear", according to Barbara Moscicki, MD, a professor of pediatrics in the Division of Adolescent Medicine at UCSF and senior author on the paper. Moscicki says that the team is proceeding cautiously since more aggressive approaches to feeding and supplementation have not yet been well studied.

Nevertheless, the researchers say that the study results are a promising start because no adverse events were seen in the study subjects on the higher calorie diets. "If we can improve weight gain with higher calories," Garber said, "then we're on the right path."

Article adapted by Medical News Today from original press release. Source: UCSF
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Hemophilia B - Single Gene Therapy Treatment Offers Significant Improvement

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Academic Journal
Main Category: Blood / Hematology
Article Date: 10 Dec 2011 - 12:00 PST

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Patients with hemophilia B experienced considerable improvements and fewer injections with clotting factor to reduce bleeding after receiving just one treatment with gene therapy, researchers from St. Jude Children's Research Hospital, Memphis, USA, and University College London (UCL), England, reported in NEJM (New England Journal of Medicine).

The small Phase I study, involving just six patients, is still proof that gene therapy is a promising treatment for the disabling and potentially dangerous consequences of painful bleeding episodes experienced by patients with hemophilia B - an inherited blood disorder.

The authors say their study will be presented in San Diego, USA, on 11th December, 2011, at the 53rd annual meeting of the American Society of Hematology.

Four out of the six participants who received gene therapy no longer require further protein injections to prevent episodes of bleeding - none of those four have suffered bouts of spontaneous bleeding either. Some of them have gone on to take part in marathon running events and other activities which would have been extremely hard to do without the gene therapy.

All the patients were treated under the care of Prof. Edward Tuddenham at the Royal Free Hospital, London. Co-author Tuddenham is a pioneer in the field of blood coagulation.

First author Dr Amit Nathwani, said:

"This is a potentially life-changing treatment for patients with this disease and an important milestone for the field of gene therapy. It could have ramifications for the treatment of haemophilia A, other protein and liver disorders and chronic diseases such as cystic fibrosis."

Hemophilia B (British spelling: haemophilia B) is a blood clotting disorder, as are all types of hemophilia. In this case it is caused by a mutation in the gene that makes Factor IX, an essential protein in the blood clotting process. It is the second most common form of hemophilia, after hemophilia A.

Hemophilia B is sometimes called Christmas disease, after Sephen Christmas, the first patient to be described with the condition. The disorder was also first published in the Christmas edition of the BMJ (British Medical Journal).

Nearly all patients with hemophilia B are male, because the mutated gene is carried on the X chromosome. The authors explain that it is a relatively rare condition, affecting approximately 1 in every 30,000 people.

Previous attempts at reducing the symptoms of hemophilia B by placing a correct copy of the gene have never been successful.

Prof. Tuddenham, Dr. Nathwani and team used AAV (adeno-associated virus) 8 to deliver the correct Factor IX gene, plus other genetic material into the liver of the patient. As the rate of natural infection with AAV8 is very low, it was picked up. AAV8 is part of a virus family that targets cells in the liver without causing illness in humans; neither does the virus integrate into human DNA.

No immunosuppressant medications were administered to the participants before the gene therapy was given; an approach pioneered jointly by scientists from St. Jude and UCL.

A one-off infusion of the vector was administered into the vein in the arm of each patient. Two patients each received gradually rising doses of the vector. Afterwards, levels of Factor IX were elevated in all participants - from between 2% and 12% compared to less than 1% before the gene therapy began.

There was a correlation between dosages of the experimental vector and Factor IX levels - two volunteers, who were given the highest dosages, had the highest Factor IX levels. Their levels rose to up to 12%. The authors explained that any gain above 1% of normal levels can significantly improve patients' quality of life and reduce the number and severity of bleeding episodes.

Trial participant Sebastian Misztal (Source: UCLH/UCL NIHR Biomedical Research Centre)

Senior author, Dr Andrew Davidoff, said:

"The first patient has been followed for the longest time, and his levels have remained at 2% for more than 18 months. These results are highly encouraging and support continued research. More patients are scheduled to be enrolled in future trials scheduled to begin later this year."

The participant with the higher dosage had to undergo short-term steroid treatment, which was effective. His liver enzyme levels had risen slightly - a sign of mild liver damage - after receiving the vector infusion. His levels of Factor IX remain above what they were before gene therapy was applied, and his liver enzyme levels are back to normal. The other participant, who received the second highest dosage, also had slightly higher liver enzyme levels, but they did not rise beyond the normal range - he was also given a short course of steroids.

The authors say the rise in enzyme levels was most likely caused by an immune response. Immune responses were reported in previous gene therapy studies when a different vector was used.

Written by Christian Nordqvist
Copyright: Medical News Today
Not to be reproduced without permission of Medical News Today

Visit our blood / hematology section for the latest news on this subject. Article - "Adenovirus-Associated Virus Vector–Mediated Gene Transfer in Hemophilia B"
Amit C. Nathwani, M.B., Ch.B., Ph.D., Edward G.D. Tuddenham, M.B., B.S., M.D., Savita Rangarajan, M.B., B.S., Cecilia Rosales, Ph.D., Jenny McIntosh, Ph.D., David C. Linch, M.B., B.Chir., Pratima Chowdary, M.B., B.S., Anne Riddell, B.Sc., Arnulfo Jaquilmac Pie, B.S.N., Chris Harrington, B.S.N., James O'Beirne, M.B., B.S., M.D., Keith Smith, M.Sc., John Pasi, M.D., Bertil Glader, M.D., Ph.D., Pradip Rustagi, M.D., Catherine Y.C. Ng, M.S., Mark A. Kay, M.D., Ph.D., Junfang Zhou, M.D., Yunyu Spence, Ph.D., Christopher L. Morton, B.S., James Allay, Ph.D., John Coleman, M.S., Susan Sleep, Ph.D., John M. Cunningham, M.D., Deokumar Srivastava, Ph.D., Etiena Basner-Tschakarjan, M.D., Federico Mingozzi, Ph.D., Katherine A. High, M.D., John T. Gray, Ph.D., Ulrike M. Reiss, M.D., Arthur W. Nienhuis, M.D., and Andrew M. Davidoff, M.D.
NEJM December 10, 2011 (10.1056/NEJMoa1108046)

Editorial - "Merry Christmas for Patients with Hemophilia B"
Katherine P. Ponder, M.D.
NEJM December 10th, 2011. DOI: 10.1056/NEJMe1111138

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Sewage Treatment Plants May Contribute To Antibiotic Resistance Problem

Main Category: Infectious Diseases / Bacteria / Viruses
Also Included In: Water - Air Quality / Agriculture;  MRSA / Drug Resistance
Article Date: 09 Dec 2011 - 1:00 PST

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Water discharged into lakes and rivers from municipal sewage treatment plants may contain significant concentrations of the genes that make bacteria antibiotic-resistant. That's the conclusion of a new study on a sewage treatment plant on Lake Superior in the Duluth, Minn., harbor that appears in ACS' journal Environmental Science & Technology.

Timothy M. LaPara and colleagues explain that antibiotic-resistant bacteria - a major problem in medicine today - are abundant in the sewage that enters municipal wastewater treatment plants. Treatment is intended to kill the bacteria, and it removes many of the bacterial genes that cause antibiotic resistance. However, genes or bacteria may be released in effluent from the plant. In an effort to determine the importance of municipal sewage treatment plants as sources of antibiotic resistance genes, the scientists studied releases of those genes at the Duluth facility.

Although the Duluth facility uses some of the most advanced technology for cleaning wastewater - so-called tertiary treatment - the study identified it as an important source of antibiotic resistance genes. Sampling of water at 13 locations detected three genes, for instance, that make bacteria resistant to the tetracycline group of antibiotics, which are used to treat conditions ranging from acne to sexually transmitted diseases to anthrax and bubonic plague. LaPara's team says their research demonstrates that even the most high-tech sewage treatment plants may be significant sources of antibiotic resistance genes in waterways.

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Visit our infectious diseases / bacteria / viruses section for the latest news on this subject. The authors acknowledge funding from the National Science Foundation and the Minnesota Environment and Natural Resources Trust Fund.
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