Medical News Today

New guidelines from the American Cancer Society say for many cancers, maintaining a healthy weight, getting adequate physical activity, and eating a healthy diet can reduce the chance of recurrence and increase the likelihood of disease-free survival after a diagnosis. The recommendations are included in newly released Nutrition and Physical Activity Guidelines for Cancer Survivors, published early online in CA: A Cancer Journal for Clinicians.

Increasing evidence shows that for many cancers, excess weight, lack of exercise, and poor nutrition increase the risk of cancer recurrence and reduce the likelihood of disease-free and overall survival for cancer patients. “The data suggests that cancer survivors, just like everyone else, benefit from these important steps,” said Colleen Doyle MS RD, American Cancer Society director of nutrition and physical activity and co-author of the guidelines. “While we’ve published previous reports outlining the evidence on the impact of nutrition and physical activity on cancer recurrence and survival, this is the first time the evidence has been strong enough to release formal guidelines for survivorship, as we’ve done for cancer prevention. Living a physically active lifestyle and eating a healthy diet should absolutely be top of mind for anyone who’s been diagnosed with cancer. ”

The report was last updated in 2006, and was first created in 2001. For the update, a group of experts in nutrition, physical activity, and cancer survivorship evaluated the scientific evidence and best clinical practices related to optimal nutrition and physical activity after the diagnosis of cancer. Among the review’s conclusions:

• Avoiding weight gain throughout treatment may be important not only for survivors who are overweight, but also those of normal weight.
• Intentional weight loss after recovering from cancer treatment among overweight and obese patients may be associated with health-related benefits.
• Evidence strongly suggests that exercise is not only safe and feasible during cancer treatment, but that it can also improve physical functioning, fatigue, multiple aspects of quality of life, and may even increase the rate of completion of chemotherapy.
• Physical activity after cancer diagnosis is associated with a reduced risk of cancer recurrence and improved overall mortality among multiple cancer survivor groups, including breast, colorectal, prostate, and ovarian cancer.
• Among breast cancer survivors, physical activity after diagnosis has consistently been associated with reduced risk of breast cancer recurrence and breast cancer-specific mortality.
• Results from observational studies suggest that diet and food choices may affect cancer progression, risk of recurrence, and overall survival in individuals who have been treated for cancer.

  For example, a dietary pattern high in fruits, vegetables, whole grains, poultry, and fish was found to be associated with reduced mortality compared with a dietary pattern characterized by a high intake of refined grains, processed and red meats, desserts, high-fat dairy products, and French fries in women after breast cancer diagnosis and treatment.

• Compelling evidence exists against the use of select supplements in certain oncology populations; therefore, health care professionals and survivors need to proceed with caution.

  “As more people survive cancer, there is increasing interest in finding information about food choices, physical activity, and dietary supplements to improve treatment outcomes, quality of life, and overall survival,” said Doyle. “Our report summarizes the findings of this expert panel, and is intended to present health care providers with the best possible information with which to help cancer survivors and their families make informed choices related to nutrition and physical activity.”

The recommendations also include specific guidance for people diagnosed with breast, colorectal, endometrial, ovarian, lung, prostate, head and neck, and hematologic cancers. It also includes a section with answers to common questions about alcohol, organic foods, sugar, supplements, and several other areas of interest.

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The genetics responsible for frequency-specific hearing loss have remained elusive until recently, when genetic loci were found that affected high-frequency hearing. Now, a study published in the open access journal BMC Genetics reports, for the first time, genetic loci with effects that are limited to specific portions of the hearing frequency map, particularly those that are most affected in ageing-related hearing loss.

Presbycusis is the loss of hearing for high-pitched sounds that gradually occurs in most individuals as they grow older. Although many genetic loci have been linked to hearing deficits in humans, many loci that contribute to tonotopy, i.e. the organization of the auditory system that permits detection and discrimination of sounds of different frequency, remain undiscovered.

A group from the National Institute on Deafness and Other Communication Disorders (NIDCD) at the National Institutes of Health (NIH), used genome-wide linkage analysis in NIH Swiss mice to successfully identify two quantitative trait loci that affect hearing at high frequencies – Hfhl1 and Hfhl3. Specifically the effect of the locus Hfhl1 is thought to be confined to hearing frequencies from 25-44kHz of the tonotopic map, whilst Hfhl3 is restricted to the 35-44kHz region.

Lead author James M Keller commented, “Our results support the hypothesis that frequency-specific hearing loss results from variation in gene activity along the cochlear partition and suggest a strategy for creating a map of genes that influence differences in hearing sensitivity and or vulnerability in restricted portions of the cochlea.”

He continued, “The high-frequency hearing loss loci, Hfhl1 and Hfhl3, explain only a portion of the variation in high-frequency hearing loss observed in these mice. Other loci, and cross talk between genes at different loci, probably account for much of the remainder – in fact we detected a number of additional loci that could account for some of the residual variation. Additional genotyping and analysis could greatly increase our understanding of the genetic architecture of the HFHL phenotype.”

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A team of American researchers have created a portable, miniature microscope in the hope of reducing the time taken to diagnose oral cancer.

The probe, which is around 20 cm long and 1 cm wide at its tip, could be used by doctors to diagnose oral cancer in real-time or as a surgical guidance tool; dentists could also use it to screen for early-stage cancer cells.

The probe has been presented in IOP Publishing’s Journal of Micromechanics and Microengineering, and has shown good agreement with images of oral cancers obtained using conventional, much slower techniques at the University of Texas Health Science Centre at San Antonio, TX.

Historically, the death rate associated with oral cancer is particularly high; not because it is hard to discover or diagnose, but due to the cancer being routinely discovered late in its development.

Lead author of the study Dr John X J Zhang at the University of Texas at Austin said: “Today, that statement is still true, as there isn’t a comprehensive programme in the US to opportunistically screen for the disease; without that, late stage discovery is more common.”

The probe uses a laser to illuminate areas of the sample and can view beneath the surface of tissue, creating full 3D images. It can also take a series of images and layer them on top of each other, much like the tiling of a mosaic, giving a large overall field-of-view.

The key component of the probe is a micromirror. Micromirrors have previously been used in barcode scanners and fibre optic switches and are controlled by a microelectromechanical system, allowing the laser beam to scan an area in a programmed fashion.

The low cost and ease of fabrication of micromirrors, along with their easy integration into electronic systems for versatile imaging operations, make them an indispensable component of the probe.

Oral cancers have traditionally been diagnosed by biopsy. Based on a doctor’s visual inspection, medical practitioners remove a sample of tissue from the patient and send it off to a pathologist who will examine the tissue under a microscope to check for abnormal or malignant cells.

Results will be sent back to the doctor for the next round of diagnoses or surgery; the whole process can take up to several weeks. Not only is this process time consuming, it can be costly, invasive and painful, often leaving scars.

“Due to the lack of real-time efficient oral cancer screening tools, it is estimated that approximately $3.2 billion is spent in the United States each year on treatment of such cancers”, Dr Zhang continued.

The researchers, from the University of Texas at Austin and the commercialization partner NanoLite Systems, Inc. are now planning clinical trials with a view to gaining approval from the Food and Drug Administration (FDA). They envisage that, with a few adjustments, the device could be built for a quarter of the price it costs to build the microscopes that are currently used in diagnosis, which is around $300 000.

Fast facts (UK)

• Oral cancer rates have risen by more than 20% in the last 30 years.
• Cigarette smoking and excessive alcohol consumption account for 90% of oral cancer cases.
• Most cases develop in people aged 40 years or over, with a steep rise in those aged 45.
• An estimated 75% of patients with mouth cancer will live for at least five years after diagnosis if diagnosed at an early stage.
• If diagnosed at a late stage, the outlook is poor: only one in five people will live for at least five years after diagnosis.

Information obtained from*

Fast facts (US)

• Approximately 40 000 Americans will be diagnosed with oral or pharyngeal cancer this year.
• It will cause over 8 000 deaths, killing roughly one person an hour, every 24 hours.
• Of those 40 000 newly diagnosed individuals, just over half (approximately 57%) will be alive in five years.
• If you include cancer of the larynx, for which the risk factors are the same, diagnosed cases grow to 54 000 with 13 500 deaths.
• Worldwide, there are 640 000 new cases of oral cancer each year.

Information obtained from the Oral Cancer Foundation**

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Prescription drug use during pregnancy is prevalent, however, not enough is known about the adverse effects they may have on the developing fetus, concludes a new review published in The Obstetrician & Gynaecologist.

The majority of women take prescriptions for pregnancy-related complaints and minor infections. However, a small proportion of women receive medication for treatment for chronic diseases such as asthma, depression or hypertension.

The prevalence of congenital malformations is estimated at 2% of all births, of which approximately 1% are considered attributable to prescription drug use during pregnancy, states the review.

Two common groups of drugs, anti-epileptics and antidepressants are explored in the review.

Anti-epileptic drugs (AEDs) are the most studied group of drugs in pregnancy, with an estimated 1 in 250 pregnancies exposed.

National Institute for Health and Clinical Excellence (NICE) guidelines state that it is not possible to comment on the risks of physical abnormalities from the drugs in view of the limited data available.

The review also looks at preliminary data collated from the UK Epilepsy and Pregnancy Register which found that the risk of congenital malformations with the use of one AED was 3.7% (n = 2598), compared with 6.0% (n = 770) in those women taking two or more AEDs.

Up to 4% of women use antidepressants during pregnancy, with 2.3% taking selective serotonin reuptake inhibitors (SSRIs).

A large birth defect registry study found no association between maternal SSRI use and cardiac malformations. However, the review states that antidepressant use in late pregnancy is associated with neonatal complications such as premature birth, feeding problems, respiratory distress syndrome, endocrine and metabolic disorders and temperature regulation disorders.

The review concludes that our evidence base for using prescription drugs in pregnancy remains limited and that drug companies do not recruit pregnant women to their clinical trials unless the drug in question is aimed at pregnancy-related disease.

Alastair Sutcliffe, Reader in Child Health, UCL Institute of Child Health and co-author of the review said:

“Many pregnant women use prescription drugs, however, the risk to the fetus remains unknown.

“Pregnant women are excluded from clinical trials, which means when new drugs are released there is almost no information on their safety and efficacy in pregnancy.”

TOG’s Editor-in-Chief, Jason Waugh said:

“The maternal physiological changes that occur during pregnancy can alter what the body does to the drug in some cases. More research is needed into the fetal effects of some drugs as there are big gaps in our knowledge.”

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Girls who start puberty very early are more likely to have psychological problems and be at risk of sexual abuse and early pregnancy, suggests a new review published in The Obstetrician & Gynaecologist (TOG).

Puberty is characterised by the maturation of the hypothalamic pituitary gonadal (HPG) axis, which plays a critical part in the development and regulation of the reproductive system.

Normal puberty commences from approximately 10 years onwards and breast development is usually the first sign of this. In Europe, the lower end of the normal range for the onset of puberty is 8 years in girls, although there are ethnic variations.

In girls, early puberty or precocious puberty is defined as the development of secondary sexual characteristics, such as the development of breasts or pubic hair before the age of 8 years. Most children with premature sexual development need referral to a paediatric endocrinologist for evaluation and management.

There are two main types of precocious puberty; the first is central precocious puberty (CPP) which results from premature activation of the HPG axis and in the majority of cases the cause is unknown. The other type is peripheral precocious puberty which results from production of sex hormones and can be caused by ovarian tumours or adrenal disorders.

Girls who start puberty early can be affected both physically and psychologically, says the review. In addition to the early physical signs of puberty, although the child may initially present with tall stature as the bones mature faster, growth may cease early and compromise final adult height.

Due to higher levels of sex steroids normally seen in older girls, psychological problems may arise resulting in adolescent behaviour. In addition, psychological problems can also arise if the child is expected to behave according to their physical maturity rather than their age. The review also states that girls are at increased risk of sexual abuse and early pregnancy.

The review also looks at the treatment for early puberty. Treatment will depend on the type of precocious puberty and the underlying cause, if known. The goal of treatment for precocious puberty is to stop, and possibly reverse the onset of puberty, improve final height and to avoid psychosocial /behavioural effects.

Most children with CPP can be treated effectively with Gonadotrophin-releasing hormone analogues (GnRHa), which control the release of the hormones responsible for the development of secondary sexual characteristics. Possible side effects include headaches, hot flushes, mood swings and rashes.

This treatment is normally stopped when it is time for normal puberty to begin. The decision to discontinue treatment should be taken jointly by the endocrinologist, the child and the parents, says the review.

The review concludes that the decision whether to provide treatment or not is a difficult one, in particular, for girls who commence puberty between 6 and 8 years old.

Sakunthala Sahithi Tirumuru, Specialist Registrar, Department of Obstetrics and Gynaecology, Alexandra Hospital, Redditch, and co-author of the review said:

“Starting puberty early can have a significant impact both psychologically and socially on both the child and her family. Puberty marks the start of a child’s sexual development and early onset could result in a higher risk of sexual abuse.

“This all needs to be considered by the healthcare team and further studies are needed to evaluate the effects of hormone treatment on quality of life and long term impact.”

TOG’s Editor-in-Chief, Jason Waugh said:

“Girls who start puberty earlier than their peers may experience difficulties and treatment may be required. However the long term effects of hormone treatment needs to be explored further.”

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Results from the largest genetic study of glaucoma, a leading cause of blindness and vision loss worldwide, showed that two genetic variations are associated with primary open angle glaucoma (POAG), a common form of the disease. The identification of genes responsible for this disease is the first step toward the development of gene-based disease detection and treatment.

About 2.2 million people in the U.S. have glaucoma. POAG is often associated with increased eye pressure but about one-third of patients have normal pressure glaucoma (NPG). Currently, no curative treatments exist for NPG.

Researchers including lead author Janey Wiggs, M.D., Ph.D., and Lou Pasquale, M.D. Co-Directors of the Glaucoma the Harvard Glaucoma Center of Excellence, analyzed DNA sequences of 6,633 participants, half of whom had POAG. Participants were part of two NIH-funded studies: GLAUGEN (Glaucoma Genes and Environment) and NEIGHBOR (NEI Glaucoma Human genetics collaBORation), conducted at 12 sites in the United States. Dr. Pasquale is also Director of the Glaucoma Service at Mass. Eye and Ear.

The results, reported online in PLoS Genetics, found that two variations were associated with POAG, including NPG. These are the first variants commonly associated with NPG. One variant is in a gene located on chromosome 9 called CDKN2BAS whereas the other variant is in a region of chromosome 8 where it may affect the expression of genes LRP12 or ZFPM2. These genes may interact with transforming growth factor beta (TGF-beta), a molecule that regulates cell growth and survival throughout the body. Previous studies have also implicated TGF-beta in glaucoma.

This study has provided important new insights into the disease pathogenesis and will make future studies focused on translating this information into the clinic possible. Ultimately we hope to prevent blindness caused by this very common eye disease,” said lead author Dr. Wiggs.

“This study has identified an important molecular pathway in the development of POAG. Control of TGF-beta might lead to more effective therapies for this blinding disease,” said Dr. Hemin Chin, associate director for Ophthalmic Genetics at the National Eye Institute.

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Scientists at The Scripps Research Institute have unraveled a complex chemical pathway that enables bacteria to form clusters called biofilms. Such improved understanding might eventually aid the development of new treatments targeting biofilms, which are involved in a wide variety of human infections and help bacteria resist antibiotics.

The report, published online ahead of print by the journal Molecular Cell, explains how nitric oxide, a signaling molecule involved in the immune system, leads to biofilm formation.

“It is estimated that about 80 percent of human pathogens form biofilms during some part of their life cycle,” said Scripps Research president and CEO Michael Marletta, PhD, who led the work. “In this study, we have detailed for the first time the signaling pathway from nitric oxide to the sensor through cellular regulators and on to the biological output, biofilm formation.”

“There’s a lot of interest right now in finding ways to influence biofilm formation in bacteria,” said lead author Lars Plate, a graduate student in Marletta’s team, which recently moved to Scripps Research from the University of California, Berkeley. “Figuring out the signaling pathway is a prerequisite for that.”

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If Pygmies are known for one trait, it is their short stature: Pygmy men stand just 4’11″ on average. But the reason why these groups are so short and neighboring groups are not remains unclear. Scientists have proposed various theories based on natural selection, including that Pygmies’ reduced size lowered nutritional requirements, helped them better handle hot climates, or allowed them to reach sexual maturity at an earlier age.

Now a new study of the Western African Pygmies in Cameroon, led by geneticists from the University of Pennsylvania, identifies genes that may be responsible for the Pygmies’ relatively small size.

The work also provides evidence based on genetic signatures of natural selection to suggest why these groups evolved to be small, with signs pointing to hormonal pathways and immune system regulation as possible drivers.

“There’s been a longstanding debate about why Pygmies are so short and whether it is an adaptation to living in a tropical environment,” said Sarah Tishkoff, senior author on the study and a Penn Integrates Knowledge professor with appointments in the genetics department of the Perelman School of Medicine and in the biology department of the School of Arts and Sciences. “I think our findings are telling us that the genetic basis of complex traits like height may be very different in globally diverse populations.”

While hundreds of studies have sought and identified genes that play a role in height variations in European populations – nearly 180 such genes have been pinpointed – this is the first genome-wide study of genes that contribute to stature in African Pygmy populations.

“By performing a detailed genetic analysis, Dr. Tishkoff and her colleagues have identified many candidate genes that have played an adaptive role in Pygmy populations, including several related to stature,” said Irene Eckstrand, who oversees evolutionary-biology grants at the National Institutes of Health’s National Institute of General Medical Sciences, which partially funded the work. “This research illustrates the value of studying human traits in their evolutionary and ecological contexts for understanding how humans adapted to their local environments.”

Tishkoff led the study with Joseph Jarvis, a Penn postdoctoral researcher at the time the study was conducted and now a senior research scientist at the Coriell Institute for Medical Research. Other Penn contributors included Laura Scheinfeldt, Sameer Soi, Charla Lambert, Bart Ferwerda and William Beggs of the Department of Genetics.

The Penn researchers collaborated with Larsson Omberg, Gabriel Hoffman and Jason Mezey of Cornell University; Alain Froment of the Musée de l’Homme in France; and Jean-Marie Bodo of the Ministère de la Recherche Scientifique et de l’Innovation in Cameroon.

Their paper was published in the journal PLoS Genetics.

Africa is the birthplace of humankind and remains a continent rife with examples of the variation within our species, including variation in body size, ranging from short-statured Pygmy hunter-gatherers to tall-statured East African pastoralists. Individuals in one of these unique groups, Western African Pygmies, are 17 centimeters shorter on average than their Bantu-speaking neighbors.

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Scientists at the Gladstone Institutes have unraveled a process by which depletion of a specific protein in the brain contributes to the memory problems associated with Alzheimer’s disease. These findings provide new insights into the disease’s development and may lead to new therapies that could benefit the millions of people worldwide suffering from Alzheimer’s and other devastating neurological disorders.

The study, led by Gladstone Investigator Jorge J. Palop, PhD, revealed that low levels of a protein, called Nav1.1, disrupt the electrical activity between brain cells. Such activity is crucial for healthy brain function and memory. Indeed, the researchers found that restoring Nav1.1 levels in mice that were genetically modified to mimic key aspects of Alzheimer’s disease (AD-mice) improved learning and memory functions and increased their lifespan. They report their findings in Cell, available online.

“It is estimated that more than 30 million people worldwide suffer from Alzheimer’s disease and that number is expected to rise dramatically in the near future,” said Lennart Mucke, MD, who directs neurological research at Gladstone, an independent and nonprofit biomedical-research organization. “This research improves our understanding of the biological processes that underlie cognitive dysfunction in this disease and could open the door for new therapeutic interventions.”

The researchers’ findings suggest that Nav1.1 levels in special regulatory nerve cells called parvalbumin cells, or PV cells, are essential to generate healthy brain-wave activity – and that problems in this process contribute to cognitive decline in AD-mice and possibly in patients with Alzheimer’s.

In the brain, neurons form highly interconnected networks, using chemical and electrical signals to communicate with each other. The researchers investigated whether this communication between neurons is disrupted in AD-mice, and if so, how this may affect the symptoms of Alzheimer’s disease.

To study this, they performed electroencephalogram (EEG) recordings – a technique that detects abnormalities in the brain’s electrical waves such as those found in patients with epilepsy. They found that similar abnormalities emerged during periods of reduced gamma-wave oscillations – a type of brain wave that is crucial to regulating learning and memory.

“Like a conductor in an orchestra, PV cells regulate brain rhythms by precisely controlling excitatory brain activity,” said Laure Verret, PhD, postdoctoral fellow and lead author. “We found that PV cells in patients with Alzheimer’s and in AD-mice have low levels of the protein Nav1.1 – likely contributing to PV cell dysfunction. As a consequence, AD-mice had abnormal brain rhythms. By restoring Nav1.1 levels, we were able to re-establish normal brain function.”

Indeed, the scientists found that increasing Nav1.1 levels in PV cells improves brain wave activity, learning, memory and survival rates in AD-mice.

“Enhancing Nav1.1 activity, and consequently improving PV cell function, may help in the treatment of Alzheimer’s disease and other neurological disorders associated with gamma-wave alterations and cognitive impairments such as epilepsy, autism and schizophrenia,” said Dr. Palop, who is also an assistant professor of neurology at the University of California, San Francisco, with which Gladstone is affiliated. “These findings may allow us to develop therapies to help patients with these devastating diseases.”

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A team of researchers has discovered a treatment for a common metabolic disorder. The study, published by Cell Press in the American Journal of Human Genetics, the official journal of the American Society of Human Genetics, reports that supplementation of nitric oxide (NO) in mice and man afflicted with argininosuccinic aciduria (ASA), a urea cycle disorder (UCD), results in long-term heart and neuropsychological improvements.

UCDs are genetic metabolic conditions resulting from a deficiency in any of the enzymes of the urea cycle, which takes place primarily in the liver and is responsible for removing ammonia (a toxic nitrogen compound) from the blood stream. When this cycle cannot proceed normally, ammonia accumulates in the blood and damages the liver and nervous system. ASA is the second-most-common UCD and is caused by a deficiency in arginosuccinate lysase (ASL), the only mammalian enzyme able to generate arginine, a precursor for the synthesis of many metabolites, including nitric oxide (NO). People with ASA often have a complex clinical phenotype even in the absence of ammonia accumulation. “Thus, we hypothesized that some of the long-term complications of ASA may result from NO deficiency rather than from ammonia accumulation,” explained Dr. Lee, a leading author of this study.

By developing a mouse model of ASA, Lee, Erez, and their team were able to test this hypothesis. Using cutting-edge gene therapy technology, they corrected the urea-cycle defect in the liver and normalized growth and survival of the mice. However, the GT-treated ASA mice remained hypertensive because they required ASL for NO production in the vasculature. Supplementation of NO treated these other disease symptoms in the mice. “Importantly, we show the translatability of our findings to humans, as we show that treatment with an NO source led to sustained normalization of blood pressure in an ASA subject,” said Dr. Lee. “Our data show that ASA is a human genetic model of NO deficiency and that NO supplementation in ASA subjects should be further investigated,” he said.

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