07.02.2015

Breast cancer feature article rubric

Researchers are gaining insight into the causes of a devastating form of muscle wasting that is often the final stage of cancer and other diseases.
As a palliative-care researcher, Susan McClement has talked to many people dying of cancer and their families a€” and some of their stories are burned into her brain. You may need a more recent browser or to install the latest version of the Adobe Flash Plugin. The woman in this case had cachexia, a metabolic disorder that affects some 9A million people worldwide, including as many as 80% of people with advanced cancer. It is now clear that a key mechanism underlying cachexia is the increased breakdown of muscle protein, along with dampened protein synthesis, which leads to overall muscle loss. For the best commenting experience, please login or register as a user and agree to our Community Guidelines. It is well established that muscle wasting in cachexia is driven by metabolic imbalance and inflammation. The Cybathlon aims to help disabled people navigate the most difficult course of all: the everyday world. Presidential candidates begin to make clear their stark differences on climate change, energy production and stem-cell research. This week, parenting tips from science, quenching a question about thirst, and a programmable quantum computer. The Conservative Cabinet minister said: "This is a long-overdue decision and marks a small but significant step towards improving media portrayal of women and girls.
One man was so concerned by the sight of his emaciated wife, whose body had been ravaged by metastatic breast cancer, that he resorted to force feeding her a€” pinching her nose and slipping in a spoonful of food when she opened her mouth.
It typically involves extreme weight- and muscle-loss, makes routine activities difficult and increases the risk of deadly complications such as infections. Studies in 2001 helped to jump-start the field when they identified genes that were more active in atrophying rodent muscles than in normal ones1, 2. You will be re-directed back to this page where you will see comments updating in real-time and have the ability to recommend comments to other users. But surely this and other examples, rather than suggesting nutritional intervention is inappropriate, suggest that a much more highly targeted approach needs to be envisaged? Convinced that food would give her the energy to fight the cancer, his daily visits became protracted battles.
Adding calories doesna€™t reverse cachexia, and McClement says that the disorder sometimes provokes extreme reactions from family members because it serves as visual confirmation of their worst fears.


These genes encode enzymes called E3 ubiquitin ligases, which tag proteins for destruction in the cell. She was the senior editor of Nature Network before becoming the editor of Nature's Research Highlights section. During cancer cachexia, optimising the amounts for an individual is likely to be especially important. She died a few weeks later.McClement, who works at the University of Manitoba in Winnipeg, Canada, says that nutritional conflicts can become a source of regret for relatives.
Mice without these enzymes were resistant to muscle loss.Muscle cells seem to make more of these ligases when hit with certain inflammatory signals from tumours or from immune cells responding to cancer or other illness. We would suggest that there could be significant impacts of re-channelling research money towards optimising and personalising nutrient intake during cachexia, instead of or in association with a primary focus on new drug design. But for many years it was overlooked, as physicians and researchers focused their attention on the primary illness instead.Now, scientists are increasingly viewing cachexia as a distinct, treatable condition. Abnormalities in apoptosis (programmed cell death) and in the muscle cella€™s energy-producing organelles, mitochondria, have also been implicated.Several drug-makers have homed in on the protein myostatin, which blocks muscle growth.
Basic research has revealed how it is driven by inflammation and metabolic imbalances, and has generated drug targets, says Stefan Anker, a cardiologist and cachexia specialist at the University Medical Center GA¶ttingen in Germany. In a 2010 paper3 that got many people excited about a possible cachexia drug, researchers from biotechnology company Amgen in Thousand Oaks, California, showed that they could reverse muscle loss and extend the lives of mice with tumours and cachexia by blocking signalling through the myostatin pathway.Research since then suggests that cachexia is more than a muscle disease. Studies4 have identified problems in the braina€™s regulation of appetite and feeding, and even ways in which the liver might be contributing to the energy imbalance that sees the body burn its own tissue to sustain itself. This has spurred investment from drug developers who aim to reduce suffering, and possibly give patients the strength to withstand chemotherapy or surgery.But some high-profile clinical trials in the past two years have produced disappointing results, prompting much self-reflection in the young field.
They showed that inflammation5 and molecules made by tumours6 cause white fat cells to turn into brown fat cells, which burn more energy to generate heat than white fat cells.
The question that researchers are now tackling is how tissues and organs a€” muscle, brain, fat, even bone a€” are communicating with one another. It is thought that Hippocrates recognized the syndrome a€” but it took until 2006 for the cachexia field to start working up a formal definition, which includes a loss of 5% or more of body weight over 12 months, and reduced muscle strength. A paper published last week7 suggests that fat signalling could be involved in muscle atrophy.All this research has brought more representatives of biotechnology and pharmaceutical companies to cachexia meetings in recent years, says Denis Guttridge, a cell biologist at the Ohio State University in Columbus, who organizes one such conference. In the clinic, it remains under-recognized by oncologists, says Egidio Del Fabbro, a palliative-care physician and researcher at Virginia Commonwealth University in Richmond. There are no standard guidelines for treatment.In the past decade, researchers have made strides in learning about the causes of cachexia, thanks to funding from the US National Cancer Institute and some advocacy groups.


New international conferences (including one that wrapped up this week in Paris) and the launch of a research journal a€” the Journal of Cachexia, Sarcopenia and Muscle a€” have also drummed up interest in the field. In 2011, biotech firm GTx of Memphis, Tennessee, launched two late-stage clinical trials of enobosarm, a molecule that binds to the same receptor as testosterone but only in muscle and bone, mimicking the hormonea€™s ability to stimulate muscle build-up but without its undesirable side effects.
Results from earlier, smaller trials looked promising: people taking the drug had increased lean body mass and improved physical function, as measured by their speed at climbing stairs8. But in the larger tests of the drug, on people with advanced lung cancer, the benefits in function disappeared. The firm has since abandoned muscle wasting, and is instead testing larger doses of enobosarm to treat breast cancer.A pair of unpublished studies on people with lung cancer and cachexia tested a compound called anamorelin, which mimics ghrelin, an appetite-stimulating peptide hormone produced mainly by the stomach.
The trials were sponsored by pharmaceutical company Helsinn in Lugano, Switzerland, which reported that participants in the treatment group put on weight and muscle mass compared with those taking a placebo, but showed no difference in hand grip strength.
Still, the company announced last week that the European Medicines Agency is reviewing its drug for approval.There is a lot of debate about why the trials failed to show functional improvements.
Some researchers say that the teams did not use the most clinically relevant measures of muscle function.
Some work has tried to make a case that the mechanisms found in rodents might be similar to those in humans, by looking at human tissue samples, says Vickie Baracos, a clinical translational researcher in muscle wasting at the University of Alberta in Edmonton, Canada. Baracos says that studies are needed that follow people with cachexia over time, collecting blood and muscle samples along the way.
GTx stopped its work on muscle wasting in part because insurers did not seem interested in covering a medication that was only going to target cachexia and not cancer, says Mary Ann Johnston, the companya€™s vice-president for clinical development. It might spur physicians to talk more to patients and their families about the troubling symptoms of cachexia. And that vacuum of information can be distressing.McClement, for her part, has been interviewing more families of people with cachexia. Given the absence of pharmacological interventions, such psychosocial ones are important, she says.



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