Researchers have discovered gene-targets (biomarkers) that may enable alternative treatments or the potential design of new drugs that target metastasis-promoting tumor genes.
This is the key finding in a study led by researchers from Georgia State University in collaboration with the University of Oklahoma College of Medicine and published in journal Oncotarget.
The spread of cancer cells from the initial site of occurrence (primary site) to other secondary tissues is called metastasis, and contributes to poor or limited response of cancer cells to treatments, which results in death. For example, cancer cells initially in the lungs can begin to spread to other organs, including the brain and liver.
While the rapid emergence of antibiotic-resistant bacteria has prompted the medical community, non-profit organizations, public health officials and the national media to educate the public to the dangers of misusing and overusing antibiotics, the University of Georgia’s J. Vaun McArthur is concerned that there’s more to the problem than the misuse of common medications.
McArthur, a senior research ecologist with the Savannah River Ecology Laboratory and Odum School of Ecology, believes environmental contaminants may be partly to blame for the rise in bacterial resistance, and he tested this hypothesis in streams on the U.S. Department of Energy’s Savannah River Site.
The 310-square mile site near Aiken, South Carolina, east of the Savannah River, was closed to the public in the early 1950s to produce materials used in nuclear weapons. This production led to legacy waste, or contamination, in limited areas of the site. This waste impacted some of the streams in the industrial areas.
Researchers at Spectrum Health Helen DeVos Children’s Hospital have completed the first clinical trial of a new treatment for children suffering from neuroblastoma. In a clinical trial led by Giselle Sholler, MD, pediatric oncologist at Helen DeVos Children’s Hospital and the Neuroblastoma and Medulloblastoma Translational Research Consortium (NMTRC), DFMO, an investigational agent, showed minimal side effects with long-term survival of three patients. This is the first clinical study of an oral dosing form of DFMO in any pediatric population.
“This DFMO trial is an important advancement in neuroblastoma research,” explained Dr. Sholler. “We believe that by using DFMO to target an important cancer stem cell pathway to ‘turn cells off,’ we may prevent children from relapsing. Cancer cells have pathways that drive the cancer to grow and DFMO targets a specific pathway to turn these cells off.”
Dr. Sholler recently published her laboratory studies describing how this drug works in neuroblastoma in preventing tumor formation in lab models and also published the full results of the phase one trial.
Results revealed today at The International Liver Congress™ 2015, show that in patients with alcohol-induced liver disease (ALD), Baclofen has a positive impact on alcohol consumption and overall measures of liver function and harm.
ALD is a major cause of alcohol-related mortality and helping patients with ALD to stop drinking is a primary goal of treatment. The primary aim of this study was to measure the effectiveness and tolerability of Baclofen in maintaining abstinence in this difficult to treat group, and to determine if this resulted in a reduction in standard measures of liver damage.
The results show promising outcomes for these patients, helping them to reduce their alcohol consumption as well as improving overall indicators of liver function and lowering physical dependence. A randomised controlled trial is now needed to confirm the benefit of Baclofen in this patient group.
About The International Liver Congress
This annual congress is the biggest event in the EASL calendar, attracting scientific and medical experts from around the world to learn about the latest in liver research.
Like a colony of bacteria or species of animals, cancer cells within a tumor must evolve to survive. A dose of chemotherapy may kill hundreds of thousands of cancer cells, for example, but a single cell with a unique mutation can survive and quickly generate a new batch of drug-resistant cells, making cancer hard to combat.
Now, scientists at the Salk Institute have uncovered details about how cancer is able to become drug resistant over time, a phenomenon that occurs because cancer cells within the same tumor aren’t identical- the cells have slight genetic variation, or diversity. The new work, published October 20 in PNAS, shows how variations in breast cancer cells’ RNA, the molecule that decodes genes and produces proteins, helps the cancer to evolve more quickly than previously thought. These new findings may potentially point to a “switch” to turn off this diversity- and thereby drug resistance- in cancer cells.
“It’s an inherent property of nature that in a community- whether it is people, bacteria or cells- a small number of members will likely survive different types of unanticipated environmental stress by maintaining diversity among its members,” says the senior author of the new work, Beverly Emerson, professor of Salk’s Regulatory Biology Laboratory and holder of the Edwin K. Hunter Chair. “Cancer co-ops this diversification strategy to foster drug resistance.”
Instead of looking at a single gene or pathway to target with cancer therapies, lead author Fernando Lopez-Diaz, Salk staff scientist, and the team aim to uncover the diversification “switch” by which cancer cells replicate but vary slightly from one another. Turning off this cellular process would strip cancer’s ability to survive drug treatment.
People in the late stages of cancer and other terminal illnesses are not only unharmed by discontinuing statins for cholesterol management, they may benefit, according to a study presented Friday by researchers at Duke Medicine representing a national research network.
The finding addresses a thorny question in treating people with life-limiting illnesses: When, if ever, is it appropriate to discontinue medications prescribed for other conditions that will likely not lead to their death?
In an analysis presented at the American Society of Clinical Oncology annual meeting in Chicago, the researchers reported that discontinuing statins in patients with advanced illnesses resulted in improved overall quality of life, lower costs and no increased deaths. In fact, the patients who stopped taking statins appeared to live slightly longer.
“When you look at the number of medications people take when they are dying, it doubles in the last year of life,” said lead author Amy Abernethy, M.D., Ph.D., director of the Center for Learning Health Care at the Duke Clinical Research Institute and a member of the Duke Cancer Institute. Abernethy represented the Palliative Care Research Cooperative Group, a national research network focused on improving care for people with serious illnesses.
People who take the common cholesterol-lowering drugs known as statins may feel a false sense of security and eat a bit more, according to a new study.
Researchers found that U.S. adults taking statins in 1999-2000 were eating fewer calories than people not taking the drugs, but statin users were eating about the same amount as non-users by 2009-2010.
“We believe that physicians need to reemphasize the importance of a healthy lifestyle to statin-users,” Dr. Takehiro Sugiyama told Reuters Health in an email.
He is the study’s lead author from the University of Tokyo in Japan.
Pfizer Inc’s Xalkori delayed progression of lung cancer longer than chemotherapy in patients who had never previously been treated for the disease, according to results of a late-stage study released on Tuesday.
The medicine, which received U.S. approval in 2011 for lung cancer patients who have a specific gene mutation, had shown in a previous Phase III trial that it significantly delayed disease progression among those who have already undergone chemotherapy for non-small-cell lung cancer, the most common form of the illness.
Pfizer said favorable results from the latest trial, combined with those from the earlier big study, establish that Xalkori is appropriate for first-line as well as second-line use, meaning for patients receiving initial treatment as well as for those who have already undergone chemotherapy.
Massachusetts General Hospital (MGH) investigators may have found a way to solve a problem that has plagued a group of drugs called ligand-mimicking integrin inhibitors, which have the potential to treat conditions ranging from heart attacks to cancer metastasis. In a Nature Structural & Molecular Biology paper receiving advance online publication, the researchers provide a structural basis for the design of new and safer integrin inhibitors.
Integrins are receptor proteins found on the surface of cells that determine whether or not cells adhere to adjacent cells and the surrounding extracellular matrix. Under normal circumstances, integrins only become activated - which allows them to bind to other cells or extracellular molecules - in response to specific signals from within the cell. If integrins become overactive, cells become too “sticky” - leading to clogged arteries, pathological inflammation, the excess tissue growth called fibrosis or the spread of cancer. Current drugs developed to inhibit integrin activation by mimicking the shape of ligands - the molecules that interact with receptors - have had unintended effects in some patients, and as a result only a handful have received FDA approval.
“Integrins have an intrinsic ability to shape-shift when they switch from an inactive to an active, adhesive state,” explains M. Amin Arnaout, MD, director of the MGH Leukocyte Biology Program and the Inflammation and Structural Biology Program, senior author of the study. “Unfortunately, under some circumstances the integrin inhibitors that have been developed to date can inadventently induce this shape shifting, and use of these drugs have produced serious, sometimes fatal side effects such as excessive bleeding.”
The Bill & Melinda Gates Foundation has awarded $23 million for research being led by University of Notre Dame biologists to prevent malaria and dengue fever, the school said.
The five-year project by biologists Neil Lobo and Nicole Achee aims to show the effectiveness of a new method of mosquito control, called spatial repellency, in quelling the illnesses, the university said in a statement this week.
According to the World Health Organization, 207 million cases of malaria were reported in 2012, and 50 million to 100 million dengue infections occur yearly.
Both the malaria parasite and dengue virus are transmitted through the bites of infected mosquitoes. Spatial repellents, such as coils or candles, release a material that drives mosquitoes away from enclosed areas.
New research shows that low doses of a cancer drug protect against the development of type 1 diabetes in mice. At the same time, the medicine protects the insulin-producing cells from being destroyed. The study is headed by researchers from the Faculty of Health and Medical Sciences at the University of Copenhagen, and has just been published in the distinguished scientific journal Proceedings of the National Academy of Sciences of the United States of America (PNAS).
Very low doses of a drug used to treat certain types of cancer protect the insulin-producing cells in the pancreas and prevent the development of diabetes mellitus type 1 in mice. The medicine works by lowering the level of so-called sterile inflammation. The findings have been made by researchers from the University of Copenhagen, the Technical University of Denmark and the University of Southern Denmark working with researchers in Belgium, Italy, Canada, Netherlands and the USA.
“Diabetes is a growing problem worldwide. Our research shows that very low doses of anticancer drugs used to treat lymphoma - so-called lysine deacetylase inhibitors - can reset the immune response to not attack the insulin-producing cells. We find fewer immune cells in the pancreas, and more insulin is produced when we give the medicine in the drinking water to mice that would otherwise develop type 1 diabetes,” says postdoc Dan Ploug Christensen, who is the first author on the article and responsible for the part of the experimental work carried out in Professor Thomas Mandrup-Poulsen’s laboratory at the Department of Biomedical Sciences, University of Copenhagen.
Scientists have taken an important step towards new malaria treatments by identifying a way to stop malaria parasites from multiplying.
In a study published in Nature Chemistry, they show that blocking the activity of an enzyme called NMT in the most common malaria parasite prevents mice from showing symptoms and extends their lifespan. The team are working to design molecules that target NMT more potently, and hope to start clinical trials of potential treatments within four years.
A recent study estimated that 1.2 million people died from malaria in 2010. Although a variety of antimalarial drugs are available, some strains of the parasite are resistant to treatment. These strains are becoming more common, with treatment failures reported across multiple frontline drugs. If acute illness is cured, the parasite can remain dormant in the blood and return to cause illness later. Malaria vaccines have been researched intensively, but none have been introduced into clinical practice.
The new study shows that NMT is involved in a wide range of essential processes in the parasite cell, including the production of proteins that enable malaria to be transmitted between humans and mosquitoes, and proteins that enable malaria to cause long-term infection.
The United States Centers for Disease Control and Prevention (CDC) was informed by Merck on Monday that the pharmaceutical company planned to recall one lot of Gardasil [Human Papillomavirus Quadrivalent (types 6, 11, 16, and 18) Vaccine, Recombinant].
The CDC media statement released yesterday states that the recall is because a number of vials may contain glass particles as a result of breakage during the vaccine manufacturing process.
GlaxoSmithKline Plc will stop paying doctors to promote its products, Chief Executive Andrew Witty said in an interview with the New York Times, in a move that could be a first for a major drug company.
GSK will also stop tying compensation of sales representatives to the number of prescriptions doctors write, the NY Times said. (link.reuters.com/kac55v)
The company’s decision comes at a time when GSK faces allegations of illegal payments to Chinese doctors and officials.
Chinese police have accused GSK of funneling up to 3 billion yuan ($494 million) to travel agencies to facilitate bribes to boost its drug sales. The accusations are the most serious against a multinational in China in years.
The FDA today approved Onglyza, a once-daily treatment for type 2 diabetes to be taken in combination with diet and exercise.
Onglyza, made by Bristol-Myers Squibb and distributed by Bristol-Myers Squibb and AstraZeneca Pharmaceuticals, was tested in diabetes patients at relatively low risk of heart disease. The FDA approval requires Bristol-Myers Squibb to conduct a postmarketing study to evaluate the drug’s heart safety in higher-risk patients.
Onglyza carries the generic name saxagliptin. It belongs to a class of type 2 diabetes drugs called DPP-4 inhibitors. The first drug in this class, Merck’s Januvia, was approved in 2006. Like Onglyza, Januvia is taken once daily and is to be used in combination with diet and exercise.
Another DPP-4 inhibitor, Takeda’s alogliptin, was rejected by the FDA last month. The U.S. regulatory agency said the company has to provide more data on heart risks before it can be approved. Takeda has said these additional studies will take two years.