People who work around the clock could actually be setting themselves back, according to Virginia Tech biologists.
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Thursday, January 08, 2015
Link between cancer and sleep cycle
People who work around the clock could actually be setting themselves back, according to Virginia Tech biologists.
Tuesday, August 12, 2014
No link between sleep apnea and cancer
Sunday, April 06, 2014
Study: Seizure medication may reduce risk for some cancers
Friday, March 28, 2014
Sleep necessary for mental health and well-being
Wednesday, January 22, 2014
Insufficient sleep epidemic
Saturday, September 21, 2013
Sleep apnea can worsen skin cancer outcomes
Saturday, August 10, 2013
People with epilepsy at elevated risk for some cancers
Sunday, May 12, 2013
Obstructive Sleep Apnea and Cancer
Wednesday, January 23, 2013
Study: Internal Clocks Can Be Modified for Treatment of Disorders
UC Irvine-led studies have revealed the cellular mechanism by which circadian rhythms -- also known as the body clock -- modify energy metabolism and also have identified novel compounds that control this action. The findings point to potential treatments for disorders triggered by circadian rhythm dysfunction, ranging from insomnia and obesity to diabetes and cancer.
Friday, May 25, 2012
Study: Sleep apnea associated with higher mortality from cancer
Sleep-disordered breathing (SDB) is associated with an increased risk of cardiovascular, metabolic and neurocognitive disorders.
New studies show that it also implies a greater risk of developing tumors, and even dying from cancer. Experimental animal studies led by researchers from the August Pi i Sunyer Biomedical Research Institute (IDIBAPS), the University of Barcelona and the Hospital ClÃnic of Barcelona have shown that repeated episodes of hypoxia (an inadequate supply of oxygen that characterizes sleep apnea) are linked to accelerated cancer progression. New experimental results are the first to suggest that sleep apnea may be associated with increased cancer mortality in humans.
Animal experiments that gave rise to this hypothesis were led by professor at the UB Ramon Farré and his team of Respiratory Biophysics and Bioengineering from the Department of Physiological Sciences I of the Faculty of Medicine of the UB and of the IDIBAPS. Now, a collaboration with the team of Dr. F. Javier Nieto, from the Department of Population Health Sciences of the School of Medicine and Public Health at the University of Wisconsin (USA), has demonstrated in a large cohort of patients that sleep apena increases the risk of cancer mortality. Dr. Ramon Farré collaborates on a regular basis with Dr. Josep Maria Montserrat, from the Pulmonology Service at the Hospital ClÃnic of Barcelona, member of the IDIBAPS and lecturer at the Department of Medicine of the UB. Experimental studies in a cohort of Spanish patients suffering from apnea, funded by the Spanish Society of Pulmonology and Thoracic Surgery (SEPAR), have demonstrated that the risk of cancer may increase in patients with sleep apnea. This research has been supported by CIBERES, a multidisciplinary research network in respiratory diseases.
In vitro and animal studies show that intermittent hypoxia promotes angiogenesis and tumor growth. Therefore, researchers have examined 22-year mortality data on 1,522 subjects from the Wisconsin sleep cohort. This prospective study has analyzed predictors and natural history of sleep disorders using techniques of polysomnography. The results of the study, whose main authors are doctors Javier Nieto and Ramon Farré, were presented on Sunday 20 May during the International Conference of the American Thoracic Society (ATS 2012) in San Francisco. They have also been published in the journal The American Journal of Respiratory and Critical Care Medicine (AJRCCM).
In this large cohort, the risk of all-cause mortality and of cancer mortality was adjusted for age, sex, body mass index, smoking, and other factors. Compared to subjects without sleep apnea, the relative hazards of cancer mortality were 1.1 for mild SDB; 2.0 for moderate SDB, and 4.8 for severe SDB. This means that, in case of developing cancer, the fact of having severe sleep apnea may accelerate cancer progression. However, further studies should be carried out to demonstrate whether patients suffering from aggressive cancer could benefit from early diagnosis and treatment of sleep-disordered breathing.
On the other hand, the cohort analyzed as part of SEPAR’s sleep study group gathers data on 5,246 patients who were diagnosed with sleep apnea in seven Spanish hospitals between 2000 and 2007. This study, carried out by Dr. Francisco Campos from the Valme Hospital (Sevilla) and co-ordinated by Dr. Josep Maria Montserrat, has shown that 5.7 % of patients with sleep-disordered breathing were diagnosed with cancer during the follow-up period, and that patients with the most severe apnea proportionally increased the risk of suffering from one. In an independent study also presented at the ATS 2012 conference, the group from the IDIBAPS-UB-ClÃnic put forward new data obtained from mice. This work shows that the effect of intermittent hypoxia on cancer growth is considerably stronger in lean mice than in obese mice.
Therefore, it is necessary to confirm with further studies the relationship between sleep-disordered breathing and cancer mortality. If these hypotheses are validated, further studies will have to analyse whether the diagnosis and treatment of SDB in patients with aggressive cancer might be indicated to prolong survival. Researchers from the IDIBAPS-UB-ClÃnic will continue working, together with renown collaborators such as those from the University of Wisconsin and the Spanish experts from SEPAR and CIBERES, to deepen knowledge about the relationship between sleep-disordered breathing, obesity and cancer mortality.
Read more here: http://www.healthcanal.com/cancers/29505-Sleep-apnea-associated-with-higher-risk-mortality-from-cancer.html
Monday, May 21, 2012
Study Claims Sleep Apnea Linked to Cancer
Two new studies have found that people with sleep apnea, a common disorder that causes snoring, fatigue and dangerous pauses in breathing at night, have a higher risk of cancer. The new research marks the first time that sleep apnea has been linked to cancer in humans.
About 28 million Americans have some form of sleep apnea, though many cases go undiagnosed. For sleep doctors, the condition is a top concern because it deprives the body of oxygen at night and often coincides with cardiovascular disease, obesity and diabetes.
“This is really big news,” said Dr. Joseph Golish, a professor of sleep medicine with the MetroHealth System in Cleveland who was not involved in the research. “It’s the first time this has been shown, and it looks like a very solid association,” he said.
Dr. Golish, the former chief of sleep medicine at the Cleveland Clinic, said that the cancer link may not prove to be as strong as the well-documented relationship between sleep apnea and cardiovascular disease, “but until disproven, it would be one more reason to get your apnea treated or to get it diagnosed if you think you might have it.”
In one of the new studies, researchers in Spain followed thousands of patients at sleep clinics and found that those with the most severe forms of sleep apnea had a 65 percent greater risk of developing cancer of any kind. The second study, of about 1,500 government workers in Wisconsin, showed that those with the most breathing abnormalities at night had five times the rate of dying from cancer as people without the sleep disorder. Both research teams only looked at cancer diagnoses and outcomes in general, without focusing on any specific type of cancer.
In both studies, being presented in San Francisco this week at an international conference organized by the American Thoracic Society, the researchers ruled out the possibility that the usual risk factors for cancer, like age, smoking, alcohol use, physical activity and weight, could have played a role. The association between cancer and disordered breathing at night remained even after they adjusted these and other variables.
Dr. Mitesh Borad, a cancer researcher and assistant professor of medicine at the Mayo Clinic who was not involved with the studies, called the findings “provocative” but said more research was needed to confirm the association. The studies were observational, and other, unknown factors may account for the correlation between sleep apnea and cancer.
Recent animal studies have suggested that sleep apnea might play a role in cancer. When mice with tumors were placed in low-oxygen environments that simulate the effects of sleep apnea, their cancers progressed more rapidly. Scientist speculate that depriving mice of oxygen may cause their bodies to develop more blood vessels to compensate, an effect that could act as a kind of fertilizer for cancer tissue and cause tumors to grow and spread more quickly.
The researchers wondered whether a similar relationship might exist in people with sleep apnea, in whom throat muscles collapse during sleep, choking off the airway and causing gasping and snoring as the body fights for air. Severe sleep apnea can produce hundreds of such episodes each night, depleting the body of oxygen.
In one study, a team at the University of Wisconsin School of Medicine and Public Health examined data on state workers taking part in the long-running Wisconsin Sleep Cohort, who since 1989 have undergone extensive overnight sleep studies and other measures of health about every four years. The landmark project was one of the first to reveal the widespread occurrence of sleep apnea in the general population.
The researchers found that the more severe a person’s breathing problems at night, the greater the likelihood of dying from cancer. People with moderate apnea were found to die of cancer at a rate double that of people without disordered breathing at night, while those in the severe category died at a rate 4.8 times that of those without the sleep disorder.
“That is really striking,” said Dr. F. Javier Nieto, one of the study’s authors and chairman of the department of population health sciences at the University of Wisconsin. “It could be something else, but it’s hard to imagine that something we didn’t control for is causing this.”
In the second study, researchers with the Spanish Sleep Network took a slightly different approach, looking not at cancer mortality among apnea patients, but at the incidence of cancer. They used a measure called the hypoxemia index, which looks at the amount of time the level of oxygen in a person’s blood drops below 90 percent at night.
About 5,200 people were followed for seven years, none of whom had a cancer diagnosis when the study began. The researchers found that the greater the extent of hypoxemia, or oxygen depletion, during sleep, the more likely a person would receive a cancer diagnosis during the study period.
People whose oxygen levels dropped below 90 percent for up to 12 percent of the total time they were asleep, for example, had a 68 percent greater likelihood of developing cancer than people whose oxygen levels did not plummet at night, said study author Dr. Miguel Angel Martinez-Garcia of La Fe University and Polytechnic Hospital in Spain. As time spent without oxygen increased, so, too, did cancer risk.
Although the study did not look for it, Dr. Martinez-Garcia speculated that treatments for sleep apnea like continuous positive airway pressure, or CPAP, which keeps the airways open at night, might reduce the association.
The Wisconsin study also did not specifically look at the impact of treatment for apnea on survival, either, but when people who were being treated with CPAP were removed from the analysis, the cancer association became stronger, “which is consistent with the hypoxemia theory,” Dr. Nieto said.
“I would say that this is one more instance that shows that sleep apnea can have profound impacts for people’s health,” he added. “Not breathing while you’re sleeping is a serious problem.”
Read more here
Friday, February 03, 2012
Genetic Breakthrough for Brain Cancer in Children
An international research team led by the Research Institute of the McGill University Health Centre (RI MUHC) has made a major genetic breakthrough that could change the way pediatric cancers are treated in the future. The researchers identified two genetic mutations responsible for up to 40 per cent of glioblastomas in children -- a fatal cancer of the brain that is unresponsive to chemo and radiotherapy treatment. The mutations were found to be involved in DNA regulation, which could explain the resistance to traditional treatments, and may have significant implications on the treatment of other cancers.
Using the knowledge and advanced technology of the team from the McGill University and Génome Québec Innovation Centre, the researchers identified two mutations in an important gene known as the histone H3.3. This gene, one of the guardians of our genetic heritage, is key in modulating the expression of our genes. "These mutations prevent the cells from differentiating normally and help protect the genetic information of the tumor, making it less sensitive to radiotherapy and chemotherapy," says Dr. Nada Jabado, hematologist-oncologist at The Montreal Children's Hospital of the McGill University Health Centre (MUHC) and principal investigator of the study.
"This research helps explain the ineffectiveness of conventional treatments against cancer in children and adolescents -- we've been failing to hit the right spot," says Dr. Jabado, who is also an Associate Professor of Pediatrics at McGill University. "It is clear now that glioblastoma in children is due to different molecular mechanisms than those in adults, and should not be treated in the same way. Importantly, we now know where to start focusing our efforts and treatments instead of working in the dark."
Inappropriate regulation of this gene has been observed in other cancers such as colon, pancreatic, lymphoma, leukemia and pancreatic neuroendocrine cancer, and future research could therefore reveal improved treatments for these diseases. "What is significant here is that for the first time in humans we have identified a mutation in one of the most important genes that regulates and protects our genetic information. This is the irrefutable proof that our genome, if modified, can lead to cancer and probably other diseases. What genomics has shown us today is only the beginning," says Dr. Jabado.
"Génome Québec is proud to have contributed to a project whose results will make a significant impact on the treatment of pediatric glioblastoma," underlines Marc Le Page, President and CEO of Génome Québec. "The outstanding contribution of experts in genomics and new sequencing technologies, made by the McGill University and Génome Québec Innovation Centre and as part of Dr. Jabado's project, is further proof that genomics has become essential for development and innovation in medical research. I wish to acknowledge the excellence of the teams involved in this study and the model of interdisciplinary collaboration that was implemented."
"Personalized medicine has amazing potential for many areas of health care, including infection, rare diseases and cancer. Researchers, like this team, play a vital role in translating discoveries into improved patient care," says Dr. Morag Park, Scientific Director of the CIHR Institute of Cancer Research. "Through research advancements like this, there is now greater emphasis on using genetic information to make medical decisions. We congratulate Dr. Jabado and her team on these results."
Brain tumours are the primary cause of death for children with cancer in Europe and North America. The diagnosis of glioblastoma in a child or adolescent remains a death sentence and about 200 children in Canada die every year of this cancer. Most children will die within the two years of their diagnosis regardless of treatment.
This work was supported by the Cole Foundation, and was funded in part by Genome Canada and the Canadian Institute for Health Research (CIHR) with co-funding from Genome BC, Génome Québec, CIHR-ICR (Institute for Cancer Research) and C17, through the Genome Canada/CIHR joint ATID Competition (project title: The Canadian Paediatric Cancer Genome Consortium: Translating next generation sequencing technologies into improved therapies for high-risk childhood cancer.
Read more: http://www.sciencedaily.com/releases/2012/01/120130102522
Sunday, January 29, 2012
Cancer Sequencing Initiative Discovers Mutations Tied to Aggressive Childhood Brain Tumors
St. Jude Children's Research Hospital - Washington University Pediatric Cancer Genome Project provides first evidence linking cancer to mutations in genes involved in DNA organization
Researchers studying a rare, lethal childhood tumor of the brainstem discovered that nearly 80 percent of the tumors have mutations in genes not previously tied to cancer. Early evidence suggests the alterations play a unique role in other aggressive pediatric brain tumors as well.
The findings from the St. Jude Children's Research Hospital - Washington University Pediatric Cancer Genome Project (PCGP) offer important insight into a poorly understood tumor that kills more than 90 percent of patients within two years. The tumor, diffuse intrinsic pontine glioma (DIPG), is found almost exclusively in children and accounts for 10 to 15 percent of pediatric tumors of the brain and central nervous system.
"We are hopeful that identifying these mutations will lead us to new selective therapeutic targets, which are particularly important since this tumor cannot be treated surgically and still lacks effective therapies," said Suzanne Baker, Ph.D., co-leader of the St. Jude Neurobiology and Brain Tumor Program and a member of the St. Jude Department of Developmental Neurobiology. She is a corresponding author of the study published in the January 29 online edition of the scientific journal Nature Genetics.
DIPG is an extremely invasive tumor that occurs in the brainstem, which is at the base of the skull and controls such vital functions as breathing and heart rate. DIPG cannot be cured by surgery and is accurately diagnosed by non-invasive imaging. As a result, DIPG is rarely biopsied in the U.S. and little is known about it.
Cancer occurs when normal gene activity is disrupted, allowing for the unchecked cell growth and spread that makes cancer so lethal. In this study, investigators found 78 percent of the DIPG tumors had alterations in one of two genes that carry instructions for making proteins that play similar roles in packaging DNA inside cells. Both belong to the histone H3 family of proteins. DNA must be wrapped around histones so that it is compact enough to fit into the nucleus. The packaging of DNA by histones influences which genes are switched on or off, as well as the repair of mutations in DNA and the stability of DNA. Disruption of any of these processes can contribute to cancer.
Researchers said that the mutations seem unique to aggressive childhood brain tumors.
"It is amazing to see that this particular tumor type appears to be characterized by a molecular 'smoking gun' and that these mutations are unique to fast-growing pediatric cancers in the brain," said Richard K. Wilson, Ph.D., director of The Genome Institute at Washington University School of Medicine in St. Louis and one of the study's corresponding authors. "This is exactly the type of result one hopes to find when studying the genomes of cancer patients."
The results are the latest from the PCGP, an ambitious three-year effort to sequence the complete normal and cancer genomes of 600 children with some of the most poorly understood and aggressive pediatric cancers. The human genome includes the complete set of instructions needed to assemble and sustain human life. The goal is to identify differences that explain why cancer develops, spreads and kills. Researchers believe the findings will provide the foundation for new tools to diagnose, treat or prevent the disease.
For this study, researchers sequenced the complete normal and cancer genomes of seven patients with DIPG. "The mutations were found at such high frequency in the cancer genomes of those seven patients that we immediately checked for the same alterations in a larger group of DIPGs," Baker said. When researchers sequenced all 16 of the related genes that make closely related variants of histone H3 proteins in an additional 43 DIPGs, they found many of the tumors contained the same mistakes in only two of these genes.
Of the 50 DIPG tumors included in this study, 60 percent had a single alteration in the makeup of the H3F3A gene. When the mutated gene was translated into a protein, the point mutation led to the substitution of methionine for lysine as the 27th amino acid in this variant of histone H3 protein. Another 18 percent of the DIPG patients carried the same mistake in a different gene, HIST1H3B.
Researchers are now working to understand how mutations in H3F3A and HIST1H3B impact cell function and contribute to cancer. Earlier research provides some clues. The lysine that is mutated is normally targeted by enzymes that attach other molecules to histone H3, influencing how it interacts with other proteins that regulate gene expression, Baker said. Mutations in the enzymes that target histone H3 have been identified in other cancers, but this is the first report showing a specific alteration of histones in cancer.
Tuesday, November 15, 2011
New Cancer Vaccine in Phase III Clinical Trials in Jerusalem
A new cancer vaccine developed by Israeli researchers has just startedPhase III clinical trials at Hadassah University Medical Center in Jerusalem.
ImMucin is a 21mer synthetic vaccine composed of the entire signal peptide domain of the MUC1 protein.
The vaccine, produced by the Vaxil BioTherapeutics firm, is being tested against a type of blood cancer known as multiple myeloma. But if the vaccine works – and so far all the signs are positive – the VaxHit basic technology that supports the vaccine might also be used to fight other forms of the disease, according to the announcement on the company's website.
If the clinical trials are successful and the vaccine is approved, ImMucin may become available to the public in about six years, not only to treat cancer, but also to prevent its recurrence.
Vaxil was founded in 2006 by Dr. Lior Carmon, a biotechnology entrepreneur with a PhD in immunology from the Weizmann Institute of Science in Rehovot. The company, based in Ness Ziona, merged in June with Sheldonco.
The new vaccine works by activating the immune system by “training” T-cells to search and destroy cells with the MUC1 molecule, typically found only on cancer cells. More than 90 percent of common solid tumor cancers bear the MUC1 molecule, as well as many non-solid tumors, including lymphoma, leukemia and multiple myeloma.
Advanced-stage cancer will still require chemotherapy or surgery to remove a large tumor, Vaxil CEO Julian Levy noted, but if the cancer is brought down to size, the body will then be able to fight it, with ImMucin seen as a long-term approach to prevent recurrence.
Read more: http://www.israelnationalnews.com/News/News.aspx/149680#.TsKS4oA9a7g
Tuesday, October 25, 2011
Biggest Ever Study Shows No Link Between Mobile Phone Use and Tumors
There is no link between long-term use of mobile phones and tumours of the brain or central nervous system, finds new research published online in the British Medical Journal.