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Genetic variant discovery to help asthma sufferers

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Research from the University of Liverpool identifies a genetic variant that could improve the safety and effectiveness of corticosteroids, drugs that are used to treat a range of common and rare conditions including asthma, and chronic obstructive pulmonary disease (COPD).
Corticosteroids are very effective in the treatment of asthma and COPD, with more than 20 million prescriptions issued in the UK annually. Unfortunately, corticosteroids can also cause side effects, one of which is adrenal suppression, seen in up to 1/3 of people tested. People with this condition do not make enough cortisol. Cortisol helps the body respond to stress, recover from infections and regulate blood pressure and metabolism.
Adrenal suppression can be very difficult to diagnose, as it can present with a spectrum of symptoms from non-specific symptoms such as tiredness, to serious illness and death. The majority of patients do not develop adrenal suppression, and the reasons why some do, and while other don’t, despite using similar doses of corticosteroids were not previously understood.
In researchers from the University’s Institute of Translational Medicine, led by Professor Sir Munir Pirmohamed, conducted a genome-wide association study (GWAS) to pinpoint the genes responsible for increasing the risk of a person developing adrenal suppression. This method searches for single nucleotide polymorphisms (SNPs). Each person carries about three million SNPs, but if a particular SNP occurs more frequently in people with a particular condition than in people without the condition, it can pinpoint the underlying reason for the difference.
The researchers identified two groups of children with asthma, and one group of adults with chronic obstructive pulmonary disease (COPD), all of whom used inhaled corticosteroid medications. Each patient’s adrenal function was tested. This is the largest published cohort of children ever tested for adrenal suppression (580 children in total).
Individuals who had a particular variation in a specific gene (platelet derived growth factor D; PDGFD) had a markedly increased risk of adrenal suppression, both in the children with asthma and adults with COPD. This risk increased if the patient had two copies of the variation (one from their mother, one from their father). Children with two copies of the high risk variation in PDGFD were nearly six times more likely to develop adrenal suppression than children with no copies.
University of Liverpoolnews.liverpool.ac.uk/2018/03/16/genetic-variant-discovery-to-help-asthma-sufferers/

Parental lifespan genes could hold clue to longer life

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A large-scale international study led by the University of Exeter Medical School has discovered new genes linked to parents’ lifespan – which could one day be targeted to help prolong human life.
How long we live is determined by a range of factors including our lifestyle and how well we treat factors including blood pressure and cholesterol from midlife. However, genetics, and how long our parental relatives lived, also plays a role.
Now, the number of genes we know influence lifespan has expanded, potentially paving the way to new therapeutic targets to prolong life.
The study, funded by the Medical Research Council and conducted in collaboration with a number of US universities, undertook a genome-wide search for variants influencing how long participants’ parents lived. The team studied 389,166 volunteers who took part in the UK Biobank, with confirmation in the US Health and Retirement Study and the Wisconsin Longitudinal Study. The DNA samples from the volunteers carry the genetics of their biological parents, so provide a practical way of studying exceptionally long lifespans.
Eight genetic variants had already been linked for lifespan, mainly involved in heart disease and dementia. The latest study has expanded this to 25 genes in all, with some specific to mothers’ or fathers’ lifespan separately.
Dr Luke Pilling, who undertook most of analyses said: “We have identified new pathways that contribute to survival, as well as confirming others. These targets, including inflammatory and cardiovascular pathways, offer potentially modifiable targets to reduce risk of an earlier death and improve health.”
Genes involved in senescence, the ‘frozen’ state that cells enter into after being damaged, played an important role in longevity. Drugs targeting senescence have already been shown to extend life in laboratory animals.
Genes related to inflammation and auto-immunity-related genes were also prominent, opening up the possibility that precision anti-inflammatory treatments may one day be helpful in extending life.
The results confirm that many genetic variants combine to influence human lifespan: no single gene variant was found to be responsible.
The study found evidence to suggest that the genetic variants for average lifespan also influence exceptionally long life expectancy. A genetic risk score combining the top ten variants was statistically associated with parents being centenarians.
Exeter Universityhttps://tinyurl.com/yakjsfoj

Beckman Coulter sponsors top-ranked sepsis clinical guide app

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Beckman Coulter has announced its exclusive sponsorship of the ESCAVO Sepsis Clinical Guide (Sepsis app), a point-of-care medical reference mobile application for healthcare professionals who manage septic patients in acute-care settings. Beckman Coulter’s sponsorship of the Sepsis app ensures this important tool will remain free for all users and that content will continue to be maintained and updated using the latest clinical practice standards.
Sepsis is a life-threatening condition that requires prompt recognition and treatment. Delayed treatment can rapidly cause cardiovascular collapse, tissue damage, organ failure and death. More than a million people are diagnosed with sepsis each year in the United States alone; the dangerous condition causes 250,000 deaths. Approximately 665,000 adults and 100,000 children visit the emergency department with sepsis-related symptoms. Patients presenting with sepsis can be in grave danger when encountering long emergency room wait times or a lack of effective or timely screening and triage protocols.
“While great strides have been made in standardizing sepsis treatment in recent years, there is still considerable variability in the quality of care among hospitals,” says Daniel Nichita, M.D., founder of ESCAVO and author of the Sepsis Clinical Guide mobile app. “One reason for this is the difficulty of diagnosing this complex disorder whose early symptoms are often very subtle and for which there is no definitive test, but also an uneven use of current clinical practice standards in sepsis care. ESCAVO developed the Sepsis app to put critical information on sepsis management—based on the most current clinical practice guidelines—in the hands of busy clinicians, who may not always have the time to familiarize themselves with current trends. Its content is delivered in a concise, actionable format to allow rapid but effective clinical decision-making at the point of care.”
The Sepsis app can benefit all medical professionals; however, it is especially valuable for those working in the emergency room, where sepsis most commonly first presents.
Healthcare providers can download the Sepsis Clinical Guide app from Google Play for Android devices, or from the App Store for the iOS platform. To find the app, users can search “sepsis.” The Sepsis Clinical Guide is recognizable by an orange-colored icon, and, as the top-ranked sepsis-related app, it appears first in the search results.  
https://tinyurl.com/njp3cswhttps://tinyurl.com/y9exh7kx

A risk factor for drug-induced skin disease identified

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Researchers have identified a type of human leukocyte antigen (HLA) that is associated with the skin disease bullous pemphigoid (BP) in diabetic patients administered with DPP-4 inhibitory drugs.
DPP-4 inhibitor (DPP-4i) is widely used to treat type 2 diabetes, but increased cases of bullous pemphigoid (BP) have been reported among patients taking the medicine. BP is the most common autoimmune blistering disorder, characterized by itchy reddening of the skin as well as tense blisters over the whole body. Afflicted patients, mostly elderly, suffer from autoimmune attacks on a type of collagen in skin, making it hard to cure and compromising their quality of life. Previously, no risk factor triggering BP in diabetic patients administered with DPP-4i had been identified.
BP is classified into two types: inflammatory and non-inflammatory, the latter of which is found more in diabetic patients administered with the drug. The research team, including Dr. Hideyuki Ujiie of Hokkaido University Hospital, examined 30 BP patients administered with DPP-4i, and investigated their symptoms and autoantibodies to group them as inflammatory or noninflammatory.
The researchers then analysed human leukocyte antigen (HLA) genes of the 30 patients to identify their white blood cell type since HLA genes are known to be involved in various immune diseases. To compare, the team also analysed the HLA of 72 BP patients who had not been administered with DPP-4i and 61 diabetic patients who were using the drug but not affected by BP. Their findings were compared with the HLA genes of 873 Japanese from the general population.
According to the results, 70 percent of the 30 BP patients administered with DPP-4i fell into the non-inflammatory type with less reddening of the skin (erythema). HLA analyses found 86 percent of the non-inflammatory BP patients administered with DPP-4i had an HLA gene called “HLA-DQB1*03:01.” The rate of having the HLA gene was much higher than was detected among the general population (18 percent) and non-BP type-2 diabetic patients administered with DPP-4i (31 percent). Meanwhile, 26 percent of BP patients who were not administered with the drug had the same HLA gene.
The findings show HLA-DQB1*03:01 is not linked to ordinary BP nor type-2 diabetes, but is closely associated with the development of BP among DPP-4i takers. “However, as the probability of patients exposed to DPP-4i to develop BP remains unclear, further research investigating a much larger number of cases is needed,” says Hideyuki Ujiie.
“Our results suggest people with HLA-DQB1*03:01 have a higher risk of developing BP when exposed to DPP-4i than those without the HLA gene. The gene could serve as a biomarker to help estimate the risk of developing BP when patients are administered with DPP-4i. The mechanism that connects the HLA gene and BP needs to be addressed to help prevent the development of the disease,” Ujiie added.
ScienceDailyhttps://tinyurl.com/y9u48zv3 

New asthma biomarkers identified from lung bacteria

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While the microbiome has gained significant attention for its impact on digestive health in recent years, its effect on lung disease has largely remained unstudied.
Dr. Patricia Finn says this is a missed opportunity.
“The microbiome is the ecosystem of good and bad bacteria living in the body,” said Finn, the Earl M. Bane Professor of Medicine at the University of Illinois at Chicago. “Because the lungs continuously and automatically draw air, and any number of environmental agents, into the body, the composition and balance of microbes in the lungs may have a profound effect on many respiratory conditions.”
New research from Finn and her colleagues in the UIC College of Medicine suggests that the lung microbiome plays a significant role in asthma severity and response to treatment.
Asthma is a chronic disease in which lung airways become swollen and narrow, making it difficult for air to move in and out of lungs. Because people with asthma have inflamed airways, they experience a range of symptoms, including shortness of breath, coughing, wheezing and chest tightness.
In a group of clinically similar patients with asthma, researchers identified two asthma phenotypes by assessing the microbiome and airway inflammation. The patients were ages 18 to 30 with mild or moderate atopic asthma.
“This tells us the microbiome has relevance beyond the gut, and that it is a potential biomarker for asthma,” said Dr. David Perkins, professor of medicine and surgery at UIC, who jointly operates the lab with Finn.
These two phenotypes, called asthma phenotype one and two, or AP1 and AP2, are demarcated by the prevalence and dominance of different bacteria in the lung. When compared, patients in the two groups performed differently on pulmonary function tests.
AP1 was associated with less severe asthma; it showed decreased T helper cytokines and increased enterococcus bacteria, but normal pulmonary function tests. In contrast, AP2 was associated with increased pro-inflammatory cytokines, increased oral taxa and strep pneumonia bacteria, and decreased pulmonary function tests, or more severe asthma.
In both AP1 and AP2, the associations between the composition of the microbiome and specific inflammatory cytokines were decreased after treatment with an inhaled corticosteroid, a common asthma therapy. Researchers say this suggests that ICS may function by dampening responses to microbes.
“The data suggest that further study of the microbiome may help to develop more personalized treatment recommendations for patients with asthma,” said Finn, the senior author on the paper.
Finn says that asthma research has increasingly focused on the differences between seemingly similar patients, and that this study adds to the growing body of evidence that patients benefit from precision medicine approaches to common chronic diseases, such as asthma.
“If we can better understand how the individual’s lung microbiome affects asthma and identify likely microbial culprits, we may get to a point where we can predict and control asthma development and severity by shifting the microbiome early in life,” Finn said. “This could be as simple as diet, probiotics or medication.”
University of Illinois – Chicago
today.uic.edu/new-asthma-biomarkers-identified-from-lung-bacteria

TAILORx trial finds most women with early breast cancer do not benefit from chemotherapy

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 New findings from the groundbreaking Trial Assigning Individualized Options for Treatment (Rx), or TAILORx trial, show no benefit from chemotherapy for 70 percent of women with the most common type of breast cancer. The study found that for women with hormone receptor (HR)-positive, HER2-negative, axillary lymph node-negative breast cancer, treatment with chemotherapy and hormone therapy after surgery is not more beneficial than treatment with hormone therapy alone. The new data will help inform treatment decisions for many women with early-stage breast cancer.
The trial was supported by the National Cancer Institute (NCI), part of the National Institutes of Health, and designed and led by the ECOG-ACRIN Cancer Research Group.
“The new results from TAILORx give clinicians high-quality data to inform personalized treatment recommendations for women,” said lead author Joseph A. Sparano, M.D., associate director for clinical research at the Albert Einstein Cancer Center and Montefiore Health System in New York City and vice chair of the ECOG-ACRIN Cancer Research Group. “These data confirm that using a 21-gene expression test to assess the risk of cancer recurrence can spare women unnecessary treatment if the test indicates that chemotherapy is not likely to provide benefit.”
TAILORx, a phase 3 clinical trial, opened in 2006 and was designed to provide an evidence-based answer to the question of whether hormone therapy alone is not inferior to hormone therapy plus chemotherapy. The trial used a molecular test (Oncotype DX Breast Recurrence Score) that assesses the expression of 21 genes associated with breast cancer recurrence to assign women with early-stage, HR- positive, HER2-negative, axillary lymph node–negative breast cancer to the most appropriate and effective post-operative treatment. The trial enrolled 10,273 women with this type of breast cancer at 1,182 sites in the United States, Australia, Canada, Ireland, New Zealand, and Peru.
When patients enrolled in the trial, their tumours were analysed using the 21-gene expression test and assigned a risk score (on a scale of 0–100) for cancer recurrence. Based on evidence from earlier trials, women in the trial who had a score in the low-risk range (0–10) received hormone therapy only, and those who had a score in the high-risk range (26 and above) were treated with hormone therapy and chemotherapy.
Women in the trial who had a score in the intermediate range (11–25) were randomly assigned to receive hormone therapy alone or hormone therapy with adjuvant chemotherapy. The goal was to assess whether women who received hormone therapy alone had outcomes that were as good as those among women who received chemotherapy in addition to hormone therapy.
“Until now, we’ve been able to recommend treatment for women with these cancers at high and low risk of recurrence, but women at intermediate risk have been uncertain about the appropriate strategy to take,” said Jeffrey Abrams, M.D., associate director of NCI’s Cancer Therapy Evaluation Program. “These findings, showing no benefit from receiving chemotherapy plus hormone therapy for most patients in this intermediate-risk group, will go a long way to support oncologists and patients in decisions about the best course of treatment.”
The researchers found that the primary endpoint of the trial, invasive disease-free survival—the proportion of women who had not died or developed a recurrence or a second primary cancer—was very similar in both groups. Five years after treatment, the rate of invasive disease-free survival was 92.8 percent for those who had hormone therapy alone and 93.1 percent for those who also had chemotherapy. At nine years, the rate was 83.3 percent for those with hormone therapy alone and 84.3 percent for the group that had both therapies. None of these differences were considered statistically significant.
The rates of overall survival were also very similar in the two groups. At five years, the overall survival rate was 98.0 percent for those who received hormone therapy alone and 98.1 percent for those who received both therapies, and at nine years the respective overall survival rates were 93.9 percent and 93.8 percent.
The researchers also found that women with a score of 0–10 had very low recurrence rates with hormone therapy alone at nine years (3 percent). This confirms similar findings from earlier studies. In addition, they found that women with a score of 26–100 had a distant recurrence rate of 13 percent despite receiving both chemotherapy and hormone therapy. This finding indicates the need to develop more effective therapies for women at high risk of recurrence.

ECOG-ACRIN Cancer Research Group
ecog-acrin.org/news-and-info/press-releases/tailorx-trial-finds-most-women-with-early-breast-cancer-do-not-benefit-from-chemotherapy

Parkinson’s gene initiates disease outside of the brain

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Until very recently, Parkinson’s had been thought a disease that starts in the brain, destroying motion centres and resulting in the tremors and loss of movement. New research shows the most common Parkinson’s gene mutation may change how immune cells react to generic infections like colds, which in turn trigger the inflammatory reaction in the brain that causes Parkinson’s. The research offers a new understanding of Parkinson’s disease.                                                     
“We know that brain cells called microglia cause the inflammation that ultimately destroys the area of the brain responsible for movement in Parkinson’s,” said Richard Smeyne, PhD, Director of the Jefferson Comprehensive Parkinson’s Disease and Movement Disorder Center at the Vickie and Jack Farber Institute for Neuroscience. “But it wasn’t clear how a common inherited mutation was involved in that process, and whether the mutation altered microglia.”
Together with Dr. Smeyne, first author Elena Kozina, PhD, looked at the mutant version of the LRRK2 gene (pronounced ‘lark’). Mutations in the LRRK2 gene are the most common cause of inherited Parkinson’s disease and are found in 40 percent of people of North African Arab descent and 18 percent of people of Ashkenazi Jewish descent with Parkinson’s. However there’s been controversy around the exact function of the LRRK2 gene in the brain.
“We know that gene mutation is not enough to cause the disease,” said Dr. Kozina, Post-Doctoral student at Jefferson.“We know that twins who both carry the mutation, won’t both necessarily develop Parkinson’s. A second ‘hit’ or initiating event is needed.”
Based on his earlier work showing that the flu might increase risk of Parkinson’s disease, Dr. Smeyne decided to investigate whether that second hit came from an infection. Suspecting that the LRRK2 mutations might be acting outside of the brain, the researchers used an agent — the outer shell of bacteria, called lippopolysaccharide (LPS) – that causes an immune reaction. LPS itself does not pass into the brain, nor do the immune cells it activates, which made it ideal for testing whether this second hit was acting directly in the brain.
When the researchers gave the bacterial fragments to the mice carrying the two most common LRRK2 gene mutations, the immune reaction became a “cytokine storm,” with inflammatory mediators rising to levels that 3-5 times higher than a normal reaction to LPS. These inflammatory mediators were produced by T and B immune cells expressing the LRRK2 mutation.
Despite the fact that LPS did not cross the blood-brain barrier, the researchers showed that the elevated cytokines were able to enter the brain, creating an environment that caused the microglia to activate pathologically and destroy the brain region involved in movement.
“Although more tests are needed to prove the link, as well as testing whether the same is true in humans, these findings give us a new way to think about how these mutations could cause Parkinson’s,” said Dr. Smeyne. “Although we can’t treat people with immunosuppressants their whole lives to prevent the disease, if this mechanism is confirmed, it’s possible that other interventions could be effective at reducing the chance of developing the disease.”
Thomas Jefferson Universitywww.jefferson.edu/university/news/2018/03/21/Parkinsons_gene_triggers_the_disease_from_outside_brain.html

Landmark genetic study better predicts stomach cancer

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A research team led by National University Health System (NUHS) and Duke-NUS Medical School has used genomic technologies to better understand intestinal metaplasia (IM), a known risk factor for gastric (stomach) cancer. Patients with IM are six times more likely to develop stomach cancer than those without. This study is an important part of an ambitious investigation to understand why some people develop stomach cancer, while others do not. The research could also help detect patients who are infected with the Helicobacter pylori bacteria, which is also linked to the disease.
Stomach cancer is the third deadliest cancer in the world according to World Health Organization (WHO) statistics, and claims more than 300 lives yearly in Singapore. The disease is believed to be caused by infection with Helicobacter pylori but is potentially treatable if detected early. Unfortunately, more than two-thirds of stomach cancer patients are only diagnosed at an advanced stage.
"Previous genetic studies on IM have mainly focused on patients who were already diagnosed with stomach cancer but these are limited in their ability to predict who are likely to develop the disease and how the disease will progress," said Professor Patrick Tan, co-lead investigator and Professor, Duke-NUS Medical School. Professor Tan is also Deputy Executive Director, Biomedical Research Council, Agency for Science, Technology, and Research, and a Senior Principal Investigator at the Cancer Science Institute of Singapore. "This new study is the first to comprehensively map out the genetic changes in IM in a cohort of stomach cancer-free subjects, which helps us better predict the possible occurrence and progression of the disease."
Dr Yeoh Khay Guan, co-lead investigator and Deputy Chief Executive, NUHS as well as Dean, NUS Yong Loo Lin School of Medicine added, "Our study is the largest series of IM to be studied in detail by genetic analysis. These new findings help us understand why some people have a higher risk of progression to stomach cancer, and identify those who may benefit from closer follow-up to prevent cancer or to detect it early so that it can be cured."
The researchers leveraged the near 3,000 participants-strong Gastric Cancer Epidemiology Programme (GCEP) cohort, recruited with the support of patients and doctors from four local public hospitals (National University Hospital, Tan Tock Seng Hospital, Singapore General Hospital, Changi General Hospital), to show that a comprehensive analysis of the genetic patterns of IM can predict its subsequent progression towards stomach cancer. The genetic analysis of IM helps to identify those with a higher risk of progression to stomach cancer, adding further information to what is available by microscopic examination alone.
The research team is using this new information to identify biomarkers that can be applied in future in the clinic to identify people who have a high risk of progression to stomach cancer.
EurekAlertwww.eurekalert.org/pub_releases/2018-01/nuos-lgs010518.php

New breast cancer targets

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Genome-wide association studies (GWAS) have identified more than 150 genetic variations associated with increased risk for breast cancer. Most of these variants are not located in protein-coding gene regions but are assumed to regulate the expression of certain genes.
One way to figure out what these variants are doing is to conduct a cis-eQTL analysis. That’s a way of detecting changes in the expression of genes presumably regulated by a nearby variant.
Using four large-scale data sets from normal and cancerous breast tissue samples, Xingyi Guo, PhD, and colleagues identified 101 candidate breast cancer susceptibility genes with variant-associated gene expression changes. In breast cancer cells grown in culture, the researchers also demonstrated how three genes promoted tumour growth by disrupting normal cell behaviour.
Their findings reveal potential target genes associated with an increased risk of breast cancer and provide additional insights into the underlying genetic and biological mechanisms that drive this common cancer.

Vanderbilt Universitynews.vanderbilt.edu/2018/05/04/new-breast-cancer-targets/

Exosomal microRNA predicts and protects against severe lung disease in extremely premature infants

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Extremely low birth-weight babies are at risk for a chronic lung disease called bronchopulmonary dysplasia, or BPD. This condition can lead to death or long-term disease, but clinical measurements are unable to predict which of the tiny infants—who get care in hospital intensive-care units and often weigh just one and a half pounds—will develop BPD.
University of Alabama at Birmingham researchers now report discovery of a strong predictive biomarker for BPD, and they show a role for the biomarker in the pathogenesis of this neonatal lung disease. These results open the path to possible future therapies to prevent or lessen BPD, which is marked by inflammation and impaired lung development.
This biomarker could also help neonatologists plan optimal management and risk stratification of their tiny patients, and it could guide targeted enrolment of high-risk infants into randomized trials of potentially novel treatment strategies.
The UAB work is an example of "bedside to bench" research. It began with prospective studies of extremely premature infants to identify potential biomarkers, and then proceeded to lab experiments using animal models and cells grown in culture to learn how the biomarker functions in disease progression.
The study was led by Charitharth Vivek Lal, M.D., assistant professor in the UAB Pediatrics Division of Neonatology, and it builds upon Lal’s 2016 report that early microbial imbalance in the airways of extremely premature infants is predictive for development of BPD.
The biomarker in the study is microRNA 876-3p.
The hunt for the biomarker began with a prospective cohort study at the UAB Regional Neonatal Intensive Care Unit, looking at exosomes obtained from tracheal aspirates of infants with severe BPD, compared with full-term controls. Exosomes are small, membrane-bound blebs or vesicles that are actively secreted by a variety of cells. They are known to contain microRNAs and proteins, and the exosomes act in cell-to-cell signalling. MicroRNAs can regulate gene expression in cells.
Lal and colleagues found that airway cells in infants with severe BPD had greater numbers of exosomes, but those exosomes were smaller sized. They also experimentally found that high oxygen exposure for newborn mice or human bronchial epithelial cells grown in culture also caused the release of more exosomes, and the exosomes were smaller in size that those secreted at normal oxygen level. Premature infants often receive extra oxygen to aid their underdeveloped lungs.
The UAB researchers then did a prospective discovery cohort study at UAB—they collected tracheal aspirate samples from extremely premature infants within six hours of birth, purified exosomes from the samples and looked for microRNAs in the exosomes. Out of 810 microRNAs that were found, 40 showed differences between infants who later developed BPD and those who were BPD-resistant.
Next, in cooperation with researchers at Thomas Jefferson University and Drexel University, a validation cohort was studied in Philadelphia. Thirty-two of the 40 microRNAs were confirmed; six had a higher statistical significance; and one biomarker, a low concentration of microRNA 876-3p, was found to have the highest sensitivity to predict severe BPD in extremely low birth-weight infants.
Medical Xpressmedicalxpress.com/news/2018-03-exosomal-microrna-severe-lung-disease.html

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