Siemens Healthineers will expand the company’s existing manufacturing operations in Shanghai, China to include a new in vitro diagnostics facility. The China manufacturing facility will enable in-country manufacturing capabilities for clinical chemistry and immunoassay reagents. “This investment demonstrates the company’s continued commitment to address the evolving needs in the Chinese market and in healthcare markets across the globe,” said Franz Walt, President, Laboratory Diagnostics, Siemens Healthineers. China is the second largest market for Siemens Healthineers. According to George Chan, President, Greater China, Siemens Healthineers, “The opening of this facility strengthens our ability to support Chinese healthcare reform as we deliver better outcomes at a lower cost to our customers.” The company expects to employ hundreds of additional employees once the project is completed.
www.healthcare.siemens.com
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The presence of certain bacteria in the mouth may reveal increased risk for pancreatic cancer and enable earlier, more precise treatment. This is the main finding of a study led by researchers at NYU Langone’s Laura and Isaac Perlmutter Cancer Center.
Pancreatic cancer patients are known to be susceptible to gum disease, cavities, and poor oral health in general, say the study authors. That vulnerability led the research team to search for direct links between the makeup of bacteria driving oral disease and subsequent development of pancreatic cancer, a disease that often escapes early diagnosis and causes 40,000 U.S. deaths annually.
“Our study offers the first direct evidence that specific changes in the microbial mix in the mouth—the oral microbiome—represent a likely risk factor for pancreatic cancer along with older age, male gender, smoking, African-American race, and a family history of the disease,” says senior investigator and epidemiologist Jiyoung Ahn, PhD.
Specifically, researchers found that men and women whose oral microbiomes included Porphyromonas gingivalis had an overall 59 percent greater risk of developing pancreatic cancer than those whose microbiomes did not contain the bacterium. Similarly, oral microbiomes containing Aggregatibacter actinomycetemcomitans were at least 50 percent more likely overall to develop the disease. Doctoral student and lead investigator Xiaozhou Fan, MS, says both types of bacteria have been tied in the past to periodontitis, a disease characterized by inflammation of the gums.
“These bacterial changes in the mouth could potentially show us who is most at risk of developing pancreatic cancer,” adds Ahn, an associate professor at NYU Langone and associate director of population sciences at the Perlmutter Cancer Center.
In another study, Ahn and her colleagues showed that cigarette smoking was linked to dramatic, although reversible, changes in the amount and mix of bacteria in the oral microbiome. But she cautions that further research is needed to determine if there is any cause-and-effect relationship, or how or whether such smoking-related changes alter the immune system or otherwise trigger cancer-causing activities in the pancreas.
Laura and Isaac Perlmutter Cancer Center
nyulangone.org/press-releases/pancreatic-cancer-risk-tied-to-specific-mouth-bacteria
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This article presents data from a multicenter evaluation of the VERIS HCV assay that runs on the DxN VERIS Molecular Diagnostics System.* The study by Braun et al. was published online at the Journal of Clinical Microbiology in February 2017, and is to be published in print in the journal’s April issue. Data includes an assessment of system performance related to precision, analytical sensitivity, analytical measurement range and clinical specificity. The study featured a large number of tests performed by ten (10) participating evaluation sites based in the United Kingdom, Germany, Italy, Spain and France.
Study results demonstrated overall precision with a standard deviation (SD) of 0.22 log IU/mL or lower for each level tested. This was despite the challenges involved with the evaluation of a high number of sites. The analytical sensitivity observed among the sites was between 6.2 and 9.0 IU/mL. A broad linear range and detection of all HCV genotypes were also demonstrated.
The data is robust owing to the large numbers of tests performed. The analytical results demonstrate that the VERIS HCV assay meets the recommendations of current clinical guidelines for patient management in terms of performance and precision. The consistency of the VERIS HCV assay’s analytical performance is, in part, ascribed to the fully automated capabilities of the DxN VERIS System.
To review the full abstract please visit http://jcm.asm.org/content/early/2017/01/27/JCM.02163-16.abstract.
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Most prostate cancer (Pca) is diagnosed through a blood test, serum PSA testing. The well appreciated down-side of PSA testing is the diagnosis of a considerable proportion of indolent cancers that are highly unlikely to progress to clinically significant, lethal disease. Our limited ability to accurately identify men destined to suffer and die from the disease from the majority of indolent cases is a major concern and contributes to the dilemma regarding Pca screening and its genetic testing. There is therefore an unmet need to develop genetic tests that can predict whether a man specifically is highly susceptible to the aggressive form of prostate cancer. In some other cancers, such as breast and ovarian cancer, certain predictors of aggressiveness (e.g. BRCA gene mutations) have proven effective in identifying subsets of patients for specific interventions. In prostate cancer, genetic testing to predict the individual risk to Pca is not performed routinely because of the absence of a marker which accurately identifies aggressive prostate cancer. In a new study, Dr. Alex Zlotta and colleagues identified a new region within the Kallikrein gene, the Kallikrein 6 gene region, detectable in the blood, that is strongly associated with aggressive prostate cancer (defined as Gleason Score ?8) in a cohort of 1858 men from three continents. The team developed a blood test at the Lunenfeld-Tanenbaum Research Institute which detects variants of this Kallikrein 6 gene. The test was validated in three independent cohorts including unique cohorts from large international screening studies for prostate cancer. The Kallikrein 6 gene variants identified also independently predicted treatment failure after surgery or radiation for prostate cancer in a fourth independent cohort. The frequency of the gene variants varied from 6 to 14% in the population and the increased risk of aggressive prostate cancer was multiplied by almost 3 times in men who harboured the mutations. Most studies to date have focused on the risk of prostate cancer, not the specific risk of aggressive lethal prostate cancer. The demonstration that germline variants of a new gene, Kallikrein 6, are strongly associated with aggressive prostate cancer, may be of high value in the management of the most common cancer in men.
Lunenfeld-Tanenbaum Research Institute research.lunenfeld.ca/rssnews/?page=2165
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People with head and neck cancers with evidence of human papillomavirus (HPV) infection generally have a better prognosis than people without evidence of infection. A new study suggests that to produce a strong, reliable prognostic signal, all that’s needed is a blood serum test for two specific HPV antibodies, rather than lab work on a biopsy. Further, the researchers said, the study shows that this blood-based biomarker is predictive of outcome for all types of head and neck cancer.
“What this adds is that it helps us know how best to measure clinically the HPV contribution to this disease,” said study senior author Karl Kelsey, a professor of epidemiology and of pathology and laboratory medicine at Brown University. Kelsey collaborated with lead author Heather Nelson of the University of Minnesota Masonic Cancer Center in making the findings.
Moreover, Nelson, Kelsey and their colleagues wrote, referring to the common HPV16 strain of the virus: “These data are among the first to demonstrate a convincing relationship between HPV16 and improved patient survival for tumours of the larynx and oral cavity.”
The study examined blood serum samples and five-year survival rates among more than 1,000 Boston-area head and neck cancer patients diagnosed between 1999 and 2011. Overall, those who tested positive for antibodies to the oncogenic HPV proteins E6 or E7 were less likely to die during the five year follow-up period after diagnosis compared to those who tested negative for the antibodies. Based on the analysis, the researchers estimated that those with evidence of an immune response to HPV were 25% less likely to die during the course of follow-up compared to those with no immune response to HPV.
The study’s purpose was to determine whether the antibodies provide a reliable indication of prognosis. In ongoing trials, doctors are testing whether patients with HPV-associated cancers can be treated less aggressively — and hopefully with fewer negative side effects — than people with non-HPV-associated cancers, Kelsey said. If trials prove successful, then it will be particularly important to determine whether cancers are HPV-associated.
“The assessment of a patient’s HPV status likely will affect treatment,” he said. “That’s why there’s real interest in getting it right; for instance, how do you test?”
Prior studies have focused primarily on the role of HPV in the oropharynx — the area of the throat right behind the mouth. An important contribution of the current study, Nelson said, is demonstration that an immune response to HPV is important for all forms of head and neck cancer, although the benefit does show some variance based on the exact cancer location. Those patients with an HPV immune response with tumours located in the oropharynx and larynx had a similar risk of dying during the follow-up period, though the reduced risk was slightly attenuated for those patients with tumours located in the oral cavity.
The results didn’t depend significantly on whether people had high or low levels of the antibodies, so long as they had some, the researchers found, though testing positive for both E6 and E7 was better than for just one.
The reduced chance of dying by five years carried through for people who tested positive for the antibodies even if they consumed tobacco and alcohol. But the worst prognoses in the study were among smokers whose cancers could not be traced to HPV.
In all, the findings controlled for the statistical influences not only of tobacco and alcohol exposure, but also of age, race, gender, education and how far advanced the cancer was.
Kelsey said the findings could help bring head and neck cancer treatment closer into line with two emerging practices of fighting the disease: personalized medicine and immunotherapy.
Brown University http://tinyurl.com/z3n94a4
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Researchers affiliated with the University of Campinas (UNICAMP) in São Paulo State, Brazil, have shown that genetic information can be used to improve early prediction of the response to drugs in patients with mesial temporal lobe epilepsy (MTLE), one of the most severe forms of epilepsy. Patients who do not respond well to treatment with antiepileptic drugs are candidates for surgery. The research was conducted at the Brazilian Research Institute for Neuroscience and Neurotechnology (BRAINN) – one of the Research, Innovation and Dissemination Centers (RIDCs) funded by FAPESP – and led by Professor Iscia Lopes-Cendes. "According to estimates, at the world’s best centres, it takes between 15 and 20 years for patients with MTLE refractory to drug treatment to be referred for surgery," Lopes-Cendes said. "Meanwhile, they continue to suffer from uncontrolled seizures. If we can shorten this process, we can improve the lives of many patients, potentially making the difference between going or not going to university, having or not having a job and a normal life." MTLE, she explained, is caused by alterations in the functioning of neurons located in the deepest structures of the brain, such as the hippocampus and amygdala, which control important functions such as memory, attention, and anxiety, among others. Seizures due to abnormal electric discharges in a large group of neurons may or may not result in convulsions but do impair memory and other brain functions, often putting the patient at risk of accident and death. Although MTLE is not the most frequent form of epilepsy, accounting for only 30-40% of cases, it is considered the hardest to treat in adults. Up to 40% of patients with MTLE do not respond to any of the available drugs. In these cases, surgical removal of the brain area that originates the seizures is often recommended. The aim of the study, according to Lopes-Cendes, was to develop a methodology for distinguishing between the two groups by analysing their genetic material. To do this, the researchers selected a set of 11 genes that have been shown to be involved in antiepileptic drug absorption, metabolism, and transport in the scientific literature. For these 11 genes, they genotyped 119 different single nucleotide polymorphism (SNP) molecular markers to see which alleles were present. "We deployed a series of statistical procedures to develop the model with the best capacity to predict whether the patient would be responsive to drug treatment," Lopes-Cendes said. "In this model, we included and excluded variables to see which ones contributed most to the power of the predictors. Besides genetic polymorphisms, we also included clinical data such as the presence or absence of hippocampal atrophy, the age at and frequency of seizures at epilepsy onset, patient gender, and so on." When only the clinical variables were taken into account, the model’s predictions were about 45% accurate, which, according to Lopes-Cendes, is less than would be achieved by tossing a coin. However, the model’s accuracy increased to 80% when only SNP markers were used and to 82% when both clinical and genetic variables were used. As Lopes-Cendes explained, in order to be sure that the two groups of patients belonged to the same population from a genetic standpoint and hence were genuinely comparable, the researchers also genotyped 90 other SNPs in different genes located on the same chromosomes as in the previous analysis. "We call this testing technique ‘genome control’," she said. "Without it, we risk selecting patient and control groups from different populations, which would invalidate the results of the analysis." In light of the model’s high level of accuracy, Lopes-Cendes revealed that she and her team at BRAINN now plan to begin a multicentre study involving patients from several countries. "The idea is to genotype these SNPs at the start of treatment and to follow the patients for two years to see what happens. If the results corroborate our findings in this first study, we’ll have sufficient evidence to include the methodology in clinical practice," she said.
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A genetic ‘switch’ has been discovered by MRC researchers at the University of Leicester that could help to prevent or delay the symptoms of Parkinson’s disease.
In a paper, the team discovered that a gene called ATF4 plays a key role in Parkinson’s disease, acting as a ‘switch’ for genes that control mitochondrial metabolism for neuron health.
Dr Miguel Martins from the MRC Toxicology Unit at the University of Leicester, who led the research, explained: “When the expression of ATF4 is reduced in flies, expression of these mitochondrial genes drops. This drop results in dramatic locomotor defects, decreased lifespan, and dysfunctional mitochondria in the brain.
“Interestingly, when we overexpressed these mitochondrial genes in fly models of Parkinson’s, mitochondrial function was re-established, and neuron loss was avoided.”
By discovering the gene networks that orchestrate this process, the researchers have singled out new therapeutic targets that could prevent neuron loss.
Some forms of Parkinson’s are caused by mutations in the genes PINK1 and PARKIN, which are instrumental in mitochondrial quality control.
Fruit flies with mutations in these genes accumulate defective mitochondria and exhibit Parkinson’s-like changes, including loss of neurons.
The researchers used PINK1 and PARKIN mutant flies to search for other critical Parkinson’s genes – and using a bioinformatics approach discovered that the ATF4 gene plays a key role.
Dr Martins added: “Studying the roles of these genes in human neurons could lead to tailored interventions that could one day prevent or delay the neuronal loss seen in Parkinson’s.”
The findings build upon recent research by the University of Leicester team, which recently discovered several genes that protect neurons in Parkinson’s disease, creating possibilities for new treatment options.
University of Leicester
www2.le.ac.uk/offices/press/press-releases/2017/february/discovery-of-genetic-2018switch2019-could-help-to-prevent-symptoms-of-parkinson2019s-disease
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24 research studies from the landmark BLUEPRINT project and IHEC consortia reveal how variation in blood cells’ characteristics and numbers can affect a person’s risk of developing complex diseases such as heart disease, and autoimmune diseases including rheumatoid arthritis, asthma, coeliac disease and type 1 diabetes.
The papers, along with another 17 in high-impact journals, represent the culmination of a five-year, £25 million (€30 million) project that brought together 42 leading European universities, research institutes and industry partners and the work of IHEC. The project’s goals were to explore and describe the range of epigenetic changes that take place in bone marrow as stem cells develop into different types of mature blood cell. It also sought to match epigenetic changes and genetic differences to the physical characteristics of each cell type and use this knowledge to understand how these can lead to blood disorders, cancer and other complex diseases*.
In the first study, Sanger Institute researchers worked closely with colleagues at the University of Cambridge and the University of Oxford to carry out the largest and most in-depth study of DNA and blood cell characteristics using the UK BioBank resource and the INTERVAL study. By comparing almost 30 million DNA sequence differences in more than 173,000 people with variation in the physical properties of blood cells the scientists identified 2,500 previously undiscovered locations in the genome that influence blood cell characteristics and functions. Further work showed that genetic differences affecting some of these characteristics are linked to increased risk of heart attack, or to rheumatoid arthritis and other common autoimmune diseases.
“The scale, resolution and homogeneity of our work were vital. Because we examined so many people we were able to discover important ‘rare and low frequency’ genetic differences that are present in fewer than 10 per cent of the population. We found that these can have a much larger impact on the characteristics of blood cells than the common differences studied previously. Of the more than 300 rare and low frequency difference we found, 74 appear to affect the structure of proteins. These give us important clues as to which biological pathways are involved in controlling the production, function and characteristics of blood cells.”
The team found that genetic differences that cause people to have more young red blood cells in their peripheral bloodstreams also increase the risk they will have a heart attack.
“When mature red blood cells rupture in our blood the body replaces them with new, young red cells – a process known as haemolysis. So we think that increased haemolysis and increased risk of coronary heart disease are affected by the same biological pathways. Identifying these pathways may offer new treatment possibilities.”
Dr Adam Butterworth, one of the study’s senior authors, from the University of Cambridge
‘By combining our detailed genetic information with data from the BLUEPRINT project, we were able to identify with high certainty ‘active’ regions of the human genome that are more likely to be involved in disease mechanisms.’
Heather Elding, one of the paper’s first authors, from the Sanger Institute
For example, in another new finding, the research team showed that genetic differences that increased the amount of certain white blood cells, known as eosinophils, also increased the risk of a person developing rheumatoid arthritis, asthma, coeliac disease and type 1 diabetes.
In the second paper, researchers collaborated with scientists at the University of Cambridge, McGill University in Canada and several UK and European institutions to explore the role that epigenetics plays in the development and function of three major human immune cell types: CD14+ monocytes, CD16+ neutrophils and naïve CD4+ T cells, from the genomes of 197 individuals. They studied the contributions of various genetic control mechanisms, including epigenetic changes such as methyl tags on promoter regions in the DNA and histone modifications, to understand how these different levels of regulation interacted with genetic differences to change the expression of genes, immune function and, ultimately, human disease.
The team identified 345 regions of the genome where they could pinpoint the likely molecular causes underlying a person’s predisposition to immune-related diseases such as inflammatory bowel disease, type 1 diabetes and multiple sclerosis.
“We have created an expansive, high-resolution atlas of variations that deepens our understanding of the interplay between the genetic and epigenetic machinery that drives the three primary cells of the human immune system. We have identified hundreds of genetic variations associated with autoimmune diseases that appear to affect the activity of genes in specific regions of the genome, pointing to biological pathways that may be involved in disease and which, ultimately, may be treatable with medication.”
Sanger Institute
www.sanger.ac.uk/news/view/landmark-project-shows-heart-disease-and-rheumatoid-arthritis-risk-raised-genetic-changes
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Researchers investigating a form of adult-onset diabetes that shares features with the two better-known types of diabetes have discovered genetic influences that may offer clues to more accurate diagnosis and treatment.
Latent autoimmune diabetes in adults (LADA) is informally called "type 1.5 diabetes" because like type 1 diabetes (T1D), LADA is marked by circulating autoantibodies, an indicator that an overactive immune system is damaging the body’s insulin-producing beta cells. But LADA also shares clinical features with type 2 diabetes (T2D), which tends to appear in adulthood. Also, as in T2D, LADA patients do not require insulin treatments when first diagnosed.
A study uses genetic analysis to show that LADA is closer to T1D than to T2D. "Correctly diagnosing subtypes of diabetes is important, because it affects how physicians manage a patient’s disease," said co-study leader Struan F.A. Grant, PhD, a genomics researcher at Children’s Hospital of Philadelphia (CHOP). "If patients are misdiagnosed with the wrong type of diabetes, they may not receive the most effective medication."
Grant collaborated with European scientists, led by Richard David Leslie of the University of London, U.K.; and Bernhard O. Boehm, of Ulm University Medical Center, Germany and the Lee Kong Chian School of Medicine, a joint medical school of Imperial College London and Nanyang Technological University, Singapore.
Occurring when patients cannot produce their own insulin or are unable to properly process the insulin they do produce, diabetes is usually classified into two major types. T1D, formerly called juvenile diabetes, generally presents in childhood, but may also appear first in adults. T2D, formerly called non-insulin-dependent diabetes, typically appears in adults, but has been increasing over the past several decades in children and teens. Some 90 percent or more of all patients with diabetes are diagnosed with T2D.
Grant and many other researchers have discovered dozens of genetic regions that increase diabetes risk, usually with different sets of variants associated with T1D compared to T2D. The current study, the largest-ever genetic study of LADA, sought to determine how established T1D- or T2D-associated variants operate in the context of LADA.
The study team compared DNA from 978 LADA patients, all adults from the U.K. and Germany, to a control group of 1,057 children without diabetes. Another set of control samples came from 2,820 healthy adults in the U.K. All samples were from individuals of European ancestry.
The researchers calculated genetic risk scores to measure whether LADA patients had genetic profiles more similar to those of T1D or T2D patients. They found several T1D genetic regions associated with LADA, while relatively few T2D gene regions added to the risk of LADA. The genetic risk in LADA from T1D risk alleles was lower than in childhood-onset T1D, possibly accounting for the fact that LADA appears later in life.
One variant, located in TCF7L2, which Grant and colleagues showed in 2006 to be among the strongest genetic risk factors for T2D reported to date, had no role in LADA. "Our finding that LADA is genetically closer to T1D than to T2D suggests that some proportion of patients diagnosed as adults with type 2 diabetes may actually have late-onset type 1 diabetes," said Grant.
Grant said that larger studies are needed to further uncover genetic influences in the complex biology of diabetes, adding, "As we continue to integrate genetic findings with clinical characteristics, we may be able to more accurately classify diabetes subtypes to match patients with more effective treatments."
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Researchers at UT Southwestern Medical Center have found a new biomarker for glioma, a common type of brain cancer, that can help doctors determine how aggressive a cancer is and that could eventually help determine the best course of treatment.
Researchers from the Harold C. Simmons Comprehensive Cancer Center found that high expression of a gene called SHOX2 predicted poor survival in intermediate grade gliomas.
“As an independent biomarker, SHOX2 expression is as potent as the currently best and widely used marker known as IDH mutations,” said Dr. Adi Gazdar, Professor of Pathology in the Nancy B. and Jake L. Hamon Center for Therapeutic Oncology and a member of the Simmons Cancer Center.
According to the National Cancer Institute, cancers of the brain and nervous system affect nearly 24,000 people annually. In 2013, there were an estimated 152,751 people living with brain and other nervous system cancer in the United States. The overall 5-year survival rate is 33.8 percent.
Knowing the probable survival status of an individual patient may help physicians choose the best treatment.
In combination with IDH mutations or several other biomarkers, SHOX2 expression helped to identify subgroups of patients with a good prognosis even though other biomarkers had predicted a bad prognosis.
“Our findings are based on analysis of previously published studies. They will have to be confirmed in prospective studies, and their clinical contribution and method of use remain to be determined,” said Dr. Gazdar, who holds the W. Ray Wallace Distinguished Chair in Molecular Oncology Research.
UT Southwestern Medical Center
http://tinyurl.com/gmpddac
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