An opportunity exists to require the rights to a real time PCR test for thirteen oncogenic HPV types (Jenkins et al, J Virol Methods 2013).
Interested parties should contact: not later than 01.09.2017
Lawyer Maria Torvund
Uniongata 18
3732 Skien
Norway
Tel: +47 35 53 20 00
Fax: +47 35 53 20 01
advokat@mariatorvund.no
A recent study has confirmed that EKF’s Quo-Test® A1c point-of-care testing (POCT) analyser shows comparable performance to a lab-based HPLC system for the measurement of glycated hemoglobin (HbA1c). Published in Practical Laboratory Medicine, the study undertaken by the Diabetes Research Unit Cymru, Swansea University, UK, also observed that under the correct circumstances using WHO guidelines Quo-Test is appropriate for the diagnosis of Type 2 diabetes.
HbA1c is routinely used as a measure for the assessment of long-term diabetes control and, more recently, it has also been recommended for diabetes diagnosis. With the increasing use of POCT devices for the measurement of HbA1c without the waiting time associated with laboratory testing, it is crucial to determine how their performance compares. The Swansea University study aimed to compare the Quo-Test POCT analyser using boronate fluorescence quenching technology with an established HPLC laboratory method.
Using whole blood EDTA samples (n=100) from subjects with and without diabetes, the study found good overall agreement between the Quo-Test and reference HPLC method (R2=0.9691; p<0.0001). A diagnostic comparison was also made in line with WHO diagnostic ranges for HbA1c. Use of the Quo-Test as a diagnostic tool, showed 97% (n=79) agreement with the HPLC analyser for glucose intolerance and 100% (n=72) agreement for Type 2 diabetes.
Gareth Dunseath, Diabetes Research Unit Cymru Laboratory Manager, commented, “Device validation and testing is an important part of the research work that the Diabetes Research Unit Cymru laboratory undertakes, especially where the findings can expand on the services that we are able to provide. In this study, our findings showed very good reproducibility and agreement between the Quo-Test and an established laboratory HPLC method across a spectrum of glucose tolerance. This gives the reassurance that the Quo-Test can be used in situations where the immediate result afforded by a POCT method is of benefit, such as screening for eligibility for clinical trials.”
The Diabetes Research Unit Cymru study follows another by scientists from the European Reference Laboratory for Glycohemoglobin. This demonstrated that Quo-Test A1c easily met International Federation of Clinical Chemistry and Laboratory Medicine (IFCC) performance criteria for HbA1c measurement. Meeting the IFCC accepted quality targets (>2 sigma at 10% total allowable error (TAE) at 48 mmol/mol HbA1c) is essential for the effective monitoring of glycemic control in diabetes patients.
EKF’s Quo-Test® analyser has been designed for easy and reliable HbA1c measurement in a point-of-care setting, such as diabetes clinics and doctors’ surgeries. It is fully automated, measuring glycated hemoglobin from a 4 μL sample taken from a finger prick or venous whole blood. Sample results are available within four minutes and reported in IFCC and DCCT standard units. It is also unaffected by most hemoglobin variants.
www.ekfdiagnostics.com
A gene called triggering receptor expressed on myeloid cells 2, or TREM2, has been associated with numerous neurodegenerative diseases, such as Alzheimer’s disease, Frontotemporal lobar degeneration, Parkinson’s disease, and Nasu-Hakola disease. Recently, a rare mutation in the gene has been shown to increase the risk for developing Alzheimer’s disease.
Independently from each other, two research groups have now revealed the molecular mechanism behind this mutation. Their research sheds light on the role of TREM2 in normal brain function and suggests a new therapeutic target in Alzheimer’s disease treatment.
Alzheimer’s disease, just like other neurodegenerative diseases, is characterized by the accumulation of specific protein aggregates in the brain. Specialized brain immune cells called microglia strive to counter this process by engulfing the toxic buildup. But as the brain ages, microglia eventually lose out and fail to rid all the damaging material.
TREM2 is active on microglia and enables them to carry out their protective function. The protein spans the microglia cell membrane and uses its external region to detect dying cells or lipids associated with toxic protein aggregates. Subsequently, TREM2 is cut in two. The external part is shed from the protein and released, while the remaining part still present in the cell membrane is degraded. To better understand TREM2 function, the two research groups took a closer look at its cleavage. They were led by Christian Haass at the German Center for Neurodegenerative Diseases at the Ludwig-Maximilians-University in Munich, Germany, and Damian Crowther of AstraZeneca’s IMED Neuroscience group in Cambridge, UK together with colleagues at the Tanz Centre for Research in Neurodegenerative Diseases, University of Toronto and the Cambridge Institute for Medical Research, University of Cambridge, UK.
Using different technological approaches, both groups first determined the exact site of protein shedding and found it to be at amino acid 157. Amino acid 157 was no unknown. Only recently, researchers from China had uncovered that a mutation at this exact position, referred to as p.H157Y, increased the risk of Alzheimer’s disease. Together, these observations indicate that protein cleavage is perturbed in the p.H157 mutant and that this alteration promotes disease development.
As a next step, Haass and Crowther’s groups investigated the biochemical properties of the p.H157Y mutant protein more closely. They found that the mutant was cleaved more rapidly than a healthy version of the protein. "Our results provide a detailed molecular mechanism for how this rare mutation alters the function of TREM2 and hence facilitates the progression of Alzheimer’s disease," said Crowther.
While most TREM2 mutations affect protein production, the mechanism behind p.H157Y is somewhat different. The p.H157Y mutation allows the protein to be correctly manufactured and transported to the microglia cell surface, but then it is cleaved too quickly. "The end result is the same. In both cases, there is too little full-length TREM protein on microglia," said Haass. "This suggests that stabilizing TREM2, by making it less susceptible to cleavage, may be a viable therapeutic strategy."
EurekAlert
www.eurekalert.org/pub_releases/2017-08/e-st-083017.php
Scientists investigating the genetic causes and altered functioning of nerve cells in motor neurone disease (MND) have discovered a new mechanism that could lead to fresh treatment approaches for one of the most common forms of the disease.
The team, based in the Sheffield Institute for Translational Neuroscience (SITraN), investigated a mutation in one particular gene, which causes sections of DNA to replicate themselves inexplicably within cells. They found a way to prevent RNA, carrying these replicated sequences, from leaving the cell’s nucleus and travelling into the surrounding cytoplasm where they cause cell death.
Patients with MND suffer progressive paralysis as the nerves supplying muscles degenerate. Although there are several different types of MND, this mutation, in a gene called C9ORF72, is responsible for the most common type of MND, called Amyotrophic Lateral Sclerosis (ALS). This accounts for about 40-50 per cent of inherited cases and 10 per cent of all MND cases. The mutations or environmental factors causing the vast majority of MND cases remain unknown.
DNA is produced in the cell’s nucleus and contains the instructions which cells use to carry out their functions. Messenger RNA, called mRNA, transcribes this information and carries it out of the cell to ‘protein factories’ in the cytoplasm surrounding the nucleus. It is quite common for some sections of repeated DNA stretches to replicate themselves for reasons that are poorly understood. These repetitions are ‘non-coding’ sections that are not responsible for building proteins and are edited out before they leave the nucleus to serve as templates for the production of proteins.
In this particular type of motor neurone disease, however, the RNA not only contains the unnecessary replicated sequences, it is able to take them out of nucleus and into the cell’s cytoplasm. Once in the cytoplasm, the RNA is used to make up repeated proteins that clump together and block the normal function of the cell, causing it to die.
In an early stage study the researchers have been able to pinpoint why the repeated RNA sequences are able to leave the cell’s nucleus to cause cell death. The team identified a particular protein called SRSF1 which binds to the pathological repeated RNA molecules and transports them out of the cell centre, effectively overriding the gatekeeping machinery within the nucleus by opening a back door.
Working in partnership with researchers at the MRC Mitochondrial Biology Unit at the University of Cambridge, the team have shown that by targeting the SRSF1 protein, it is possible to reduce the amount of rogue RNA escaping into the cell’s cytoplasm.
“This is a completely new approach to tackling the most common type of motor neurone disease. No one has yet attempted to prevent these repeated sequences of RNA from leaving the cell’s nucleus and it opens up new areas of investigation for gene therapy,” explains University of Sheffield’s Dr Guillaume Hautbergue, who conceived the study and led the research jointly with Dr Alexander Whitworth, of the University of Cambridge, and SITraN Director, Professor Dame Pamela Shaw.
The University of Sheffield
www.sheffield.ac.uk/news/nr/motor-neurone-disease-1.716303
Interactions among proteins that relay information from one immune cell to another are weakened in the blood of brain cancer patients within five years before the cancer is diagnosed, said lead researcher Judith Schwartzbaum of The Ohio State University.
That information could one day lead to earlier diagnosis of brain cancer, said Schwartzbaum, an associate professor of epidemiology and member of Ohio State’s Comprehensive Cancer Center.
The study focused on gliomas, which make up about 80 percent of brain cancer diagnoses. Average survival time for the most common type of glioma is 14 months.
Symptoms vary and include headaches, memory loss, personality changes, blurred vision and difficulty speaking. On average, the cancer is diagnosed three months after the onset of symptoms and when tumours are typically advanced.
“It’s important to identify the early stages of tumour development if we hope to intervene more effectively,” Schwartzbaum said. “If you understand those early steps, maybe you can design treatments to block further tumour growth.”
While widespread blood testing of people without symptoms of this rare tumour would be impractical, this research could pave the way for techniques to identify brain cancer earlier and allow for more-effective treatment, Schwartzbaum said.
Schwartzbaum evaluated blood samples from 974 people, half of whom went on to receive a brain-cancer diagnosis in the years after their blood was drawn. The samples came from Norway’s Janus Serum Bank.
Because of previous research – including her own on the relationship between allergies and brain cancer – Schwartzbaum was interested in the role of cytokines, proteins that communicate with one another and with immune cells to spark immune responses. Schwartzbaum’s previous work found that allergies appeared to offer protection against brain cancer.
In this study, Schwartzbaum evaluated 277 cytokines in the blood samples and found less cytokine interaction in the blood of people who developed cancer.
“There was a clear weakening of those interactions in the group who developed brain cancer and it’s possible this plays a role in tumour growth and development,” Schwartzbaum said.
Cytokine activity in cancer is especially important to understand because it can play a good-guy role in terms of fighting tumour development, but it also can play a villain and support a tumour by suppressing the immune system, she said.
In addition to discovering the weakening of cytokine interactions in the blood of future cancer patients, the researchers found a handful of cytokines that appear to play an especially important role in glioma development.
The results of this study must be confirmed and further evaluated before it could translate to changes in the earlier diagnosis of brain cancer, but the discovery offers important insights, Schwartzbaum said.
“It’s possible this could also happen with other tumours – that this is a general sign of tumour development,” she said.
Ohio State Universityhttps://news.osu.edu/news/2015/09/09/a-hint-of-increased-brain-tumor-risk-5-years-before-diagnosis/
A DNA variant—located in the DNMT3B gene and commonly found in people of European and African descent—increases the likelihood of developing nicotine dependence, smoking heavily, and developing lung cancer, according to a new study led by RTI International.
Nearly 1 billion people smoke and 6 million premature deaths occur worldwide each year from cigarette smoking, according to the World Health Organization. Smoking is the leading cause of preventable death and one person dies approximately every 6 seconds from smoking-related causes, according to the WHO.
The new study is the largest genome-wide association study of nicotine dependence. Researchers studied more than 38,600 former and current smokers from the United States, Iceland, Finland, and the Netherlands.
“This new finding widens the scope of how genetic factors are known to influence nicotine dependence,” said Dana Hancock, Ph.D., genetic epidemiologist at RTI and lead author of the study. “The variant that we identified is common, occurring in 44 percent of Europeans or European Americans and 77 percent of African Americans, and it exerts important effects on gene regulation in human brain, specifically in the cerebellum, which has long been overlooked in the study of addiction.”
The genetic variant was linked to an increased risk of nicotine dependence by testing nearly 18 million variants across the genome for association with nicotine dependence. The variant was also tested in independent studies and found to associate with heavier smoking and with increased risk of lung cancer.
RTI International
www.rti.org/news/researchers-identify-gene-influences-nicotine-dependence
Yale experts and their partners in a national research consortium have identified several genes and gene clusters associated with the immune response to influenza (“flu”) vaccination. The findings point to the prospect of using genetic profiles to predict individual responses to the flu vaccine.
The global impact of influenza is substantial, with seasonal epidemics estimated to result in 3-5 million cases of severe illness, and 250,000 to 500,000 deaths annually worldwide. Vaccination is the best way to protect against flu infection, but the composition of the seasonal vaccine changes from year to year. Moreover, effectiveness of the vaccine varies widely among individuals.
Previous studies, including a study done at Yale, have sought to identify changes in gene expression associated with successful flu vaccination but focused on relatively small numbers of participants. The new study included six different cohorts receiving the flu vaccine from across the country; research centres included Yale, the Baylor Research Institute, Emory University, the Mayo Clinic, and the National Institutes of Health. The size of the cohort — more than 500 individuals — allowed researchers to not only identify genes and gene clusters associated with vaccine response, but also confirm these findings in an independent cohort of participants.
Analysing the data, the research team identified several gene “signatures,” or groups of genes, that were associated with a stronger response to the flu vaccine. The response was determined by increases in antibodies that protect against infection.
We “were able to identify genes at baseline, before vaccination, that would predict how individuals would respond to the vaccine,” said Ruth Montgomery, associate professor of medicine at Yale School of Medicine and a co-author.
The researchers also found that the while the genes were predictive of a robust vaccine response in adults younger than age 35, those same genes did not improve responses in adults over age 60. “Another finding is that genes that contribute to good immune response are different in young and older people,” Montgomery noted.
“Surprisingly, we found that baseline differences, both at the gene and module level, were inversely correlated between young and older participants,” added Steven Kleinstein, associate professor of pathology at Yale School of Medicine and a corresponding author on the study. The reasons for these age differences warrant further study, said the researchers.
The findings offer new insights into the biology of vaccine response. They may also help investigators predict responses in individuals and develop strategies to improve vaccines, or treatments to boost the immune system’s response to vaccination, the researchers noted.
Yale University
news.yale.edu/2017/08/25/study-identifies-genes-linked-better-immune-response-flu-vaccine
Researchers at the University of Helsinki, in cooperation with two research groups in the United States, have discovered that some Finnish mothers carry rare gene variants that protect them from pre-eclampsia, also known as toxaemia of pregnancy. This is the first time that mothers’ genotypes have been proven to contain factors that protect against pre-eclampsia.
Around 5 per cent of pregnant women get pre-eclampsia, which is one of the most common causes of maternal deaths and premature births. The underlying cause of pre-eclampsia is not yet known in detail, but the disease is known to increase the risk of cardiovascular diseases among mothers and their children later in life. Susceptibility to pre-eclampsia is hereditary: family history of this disease on the mother’s or father’s side increases its risk.
Researchers at the University of Helsinki have studied the effects of mothers’ genetic variations on developing pre-eclampsia. The study was based on the Finnish FINNPEC (Finnish Genetics of Pre-eclampsia Consortium) and FINRISK cohorts and compared samples from more than 600 pre-eclampsia patients and 2,000 non-pre-eclamptic controls.
“We chose candidate genes that were interesting in terms of pre-eclampsia, and studied the variation found in them among patients and controls,” says Inkeri Lokki, who is completing her doctoral dissertation on the subject. “The sFlt-1 protein is known to be linked to pre-eclampsia, and we found two single nucleotide polymorphisms in the gene that codes this protein. Pre-eclampsia is less common among mothers who carry these mutations than it is among other mothers.”
Too high an amount of sFlt-1 protein in the body causes vascular disorders. It is known that the amount of the sFlt-1 protein in the blood of the women who developed pre-eclampsia had increased before they fell ill.
The study also examined Finnish mothers’ health over the longer term, based on the FINRISK material.
“It seems that the women who carry gene variants that protect them from pre-eclampsia were also less likely to develop cardiac failure later in life than other women,” says Lokki.
University of Helsinki
www.helsinki.fi/en/news/rare-gene-variant-discovered-to-contribute-to-lower-risk-of-pre-eclampsia-in-finnish-mothers
ClearLLab reagents are the first to receive Food and Drug Administration (FDA) clearance (via the De Novo Process) to market them in the US. They deliver the first preformulated, IVD antibody cocktails for leukemia and lymphoma immunophenotyping in the clinical lab. For clinical laboratories it means they no longer have to develop their own laboratory developed test (LDT), a technically demanding, manual, time-consuming, and potentially error-prone process. Previously, labs would have had to make and validate their own antibody cocktails. ClearLLab reagents simplify and standardize the process.
‘FDA allows marketing of test to aid in the detection of certain leukemias and lymphomas’ with the FDA confirming that the test ‘provides consistent results to aid in the diagnoses of these serious cancers’. The FDA evaluated data from a multi-site clinical study which compared panel results to alternative detection methods.
Dr Mario Koksch, Vice President and General Manager of Beckman Coulter’s Cytometry Business Unit said: “Flow cytometry is a powerful tool for the detailed and fast analysis of complex populations, with the technique becoming increasingly valuable to the clinical hematology laboratory. “Clearance to market the first IVD L&L reagents in the US has opened the door to the expansion globally of our clinical reagent and instrument portfolio.”
ClearLLab reagents deliver fast and accurate qualitative identification of various hematolymphoid cell populations by immunophenotyping on the FC500 flow cytometer. With the reliability of a standardized kit and protocols, the preformulated combinations offer LEAN-focused benefits which reduce manual preparation and validation time, accelerate sample preparation time, improve workflow, streamline lab inventory management and provide confidence in the accuracy and reliability of results.
As Dr Koksch added: “The routine use of ready-to-use ClearLLab reagents delivers greater efficiency and cost savings. Preformulated antibody combinations enable the lab to avoid the potential errors of manual antibody cocktail preparation, with the reassurance of standardized reporting to international guidelines.”
ClearLLab reagents follow the 2006 Bethesda International Consensus Recommendations on the Flow Cytometric Immunophenotypic Analysis of Hematolymphoid Neoplasia. They are compatible with the World Health Organization (WHO) 2016-revised classification of myeloid neoplasms and acute leukemia. WHO, in collaboration with the European Association for Hematopathology and the Society for Hematopathology, recently made important changes to the classification of these diseases. These included new criteria for the recognition of some previously described neoplasms as well as clarification and refinement of the defining criteria for others.
www.beckman.com
Every year, just over 1000 people are diagnosed with kidney cancer in Sweden. The three most common variants are clear cell, papillary and chromophobe renal cancer. Researchers compare the gene expression in tumour cells from a kidney cancer patient with cells from healthy tissue to figure out in which part of the kidney the cancer began and what went wrong in these cells. Now, a research team at Lund University in Sweden has discovered that in the Cancer Genome Atlas database, the gene expression in reference samples from normal tissue varies, depending on where in the kidney the samples happen to have been taken. The analyses can be improved by clarifying which samples correspond to the correct tissue.
The part of the kidney which purifies the blood and generates urine is called the nephron and functions as a kind of tubing system. Each kidney contains around a million nephrons which collectively filter 180 litres of primary urine (waste products, water and salts) every day. This results in 1.5 litres of concentrated liquid, which is excreted through urination.
“Everything is very specifically regulated and the cells have different gene expression and hence properties depending on their location in the tubing.”, explains Håkan Axelson, research team leader and professor of molecular tumour biology.
When a tumour biopsy is taken from a patient and compared with healthy kidney tissue, it serves to map how the various genes are expressed so as to clarify what has gone wrong in the tumour cells. The Cancer Genome Atlas – an international database containing almost 1000 samples from kidney tumours and healthy tissue – is a tool in this process.
“But when our research team studied the samples from the database, we noticed a great range of gene expressions between normal tissue samples. It emerged that the samples in the Cancer Genome Atlas were taken at different depths in the kidney and therefore contain different types of cells, which means that their gene expressions also vary”, says Håkan Axelson.
The normal reference samples thus contain various types of cells depending on where in the kidney they happen to have been taken. Since the Atlas does not state the location in the kidney the reference sample was collected, the comparison risks being unreliable and sometimes completely incorrect.
“Since the gene expression in the cells varies depending on their location, it is important that the normal samples contained in the database should also be taken from the location corresponding to that of the patient’s tumour”, says David Lindgren, who is the lead author of the study.
As an example, it was previously suspected that clear cell tumours occur in the first part of the nephron, but if these tumour cells are compared with a normal sample taken deeper inside the nephron, the cells will not correspond to the tumour sample. The gene expression is thereby different. Although each patient is unique, the various types of tumours have different specific genetic changes which occur as a consequence of properties in the cell in which the tumour originated.
“It is extremely important to know what characterises the cells in which the tumour occurs. Through better understanding of this interaction, we can increase our understanding of the course of the disease, which could be significant for diagnostics and, in the longer term, also for the choice of treatment”, concludes Håkan Axelson.
Lund University
www.lunduniversity.lu.se/article/improved-analysis-of-kidney-cancer
November 2025
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