Siemens Healthineers is developing “The Enterprise Project” with the Hermes Pardini Group of Minas Gerais, Brazil. The Enterprise Project is the largest and most complex clinical analysis laboratory known to date and is expected to be capable of handling 110 million sample tubes per year upon completion. Siemens Healthineers, in collaboration with Inpeco, has designed and will deliver this fully automated multidisciplinary solution on an unprecedented scale, which will include at least 100 analysers—including more than 50 Atellica Solution clinical chemistry and immunoassay analysers from Siemens Healthineers, the largest IVD supplier in this project. The highly sophisticated solution will provide automation of clinical and operational workflow, from sample reception through testing to disposal. Sited in Vespasiano, Grande Belo Horizonte in Minas Gerais, the lab will occupy 3,500 square meters of floor space, will conduct operations 24 hours a day, and is expected to be fully operational during 2019. “The automation track will be more than 330 meters long upon completion and will be used to automatically transport and distribute sample tubes to specific analysers that can run the specific type of test requested by clinicians,” said Guilherme Collares, Chef Operations Officer of the Hermes Pardini Group. “Unlike conventional laboratory set-ups, where sample tubes have to be moved manually between different analysers, our enterprise lab is designed to employ a ‘one-touch, one workflow’ concept to eliminate the need for manual interventions, ensure sample traceability, and reduce the turnaround time to results. The Enterprise Project also will rely on Atellica Process Manager, an IT solution that delivers a 3D view of the laboratory configuration, to enable operators to manage alerts, control instruments and reagent monitoring remotely, and see test progression in real time. Siemens Healthineers will implement the first Laboratory Control Room, which will centralize management and provide holistic visibility of operations in the central Vespasiano laboratory, and other Hermes Pardini satellite lab units in São Paulo, Rio de Janeiro, Goiania, and Belo Horizonte.
https://tinyurl.com/y9h4mtgm
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There is as yet no cure for Alzheimer’s disease. It is often argued that progress in drug research has been hampered by the fact that the disease can only be diagnosed when it is too late for an effective intervention. Alzheimer’s disease is thought to begin long before patients show typical symptoms like memory loss. Scientists have now developed a blood test for Alzheimer’s disease and found that it can detect early indicators of the disease long before the first symptoms appear in patients. The blood test would thus offer an opportunity to identify those at risk and may thereby open the door to new avenues in drug discovery. One of the hallmarks of Alzheimer’s disease is the accumulation of amyloid-β plaques in the patient’s brain. The blood test, developed by Klaus Gerwert and his team at Ruhr University Bochum, Germany, works by measuring the relative amounts of a pathological and a healthy form of amyloid-β in the blood. The pathological form is a misfolded version of this molecule and known to initiate the formation of toxic plaques in the brain. Toxic amyloid-β molecules start accumulating in the patients’ body 15-20 years before disease onset. In the present study, Gerwert and colleagues from Germany and Sweden addressed whether the blood test would be able to pick up indications of pathological amyloid-β in very early phases of the disease. The researchers first focused on patients in the early, so called prodromal stages of the disease from the Swedish BioFINDER cohort conducted by Oskar Hanson. They found that the test reliably detected amyloid-β alterations in the blood of participants with mild cognitive impairment that also showed abnormal amyloid deposits in brain scans. In a next step, Gerwert and colleagues investigated if their assay was able to detect blood changes well ahead of disease onset. They used data from the ESTHER cohort study, which Hermann Brenner started in 2000 at DKFZ, comparing blood samples of 65 participants that were later in the follow-up studies diagnosed with Alzheimer’s disease with 809 controls. The assay was able to detect signs of the disease on average eight years before diagnosis in individuals without clinical symptoms. It correctly identified those with the disease in almost 70% of the cases, while about 9% of true negative subjects would wrongly be detected as positive. The overall diagnostic accuracy was 86%. Currently available diagnostic tools for Alzheimer’s disease either involve expensive positron emission tomography (PET) brain scans, or analyse samples of cerebrospinal fluid that are extracted via lumbar puncture. The researchers suggest that their blood test serves as a cheap and simple option to pre-select individuals from the general population for further testing by these more invasive and costly methods to exclude the falsely positive subjects. EMBOwww.embo.org/news/press-releases/2018/a-new-blood-test-useful-to-detect-people-at-risk-of-developing-alzheimer-s-disease
https://clinlabint.com/wp-content/uploads/sites/2/2020/06/clinlab-logo.png003wmediahttps://clinlabint.com/wp-content/uploads/sites/2/2020/06/clinlab-logo.png3wmedia2020-08-26 09:32:182021-01-08 11:08:46A new blood test useful to detect people at risk of developing Alzheimer’s disease
An urgent question for cancer scientists is why immunotherapy achieves dramatic results in some cases but doesn’t help most patients. Now, two research groups from Dana-Farber Cancer Institute have independently discovered a genetic mechanism in cancer cells that influences whether they resist or respond to immunotherapy drugs known as checkpoint inhibitors. The scientists say the findings reveal potential new drug targets and might aid efforts to extend the benefits of immunotherapy treatment to more patients and additional types of cancer. One report, focusing on clinical trial patients with advanced kidney cancer treated with checkpoint inhibitors, is from scientists at Dana-Farber Cancer Institute and the Broad Institute of MIT and Harvard, led by Eliezer Van Allen, MD, of Dana-Farber and the Broad, and Toni Choueiri, MD, director of the Lank Center for Genitourinary Oncology at Dana-Farber. The second report, which identifies the immunotherapy resistance mechanism in melanoma cells, is from a group led by Kai Wucherpfennig, MD, PhD, director of Dana-Farber’s Center for Cancer Immunotherapy Research, and Shirley Liu, PhD, of Dana-Farber. The two groups converged on a discovery that resistance to immune checkpoint blockade is critically controlled by changes in a group of proteins that regulate how DNA is packaged in cells. The collection of proteins, called a chromatin remodelling complex, is known as SWI/SNF; its components are encoded by different genes, among them ARID2, PBRM1, and BRD7. SWI/SNF’s job is to open up stretches of tightly wound DNA so that its blueprints can be read by the cell to activate certain genes to make proteins. Researchers led by Van Allen and Choueiri sought an explanation for why some patients with a form of metastatic kidney cancer called clear cell renal cell cancer (ccRCC) gain clinical benefit — sometimes durable — from treatment with immune checkpoint inhibitors that block the PD-1 checkpoint, while other patients don’t. The scientists’ curiosity was piqued by the fact that ccRCC differs from other types of cancer that respond well to immunotherapy, such as melanoma, non-small cell lung cancer, and a specific type of colorectal cancer. Cells of the latter cancer types contain many DNA mutations, which are thought to make distinctive "neoantigens" that help the patient’s immune system recognize and attack tumours, and make the cancer cells’ “microenvironment” hospitable to tumour-fighting T cells. By contrast, ccRCC kidney cancer cells contain few mutations, yet some patients even with advanced, metastatic disease respond well to immunotherapy. To search for other characteristics of ccRCC tumours that influence immunotherapy response or resistance, the researchers used whole-exome DNA sequencing to analyse tumour samples from 35 patients treated in a clinical trial with the checkpoint blocker nivolumab (Opdivo). They also analysed samples from another group of 63 patients with metastatic ccRCC treated with similar drugs. When the data was sorted and refined, the scientists discovered that patients who benefited from the immunotherapy treatment with longer survival and progression-free survival were those whose tumours lacked a functioning PRBM1 gene. (About 41 percent of patients with ccRCC kidney cancer have a non-functioning PRBM1 gene.) That gene encodes a protein called BAF 180, which is a subunit of the PBAF subtype of the SWI/SNF chromatin remodelling complex. Loss of the PRBM1 gene function caused the cancer cells to have increased expression of other genes, including a gene pathway known as IL6/JAK-STAT3, which are involved in immune system stimulation. While the finding does not directly lead to a test for immunotherapy response yet, Choueiri said, "We intend to look at these specific genomic alterations in larger, randomized controlled trials, and we hope that one day these findings will be the impetus for prospective clinical trials based on these alterations." In the second report, the scientists led by Wucherpfennig came at the issue from a different angle. They used the gene-editing CRISPR/Cas9 technique to sift the genomes of melanoma cells for changes that made tumours resistant to being killed by immune T cells, which are the main actors in the immune system response against infections and cancer cells. The search turned up about 100 genes which appeared to govern melanoma cells’ resistance to being killed by T cells. Inactivating those genes rendered the cancer cells sensitive to T-cell killing. Narrowing down their search, the Wucherpfennig team identified the PBAF subtype of the SWI/SNF chromatin remodelling complex — the same group of proteins implicated by the Van Allen and Choueiri team in kidney cancer cells — as being involved in resistance to immune T cells. When the PRBM1 gene was knocked out in experiments, the melanoma cells became more sensitive to interferon-gamma produced by T cells, and in response produced signaling molecules that recruited more tumor-fighting T cells into the tumor. The two other genes in the PBAF complex — ARID2 and BRD7 — are also found mutated in some cancers, according to the researchers, and those cancers, like the melanoma lacking ARID2 function, may also respond better to checkpoint blockade. The protein products of these genes, the authors note, "represent targets for immunotherapy, because inactivating mutations sensitize tumor cells to T-cell mediated attack." Finding ways to alter those target molecules, they add, "will be important to extend the benefit of immunotherapy to larger patient populations, including cancers that thus far are refractory to immunotherapy." Dana-Farber Cancer Institutewww.dana-farber.org/newsroom/news-releases/2018/mechanism-for-resistance-to-immunotherapy-treatment-discovered/
https://clinlabint.com/wp-content/uploads/sites/2/2020/06/clinlab-logo.png003wmediahttps://clinlabint.com/wp-content/uploads/sites/2/2020/06/clinlab-logo.png3wmedia2020-08-26 09:32:182021-01-08 11:08:53Mechanism for resistance to immunotherapy treatment discovered
Cancer drops sparse chemical hints of its presence early on, but unfortunately, many of them are in a class of biochemicals that could not be detected thoroughly, until now. Researchers at the Georgia Institute of Technology have engineered a chemical trap that exhaustively catches what are called glycoproteins, including minuscule traces that have previously escaped detection. Glycoproteins are protein molecules bonded with sugar molecules, and they’re very common in all living things. Glycoproteins come in myriad varieties and sizes and make up important cell structures like cell receptors. They also wander around our bodies in secretions like mucus or hormones. But some glycoproteins are very, very rare and can serve as an early signal, or biomarker, indicating there’s something wrong in the body – like cancer. Existing methods to reel in glycoproteins for laboratory examination are relatively new and have had big holes in their nets, so many of these molecules, especially those very rare ones produced by cancer, have tended to slip by. “These tiny traces are critically important for early disease detection,” said principal investigator Ronghu Wu, a professor in Georgia Tech’s School of Chemistry and Biochemistry. “When cancer is just getting started, aberrant glycoproteins are produced and secreted into body fluids such as blood and urine. Often their abundances are extremely low, but catching them is urgent.” This new chemical trap, which took Georgia Tech chemists several years to develop and is based on a boronic acid, has proven extremely effective in lab tests including on cultured human cells and mouse tissue samples. “This method is very universal,” said first author Haopeng Xiao, a graduate research assistant. “We get over 1,000 glycoproteins in a really small lab sample.” In comparison tests with existing methods, the chemical trap, a complex molecular construction reminiscent of an octopus, captured exponentially more glycoproteins, especially more of those trace glycoproteins. Wu, Xiao and Weixuan Chen, a former Georgia Tech postdoctoral researcher, who was also first author of the study alongside Xiao. For chemistry whizzes, here’s a short summary of how the researchers made the octopus. They took a good thing and doubled then tripled down on it. Those who recall high school chemistry class may still know what boric acid is, as do people who use it to kill roaches. Its chemical structure is an atom of boron bonded with three hydroxyl groups (H3BO3). Boronic acids are a family of organic compounds that build on boric acid. There are many members of the boronic acid family, and they tend to bond well with glycoproteins, but their bonds can be less reliable than needed. “Most boronic acids let too many low-abundance glycoproteins get away,” Wu said. “They can catch glycoproteins that are in high abundance but not those in low abundance, the ones that tell us more valuable things about cell development or about human disease.” But the Georgia Tech chemists were able to leverage the strengths of boronic acids to develop a glycoprotein capturing method that works exceptionally well. First, they tested several boronic acid derivatives and found that one called benzoboroxole strongly bound with each sugar component on the glycopeptide. (“Peptide” refers to the basic chemical composition of a protein.) Then they stitched many benzoboroxole molecules together with other components to form a "dendrimer," which refers to the resulting branch- or tentacle-like structure. The finished large molecule resembled an octopus ready to go after those sugar components. In its middle, similarly positioned to an octopus’s head, was a magnetic bead, which acted as a kind of handle. Once the dendrimer caught a glycoprotein, the researchers used a magnet to grab the bead and pull out their chemical octopus along with its ensnared glycopeptides (e.g. glycoproteins). “Then we washed the dendrimer off with a low pH solution, and we had the glycoproteins analysed with things like mass spectrometry,” Wu said. The researchers have some ideas about how medical laboratory researchers could make practical use of the new Georgia Tech method to detect odd biomolecules emitted by cancer, such as antigens. For example, the chemical octopus could improve detection of prostate-specific antigens (PSA) in prostate cancer screenings. “PSA is a glycoprotein. Right now, if the level is very high, we know that the patient may have cancer, and if it’s very low, we know cancer is not likely,” Wu said. “But there is a gray area in between, and this method could lead to much more detailed information in that gray area.” The researchers also believe that developers could leverage the chemical invention to produce targeted cancer treatments. Immune cells could be trained to recognize the aberrant glycoproteins, track down their source cancer cells in the body and kill them.
Georgia Institute of Technologywww.news.gatech.edu/2018/05/04/chemical-octopus-catches-sneaky-cancer-clues-trace-glycoproteins
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The role of the placenta in healthy foetal development is being seriously under-appreciated according to a new paper The study was part of the Wellcome-funded “Deciphering the Mechanisms of Developmental Disorders (DMDD)” consortium. Dr Myriam Hemberger at the Babraham Institute, Cambridge led the research, working with colleagues at the Wellcome Sanger Institute, Cambridge, the Francis Crick Institute, London, the University of Oxford and the Medical University of Vienna, Austria. The team studied 103 genetic mutations in mice that cause embryos to die before birth. The results showed that the majority, almost 70 per cent, cause defects in the placenta. Each of the 103 gene mutations causes the loss of a particular factor. Many of these had not been previously linked to placenta development, and hence the study highlights the unexpected number of genes that affect development of the placenta. By studying a select group of three genes in further detail, the team went on to show that the death of the embryo could be directly linked to defects in the placenta in one out of these three cases. This may mean that a significant number of genetic defects that lead to prenatal death may be due to abnormalities of the placenta, not just the embryo. Although this research uses mice, the findings are likely to be highly relevant to complications during human pregnancy and the study highlights the need for more work to be done on investigating development of the placenta during human pregnancies. The placenta is vital for normal pregnancy progression and embryo development in most animals that give birth to live young, including humans. It provides a unique and highly specialised interface between the embryo and the mother, ensuring an adequate provision of nutrients and oxygen to the embryo. The placenta is also involved in waste disposal from the embryo and produces important hormones that help sustain pregnancy and promote foetal growth. Although previous research has highlighted the pivotal role of the placenta for a healthy pregnancy, its potential contribution to pregnancy complications and birth defects continues to be overlooked. Scientists call mutations that cause death in the womb embryonic lethal. Mouse lethal genes are enriched for human disease genes and the affected embryos often show morphological abnormalities, i.e. changes to their shape and structure. Around one-third of all gene mutants studied in mouse are lethal or subviable (i.e. mutant offspring are less likely to survive than non-mutant pups). “Analysis of embryonic lethal mutants has largely focused on the embryo and not the placenta, despite its critical role in development. Of the mutations we’ve studied, far more than expected showed defects in the placenta and this is particularly true for mutations that cause death during the early stages of pregnancy. Intriguingly, our analysis also indicates that issues in the placenta often occur alongside specific defects in the embryo itself.”
“Our data highlight the hugely under-appreciated importance of placental defects in contributing to abnormal embryo development and suggest key molecular nodes governing placentation. The importance of a healthy placenta has often been overlooked in these studies and it is important that we start doing more to understand its contribution to developmental abnormalities.” Wellcome Sanger Institutewww.sanger.ac.uk/news/view/placenta-defects-critical-factor-prenatal-deaths
https://clinlabint.com/wp-content/uploads/sites/2/2020/06/clinlab-logo.png003wmediahttps://clinlabint.com/wp-content/uploads/sites/2/2020/06/clinlab-logo.png3wmedia2020-08-26 09:32:182021-01-08 11:08:48Placenta defects critical factor in prenatal deaths
Researchers from Case Western Reserve University School of Medicine have discovered how unusually long pieces of RNA work in skin cells. The RNA pieces, called “long non-coding RNAs” or “lncRNAs,” help skin cells modulate connective tissue proteins, like collagen, and could represent novel therapeutic targets to promote skin repair. In a recent study, researchers identified specific lncRNAs that control genes and behaviour of mouse skin cells. The team found 111 lncRNAs that work with a highly conserved protein network called the Wnt/β-catenin pathway. The Wnt/β-catenin pathway serves as a signalling hub that helps cells across species adjust gene expression in response to their environment. The new study connects this important pathway to a new form of genetic control—lncRNAs. “LncRNAs are a newly discovered class of genes, and we’ve been working to elucidate their functions and mechanisms as they appear to be critical for human health,” said Ahmad Khalil, PhD, assistant professor of genetics and genome sciences and member of the Case Comprehensive Cancer Center at Case Western Reserve University School of Medicine. “Our findings show that the Wnt/β-catenin pathway activates certain lncRNAs to directly control gene expression in skin fibroblast cells.” The team studied skin cells, called dermal fibroblasts, that help hair follicles develop, wounds heal, and generally maintain the structural integrity of skin. Fibroblasts orchestrate these important functions with the help of the Wnt/β-catenin pathway, among others. Sustained activation of the Wnt/β-catenin pathway can cause fibroblasts to overproduce connective tissue proteins, like collagen, causing harmful skin fibrosis. According to the new study, lncRNAs serve as an intermediary between Wnt/β-catenin and fibroblast genes. The researchers showed fibroblasts genetically modified to overproduce β-catenin had 8-14 times higher levels of two specific lncRNAs when compared to control fibroblasts. The researchers named the lncRNAs Wincr1 and Wincr2—Wnt signalling induced non-coding RNA.” The lncRNA levels correlated with significantly higher levels of proteins that help fibroblasts move and contract. The findings suggest disrupting lncRNA levels could change how fibroblasts function in skin. The study adds to a growing body of evidence that lncRNAs could represent a new arena for drug developers. LncRNAs are intriguing therapeutic targets—recent studies by Khalil and others have implicated lncRNAs defects in all kinds of diseases, including infertility and cancer. Said Atit, “Specific lncRNAs that operate downstream of the Wnt/β-catenin pathway could serve as drug targets for chronic and acute skin fibrosis conditions.” The researchers are now working to understand how lncRNAs work in various animal models, and how their dysfunction may promote disease.
Case Western Reserve University School of Medicinehttps://tinyurl.com/yan5xss9
https://clinlabint.com/wp-content/uploads/sites/2/2020/06/clinlab-logo.png003wmediahttps://clinlabint.com/wp-content/uploads/sites/2/2020/06/clinlab-logo.png3wmedia2020-08-26 09:32:182021-01-08 11:08:55Finding long strands of RNA in skin development and disease
New findings will help to identify the genetic causes of brain disorders: researchers at the Universities of Basel, Bonn and Cologne have presented a systematic catalogue of specific variable locations in the genome that influence gene activity in the human hippocampus. Individual differences in gene regulation contribute to the development of numerous multifactorial disorders. Researchers are therefore attempting to clarify the influence of genetic variants (single-nucleotide polymorphisms, or SNPs) on gene expression and on the epigenetic modification of regulatory sections of the genome (DNA methylation). The German–Swiss team has now studied the genetic determinants of gene expression, as well as the process of DNA methylation in the human hippocampus. The researchers have presented an extensive catalogue of variable locations in the genome – that is, of SNPs – that affect the activity of genes in the human hippocampus. Specifically, they have analysed the influence of more than three million SNPs, spread throughout the genome, on activity in nearby genes and the methylation of adjacent DNA sections. The special thing about their work is that the researchers used freshly frozen hippocampus tissue obtained during surgery on 110 treatment-resistant epilepsy patients. They extracted DNA and RNA from the hippocampus tissue and, for all of the obtained samples, used microchips to determine several hundred thousand SNPs, as well as the degree of methylation at several hundred thousand locations (known as CpG dinucleotides) in the genome. Among other analyses, they measured the gene expression of over 15,000 genes using RNA microchips. The researchers also demonstrated the preferred areas in which variably methylated CpG dinucleotides appear in the genome, and they were able to assign these to specific regulatory elements, revealing a link to brain disorders: a significant proportion of the identified SNPs that individually influence DNA methylation and gene expression in the hippocampus also contribute to the development of schizophrenia. This underlines the potentially significant role played by SNPs with a regulatory effect in the development of brain disorders. The study’s findings will make it considerably easier to interpret evidence of genetic associations with brain disorders in the future. Of the SNPs involved in the development of brain disorders, many of those identified in recent years are located in the non-coding part of the genome. Their functional effect in cells is therefore largely unclear.
University of Baselhttps://tinyurl.com/y9uveu98
https://clinlabint.com/wp-content/uploads/sites/2/2020/06/clinlab-logo.png003wmediahttps://clinlabint.com/wp-content/uploads/sites/2/2020/06/clinlab-logo.png3wmedia2020-08-26 09:32:182021-01-08 11:08:44Tracking down genetic influences on brain disorders
Blood stem cells give rise to all of our blood cells: the red blood cells that transport oxygen, the platelets that enable blood coagulation, and our immune cells that protect us from infections. Immune cells can, in turn, be divided into two groups; one that consists of cells with a very short life expectancy and a natural but rather unspecific ability to counteract infections (myeloid cells), and another that, in contrast, consists of very long-lived cells (lymphocytes) that specialize in combatting specific bacteria and viruses. “The ability of blood stem cells to form all types of blood cells is a fundamental property that is also utilized in connection with bone marrow transplants. An increased understanding of these processes is crucial as immune cells in patients who undergo bone marrow transplants are regenerated very slowly, which results in a long period of immune sensitivity”, says David Bryder who was in charge of the study. Despite the fact that all of our genes have been mapped, it is still largely unknown how the genes are controlled. What a cell can and cannot do is governed entirely by how the cell uses its genome. David Bryder and his colleagues have searched for genes expressed in immature blood cells but which disappear in connection with their further maturation. They then discovered the HLF gene, which caught their attention for two reasons: one, the gene controls what parts of our DNA are to be used, and two, the gene is directly involved in a rare but very aggressive type of blood cancer. “Our studies revealed that if the immature blood cells are unable to shut down the HLF gene at the correct stage of development, the lymphocytes – the long-lived immune cells – are unable to form. As a result, you will only have one type of immune defence.” A single cell must undergo a variety of changes to become cancerous. However, the earliest changes may involve the HLF gene, which give rise to a precursor to leukemia. Patients with leukemia in which the HLF gene is involved have a very poor prognosis, but it has been difficult to generate reliable models for studying the emergence, development and possible treatment of these leukemia more thoroughly. The researchers’ long-term goal is now to identify the mechanisms that can be used to break down these aggressive leukemia. “The knowledge and experimental model systems we developed concerning how HLF affects blood cell development enables us to map the order of gene mutations that lead to HLF-generated leukemia, which is an important next step towards our goal”, concludes David Bryder.
Lund Universityhttps://tinyurl.com/yd2xl6b2
https://clinlabint.com/wp-content/uploads/sites/2/2020/06/clinlab-logo.png003wmediahttps://clinlabint.com/wp-content/uploads/sites/2/2020/06/clinlab-logo.png3wmedia2020-08-26 09:32:182021-01-08 11:08:51The HLF-gene controls the generation of our long-term immune system
Both environmental and genetic risk factors contribute to development of lung cancer. Tobacco smoking is the most well-known environmental risk factor associated with lung cancer. A Dartmouth research team led by Yafang Li, PhD, has conducted a study to display that gene-smoking interactions play important roles in the etiology of lung cancer. In their study, three novel SNPs (single-nucleotide polymorphisms), or variations in our DNA that underlie our susceptibility to developing disease, were identified in the interaction analysis, including two SNPs for non-small cell lung cancer risk and one SNP for squamous cell lung cancer risk. The three identified novel SNPs provide potential candidate biomarkers for lung cancer risk screening and intervention. The team’s findings, "Genome-wide interaction study of smoking behaviour and non-small cell lung cancer risk in Caucasian population," have been published in Carcinogenesis. The genotype and phenotype data used in this analysis came from OncoArray Consortium. "Genome-wide interaction scanning remains a challenge as most genome-wide association studies are designed for main effect association analysis and have limited power for interaction analysis," said Li. "This study is by far the largest genome-wide SNP-smoking interaction analysis reported for lung cancer. We also adopted a two-step strategy in the analysis to reduce the power loss from ordinary gene-environment interaction analysis." The three SNPs, identified in the team’s study, stratify lung cancer risk by smoking behavior. These three SNPs can be potential biomarkers used to improve the precision to which researchers can categorize an individual’s risk of lung cancer disease by smoking behavior, which are helpful for individualized prognosis and prediction of treatment plan. While this reported study was restricted to a Caucasian population and the results may not be generalized to other ethnicities because of the different genetic backgrounds, the team aims to further test the identified interaction effect using genotype from other populations. "The limited overlap between discovery genotype and replication genotype may have reduced the power in our validation study," says Li. "We believe as more genotype data becomes available in the future we can discover more important gene-smoking interaction in lung cancer disease." EurekAlert www.eurekalert.org/pub_releases/2017-10/dmc-tnl102617.php
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R-Biopharm Group recently announced a collaborative agreement with SSI, focusing on discovery and development of novel diagnostic approaches for the detection of tuberculosis infection. The development of new diagnostic assays in the area of infectious diseases is a priority for R-Biopharm, a company with 30 years of experience in providing testing solutions for Clinical Diagnostics and Food & Feed analysis. R-Biopharm Group operates in various countries including subsidiaries in the UK, USA, Italy, France, Latin America, Brazil, Spain, Belgium, Australia, India and China as well as by a worldwide extensive network of more than 120 distributors. “This collaborative agreement creates an opportunity to work with the world-leading scientists and inventors of novel biomarkers and vaccines in the area of tuberculosis research. Our Infectious Diseases Team is inspired to join efforts for the development of novel diagnostics for the tuberculosis patients throughout the world. At R-Biopharm we are concerned about rising numbers of tuberculosis cases and escalation of multidrug-resistant (MDR-TB) and extensively drug-resistant TB (XDR-TB). In cooperation with Statens Serum Institute we will have the potential to transform the current underserved market of tuberculosis diagnostics and provide alternative solutions for the detection of TB infection,” said Dr. Ralf Dreher, CEO and Founder of R-Biopharm Group. SSI is one of Denmark’s largest research institutions in the health sector with over a century of experience in research, development and manufacturing of biologics. Led by Professor Peter Andersen, the research and development team at SSI are at the forefront in the development of novel vaccines and diagnostic agents for major diseases affecting global health. The program has brought several novel vaccine candidates in clinical trial within TB and Chlamydia as well as provided the ground work for the current industry standard in diagnostic tests for tuberculosis infection (IGRAs). “We are excited for our collaboration with R-Biopharm, a leading industry partner in the field of infectious disease diagnostics. As a government research organization under the ministry of health, industrial involvement is pivotal to get our projects from the lab out to the benefit of patients. The strong research base at R-Biopharm is a great match for the SSI team and has been a fruitful synergy,” said Prof. Peter Andersen, Executive Vice President, Center for Vaccine Research at Statens Serum Institute. Under the agreement, R-Biopharm and SSI will collaborate on research and development and responsibility for the commercialization of potential products.
www.r-biopharm.com
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