DNA mutations driving cancer development are caused by different mechanisms, each of them leaving behind specific patterns, or “scars” in the genome. Using CRISPR-Cas9 technology, researchers at CeMM and the Wellcome Trust Sanger Institute at Cambridge, UK were able to show for the first time in cell culture that specific genetic alterations indeed lead to the predicted pattern of mutational signatures observed in human cancers. When a cell develops into a tumour, something has gone terribly wrong: the uncontrolled growth, invasion of nearby tissues and finally metastasis are the result of many consecutive DNA mutations. Such an accumulation of demolished genetic material often derives from initial environmental exposures, enzymatic activities or defects in DNA replication or DNA repair mechanisms. Each of those initial mutagenic conditions creates their own pattern of DNA damage called mutational signature. Deciphering them could theoretically allow us to trace back the initial cause of a tumour, profile its properties and help find a therapeutic strategy. However, reading those mutational signatures in tumour samples is a difficult task, as the large amount of mutations that a patient acquires during its lifetime create a noisy and uncontrolled system – even the best clinical data will, at most, provide only associations. Therefore, the group of Joanna Loizou, Principal Investigator at CeMM in collaboration with researchers from the Wellcome Trust Sanger Institute, developed an experimental setup to validate the concept of mutational signatures in cell culture. The findings of this study not only confirm an analytical principle that describes mutational processes and cancer development, mutational signatures are a direct mechanistic read-out of specific dysfunctions of a cell. Thus, even if the underlying gene defect is unknown, mutational signatures could be used as biomarkers for the molecular characterization of tumors – a new diagnostic tool to improve the precise and personalized treatment of cancer.
CeMM cemm.at/news/
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A new study from BUSM and BUSPH identifies a pattern of inflammation associated with cardio-metabolic risks among participants in the Black Women’s Health Study, as well as two independent groups of vulnerable women. These findings could help underserved patients benefit from precision medicine and personalized profiles of disease risk. According to the researchers, body mass index alone is an imperfect measure of obesity-associated disease risks, such as for Type 2 diabetes, because there are some individuals with chronic obesity who are apparently protected from cardio-metabolic complications and lean individuals with high cardiovascular and diabetes risks. Abnormal, unresolved inflammation in blood and adipose (fat) tissue, rather than obesity per se, is thought to be important for development of disease. Certain biomarkers show promise in predicting obesity-associated diabetes risk; however, the clinical utility of single biomarkers is limited for complex disease phenotypes such as these. The research team took a data-driven, systems biology approach to discover six cytokine signatures associated with Type 2 diabetes risk in a vulnerable population: African American women with obesity and varying degrees of metabolic health. These six distinct signatures are patterns of sixteen cytokines/chemokines that promote or reduce inflammation. Analyses of plasma samples from participants in the Black Women’s Health Study, formed the basis for the discovery dataset, which was then validated in two separate groups, African American women volunteers with obesity who had donated plasma to the Komen Tissue Bank, and African American women with obesity who were breast reduction surgical patients at a safety net hospital in Greater Boston. The patterns or signatures in the validation cohorts closely resembled the distributions in the discovery cohort. “These findings are highly relevant to an understudied and underserved population that experiences elevated risks for co-morbidities of obesity. The overall impact of this report is high because of the potential utility of the new signatures just discovered and validated, which could assist clinical decision making with more personalized information,” explained corresponding author Gerald V. Denis, PhD, Associate Professor of Pharmacology and Medicine at BUSM.
Boston University School of Medicine www.bumc.bu.edu/busm/2018/05/08/new-study-provides-insight-into-blood-signatures-of-inflammation/
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A Vanderbilt-led research team has discovered genetic variations that increase the risk of heart attack even when patients are receiving a statin drug like Lipitor or Crestor to lower their blood cholesterol. The finding helps explain why some patients experience a heart attack or the need for coronary revascularization to open blocked heart arteries while taking statins. It suggests that drugs targeting the genetic variations could lower the heart risk in these patients. The study demonstrates the power of genome-wide association studies and longitudinal electronic health records (EHRs) to find links between genetic variation and disease, said the paper’s first author, Wei-Qi Wei, MD, PhD, assistant professor of Biomedical Informatics in the Vanderbilt University School of Medicine. Some of the patients were followed for heart disease for up to a decade after starting on their statin drug. The study found that the effect of the genetic variations or variants was independent of how much their cholesterol improved while taking statins. “People with these genetic variants were at a higher risk for heart disease, even considering those who have ideal cholesterol levels on their statin,” said Joshua Denny, MD, MS, Vice President of Personalized Medicine at Vanderbilt University Medical Center (VUMC) and the paper’s corresponding author. The researchers searched four sites in the Electronic Medical Records and Genomics (eMERGE) network, a nationwide consortium of experts, biorepositories and electronic medical record systems supported by the National Institutes of Health (NIH), including BioVU, VUMC’s DNA databank. They found 3,099 people who had experienced a heart attack or the need for revascularization while on statins, and compared them to 7,681 “control” patients on statins who did not experience heart events. From this comparison, the researchers were able to identify seven genetic variations, called single nucleotide polymorphisms or SNPs, in the LPA locus of genes that were associated with these heart events in patients receiving statin treatment. The LPA gene encodes apolipoprotein (a), a fatty protein that binds to low-density lipoprotein (LDL), the form of blood cholesterol that is the target of statin drugs. High levels of bound LDL, called Lp(a) for short, is well known to be an independent risk factor for heart disease. One of the SNPs was highly associated with an increased risk of heart events. When the researchers examined the full EHRs of 11,566 individuals who carried the SNP for more than 1,000 physical conditions, they found significantly higher rates of coronary heart disease and heart attack but not of other diseases. The approach, called a phenome-wide association study, was pioneered by Denny and his colleagues at Vanderbilt. “The study highlights the need to consider targeting Lp(a) levels as an important independent factor to reduce cardiovascular risk in patients on statin therapy,” Wei concluded. Efforts to reduce Lp(a) levels using existing or new drugs could reduce heart events in the proportion of patients on statins who carry LPA variations, he added, although clinical trials would be needed to detect potential side effects and confirm the safety of any such treatment.
Vanderbilt University Medical Centre news.vanderbilt.edu/2018/05/03/gene-study-spots-clues-to-heart-risk-for-statin-patients/
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An international team of researchers from the Hopp Children’s Cancer Center at the NCT Heidelberg (KiTZ), the European Molecular Biology Laboratory (EMBL) and the German Cancer Consortium (DKTK) together with colleagues at the St. Jude Children’s Research Hospital in Memphis and the Hospital for Sick Children in Toronto has summarized hereditary gene defects which can trigger the development of certain malignant brain tumours (medulloblastoma). From their findings, the team has derived recommendations for routine genetic screening in medulloblastoma patients. Medulloblastoma is a rare malignant tumour of the cerebellum and occurs predominantly in children. Scientists believe that in many cases hereditary gene defects trigger the development of this malignant disease. However, there are no standards for routine genetic screening of patients, nor are there guidelines and a corresponding nationwide infrastructure for genetic counselling of affected families. Scientists have now been able to characterize medulloblastoma more accurately and to derive recommendations for genetic testing based on analysis of 1022 patients with medulloblastoma. "We analysed genes that have been previously implicated in predisposition to any type of paediatric and adult cancer", says Sebastian Waszak from the EMBL Heidelberg who is one of the study’s lead authors. It turned out that six genes were also frequently affected by genetic alterations in patients with medulloblastoma. Considering the six significantly enriched genes, about five percent of patients had an increased risk of cancer. Taking into account all cancer risk genes, about eleven percent of the patients had an increased cancer risk. Looking at a particular tumour subgroup, the so called "SHH-activated medulloblastoma", even 20 percent were identified to harbour a genetic predisposition to cancer. These predisposing mutations occur in every single cell of the patient and can be also passed on to offspring. "Mutations of this kind often indicate a familial predisposition to cancer and therefore place special demands on the treatment of patients and the counselling of families", said Paul Northcott from the St. Jude Children’s Research Hospital in Memphis, who shares the lead authorship. The results are particularly important because both, materials from previous studies and patient data from four current or recently completed clinical trials were included in the analysis. Based on these findings and other tumour features, the scientists developed criteria for routine genetic screening. "Hereditary disease factors usually have a significant impact on the whole family of the patient, We want to make genetic analysis available as a standard of care for patients with specific medulloblastoma", says Stefan Pfister, KiTZ director, scientist at the German Cancer Research Center, and senior physician at the Heidelberg University Hospital. To make this possible, Stefan Pfister and Christian Kratz from the Hannover Medical School have created a registry for patients with a hereditary cancer predisposition and a website that contains information for patients, families, and physicians (www.krebs-praedisposition.de).
The German Cancer Research Center (DKFZ) www.dkfz.de/en/presse/pressemitteilungen/2018/dkfz-pm-18-30-Genetic-analysis-for-certain-childhood-brain-tumors-soon-a-standard-of-care.php
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Researchers have identified that enlargement of the left atrium of the heart is linked to abnormal activity of molecules that are associated with adverse changes in the heart’s size, shape, structure, and function — conditions that can lead to atrial fibrillation and death. The new study, conducted by researchers at the Intermountain Medical Center Heart Institute in Salt Lake City, is the first time this association has been connected to the human heart in a clinical setting. In conducting the study, researchers noted that under stress conditions, cardiac fibroblasts, which play a role in normal cardiac function and changes in the heart, release greater quantities of exosomes, which are small pieces of cells circulating in the blood that contain cellular components and convey information to distant tissues. The Intermountain Medical Center Heart Institute researchers found that in patients with atrial fibrillation, exosomes and plasma are enriched with MicroRNA (miR)-21-3p — which is associated to abnormal enlargement of the heart muscle. Scientists are interested in exosomes because initially they were thought to be a waste by-product as cells shed. But now researchers are learning that not only are exosomes communicators between cells, but they influence the spread of proteins, lipids, mRNA, miRNA, and DNA and are contributing factors in the development of several diseases. “Our study gives us a better understanding of the process of how atrial fibrillation begins and advances,” says Victoria Jacobs, NP, PhD, a member of the Intermountain Medical Center Heart Institute research team. “Once atrial fibrillation happens, we have some ‘band-aids’ to fix its symptoms, but we want to learn how to keep atrial fibrillation and atrial enlargement from happening in the first place.” While an enlarged atria may have several causes, recent studies have linked enlargement to an increased risk of atrial fibrillation. Researchers are interested in learning more about atrial fibrillation because it, along with coronary artery disease, is the number one killer of people in America. Atrial fibrillation affects more than 3.4 million Americans, primarily older adults. An enlarged left atrium has been linked to atrial fibrillation, as it can prevent the heart from pumping blood properly and may increase risk of an irregular heartbeat. Researchers at the Intermountain Medical Center Heart Institute examined biomarkers, which are biological molecules used to see how well the body responds to a treatment for a disease or condition, that could specifically predict the occurrence and severity of adverse growth in the left atrium of the heart. A basic study previously done in Germany that focused on cell cultures and small lab rodents suggested that miR-21-3p played a role in that growth. But no one has connected it to the human heart in a clinical setting until now. “We know patients with atrial fibrillation develop thickening of heart tissue, or fibrosis,” said Dr. Jacobs. “As atrial fibrillation progresses, we know there’s more fibrosis in the left atrium. But this is the first time we’ve shown miR-21-3p is associated with left atrial fibrillation in patients.”
The Intermountain Medical Center intermountainhealthcare.org/news/2018/05/rna-molecules-predict-adverse-heart-growth-function/
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Rheumatoid arthritis (RA) is an autoimmune disorder that occurs when the immune system mistakenly attacks the body’s tissues. Unlike the wear-and-tear damage of osteoarthritis, rheumatoid arthritis affects the lining of the joints, causing painful swelling that can eventually result in bone erosion and joint deformity. Most RA patients are positive for anticitrullinated protein antibodies (ACPA), and these antibodies are highly specific for RA diagnosis. ACPA recognizes various citrullinated proteins, such as fibrinogen, vimentin and glucose- 6-phosphate isomerase. Citrullinated proteins are proteins that have the amino acid arginine converted into the citrulline, which is not one of the 20 standard amino acids encoded by DNA in the genetic code. Autoreactivity to citrullinated protein may increase susceptibility to RA. While many candidate citrullinated antigens have been identified in RA joints, the involvement of citrullinated proteins in blood serum remains mostly uninvestigated. To that end, a team of University of Tsukuba-centred researchers set out to explore the expression and commonality of citrullinated proteins in peptide glucose-6-phosphate isomerase-induced arthritis (pGIA) and patients with RA, and went one step further to investigate its correlation with RA disease activity. "We examined serum citrullinated proteins from pGIA by western blotting, and the sequence was identified by mass spectrometry. With the same methods, serum citrullinated proteins were analysed in patients with RA, primary Sjögren’s syndrome, systemic lupus erythematosus, and osteoarthritis as well as in healthy subjects," study corresponding author Isao Matsumoto explains. "In patients with RA, the relationship between the expression of the identified protein inter-alpha-trypsin inhibitor heavy chain 4 (ITIH4) and clinical features was also evaluated, and the levels of citrullinated ITIH4 were compared before and after biological treatment." The researchers found that citrullinated ITIH4 was highly specific to patients with RA, compared with patients with other autoimmune and arthritic diseases or in healthy subjects, indicating a potential role for citrullinated ITIH4 in RA pathogenesis. Notably, its levels were decreased in correlation with the reduction of disease activity score after effective treatment in patients with RA. Moreover, antibody response to citrullinated epitope in ITIH4 was specifically observed in patients with RA. "Our results suggest that citrullinated ITIH4 might be a novel biomarker to distinguish RA from other rheumatic diseases and for assessing disease activity in patients with RA," Matsumoto says. "To our knowledge, this is the first report of its kind in the literature."
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Kidney cancer, one of the ten most prevalent malignancies in the world, has increased in incidence over the last decade, likely due to rising obesity rates. The most common subtype of this cancer is “clear cell” renal cell carcinoma (ccRCC), which exhibits multiple metabolic abnormalities, such as highly elevated stored sugar and fat deposition. By integrating data on the function of essential metabolic enzymes with genetic, protein, and metabolic abnormalities associated with ccRCC, researchers at the Perelman School of Medicine at the University of Pennsylvania determined that enzymes important in multiple pathways are universally depleted in ccRCC tumors. “Kidney cancer develops from an extremely complex set of cellular malfunctions,” said senior author Celeste Simon, PhD, the scientific director of the Abramson Family Cancer Research Institute and a professor of Cell and Developmental Biology. “That’s why we approached studying its cause from many perspectives.” Using human tissue provided by the National Cancer Institute’s Cooperative Human Tissue Network and Penn Medicine physicians Naomi Haas, MD, an associate professor of Hematology/Oncology, and Priti Lal, MD, an associate professor of Pathology and Laboratory Medicine, the team found that the expression of certain enzymes is strongly repressed in ccRCC tumors. For example, reduced activity of one enzyme, arginase, promotes ccRCC tumour growth through at least two distinct biochemical pathways. One is by conserving a critical molecular cofactor and the second is by avoiding toxic accumulation of organic compounds. The enzymes whose activities are depressed are involved in the breakdown of urea, a by-product of protein being used in the human body. In addition, loss of these enzymes results in decreased ability of the immune system to eradicate these tumours. “Pharmacological approaches to restore the expression of urea cycle enzymes would greatly expand treatment options for ccRCC patients, whose current therapies only benefit a small subset,” Simon said.
Penn Medicine www.pennmedicine.org/news/news-releases/2018/may/depleted-metabolic-enzymes-promote-tumor-growth-in-kidney-cancer-1
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Scientists have identified a mutation that gives cancer cells resistance to the breakthrough cancer treatment olaparib and other PARP inhibitors. The study findings could help predict which patients will develop resistance to PARP inhibitors and allow doctors to alter treatment at the earliest possible opportunity. A team at The Institute of Cancer Research, London, used gene editing to identify a specific mutation in the PARP1 protein that prevents PARP inhibitors from working. Testing for this mutation could add another level of personalisation to an already targeted treatment – helping guide decisions about whether to use PARP inhibitors in the first place, and when to switch to other drugs, such as platinum-based therapies. PARP1 is crucial for the repair of damaged DNA and is an important target for olaparib and other PARP inhibitors. These drugs are especially effective in patients who already have weaknesses in DNA repair because of inherited errors in the BRCA genes – a discovery that was made at the ICR. The scientists used new ‘CRIPSR-Cas9’ gene editing technology to generate mutations in small, targeted sections of the PARP1 gene, and tagged the mutant protein with a fluorescent protein so their effects could be tracked. This approach allowed the researchers to observe the effect of specific mutations on PARP1 and on the sensitivity of cancer cells to PARP inhibitors, such as olaparib and talazoparib. Olaparib is available on the NHS for women with ovarian cancer who have inherited BRCA mutations, and is currently being evaluated for breast cancer. It was the first ever cancer drug to be approved that is targeted against an inherited genetic fault. The study identified specific PARP1 mutations which disrupt the ability of the protein to bind to DNA, which means PARP inhibitors can no longer trap them at the site of DNA damage. The researchers found that, contrary to their original predictions, cancer cells with certain mutations in the BRCA1 gene could survive this loss of PARP1’s DNA repair function – making them resistant to PARP inhibitors. It is thought that in these cases the BRCA1 gene retains some function, providing some residual ability to repair DNA despite the loss of PARP1. The scientists emphasised that further research needs to be carried out to examine more PARP1 mutations in patients as only one example in humans was found in this study. The team is looking to apply this same gene editing approach to study how resistance arises to other drugs, and if it is possible to predict how quickly this resistance will progress.
Institute of Cancer Researchwww.icr.ac.uk/news-archive/scientists-identify-cause-of-resistance-to-breakthrough-breast-and-ovarian-cancer-drug
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ZenTech has signed a strategic agreement to transfer its portfolio of radioimmunoassays (RIA) to DIAsource ImmunoAssays, a BioVendor group company.
ZenTech, a Belgian biotech company specialized in the development, production and commercialization of solutions for clinical diagnostics of early life stage diseases and newborn screening, and DIAsource ImmunoAssays, a leading diagnostics company delivering manual RIA and ELISA kits and open automation solutions to international markets, today announced a strategic agreement, under which ZenTech will transfer its portfolio of RIA products to DIAsource, securing the continued production and sales of these products.
ZenTech has strategically reoriented itself to focus on newborn screening and early life stage diseases. DIAsource is the second largest supplier of radioimmunoassays in the world, committed to servicing customers worldwide that use manual ELISA and RIA assays and open automation to complement their portfolio on closed automated systems.
Both Belgian companies have long standing collaborations for more than 15 years, whereby DIAsource already managed part of the commercialization of the Zentech portfolio successfully. The current transfer of the RIA products from Zentech to DIAsource is a logical next step in line with the strategies of both companies. The portfolio to be transferred includes the complete line of specialty radioimmunoassays with thyroid markers and markers for fertility and salt balance.
In order to support a smooth transition with minimal disruption for customers, the companies have agreed to a transition period. Effective today 24th of July 2018 DIAsource Immunoassays assumes commercial ownership of the RIA product portfolio and will service clients from order to shipment, whereby ZenTech remains the manufacturer during the transition period in which the production will be transferred to DIAsource. The latter will be done in close collaboration and in phases and concluded by 30 September 2019.
Jean-Claude Havaux, Chaiman of the Board, ZenTech, said: “Historically, ZenTech had a background and expertise in radioimmunoassays. However, when ZenTech acquired the Belgian company Gamma in 2011, it got access to new technologies and entered the market of newborn screening and early life stage diseases. Today’s acquisition of the RIA products by ZenTech’s commercial partner DIAsource will guarantee RIA customers are offered long term service and excellence in logistics worldwide. This transaction will give ZenTech the opportunity to focus on new innovative product lines and other technologies such as molecular diagnostics and mass spectrometry. ZenTech strives to "make innovation affordable for most" within a worldwide strategy.”
Jef Vangenechten, CEO of DIAsource Immunoassays, said: "This acquisition is yet another step in our strategy to position DIAsource as a consolidator of manual specialty assays, after previous acquisitions of the Intertech RIA product line in 2012 and Viro-Immun ELISA and IFA product lines in 2017. DIAsource also acquired the RIA client businesses from distribution partners in France and Spain in 2015 and 2016. This fourth acquisition in the RIA space demonstrates our commitment to the long term future servicing and support of our large RIA customer base worldwide We experience that RIA remains important as the gold standard for assays that are not available on automated systems or for parameters that require a higher analytical accuracy, whereby manual assays offer benefits in terms of quality and flexibility versus price. DIAsource now has a unique position by combining the most complete offering of RIA specialty assays on the market with the ability to offer various RIA automation solutions. Furthermore our manual assays also allow customization for life science research and screening."
www.diasource-diagnostics.comwww.zentech.be
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The way healthcare is delivered around the globe is changing. Patients are now at the centre of how medical care is delivered and recent advances in medical technology have allowed medical laboratory testing to move in parallel with this course. Keeping up-to-date with latest industry trends emerging from within the medical laboratory industry is critical to the lab professional, particularly in Europe, where the In-Vitro Diagnostics (IVD), clinical laboratory, molecular diagnostics and Point-of-Care Testing markets are some of the fastest growing in the world. Regulations around medical and IVD devices in Europe are also evolving which involves important improvements to modernise the current system including risk-classification, improved transparency and new rules on clinical evidence. Under these new regulations, the classification of devices is based on risk and manufacturers need to demonstrate that their medical device meets the requirements by carrying out a conformity assessment. Essentially, the European medical laboratory-testing ecosystem is becoming safer, faster and more efficient, and technology and regulations are evolving to put patient safety and care at the heart of healthcare delivery. Here are some of the top trends that are shaping the European medical laboratory industry in 2018: Point-of-Care Testing (POC) As the world becomes more connected, POC testing enters a rapid phase of development. Medical decisions can be made quickly as the disease can be diagnosed at an earlier stage. Next generation POC testing is entering the market with prospective label-free biosensors, such as electrochemical, surface plasmon resonance (SPR), white light reflectance spectroscopy (WLRS), etc., being used for improved devices. Also, a wide range of POC assays for the quantitative determination of biomarkers has been developed using portable and easy-to-use POC clinical and biochemical analysers. 3D printing also shows huge potential to improving the performance of POC devices. The Internet of Things (IoT) The IoT can help to reduce the rising costs in laboratory testing while also increasing access to patient care. According to a report by ABI Research, connectivity to lab equipment and the services enabled by that connectivity will increase total global laboratory test throughput to over 3.02 billion more diagnostic tests by 2020. Laboratory Automation Increasing the efficiency to maximise the productivity and manage costs has become critical for the long-term success of the clinical laboratory. Robotic automation is an area where patient-focused technology can make a real difference. The future lies in automated phlebotomy, transportation processes using drones and Artificial Intelligence (AI) with these advancements providing increased access to healthcare. Next-generation DNA sequencing (NGS)
Since the introduction of many next-generation sequencing (NGS), the cost of DNA sequencing has significantly reduced and huge improvements have been made in the unraveling the complexities of sequencing data. In situ sequencing (ISS) offers incredible new opportunities for studying tissue heterogeneity, for example. NGS provides cheaper, friendlier, and more flexible high-throughput sequencing options with a quantum leap towards the generation of much more data on genomics, transcriptomics, and methylomics that translate more productively into proteomics, metabolomics, and systeomics.
www.medlabeurope.com
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Tracing the footprints of a tumour: genomic “scars” allow cancer profiling
, /in E-News /by 3wmediaDNA mutations driving cancer development are caused by different mechanisms, each of them leaving behind specific patterns, or “scars” in the genome. Using CRISPR-Cas9 technology, researchers at CeMM and the Wellcome Trust Sanger Institute at Cambridge, UK were able to show for the first time in cell culture that specific genetic alterations indeed lead to the predicted pattern of mutational signatures observed in human cancers.
When a cell develops into a tumour, something has gone terribly wrong: the uncontrolled growth, invasion of nearby tissues and finally metastasis are the result of many consecutive DNA mutations. Such an accumulation of demolished genetic material often derives from initial environmental exposures, enzymatic activities or defects in DNA replication or DNA repair mechanisms. Each of those initial mutagenic conditions creates their own pattern of DNA damage called mutational signature. Deciphering them could theoretically allow us to trace back the initial cause of a tumour, profile its properties and help find a therapeutic strategy.
However, reading those mutational signatures in tumour samples is a difficult task, as the large amount of mutations that a patient acquires during its lifetime create a noisy and uncontrolled system – even the best clinical data will, at most, provide only associations. Therefore, the group of Joanna Loizou, Principal Investigator at CeMM in collaboration with researchers from the Wellcome Trust Sanger Institute, developed an experimental setup to validate the concept of mutational signatures in cell culture.
The findings of this study not only confirm an analytical principle that describes mutational processes and cancer development, mutational signatures are a direct mechanistic read-out of specific dysfunctions of a cell. Thus, even if the underlying gene defect is unknown, mutational signatures could be used as biomarkers for the molecular characterization of tumors – a new diagnostic tool to improve the precise and personalized treatment of cancer.
CeMM
cemm.at/news/
Insight into blood signatures of inflammation
, /in E-News /by 3wmediaA new study from BUSM and BUSPH identifies a pattern of inflammation associated with cardio-metabolic risks among participants in the Black Women’s Health Study, as well as two independent groups of vulnerable women. These findings could help underserved patients benefit from precision medicine and personalized profiles of disease risk.
According to the researchers, body mass index alone is an imperfect measure of obesity-associated disease risks, such as for Type 2 diabetes, because there are some individuals with chronic obesity who are apparently protected from cardio-metabolic complications and lean individuals with high cardiovascular and diabetes risks. Abnormal, unresolved inflammation in blood and adipose (fat) tissue, rather than obesity per se, is thought to be important for development of disease. Certain biomarkers show promise in predicting obesity-associated diabetes risk; however, the clinical utility of single biomarkers is limited for complex disease phenotypes such as these.
The research team took a data-driven, systems biology approach to discover six cytokine signatures associated with Type 2 diabetes risk in a vulnerable population: African American women with obesity and varying degrees of metabolic health. These six distinct signatures are patterns of sixteen cytokines/chemokines that promote or reduce inflammation.
Analyses of plasma samples from participants in the Black Women’s Health Study, formed the basis for the discovery dataset, which was then validated in two separate groups, African American women volunteers with obesity who had donated plasma to the Komen Tissue Bank, and African American women with obesity who were breast reduction surgical patients at a safety net hospital in Greater Boston. The patterns or signatures in the validation cohorts closely resembled the distributions in the discovery cohort.
“These findings are highly relevant to an understudied and underserved population that experiences elevated risks for co-morbidities of obesity. The overall impact of this report is high because of the potential utility of the new signatures just discovered and validated, which could assist clinical decision making with more personalized information,” explained corresponding author Gerald V. Denis, PhD, Associate Professor of Pharmacology and Medicine at BUSM.
Boston University School of Medicine
www.bumc.bu.edu/busm/2018/05/08/new-study-provides-insight-into-blood-signatures-of-inflammation/
Gene study spots clues to heart risk for statin patients
, /in E-News /by 3wmediaA Vanderbilt-led research team has discovered genetic variations that increase the risk of heart attack even when patients are receiving a statin drug like Lipitor or Crestor to lower their blood cholesterol.
The finding helps explain why some patients experience a heart attack or the need for coronary revascularization to open blocked heart arteries while taking statins. It suggests that drugs targeting the genetic variations could lower the heart risk in these patients.
The study demonstrates the power of genome-wide association studies and longitudinal electronic health records (EHRs) to find links between genetic variation and disease, said the paper’s first author, Wei-Qi Wei, MD, PhD, assistant professor of Biomedical Informatics in the Vanderbilt University School of Medicine.
Some of the patients were followed for heart disease for up to a decade after starting on their statin drug. The study found that the effect of the genetic variations or variants was independent of how much their cholesterol improved while taking statins.
“People with these genetic variants were at a higher risk for heart disease, even considering those who have ideal cholesterol levels on their statin,” said Joshua Denny, MD, MS, Vice President of Personalized Medicine at Vanderbilt University Medical Center (VUMC) and the paper’s corresponding author.
The researchers searched four sites in the Electronic Medical Records and Genomics (eMERGE) network, a nationwide consortium of experts, biorepositories and electronic medical record systems supported by the National Institutes of Health (NIH), including BioVU, VUMC’s DNA databank.
They found 3,099 people who had experienced a heart attack or the need for revascularization while on statins, and compared them to 7,681 “control” patients on statins who did not experience heart events.
From this comparison, the researchers were able to identify seven genetic variations, called single nucleotide polymorphisms or SNPs, in the LPA locus of genes that were associated with these heart events in patients receiving statin treatment.
The LPA gene encodes apolipoprotein (a), a fatty protein that binds to low-density lipoprotein (LDL), the form of blood cholesterol that is the target of statin drugs. High levels of bound LDL, called Lp(a) for short, is well known to be an independent risk factor for heart disease.
One of the SNPs was highly associated with an increased risk of heart events. When the researchers examined the full EHRs of 11,566 individuals who carried the SNP for more than 1,000 physical conditions, they found significantly higher rates of coronary heart disease and heart attack but not of other diseases.
The approach, called a phenome-wide association study, was pioneered by Denny and his colleagues at Vanderbilt.
“The study highlights the need to consider targeting Lp(a) levels as an important independent factor to reduce cardiovascular risk in patients on statin therapy,” Wei concluded.
Efforts to reduce Lp(a) levels using existing or new drugs could reduce heart events in the proportion of patients on statins who carry LPA variations, he added, although clinical trials would be needed to detect potential side effects and confirm the safety of any such treatment.
Vanderbilt University Medical Centre
news.vanderbilt.edu/2018/05/03/gene-study-spots-clues-to-heart-risk-for-statin-patients/
Genetic analysis for certain childhood brain tumours soon a standard-of-care?
, /in E-News /by 3wmediaAn international team of researchers from the Hopp Children’s Cancer Center at the NCT Heidelberg (KiTZ), the European Molecular Biology Laboratory (EMBL) and the German Cancer Consortium (DKTK) together with colleagues at the St. Jude Children’s Research Hospital in Memphis and the Hospital for Sick Children in Toronto has summarized hereditary gene defects which can trigger the development of certain malignant brain tumours (medulloblastoma). From their findings, the team has derived recommendations for routine genetic screening in medulloblastoma patients.
Medulloblastoma is a rare malignant tumour of the cerebellum and occurs predominantly in children. Scientists believe that in many cases hereditary gene defects trigger the development of this malignant disease. However, there are no standards for routine genetic screening of patients, nor are there guidelines and a corresponding nationwide infrastructure for genetic counselling of affected families.
Scientists have now been able to characterize medulloblastoma more accurately and to derive recommendations for genetic testing based on analysis of 1022 patients with medulloblastoma. "We analysed genes that have been previously implicated in predisposition to any type of paediatric and adult cancer", says Sebastian Waszak from the EMBL Heidelberg who is one of the study’s lead authors. It turned out that six genes were also frequently affected by genetic alterations in patients with medulloblastoma.
Considering the six significantly enriched genes, about five percent of patients had an increased risk of cancer. Taking into account all cancer risk genes, about eleven percent of the patients had an increased cancer risk. Looking at a particular tumour subgroup, the so called "SHH-activated medulloblastoma", even 20 percent were identified to harbour a genetic predisposition to cancer.
These predisposing mutations occur in every single cell of the patient and can be also passed on to offspring. "Mutations of this kind often indicate a familial predisposition to cancer and therefore place special demands on the treatment of patients and the counselling of families", said Paul Northcott from the St. Jude Children’s Research Hospital in Memphis, who shares the lead authorship. The results are particularly important because both, materials from previous studies and patient data from four current or recently completed clinical trials were included in the analysis.
Based on these findings and other tumour features, the scientists developed criteria for routine genetic screening. "Hereditary disease factors usually have a significant impact on the whole family of the patient, We want to make genetic analysis available as a standard of care for patients with specific medulloblastoma", says Stefan Pfister, KiTZ director, scientist at the German Cancer Research Center, and senior physician at the Heidelberg University Hospital. To make this possible, Stefan Pfister and Christian Kratz from the Hannover Medical School have created a registry for patients with a hereditary cancer predisposition and a website that contains information for patients, families, and physicians (www.krebs-praedisposition.de).
The German Cancer Research Center (DKFZ)
www.dkfz.de/en/presse/pressemitteilungen/2018/dkfz-pm-18-30-Genetic-analysis-for-certain-childhood-brain-tumors-soon-a-standard-of-care.php
RNA molecules predict adverse heart growth and function that can lead to atrial fibrillation and death
, /in E-News /by 3wmediaResearchers have identified that enlargement of the left atrium of the heart is linked to abnormal activity of molecules that are associated with adverse changes in the heart’s size, shape, structure, and function — conditions that can lead to atrial fibrillation and death.
The new study, conducted by researchers at the Intermountain Medical Center Heart Institute in Salt Lake City, is the first time this association has been connected to the human heart in a clinical setting.
In conducting the study, researchers noted that under stress conditions, cardiac fibroblasts, which play a role in normal cardiac function and changes in the heart, release greater quantities of exosomes, which are small pieces of cells circulating in the blood that contain cellular components and convey information to distant tissues.
The Intermountain Medical Center Heart Institute researchers found that in patients with atrial fibrillation, exosomes and plasma are enriched with MicroRNA (miR)-21-3p — which is associated to abnormal enlargement of the heart muscle.
Scientists are interested in exosomes because initially they were thought to be a waste by-product as cells shed. But now researchers are learning that not only are exosomes communicators between cells, but they influence the spread of proteins, lipids, mRNA, miRNA, and DNA and are contributing factors in the development of several diseases.
“Our study gives us a better understanding of the process of how atrial fibrillation begins and advances,” says Victoria Jacobs, NP, PhD, a member of the Intermountain Medical Center Heart Institute research team. “Once atrial fibrillation happens, we have some ‘band-aids’ to fix its symptoms, but we want to learn how to keep atrial fibrillation and atrial enlargement from happening in the first place.”
While an enlarged atria may have several causes, recent studies have linked enlargement to an increased risk of atrial fibrillation. Researchers are interested in learning more about atrial fibrillation because it, along with coronary artery disease, is the number one killer of people in America. Atrial fibrillation affects more than 3.4 million Americans, primarily older adults.
An enlarged left atrium has been linked to atrial fibrillation, as it can prevent the heart from pumping blood properly and may increase risk of an irregular heartbeat.
Researchers at the Intermountain Medical Center Heart Institute examined biomarkers, which are biological molecules used to see how well the body responds to a treatment for a disease or condition, that could specifically predict the occurrence and severity of adverse growth in the left atrium of the heart. A basic study previously done in Germany that focused on cell cultures and small lab rodents suggested that miR-21-3p played a role in that growth. But no one has connected it to the human heart in a clinical setting until now.
“We know patients with atrial fibrillation develop thickening of heart tissue, or fibrosis,” said Dr. Jacobs. “As atrial fibrillation progresses, we know there’s more fibrosis in the left atrium. But this is the first time we’ve shown miR-21-3p is associated with left atrial fibrillation in patients.”
The Intermountain Medical Center
intermountainhealthcare.org/news/2018/05/rna-molecules-predict-adverse-heart-growth-function/
Biomarker with remarkable specificity to rheumatoid arthritis
, /in E-News /by 3wmediaRheumatoid arthritis (RA) is an autoimmune disorder that occurs when the immune system mistakenly attacks the body’s tissues. Unlike the wear-and-tear damage of osteoarthritis, rheumatoid arthritis affects the lining of the joints, causing painful swelling that can eventually result in bone erosion and joint deformity.
Most RA patients are positive for anticitrullinated protein antibodies (ACPA), and these antibodies are highly specific for RA diagnosis. ACPA recognizes various citrullinated proteins, such as fibrinogen, vimentin and glucose- 6-phosphate isomerase. Citrullinated proteins are proteins that have the amino acid arginine converted into the citrulline, which is not one of the 20 standard amino acids encoded by DNA in the genetic code. Autoreactivity to citrullinated protein may increase susceptibility to RA.
While many candidate citrullinated antigens have been identified in RA joints, the involvement of citrullinated proteins in blood serum remains mostly uninvestigated. To that end, a team of University of Tsukuba-centred researchers set out to explore the expression and commonality of citrullinated proteins in peptide glucose-6-phosphate isomerase-induced arthritis (pGIA) and patients with RA, and went one step further to investigate its correlation with RA disease activity.
"We examined serum citrullinated proteins from pGIA by western blotting, and the sequence was identified by mass spectrometry. With the same methods, serum citrullinated proteins were analysed in patients with RA, primary Sjögren’s syndrome, systemic lupus erythematosus, and osteoarthritis as well as in healthy subjects," study corresponding author Isao Matsumoto explains. "In patients with RA, the relationship between the expression of the identified protein inter-alpha-trypsin inhibitor heavy chain 4 (ITIH4) and clinical features was also evaluated, and the levels of citrullinated ITIH4 were compared before and after biological treatment."
The researchers found that citrullinated ITIH4 was highly specific to patients with RA, compared with patients with other autoimmune and arthritic diseases or in healthy subjects, indicating a potential role for citrullinated ITIH4 in RA pathogenesis. Notably, its levels were decreased in correlation with the reduction of disease activity score after effective treatment in patients with RA. Moreover, antibody response to citrullinated epitope in ITIH4 was specifically observed in patients with RA.
"Our results suggest that citrullinated ITIH4 might be a novel biomarker to distinguish RA from other rheumatic diseases and for assessing disease activity in patients with RA," Matsumoto says. "To our knowledge, this is the first report of its kind in the literature."
MedicalXpressmedicalxpress.com/news/2018-04-discovery-biomarker-remarkable-specificity-rheumatoid.html
Depleted metabolic enzymes promote tumour growth in kidney cancer
, /in E-News /by 3wmediaKidney cancer, one of the ten most prevalent malignancies in the world, has increased in incidence over the last decade, likely due to rising obesity rates. The most common subtype of this cancer is “clear cell” renal cell carcinoma (ccRCC), which exhibits multiple metabolic abnormalities, such as highly elevated stored sugar and fat deposition.
By integrating data on the function of essential metabolic enzymes with genetic, protein, and metabolic abnormalities associated with ccRCC, researchers at the Perelman School of Medicine at the University of Pennsylvania determined that enzymes important in multiple pathways are universally depleted in ccRCC tumors.
“Kidney cancer develops from an extremely complex set of cellular malfunctions,” said senior author Celeste Simon, PhD, the scientific director of the Abramson Family Cancer Research Institute and a professor of Cell and Developmental Biology. “That’s why we approached studying its cause from many perspectives.”
Using human tissue provided by the National Cancer Institute’s Cooperative Human Tissue Network and Penn Medicine physicians Naomi Haas, MD, an associate professor of Hematology/Oncology, and Priti Lal, MD, an associate professor of Pathology and Laboratory Medicine, the team found that the expression of certain enzymes is strongly repressed in ccRCC tumors. For example, reduced activity of one enzyme, arginase, promotes ccRCC tumour growth through at least two distinct biochemical pathways. One is by conserving a critical molecular cofactor and the second is by avoiding toxic accumulation of organic compounds. The enzymes whose activities are depressed are involved in the breakdown of urea, a by-product of protein being used in the human body. In addition, loss of these enzymes results in decreased ability of the immune system to eradicate these tumours.
“Pharmacological approaches to restore the expression of urea cycle enzymes would greatly expand treatment options for ccRCC patients, whose current therapies only benefit a small subset,” Simon said.
Penn Medicine
www.pennmedicine.org/news/news-releases/2018/may/depleted-metabolic-enzymes-promote-tumor-growth-in-kidney-cancer-1
Cause of resistance to breakthrough breast and ovarian cancer drug
, /in E-News /by 3wmediaScientists have identified a mutation that gives cancer cells resistance to the breakthrough cancer treatment olaparib and other PARP inhibitors.
The study findings could help predict which patients will develop resistance to PARP inhibitors and allow doctors to alter treatment at the earliest possible opportunity.
A team at The Institute of Cancer Research, London, used gene editing to identify a specific mutation in the PARP1 protein that prevents PARP inhibitors from working.
Testing for this mutation could add another level of personalisation to an already targeted treatment – helping guide decisions about whether to use PARP inhibitors in the first place, and when to switch to other drugs, such as platinum-based therapies.
PARP1 is crucial for the repair of damaged DNA and is an important target for olaparib and other PARP inhibitors. These drugs are especially effective in patients who already have weaknesses in DNA repair because of inherited errors in the BRCA genes – a discovery that was made at the ICR.
The scientists used new ‘CRIPSR-Cas9’ gene editing technology to generate mutations in small, targeted sections of the PARP1 gene, and tagged the mutant protein with a fluorescent protein so their effects could be tracked.
This approach allowed the researchers to observe the effect of specific mutations on PARP1 and on the sensitivity of cancer cells to PARP inhibitors, such as olaparib and talazoparib.
Olaparib is available on the NHS for women with ovarian cancer who have inherited BRCA mutations, and is currently being evaluated for breast cancer. It was the first ever cancer drug to be approved that is targeted against an inherited genetic fault.
The study identified specific PARP1 mutations which disrupt the ability of the protein to bind to DNA, which means PARP inhibitors can no longer trap them at the site of DNA damage.
The researchers found that, contrary to their original predictions, cancer cells with certain mutations in the BRCA1 gene could survive this loss of PARP1’s DNA repair function – making them resistant to PARP inhibitors.
It is thought that in these cases the BRCA1 gene retains some function, providing some residual ability to repair DNA despite the loss of PARP1.
The scientists emphasised that further research needs to be carried out to examine more PARP1 mutations in patients as only one example in humans was found in this study.
The team is looking to apply this same gene editing approach to study how resistance arises to other drugs, and if it is possible to predict how quickly this resistance will progress.
Institute of Cancer Researchwww.icr.ac.uk/news-archive/scientists-identify-cause-of-resistance-to-breakthrough-breast-and-ovarian-cancer-drug
DIAsource Immunoassays to assume production and sales of ZenTech RIA product portfolio
, /in E-News /by 3wmediaZenTech has signed a strategic agreement to transfer its portfolio of radioimmunoassays (RIA) to DIAsource ImmunoAssays, a BioVendor group company.
ZenTech, a Belgian biotech company specialized in the development, production and commercialization of solutions for clinical diagnostics of early life stage diseases and newborn screening, and DIAsource ImmunoAssays, a leading diagnostics company delivering manual RIA and ELISA kits and open automation solutions to international markets, today announced a strategic agreement, under which ZenTech will transfer its portfolio of RIA products to DIAsource, securing the continued production and sales of these products.
ZenTech has strategically reoriented itself to focus on newborn screening and early life stage diseases. DIAsource is the second largest supplier of radioimmunoassays in the world, committed to servicing customers worldwide that use manual ELISA and RIA assays and open automation to complement their portfolio on closed automated systems.
Both Belgian companies have long standing collaborations for more than 15 years, whereby DIAsource already managed part of the commercialization of the Zentech portfolio successfully. The current transfer of the RIA products from Zentech to DIAsource is a logical next step in line with the strategies of both companies. The portfolio to be transferred includes the complete line of specialty radioimmunoassays with thyroid markers and markers for fertility and salt balance.
In order to support a smooth transition with minimal disruption for customers, the companies have agreed to a transition period. Effective today 24th of July 2018 DIAsource Immunoassays assumes commercial ownership of the RIA product portfolio and will service clients from order to shipment, whereby ZenTech remains the manufacturer during the transition period in which the production will be transferred to DIAsource. The latter will be done in close collaboration and in phases and concluded by 30 September 2019.
Jean-Claude Havaux, Chaiman of the Board, ZenTech, said: “Historically, ZenTech had a background and expertise in radioimmunoassays. However, when ZenTech acquired the Belgian company Gamma in 2011, it got access to new technologies and entered the market of newborn screening and early life stage diseases. Today’s acquisition of the RIA products by ZenTech’s commercial partner DIAsource will guarantee RIA customers are offered long term service and excellence in logistics worldwide. This transaction will give ZenTech the opportunity to focus on new innovative product lines and other technologies such as molecular diagnostics and mass spectrometry. ZenTech strives to "make innovation affordable for most" within a worldwide strategy.”
Jef Vangenechten, CEO of DIAsource Immunoassays, said: "This acquisition is yet another step in our strategy to position DIAsource as a consolidator of manual specialty assays, after previous acquisitions of the Intertech RIA product line in 2012 and Viro-Immun ELISA and IFA product lines in 2017. DIAsource also acquired the RIA client businesses from distribution partners in France and Spain in 2015 and 2016. This fourth acquisition in the RIA space demonstrates our commitment to the long term future servicing and support of our large RIA customer base worldwide
www.diasource-diagnostics.comwww.zentech.beWe experience that RIA remains important as the gold standard for assays that are not available on automated systems or for parameters that require a higher analytical accuracy, whereby manual assays offer benefits in terms of quality and flexibility versus price.
DIAsource now has a unique position by combining the most complete offering of RIA specialty assays on the market with the ability to offer various RIA automation solutions. Furthermore our manual assays also allow customization for life science research and screening."
Top Trends Changing The Medical Laboratory Industry In Europe
, /in E-News /by 3wmediaThe way healthcare is delivered around the globe is changing. Patients are now at the centre of how medical care is delivered and recent advances in medical technology have allowed medical laboratory testing to move in parallel with this course.
www.medlabeurope.comKeeping up-to-date with latest industry trends emerging from within the medical laboratory industry is critical to the lab professional, particularly in Europe, where the In-Vitro Diagnostics (IVD), clinical laboratory, molecular diagnostics and Point-of-Care Testing markets are some of the fastest growing in the world.
Regulations around medical and IVD devices in Europe are also evolving which involves important improvements to modernise the current system including risk-classification, improved transparency and new rules on clinical evidence. Under these new regulations, the classification of devices is based on risk and manufacturers need to demonstrate that their medical device meets the requirements by carrying out a conformity assessment.
Essentially, the European medical laboratory-testing ecosystem is becoming safer, faster and more efficient, and technology and regulations are evolving to put patient safety and care at the heart of healthcare delivery. Here are some of the top trends that are shaping the European medical laboratory industry in 2018:
Point-of-Care Testing (POC)
As the world becomes more connected, POC testing enters a rapid phase of development. Medical decisions can be made quickly as the disease can be diagnosed at an earlier stage. Next generation POC testing is entering the market with prospective label-free biosensors, such as electrochemical, surface plasmon resonance (SPR), white light reflectance spectroscopy (WLRS), etc., being used for improved devices. Also, a wide range of POC assays for the quantitative determination of biomarkers has been developed using portable and easy-to-use POC clinical and biochemical analysers. 3D printing also shows huge potential to improving the performance of POC devices.
The Internet of Things (IoT)
The IoT can help to reduce the rising costs in laboratory testing while also increasing access to patient care. According to a report by ABI Research, connectivity to lab equipment and the services enabled by that connectivity will increase total global laboratory test throughput to over 3.02 billion more diagnostic tests by 2020.
Laboratory Automation
Increasing the efficiency to maximise the productivity and manage costs has become critical for the long-term success of the clinical laboratory. Robotic automation is an area where patient-focused technology can make a real difference. The future lies in automated phlebotomy, transportation processes using drones and Artificial Intelligence (AI) with these advancements providing increased access to healthcare.
Next-generation DNA sequencing (NGS)
Since the introduction of many next-generation sequencing (NGS), the cost of DNA sequencing has significantly reduced and huge improvements have been made in the unraveling the complexities of sequencing data. In situ sequencing (ISS) offers incredible new opportunities for studying tissue heterogeneity, for example. NGS provides cheaper, friendlier, and more flexible high-throughput sequencing options with a quantum leap towards the generation of much more data on genomics, transcriptomics, and methylomics that translate more productively into proteomics, metabolomics, and systeomics.