There are nine genes that make you gain more weight if you already have a high body mass index, McMaster University researchers have found. “It’s similar to a tiny snow ball at a top of a hill that becomes bigger and bigger when rolling down the hill,” said senior author David Meyre, an associate professor of health research methods, evidence and impact at McMaster University. He also holds the Canada Research Chair in Genetics of Obesity. “The effect of these genes may be amplified by four times, if we compare the 10% of the population at the low end of the body mass index, compared to the 10% at the high end,” he added. The study’s co-first authors are postdoctoral fellow Arkan Abadi and PhD student Akram Alyass, who both work in the Meyre laboratory. Although the increasing average body mass index of the population of several high-income countries has recently plateaued, the researchers note in the study, the cases of extreme forms of obesity are still growing. People who are morbidly obese are at risk of health complications such as diabetes, cardiovascular disease, hypertension and cancers and early death. On top of lifestyle factors such as unhealthy diet and physical inactivity, genetic factors are also known to play an important role, with 50 to 80 per cent of body mass index related to genetics. The researchers looked at 37 genes that are well established as modulating the body mass in 75,230 adults with European ancestry and found the nine with the snowball effect. “These genes may, in part, explain why some individuals experience uncontrolled and constant weight gain across their life, despite the availability of different therapeutic approaches,” said Meyre. “The plausible explanation is that there are interactions between the snowball obesity genes and risk environmental factors.” He added that the idea of preventing obesity in the first place is a good strategy for people with a high genetic risk for obesity. “We have an important message of hope that the carriers of these genes, if they stay in the low end of body mass index through appropriate lifestyle, may minimize the effect of the snowball obesity genes.”
McMaster Universityhttps://tinyurl.com/ya247466
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 11:08:56Researchers find genes may ‘snowball’ obesity
When researchers at the University of São Paulo (USP) in Brazil treated human melanoma cell lines with a synthetic compound similar to curcumin, one of the pigments that give turmeric (Curcuma longa) its orange colour, they identified genes with altered expression in potentially invasive tumours and malignant cells resistant to chemotherapy. According to the scientists, if further studies confirm the importance of these genes to disease progression and increasing chemoresistance, it will be possible to explore their future use as biomarkers to assist diagnosis and even as therapeutic targets. “Previous research by collaborators had already shown that DM-1, a compound analogous to curcumin, has anti-tumour activity at low doses. We set out to understand which genes this substance modulates and why it is toxic to melanoma but not to normal cells,” said Érica Aparecida de Oliveira, a postdoctoral scholar at USP’s School of Pharmaceutical Sciences (FCF). As Oliveira explained, there are hundreds of papers attesting to the anti-oxidant, anti-tumoural, anti-microbial and anti-inflammatory properties of curcumin in the scientific literature. However, the therapeutic usefulness of this compound in its natural form is limited owing to poor absorption, rapid metabolization, and water insolubility. To solve this problem, scientists have developed synthetic analogues with minor structural modifications to make the molecule more stable in the organism. DM-1 (sodium 4-[5-(4-hydroxy-3-methoxyphenyl)-3-oxo-penta-1,4-dienyl]-2-methoxy-phenolate) was synthesized some years ago by José Agustín Pablo Quincoces Suárez, a professor at Bandeirantes University (UNIBAN). “Experiments with animals conducted by collaborators showed that treatment with DM-1 can promote a reduction in tumour volume. DM-1 has also proved toxic to chemoresistant melanoma cells,” Oliveira said. To unpack DM-1’s mechanism of action, Oliveira resorted to a toxicogenomics platform developed by the research group of FCF-USP professor Gisele Monteiro, a fellow researcher at the investigation. Such platform is comprised of a collection of 6,000 frozen yeast strains, all mutants of the species Saccharomyces cerevisiae, widely used as baker’s and brewer’s yeast. “This yeast’s genome has 6,000 genes, and a different gene has been knocked out in each of these mutants, so we were able to study the effects of the compound in a highly specific manner, gene by gene,” Oliveira said. The 6,000 mutant yeast strains were thawed, spread on plates with 96 small wells, and treated with DM-1. The strains that did not grow in the presence of the curcumin analogue were discarded, leaving an initial group of 211 genes that were affected by the treatment. The next step was to filter the genes in order to identify those with homologues in the human genome since some might be associated with functions specific to yeast. The researchers came up with a second list containing 79 candidate genes, thanks to the aid from bioinformatics tools and from the expertise of Helder Nakaya , another fellow researcher and also a professor at FCF-USP. “We then began to look at public repositories of genomic data from cancer patients, such as The Cancer Genome Atlas (TCGA) and the Gene Expression Omnibus (GEO), to understand how these genes talked to each other,” Oliveira said. The analysis showed most to be associated with cell signalling pathways that favoured tumour progression when active. Examples included the pathways mediated by mitogen-activated protein (MAP) kinase and epidermal growth factor receptor (EGFR). The next step was to investigate which genes were important to the progression of melanoma specifically. This entailed using bioinformatics to focus on the analysis of genomic sequences from melanoma patients. “We performed a data mining exercise to find genes with altered expression during melanoma progression,” Oliveira said. “We identified seven genes that appeared to be important, and when we looked at the public databases, we could see that the expression of these genes was indeed altered in many patients.” In vitro tests with non-chemoresistant parent melanoma cells showed that treatment with DM-1 induced cell death, mainly because it increased expression of a gene known as TOP-1. When this gene is active, it leads to DNA transcription errors and hence causes genomic instability in cells. In chemoresistant melanoma cells, cytotoxicity was caused mainly by increased expression of the gene ADK, which is involved in energy production for cells. “Like curcumin, which can interact with multiple cellular targets and modulate multiple signaling pathways, DM-1 also acts in different ways to promote toxicity in both parent and drug-resistant melanoma cells,” Oliveira said.
EurekAlerthttps://tinyurl.com/ya7hhwwk
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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
In a new study New York University College of Dentistry (NYU Dentistry) researchers investigating the catabolic effect of parathyroid hormone (PTH) in hyperparathyroidism (HPT) showed, for the first time, that monocyte chemoattractant protein-1 (MCP-1) is required for catabolic responses to PTH. HPT is a condition in which an abnormally high concentration of PTH in the blood accelerates bone loss. The research team, led by Nicola C. Partridge, PhD, professor and chair of the Department of Basic Science and Craniofacial Biology at NYU Dentistry, had previously found that MCP-1 is important in producing an anabolic effect of PTH, in which bone formation is increased, and they wanted to know if it was also important in causing a catabolic effect, in which bone is broken down. In the present study, the researchers focused on the role of MCP-1 in PTH-induced osteoclast formation. Osteoclasts are cells that break down the bone. Increased osteoclast formation causes bones to become thinner and weaker. The researchers recreated the hyperparathyroid state in mice by constantly elevating their hyperparathyroid levels. Over a two-week period, they continuously infused female wild-type and MCP-1 knockout mice with human PTH. They showed that the ability of PTH to increase osteoclast formation in vitro is markedly impaired in cells from MCP-1 knockout mice and concluded that MCP-1 is an important chemokine, or signalling protein, in PTH-induced osteoclast formation and bone resorption. The findings support the possibility that MCP-1 could be a marker for how PTH works in humans with hyperparathyroidism, as elevated serum MCP-1 has been shown to be correlated with elevated serum PTH levels in women. Notably, within minutes after humans undergo parathyroid adenoma surgery, MCP-1 serum levels decrease. Because high serum levels of MCP-1 cause the white cells and osteoclasts to be stimulated, this process could have systemic effects as well as effects on bone. “MCP-1 is a chemokine, which induces cells to move along a gradient recruiting white cells and osteoclasts in tissues,” says Dr. Partridge. “Accordingly, there could also be effects on adipose tissue, the heart, and inflammatory conditions.” In the United States, about 1,000 people develop HPT each year, with osteoporosis the most common manifestation. According to the National Institutes of Health, there are approximately 1.5 million osteoporotic fractures in the U.S. each year that lead to half a million hospitalizations, over 800,000 emergency room encounters, more than 2,600,000 physician office visits, and the placement of nearly 180,000 individuals in nursing homes. Hip fractures are by far the most devastating type of fracture, accounting for about 300,000 hospitalizations each year. About one in five people sustaining a hip fracture ends up in a nursing home.
NYU College of Dentistryhttps://tinyurl.com/y7nzipw9
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Investigators at The Feinstein Institute for Medical Research discovered dozens of new genetic variations associated with a person’s general cognitive ability. The findings have the potential to help researchers develop more targeted treatment for cognitive and memory disorders. “For the first time, we were able to use genetic information to point us towards specific drugs that might aid in cognitive disorders of the brain, including Alzheimer’s disease, schizophrenia and attention deficit hyperactivity disorder,” said Todd Lencz, PhD, senior author of the study and professor at the Feinstein Institute and the Donald and Barbara Zucker School of Medicine at Hofstra/Northwell. In the largest peer-reviewed study of its kind, an international team of 65 scientists, led by Dr. Lencz, studied the genomes of more than 100,000 individuals who had their brain function measured by neuropsychological tests. These data were then combined with genomes from 300,000 people measured for the highest level of education achieved, which serves as an estimate for cognitive ability, or how the brain acquires knowledge. While profiling cognitive ability, researchers also discovered a genetic overlap with longevity. They found when examining an individual’s family that a genetic predisposition towards higher cognitive ability was associated with longer lifespan. A new genetic overlap between cognitive ability and risk for autoimmune disease was also identified. This study appears less than a year after Dr. Lencz and his colleagues published a similar, smaller study that was only able to identify a few key genes associated with cognitive ability. “The field of genomics is growing by leaps and bounds,” Dr. Lencz said. “Because the number of genes we can discover is a direct function of the sample size available, further research with additional samples is likely to provide even more insight into how our genes play a role in cognitive ability.”
Feinstein Institute – Northwell Healthhttps://tinyurl.com/y8649b9o
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 11:08:55Researchers identify new genes associated with cognitive ability
A simple blood test that detects tumour cells circulating in the blood shows promise as a new way to predict high or low risk of a breast cancer relapse. “Late recurrence five or more years after surgery accounts for at least one-half of recurrences of breast cancer, and there are no tests that identify who is at highest risk. We found that in women who were cancer-free five years after diagnosis, about 5 percent had a positive circulating tumour cells (CTC) test,” said lead researcher Joseph A. Sparano, MD, vice chair of the ECOG-ACRIN Cancer Research Group, Philadelphia, and associate director for clinical research at Montefiore Medical Center, Albert Einstein Cancer Center, New York. “More importantly …”, Dr. Sparano continued, “…we also found that a positive test was associated with a 35 percent recurrence risk after two years, compared with only 2 percent for those with a negative CTC test.” The concept is to explore the use of the CTC blood test in a new way. Currently, the test is FDA-approved for use by physicians to monitor response to treatment in patients with advanced breast, colon or prostate cancer, but not early stage cancer. A rise in the number of circulating tumour cells in the blood in patients with advanced disease may indicate trouble before it shows up on a scan. In this study, the research team evaluated this test in a different setting—individuals alive and cancer-free about five years after their diagnosis and potentially cured, but still at risk for having a recurrence of their disease. ”Our ultimate goal is to use blood tests like this to tailor treatment in a way that minimizes recurrence risk for those at high risk, and spare treatment for those at low risk who may be unlikely to benefit from it,” Dr. Sparano said. “The findings of this analysis provide strong evidence to further evaluate this new risk assessment approach using CTC and other blood-based tests in this setting”. The test was done on a single blood sample provided by 547 breast cancer patients who had been diagnosed more than five years prior and treated as part of a large ECOG-ACRIN breast cancer treatment trial, E5103. This group of patients had stage two or three breast cancer, and the cells in their tumours were HER2-negative. Many women in E5103 remain cancer free and are being followed for their breast cancer status as part of standard care. Dr. Sparano and colleagues set up a biobank and invited these patients to contribute additional specimens for future research into the reasons for late recurrence. The biobank was established by ECOG-ACRIN and the Coalition of Cancer Cooperative Groups with funding from the Breast Cancer Research Foundation, National Cancer Institute, and Susan G. Komen.
ECOG-ACRIN Cancer Research Grouphttps://tinyurl.com/ydgym4c3
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Clearbridge BioMedics and Leica Biosystems have today announced a partnership, co-marketing each other’s products to support circulating tumour cell (CTC) research. This is specifically for the Clearbridge BioMedics ClearCell® FX CTC enrichment system and the Leica Biosystems’ BOND RX staining platform. This new partnership provides an integrated and automated workflow for CTC enrichment and immunostaining, improving on major challenges in CTC liquid biopsy testing, such as handling and standardization. The ClearCell® FX System is an automated CTC enrichment system, powered by the patented CTChip® FR1 microfluidics biochip. Using a label-free approach, the ClearCell® FX System retrieves wholly-intact and viable CTCs from a standard blood draw. The gentle sorting principle retains high cell integrity and cell surface antigen expression. This coupled with single-step CTC retrieval, provides a seamless integration into pathology lab workflows. Automated CTC staining on a glass slide is then performed on Leica Biosystems’ BOND RX. The BOND RX platform is an open and flexible system that efficiently automates staining for immunofluorescence (IF), immunohistochemistry (IHC) and fluorescent in-situ hybridization (FISH) assays. It provides a high-throughput workflow with exceptional consistency and minimal hands-on time. Linking these two advanced technologies will empower researchers and laboratories with an integrated solution for CTC enrichment and immunostaining, accelerating the development of clinical applications using CTCs. “The global liquid biopsy market has been growing significantly and will continue to grow, due to trends such as rising prevalence of cancer, preference for personalized medicine and the move towards non-invasive procedures. Today’s partnership announcement between Leica Biosystems and Clearbridge BioMedics provides clinical research laboratories with a seamless end-to-end enrichment and immunostaining solution for CTCs. This will support the development of new therapies and diagnostics for cancer patients,” said Dr Michael Paumen, CEO of Clearbridge BioMedics.
www.clearbridgebiomedics.comwww.leicabiosystems.com
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 11:08:54Clearbridge BioMedics and Leica Biosystems to co-market automated solutions for circulating tumour cell (CTC) analysis
Siemens Healthineers has now confirmed that it has completed the acquisition of Epocal Inc. from Abbott to complete its blood gas portfolio. The closing of the deal occurred October 31, 2017. Financial details of the transaction were not disclosed. In integrating Epocal Inc.’s offerings into its POC Ecosystem™ solution, Siemens Healthineers enables customized testing offerings based on individual facility needs – whether that is handheld testing, benchtop solutions or central lab applications – to help improve process efficiency. The epoc® product line will integrate seamlessly into the Siemens Healthineers POC Ecosystem solution for easy connection from many manufacturers’ point-of-care analysers to hospital information systems, providing a flexible, long-term solution. “Health networks have varying needs for blood gas testing across physicians’ offices, clinics, emergency departments, laboratories and even in ambulances. Having any one solution is limiting and may not meet all patient needs, which is why customized testing solutions are so important for improving patient care,” said Peter Koerte, President, Point of Care Diagnostics, Siemens Healthineers. “With a complete offering for blood gas diagnostics, we can help healthcare providers and point-of-care coordinators improve their workflows by offering the right test in the right setting at the right time.”
www.siemens.com/epoc
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EKF Diagnostics announces that its Stanbio Chemistry Procalcitonin (PCT) LiquiColor® assay has been FDA cleared and validated for use on Beckman AU 480, 680 and 5800 clinical chemistry analysers. EKF is pleased to confirm the immediate availability of a user-defined application (UDA) for running this 10-minute test for bacterial infection and sepsis on these Beckman AU analysers. PCT is a widely accepted marker for use in conjunction with other tests to quickly identify sepsis and monitor progression/severity over time. EKF’s PCT test is designed to be used on an open channel of most main brand clinical chemistry analysers, including Roche Cobas, Abbott Architect and Hitachi systems. Therefore, the availability of the user-defined application (UDA) on Beckman AU analysers further increases the breadth of application of the LiquiColor PCT assay. Trevor McCarthy, Sales Manager, EKF Central Laboratory Products, EMEA/APAC said, “The news regarding the FDA clearance and Beckman AU analyser validated application for the PCT LiquiColor assay will bolster trust in the quality and reliability of our product. Having EKF’s PCT assay validated on Beckman AU chemistry analysers allows us to provide a competitive alternative product for hospital labs and should open up new markets and opportunities for us to support improved and early detection of sepsis.” The cost-effective, immunoturbidimetric assay, which features the use of monoclonal antibodies coated to latex particles, can determine PCT from just 20µL of serum and plasma specimens. Conveniently, the reagent set requires no reagent preparation and is designed to be used on open chemistry systems. It is available in a liquid-stable format, meaning that it can remain on-board a clinical chemistry analyser for up to four weeks. PCT is a quick and effective adjunct marker in sepsis diagnosis which helps to differentiate between viral and bacterial infections, so enabling early administration of antimicrobial therapy. It is an important test, as the Surviving Sepsis Campaign (SSC) estimates that the incidence of sepsis is 3 per 1,000 worldwide. There has been a steady rise in the number of patients with sepsis; globally there are now over 18 million cases per year. Due to its high mortality, sepsis is a primary cause of death, accounting for over 60% of deaths per year in the developing world. It kills over 6 million new-borns and children each year and there are over 100,000 cases of maternal sepsis. In addition to improving sepsis survival rates and improving antibiotic stewardship, studies have also shown that PCT testing reduces hospital costs and length of stay. For example, a recent large cohort study examined whether PCT testing helps to more effectively manage sepsis care. The study found that use of PCT testing on day one of admission into the ICU lead to an average of 1.2 fewer hospital days than patients who were not screened and saved an average of $2,759 (€2,337) on their total hospital costs.
www.ekfdiagnostics.com
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 11:08:54EKF procalcitonin assay validated for Beckman AU chemistry analysers
A research team led by National University Health System (NUHS) and Duke-NUS Medical School has used genomic technologies to better understand intestinal metaplasia (IM), a known risk factor for gastric (stomach) cancer. Patients with IM are six times more likely to develop stomach cancer than those without. This study is an important part of an ambitious investigation to understand why some people develop stomach cancer, while others do not. The research could also help detect patients who are infected with the Helicobacter pylori bacteria, which is also linked to the disease. Stomach cancer is the third deadliest cancer in the world according to World Health Organization (WHO) statistics, and claims more than 300 lives yearly in Singapore. The disease is believed to be caused by infection with Helicobacter pylori but is potentially treatable if detected early. Unfortunately, more than two-thirds of stomach cancer patients are only diagnosed at an advanced stage. "Previous genetic studies on IM have mainly focused on patients who were already diagnosed with stomach cancer but these are limited in their ability to predict who are likely to develop the disease and how the disease will progress," said Professor Patrick Tan, co-lead investigator and Professor, Duke-NUS Medical School. Professor Tan is also Deputy Executive Director, Biomedical Research Council, Agency for Science, Technology, and Research, and a Senior Principal Investigator at the Cancer Science Institute of Singapore. "This new study is the first to comprehensively map out the genetic changes in IM in a cohort of stomach cancer-free subjects, which helps us better predict the possible occurrence and progression of the disease." Dr Yeoh Khay Guan, co-lead investigator and Deputy Chief Executive, NUHS as well as Dean, NUS Yong Loo Lin School of Medicine added, "Our study is the largest series of IM to be studied in detail by genetic analysis. These new findings help us understand why some people have a higher risk of progression to stomach cancer, and identify those who may benefit from closer follow-up to prevent cancer or to detect it early so that it can be cured." The researchers leveraged the near 3,000 participants-strong Gastric Cancer Epidemiology Programme (GCEP) cohort, recruited with the support of patients and doctors from four local public hospitals (National University Hospital, Tan Tock Seng Hospital, Singapore General Hospital, Changi General Hospital), to show that a comprehensive analysis of the genetic patterns of IM can predict its subsequent progression towards stomach cancer. The genetic analysis of IM helps to identify those with a higher risk of progression to stomach cancer, adding further information to what is available by microscopic examination alone. The research team is using this new information to identify biomarkers that can be applied in future in the clinic to identify people who have a high risk of progression to stomach cancer. EurekAlertwww.eurekalert.org/pub_releases/2018-01/nuos-lgs010518.php
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 11:08:54Landmark genetic study better predicts stomach cancer
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Researchers find genes may ‘snowball’ obesity
, /in E-News /by 3wmediaThere are nine genes that make you gain more weight if you already have a high body mass index, McMaster University researchers have found.
“It’s similar to a tiny snow ball at a top of a hill that becomes bigger and bigger when rolling down the hill,” said senior author David Meyre, an associate professor of health research methods, evidence and impact at McMaster University. He also holds the Canada Research Chair in Genetics of Obesity.
“The effect of these genes may be amplified by four times, if we compare the 10% of the population at the low end of the body mass index, compared to the 10% at the high end,” he added.
The study’s co-first authors are postdoctoral fellow Arkan Abadi and PhD student Akram Alyass, who both work in the Meyre laboratory.
Although the increasing average body mass index of the population of several high-income countries has recently plateaued, the researchers note in the study, the cases of extreme forms of obesity are still growing. People who are morbidly obese are at risk of health complications such as diabetes, cardiovascular disease, hypertension and cancers and early death.
On top of lifestyle factors such as unhealthy diet and physical inactivity, genetic factors are also known to play an important role, with 50 to 80 per cent of body mass index related to genetics.
The researchers looked at 37 genes that are well established as modulating the body mass in 75,230 adults with European ancestry and found the nine with the snowball effect.
“These genes may, in part, explain why some individuals experience uncontrolled and constant weight gain across their life, despite the availability of different therapeutic approaches,” said Meyre. “The plausible explanation is that there are interactions between the snowball obesity genes and risk environmental factors.”
He added that the idea of preventing obesity in the first place is a good strategy for people with a high genetic risk for obesity.
“We have an important message of hope that the carriers of these genes, if they stay in the low end of body mass index through appropriate lifestyle, may minimize the effect of the snowball obesity genes.”
McMaster Universityhttps://tinyurl.com/ya247466
Genes associated with progression of melanoma are identified
, /in E-News /by 3wmediaWhen researchers at the University of São Paulo (USP) in Brazil treated human melanoma cell lines with a synthetic compound similar to curcumin, one of the pigments that give turmeric (Curcuma longa) its orange colour, they identified genes with altered expression in potentially invasive tumours and malignant cells resistant to chemotherapy.
According to the scientists, if further studies confirm the importance of these genes to disease progression and increasing chemoresistance, it will be possible to explore their future use as biomarkers to assist diagnosis and even as therapeutic targets.
“Previous research by collaborators had already shown that DM-1, a compound analogous to curcumin, has anti-tumour activity at low doses. We set out to understand which genes this substance modulates and why it is toxic to melanoma but not to normal cells,” said Érica Aparecida de Oliveira, a postdoctoral scholar at USP’s School of Pharmaceutical Sciences (FCF).
As Oliveira explained, there are hundreds of papers attesting to the anti-oxidant, anti-tumoural, anti-microbial and anti-inflammatory properties of curcumin in the scientific literature. However, the therapeutic usefulness of this compound in its natural form is limited owing to poor absorption, rapid metabolization, and water insolubility. To solve this problem, scientists have developed synthetic analogues with minor structural modifications to make the molecule more stable in the organism.
DM-1 (sodium 4-[5-(4-hydroxy-3-methoxyphenyl)-3-oxo-penta-1,4-dienyl]-2-methoxy-phenolate) was synthesized some years ago by José Agustín Pablo Quincoces Suárez, a professor at Bandeirantes University (UNIBAN).
“Experiments with animals conducted by collaborators showed that treatment with DM-1 can promote a reduction in tumour volume. DM-1 has also proved toxic to chemoresistant melanoma cells,” Oliveira said.
To unpack DM-1’s mechanism of action, Oliveira resorted to a toxicogenomics platform developed by the research group of FCF-USP professor Gisele Monteiro, a fellow researcher at the investigation. Such platform is comprised of a collection of 6,000 frozen yeast strains, all mutants of the species Saccharomyces cerevisiae, widely used as baker’s and brewer’s yeast.
“This yeast’s genome has 6,000 genes, and a different gene has been knocked out in each of these mutants, so we were able to study the effects of the compound in a highly specific manner, gene by gene,” Oliveira said.
The 6,000 mutant yeast strains were thawed, spread on plates with 96 small wells, and treated with DM-1. The strains that did not grow in the presence of the curcumin analogue were discarded, leaving an initial group of 211 genes that were affected by the treatment.
The next step was to filter the genes in order to identify those with homologues in the human genome since some might be associated with functions specific to yeast. The researchers came up with a second list containing 79 candidate genes, thanks to the aid from bioinformatics tools and from the expertise of Helder Nakaya , another fellow researcher and also a professor at FCF-USP.
“We then began to look at public repositories of genomic data from cancer patients, such as The Cancer Genome Atlas (TCGA) and the Gene Expression Omnibus (GEO), to understand how these genes talked to each other,” Oliveira said.
The analysis showed most to be associated with cell signalling pathways that favoured tumour progression when active. Examples included the pathways mediated by mitogen-activated protein (MAP) kinase and epidermal growth factor receptor (EGFR).
The next step was to investigate which genes were important to the progression of melanoma specifically. This entailed using bioinformatics to focus on the analysis of genomic sequences from melanoma patients.
“We performed a data mining exercise to find genes with altered expression during melanoma progression,” Oliveira said. “We identified seven genes that appeared to be important, and when we looked at the public databases, we could see that the expression of these genes was indeed altered in many patients.”
In vitro tests with non-chemoresistant parent melanoma cells showed that treatment with DM-1 induced cell death, mainly because it increased expression of a gene known as TOP-1. When this gene is active, it leads to DNA transcription errors and hence causes genomic instability in cells.
In chemoresistant melanoma cells, cytotoxicity was caused mainly by increased expression of the gene ADK, which is involved in energy production for cells.
“Like curcumin, which can interact with multiple cellular targets and modulate multiple signaling pathways, DM-1 also acts in different ways to promote toxicity in both parent and drug-resistant melanoma cells,” Oliveira said.
EurekAlerthttps://tinyurl.com/ya7hhwwk
Finding long strands of RNA in skin development and disease
, /in E-News /by 3wmediaResearchers 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
Evidence that MCP-1 may determine bone loss responses to parathyroid hormone
, /in E-News /by 3wmediaIn a new study New York University College of Dentistry (NYU Dentistry) researchers investigating the catabolic effect of parathyroid hormone (PTH) in hyperparathyroidism (HPT) showed, for the first time, that monocyte chemoattractant protein-1 (MCP-1) is required for catabolic responses to PTH. HPT is a condition in which an abnormally high concentration of PTH in the blood accelerates bone loss.
The research team, led by Nicola C. Partridge, PhD, professor and chair of the Department of Basic Science and Craniofacial Biology at NYU Dentistry, had previously found that MCP-1 is important in producing an anabolic effect of PTH, in which bone formation is increased, and they wanted to know if it was also important in causing a catabolic effect, in which bone is broken down.
In the present study, the researchers focused on the role of MCP-1 in PTH-induced osteoclast formation. Osteoclasts are cells that break down the bone. Increased osteoclast formation causes bones to become thinner and weaker. The researchers recreated the hyperparathyroid state in mice by constantly elevating their hyperparathyroid levels. Over a two-week period, they continuously infused female wild-type and MCP-1 knockout mice with human PTH. They showed that the ability of PTH to increase osteoclast formation in vitro is markedly impaired in cells from MCP-1 knockout mice and concluded that MCP-1 is an important chemokine, or signalling protein, in PTH-induced osteoclast formation and bone resorption.
The findings support the possibility that MCP-1 could be a marker for how PTH works in humans with hyperparathyroidism, as elevated serum MCP-1 has been shown to be correlated with elevated serum PTH levels in women. Notably, within minutes after humans undergo parathyroid adenoma surgery, MCP-1 serum levels decrease.
Because high serum levels of MCP-1 cause the white cells and osteoclasts to be stimulated, this process could have systemic effects as well as effects on bone. “MCP-1 is a chemokine, which induces cells to move along a gradient recruiting white cells and osteoclasts in tissues,” says Dr. Partridge. “Accordingly, there could also be effects on adipose tissue, the heart, and inflammatory conditions.”
In the United States, about 1,000 people develop HPT each year, with osteoporosis the most common manifestation. According to the National Institutes of Health, there are approximately 1.5 million osteoporotic fractures in the U.S. each year that lead to half a million hospitalizations, over 800,000 emergency room encounters, more than 2,600,000 physician office visits, and the placement of nearly 180,000 individuals in nursing homes. Hip fractures are by far the most devastating type of fracture, accounting for about 300,000 hospitalizations each year. About one in five people sustaining a hip fracture ends up in a nursing home.
NYU College of Dentistryhttps://tinyurl.com/y7nzipw9
Researchers identify new genes associated with cognitive ability
, /in E-News /by 3wmediaInvestigators at The Feinstein Institute for Medical Research discovered dozens of new genetic variations associated with a person’s general cognitive ability. The findings have the potential to help researchers develop more targeted treatment for cognitive and memory disorders.
“For the first time, we were able to use genetic information to point us towards specific drugs that might aid in cognitive disorders of the brain, including Alzheimer’s disease, schizophrenia and attention deficit hyperactivity disorder,” said Todd Lencz, PhD, senior author of the study and professor at the Feinstein Institute and the Donald and Barbara Zucker School of Medicine at Hofstra/Northwell.
In the largest peer-reviewed study of its kind, an international team of 65 scientists, led by Dr. Lencz, studied the genomes of more than 100,000 individuals who had their brain function measured by neuropsychological tests. These data were then combined with genomes from 300,000 people measured for the highest level of education achieved, which serves as an estimate for cognitive ability, or how the brain acquires knowledge.
While profiling cognitive ability, researchers also discovered a genetic overlap with longevity. They found when examining an individual’s family that a genetic predisposition towards higher cognitive ability was associated with longer lifespan. A new genetic overlap between cognitive ability and risk for autoimmune disease was also identified.
This study appears less than a year after Dr. Lencz and his colleagues published a similar, smaller study that was only able to identify a few key genes associated with cognitive ability.
“The field of genomics is growing by leaps and bounds,” Dr. Lencz said. “Because the number of genes we can discover is a direct function of the sample size available, further research with additional samples is likely to provide even more insight into how our genes play a role in cognitive ability.”
Feinstein Institute – Northwell Healthhttps://tinyurl.com/y8649b9o
Simple blood test may predict recurrence of breast cancer
, /in E-News /by 3wmediaA simple blood test that detects tumour cells circulating in the blood shows promise as a new way to predict high or low risk of a breast cancer relapse.
“Late recurrence five or more years after surgery accounts for at least one-half of recurrences of breast cancer, and there are no tests that identify who is at highest risk. We found that in women who were cancer-free five years after diagnosis, about 5 percent had a positive circulating tumour cells (CTC) test,” said lead researcher Joseph A. Sparano, MD, vice chair of the ECOG-ACRIN Cancer Research Group, Philadelphia, and associate director for clinical research at Montefiore Medical Center, Albert Einstein Cancer Center, New York.
“More importantly …”, Dr. Sparano continued, “…we also found that a positive test was associated with a 35 percent recurrence risk after two years, compared with only 2 percent for those with a negative CTC test.”
The concept is to explore the use of the CTC blood test in a new way. Currently, the test is FDA-approved for use by physicians to monitor response to treatment in patients with advanced breast, colon or prostate cancer, but not early stage cancer. A rise in the number of circulating tumour cells in the blood in patients with advanced disease may indicate trouble before it shows up on a scan. In this study, the research team evaluated this test in a different setting—individuals alive and cancer-free about five years after their diagnosis and potentially cured, but still at risk for having a recurrence of their disease.
”Our ultimate goal is to use blood tests like this to tailor treatment in a way that minimizes recurrence risk for those at high risk, and spare treatment for those at low risk who may be unlikely to benefit from it,” Dr. Sparano said. “The findings of this analysis provide strong evidence to further evaluate this new risk assessment approach using CTC and other blood-based tests in this setting”.
The test was done on a single blood sample provided by 547 breast cancer patients who had been diagnosed more than five years prior and treated as part of a large ECOG-ACRIN breast cancer treatment trial, E5103. This group of patients had stage two or three breast cancer, and the cells in their tumours were HER2-negative.
Many women in E5103 remain cancer free and are being followed for their breast cancer status as part of standard care. Dr. Sparano and colleagues set up a biobank and invited these patients to contribute additional specimens for future research into the reasons for late recurrence. The biobank was established by ECOG-ACRIN and the Coalition of Cancer Cooperative Groups with funding from the Breast Cancer Research Foundation, National Cancer Institute, and Susan G. Komen.
ECOG-ACRIN Cancer Research Grouphttps://tinyurl.com/ydgym4c3
Clearbridge BioMedics and Leica Biosystems to co-market automated solutions for circulating tumour cell (CTC) analysis
, /in E-News /by 3wmediaClearbridge BioMedics and Leica Biosystems have today announced a partnership, co-marketing each other’s products to support circulating tumour cell (CTC) research. This is specifically for the Clearbridge BioMedics ClearCell® FX CTC enrichment system and the Leica Biosystems’ BOND RX staining platform. This new partnership provides an integrated and automated workflow for CTC enrichment and immunostaining, improving on major challenges in CTC liquid biopsy testing, such as handling and standardization.
The ClearCell® FX System is an automated CTC enrichment system, powered by the patented CTChip® FR1 microfluidics biochip. Using a label-free approach, the ClearCell® FX System retrieves wholly-intact and viable CTCs from a standard blood draw. The gentle sorting principle retains high cell integrity and cell surface antigen expression. This coupled with single-step CTC retrieval, provides a seamless integration into pathology lab workflows.
Automated CTC staining on a glass slide is then performed on Leica Biosystems’ BOND RX. The BOND RX platform is an open and flexible system that efficiently automates staining for immunofluorescence (IF), immunohistochemistry (IHC) and fluorescent in-situ hybridization (FISH) assays. It provides a high-throughput workflow with exceptional consistency and minimal hands-on time.
Linking these two advanced technologies will empower researchers and laboratories with an integrated solution for CTC enrichment and immunostaining, accelerating the development of clinical applications using CTCs.
“The global liquid biopsy market has been growing significantly and will continue to grow, due to trends such as rising prevalence of cancer, preference for personalized medicine and the move towards non-invasive procedures. Today’s partnership announcement between Leica Biosystems and Clearbridge BioMedics provides clinical research laboratories with a seamless end-to-end enrichment and immunostaining solution for CTCs. This will support the development of new therapies and diagnostics for cancer patients,” said Dr Michael Paumen, CEO of Clearbridge BioMedics. www.clearbridgebiomedics.comwww.leicabiosystems.com
Siemens Healthineers announces closing of Epocal acquisition
, /in E-News /by 3wmediaSiemens Healthineers has now confirmed that it has completed the acquisition of Epocal Inc. from Abbott to complete its blood gas portfolio. The closing of the deal occurred October 31, 2017. Financial details of the transaction were not disclosed.
In integrating Epocal Inc.’s offerings into its POC Ecosystem™ solution, Siemens Healthineers enables customized testing offerings based on individual facility needs – whether that is handheld testing, benchtop solutions or central lab applications – to help improve process efficiency. The epoc® product line will integrate seamlessly into the Siemens Healthineers POC Ecosystem solution for easy connection from many manufacturers’ point-of-care analysers to hospital information systems, providing a flexible, long-term solution.
“Health networks have varying needs for blood gas testing across physicians’ offices, clinics, emergency departments, laboratories and even in ambulances. Having any one solution is limiting and may not meet all patient needs, which is why customized testing solutions are so important for improving patient care,” said Peter Koerte, President, Point of Care Diagnostics, Siemens Healthineers. “With a complete offering for blood gas diagnostics, we can help healthcare providers and point-of-care coordinators improve their workflows by offering the right test in the right setting at the right time.” www.siemens.com/epoc
EKF procalcitonin assay validated for Beckman AU chemistry analysers
, /in E-News /by 3wmediaEKF Diagnostics announces that its Stanbio Chemistry Procalcitonin (PCT) LiquiColor® assay has been FDA cleared and validated for use on Beckman AU 480, 680 and 5800 clinical chemistry analysers. EKF is pleased to confirm the immediate availability of a user-defined application (UDA) for running this 10-minute test for bacterial infection and sepsis on these Beckman AU analysers.
PCT is a widely accepted marker for use in conjunction with other tests to quickly identify sepsis and monitor progression/severity over time. EKF’s PCT test is designed to be used on an open channel of most main brand clinical chemistry analysers, including Roche Cobas, Abbott Architect and Hitachi systems. Therefore, the availability of the user-defined application (UDA) on Beckman AU analysers further increases the breadth of application of the LiquiColor PCT assay.
Trevor McCarthy, Sales Manager, EKF Central Laboratory Products, EMEA/APAC said, “The news regarding the FDA clearance and Beckman AU analyser validated application for the PCT LiquiColor assay will bolster trust in the quality and reliability of our product. Having EKF’s PCT assay validated on Beckman AU chemistry analysers allows us to provide a competitive alternative product for hospital labs and should open up new markets and opportunities for us to support improved and early detection of sepsis.”
The cost-effective, immunoturbidimetric assay, which features the use of monoclonal antibodies coated to latex particles, can determine PCT from just 20µL of serum and plasma specimens. Conveniently, the reagent set requires no reagent preparation and is designed to be used on open chemistry systems. It is available in a liquid-stable format, meaning that it can remain on-board a clinical chemistry analyser for up to four weeks.
PCT is a quick and effective adjunct marker in sepsis diagnosis which helps to differentiate between viral and bacterial infections, so enabling early administration of antimicrobial therapy. It is an important test, as the Surviving Sepsis Campaign (SSC) estimates that the incidence of sepsis is 3 per 1,000 worldwide. There has been a steady rise in the number of patients with sepsis; globally there are now over 18 million cases per year. Due to its high mortality, sepsis is a primary cause of death, accounting for over 60% of deaths per year in the developing world. It kills over 6 million new-borns and children each year and there are over 100,000 cases of maternal sepsis.
In addition to improving sepsis survival rates and improving antibiotic stewardship, studies have also shown that PCT testing reduces hospital costs and length of stay. For example, a recent large cohort study examined whether PCT testing helps to more effectively manage sepsis care. The study found that use of PCT testing on day one of admission into the ICU lead to an average of 1.2 fewer hospital days than patients who were not screened and saved an average of $2,759 (€2,337) on their total hospital costs. www.ekfdiagnostics.com
Landmark genetic study better predicts stomach cancer
, /in E-News /by 3wmediaA research team led by National University Health System (NUHS) and Duke-NUS Medical School has used genomic technologies to better understand intestinal metaplasia (IM), a known risk factor for gastric (stomach) cancer. Patients with IM are six times more likely to develop stomach cancer than those without. This study is an important part of an ambitious investigation to understand why some people develop stomach cancer, while others do not. The research could also help detect patients who are infected with the Helicobacter pylori bacteria, which is also linked to the disease.
Stomach cancer is the third deadliest cancer in the world according to World Health Organization (WHO) statistics, and claims more than 300 lives yearly in Singapore. The disease is believed to be caused by infection with Helicobacter pylori but is potentially treatable if detected early. Unfortunately, more than two-thirds of stomach cancer patients are only diagnosed at an advanced stage.
"Previous genetic studies on IM have mainly focused on patients who were already diagnosed with stomach cancer but these are limited in their ability to predict who are likely to develop the disease and how the disease will progress," said Professor Patrick Tan, co-lead investigator and Professor, Duke-NUS Medical School. Professor Tan is also Deputy Executive Director, Biomedical Research Council, Agency for Science, Technology, and Research, and a Senior Principal Investigator at the Cancer Science Institute of Singapore. "This new study is the first to comprehensively map out the genetic changes in IM in a cohort of stomach cancer-free subjects, which helps us better predict the possible occurrence and progression of the disease."
Dr Yeoh Khay Guan, co-lead investigator and Deputy Chief Executive, NUHS as well as Dean, NUS Yong Loo Lin School of Medicine added, "Our study is the largest series of IM to be studied in detail by genetic analysis. These new findings help us understand why some people have a higher risk of progression to stomach cancer, and identify those who may benefit from closer follow-up to prevent cancer or to detect it early so that it can be cured."
The researchers leveraged the near 3,000 participants-strong Gastric Cancer Epidemiology Programme (GCEP) cohort, recruited with the support of patients and doctors from four local public hospitals (National University Hospital, Tan Tock Seng Hospital, Singapore General Hospital, Changi General Hospital), to show that a comprehensive analysis of the genetic patterns of IM can predict its subsequent progression towards stomach cancer. The genetic analysis of IM helps to identify those with a higher risk of progression to stomach cancer, adding further information to what is available by microscopic examination alone.
The research team is using this new information to identify biomarkers that can be applied in future in the clinic to identify people who have a high risk of progression to stomach cancer.
EurekAlertwww.eurekalert.org/pub_releases/2018-01/nuos-lgs010518.php