Join southeast Asia’s premier laboratory and healthcare exhibition and take part in the free educational sessions, attend the CME accredited conferences, visit the scientific poster zone and explore so much more at Level 4 at Suntec Singapore Convention & Exhibition Centre.
www.medlabasia.com
An international team of researchers from the Hopp Children’s Cancer Centre 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 pediatric 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 Centre, 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)https://tinyurl.com/ya5akv4j
The largest genetic study of its kind ever to use accelerometer data to examine how we slumber has uncovered a number of parts of our genetic code that could be responsible for causing poor sleep quality and duration.
The international collaboration, led by the University of Exeter, has found 47 links between our genetic code and the quality, quantity and timing of how we sleep. They include ten new genetic links with sleep duration and 26 with sleep quality.
The Medical Research Council-funded study looked at data from 85,670 participants of UK Biobank and 5,819 individuals from three other studies, who wore accelerometers – wrist-worn devices (similar to a Fitbit) which record activity levels continuously. They wore the accelerometers continuously for seven days, giving more detailed sleep data than previous studies, which have relied on people accurately reporting their own sleep habits.
Among the genomic regions uncovered is a gene called PDE11A. The research team discovered than an uncommon variant of this gene affects not only how long you sleep but your quality of sleep too. The gene has previously been identified as a possible drug target for treatment of people with neuropsychiatric disorders associated with mood stability and social behaviours.
The study also found that among people with the same hip circumference, a higher waist circumference resulted in less time sleeping, although the effect was very small – around 4 seconds less sleep per 1cm waist increase in someone with the average hip circumference of around 100cm.
The team involved colleagues from the Center for Sleep and Circadian Neurobiology in Pennsylvania, Massachusetts General Hospital as well as the Netherlands, France and Switzerland. They found that collectively, the genetic regions linked to sleep quality are also linked to the production of serotonin – a neurotransmitter associated with feelings of happiness and wellbeing. Serotonin is known to play a key role in sleep cycles and is theorised to help promote deeper and more restful sleep.
Senior author Dr Andrew Wood, of the University of Exeter Medical School, said: “We know that getting enough sleep improves our health and wellbeing, yet we still know relatively little about the mechanisms in our bodies that influence how we sleep. Changes in sleep quality, quantity and timing are strongly associated with several human diseases such as diabetes and obesity, and psychiatric disorders.
The group also found further evidence that Restless Leg Syndrome is linked to poorer sleep from the genetic variants they found to be associated with sleep measures derived from the accelerometer data.
University of Exeter
https://www.exeter.ac.uk/news/research/title_711082_en.html
Dubai, United Arab Emirates, 12th December 2018: Ahead of the upcoming MEDLAB Exhibition & Congress, the MENA region’s largest medical laboratory event, experts are highlighting the need for advancing genetic and disease research in the Arab world in order to provide targeted gene therapies for certain cancers for citizens in the UAE.
This is in line with the UAE Vision 2021 National Agenda, which aims to reduce cancer-related deaths in the country, with the World Health Organisation (WHO) estimating 25.6 deaths per 100,000 population in the UAE in 2017. To achieve this aim, the UAE government regularly launches national awareness and preventative campaigns within the framework of ‘Itmenan’ which involves the ‘Universal Periodic Examination’ and ‘Early Detection of Cancer’ initiatives adopted by the Council of Ministers.
Targeted therapies, or precision medicine, is defined as tailoring of medical treatment to the individual characteristics of each patient. It is an emerging approach for disease treatment and prevention that takes into account individual variability in genes, environment, and lifestyle for each person. For example, for cancer treatments, based on genetic testing, a physician can choose the most effective chemotherapy based on the mutation or biomarker identified.
According to the WHO, while 70% of deaths from cancer occur in low and middle-income countries, only one in five low and middle-income countries have the necessary data to drive cancer policy. More than 90% of high-income countries reported available treatment services compared to less than 30% in low-income countries. While a portion of countries in MENA do have a high GDP, they are still considered developing economies according to the United Nations.
Commenting, Dr Sara Sorrell, Consultant Family Medicine, Intercare Health Center, Abu Dhabi, UAE, said: “It is well recognised that Middle Eastern populations are underrepresented in disease research and, to date, there is no research to indicate the impact of precision medicine in the UAE. But I think that this is still premature as we don’t even have enough data on the general population genetics of this part of the world, so this is really the first step.
“For instance, if a different mutation is found to cause a particular cancer here, compared to European descent populations, this may present a novel target for new cancer therapies for local populations. Or, if a new drug comes on the market, what’s the effect in the local population? Therefore, advancing genetic and disease research in the UAE and the Arab world is very important. For this to occur, there needs to be both a focus on funding research as well as formulating policies around research and healthcare innovation to protect patients, scientists, and physicians,” she added.
Molecular diagnostics and genetics experts from the MENA region will gather at the upcoming MEDLAB Congress taking place from 4 – 7 February 2019 at Dubai World Trade Centre to discuss topics such as barriers to providing precision medicine in the Arab World, strategies for the prevention of genetic diseases, and Next-Generation Sequencing in oncology, among others.
Commenting on the importance of scientific exchange in the regional medical laboratory industry, Rejoy Penacerrada, Conference Director, MEDLAB Congress, said: “The conferences provide an important platform for the region’s medical laboratory community to engage in discussion that will promote the role of genetic and population research in advancing the health of citizens across the region. This is led by the intense interest in precision medicine, with the region’s laboratories now actively expanding their test menus for more personalised diagnostic services.”
Organised by Informa Exhibitions, the MEDLAB Congress brings together more than 6,700 conference delegates to hear from more than 110 speakers from 20 countries in an effort to provide advanced medical laboratory techniques for better health.
For a closer look at MEDLAB 2019, please visit www.medlabme.com
Beckman Coulter Diagnostics has embarked on a strategic collaboration with the University of California, Irvine – one of the first targeted academic partnerships the company envisions around the globe.
Beckman Coulter Diagnostics will access UCI research in innovative diagnostic platforms, life sciences applications, devices, and data analytics to further its mission of advancing healthcare. UCI faculty, students and entrepreneurs will benefit from Beckman Coulter Diagnostics’ expertise in accelerating the commercialization of technology and other world-class UCI breakthroughs.
“We are honoured that Beckman Coulter Diagnostics has selected UCI as a strategic innovation partner,” said Richard Sudek, Ph.D., chief innovation officer and executive director at UCI Applied Innovation. “This is a new type of industry collaboration which aims to significantly change how industry and universities partner together. We look forward to teaming up with Beckman Coulter to increase the speed and quality of how UCI discoveries make it to market.”
“We are excited to tap into the broad expertise of UCI researchers as we focus on identifying innovative solutions to clinical unmet needs“ said Fiona Adair, Ph.D., vice president of strategy and innovation at Beckman Coulter Diagnostics. “We believe this type of academic-industry partnership can lead to development of innovative diagnostic technologies to improve healthcare. UCI Applied Innovation is a place where valuable new ideas are incubated. In turn, we can provide promising students, researchers, and entrepreneurs industry-specific feedback and mentorship opportunities. We will have a Beckman Coulter office at the Cove @ UCI Applied Innovation for seamless collaboration with academic units as well as to integrate into the innovation ecosystem.”
This level of collaboration is an industry model of synthesizing research, commercial expertise and clinical needs to produce beneficial results. As a first step, Beckman Coulter will fund Proof of Product grants to help UCI innovations bridge the gap between the lab and early commercialization. Through these grants, Beckman Coulter will determine a specific focus area for university entrepreneurial teams.
Additionally, Beckman Coulter will also seek eligible UCI graduate students to enter its competitive talent onboarding program, in which they’ll get the opportunity to work across multiple divisions of the company.
“The partnership with UCI represents a landmark in Beckman Coulter’s strategic initiatives to drive translational innovation and extend the company’s leadership in clinical diagnostics.” said John Blackwood, senior vice president and general manager of products and services at Beckman Coulter. “Beckman Coulter is engaging with academic partners that excel in applying the latest technology to develop superior solutions for better patient outcomes. UCI maintains an ecosystem of innovation that facilitates academic-industry partnerships and we are excited about the opportunity to leverage UCI’s research expertise for the benefit of patients around the world.”
Braunschweig Municipal Hospital has put new technology in place for molecular diagnostics that will recognize genetic changes in cancer cells. Pathologists can thus accurately identify patients eligible for targeted treatment based on the genetic make-up of their tumours. The method was developed by Neo New Oncology, a subsidiary of Siemens Healthineers. Braunschweig Municipal Hospital, with 38 clinics making it one of the largest hospitals in northern Germany, will thus boost its position as a top oncology provider in the region. This concept serves as a model for regional clinics in Germany.
The technology from Neo enables hospital pathologists to demonstrate many genetic changes relevant to a treatment decision with just a single diagnostic test. Conversely, standard diagnostic procedures usually involve a combination of many different diagnostic procedures to obtain all information about a tumour’s genetic make-up. The analysis can be time-consuming as a result, which prevents the treating oncologists from beginning treatment directly. In addition, with the standard procedure the tumour sample often is not enough to enable a full, end-to-end analysis. This creates the risk that patients who could benefit from targeted treatment will fail to be identified.
Cancer patients are now living longer and also living better with their disease. One reason is the constant refinement of individual treatment options that modern medicine now makes available. This also includes “targeted medications”: In contrast to chemotherapy, which non-selectively targets all dividing cells, these substances act specifically on particular changes in a tumour’s genetic information. This not only makes them highly efficient, but also substantially reduces the risk of adverse drug reactions compared to chemotherapy. If tumours lack the relevant genetic changes, however, these targeted medications are virtually ineffective. Targeted treatment must therefore be coordinated with the specific characteristics of the cancer cells in a given patient. For lung cancer, for example, more than a dozen genetic changes are known, which can have different consequences for treatment. Patient treatment is therefore increasingly tailored to the individual tumour, which makes it more effective. For physicians to make the best possible treatment decision, therefore, it is essential that they understand the individual patient’s cancer down to molecular level.
The Neo procedure is based on the method of “next generation sequencing.” This selects and analyses relevant parts of the tumour DNA at high resolution. The resulting large volumes of data are processed by software developed by Neo New Oncology using a quality-assured system. Hospital pathologists then evaluate the data. They analyse the changes in the patient’s tumour, the medications that can be used against it, and establish whether there are appropriate clinical studies for which the inclusion criteria are met, enabling the patient to benefit from innovative new treatment options.
The results of this evaluation are then discussed by the hospital’s Tumour Board. This is where all the relevant medical disciplines at the hospital review all the radiological and molecular diagnostic results and discuss which treatment option would be the best for the patient in question. This ensures that every individual patient benefits from the all of the hospital’s medical expertise.
www.siemens-healthineers.com
Glaucoma, a disease that afflicts nearly 70 million people worldwide, is something of a mystery despite its prevalence. Little is known about the origins of the disease, which damages the retina and optic nerve and can lead to blindness.
A new study from MIT and Massachusetts Eye and Ear has found that glaucoma may in fact be an autoimmune disorder. In a study of mice, the researchers showed that the body’s own T cells are responsible for the progressive retinal degeneration seen in glaucoma. Furthermore, these T cells appear to be primed to attack retinal neurons as the result of previous interactions with bacteria that normally live in our body.
The discovery suggests that it could be possible to develop new treatments for glaucoma by blocking this autoimmune activity, the researchers say.
“This opens a new approach to prevent and treat glaucoma,” says Jianzhu Chen, an MIT professor of biology, a member of MIT’s Koch Institute for Integrative Cancer Research, and one of the senior authors of the study.
Dong Feng Chen, an associate professor of ophthalmology at Harvard Medical School and the Schepens Eye Research Institute of Massachusetts Eye and Ear, is also a senior author of the study. The paper’s lead authors are Massachusetts Eye and Ear researchers Huihui Chen, Kin-Sang Cho, and T.H. Khanh Vu.
One of the biggest risk factors for glaucoma is elevated pressure in the eye, which often occurs as people age and the ducts that allow fluid to drain from the eye become blocked. The disease often goes undetected at first; patients may not realize they have the disease until half of their retinal ganglion cells have been lost.
Most treatments focus on lowering pressure in the eye (also known as intraocular pressure). However, in many patients, the disease worsens even after intraocular pressure returns to normal. In studies in mice, Dong Feng Chen found the same effect.
“That led us to the thought that this pressure change must be triggering something progressive, and the first thing that came to mind is that it has to be an immune response,” she says.
To test that hypothesis, the researchers looked for immune cells in the retinas of these mice and found that indeed, T cells were there. This is unusual because T cells are normally blocked from entering the retina, by a tight layer of cells called the blood-retina barrier, to suppress inflammation of the eye. The researchers found that when intraocular pressure goes up, T cells are somehow able to get through this barrier and into the retina.
The Mass Eye and Ear team then enlisted Jianzhu Chen, an immunologist, to further investigate what role these T cells might be playing in glaucoma. The researchers generated high intraocular pressure in mice that lack T cells and found that while this pressure induced only a small amount of damage to the retina, the disease did not progress any further after eye pressure returned to normal.
Further studies revealed that the glaucoma-linked T cells target proteins called heat shock proteins, which help cells respond to stress or injury. Normally, T cells should not target proteins produced by the host, but the researchers suspected that these T cells had been previously exposed to bacterial heat shock proteins. Because heat shock proteins from different species are very similar, the resulting T cells can cross-react with mouse and human heat shock proteins.
To test this hypothesis, the team brought in James Fox, a professor in MIT’s Department of Biological Engineering and Division of Comparative Medicine, whose team maintains mice with no bacteria. The researchers found that when they tried to induce glaucoma in these germ-free mice, the mice did not develop the disease.
The researchers then turned to human patients with glaucoma and found that these patients had five times the normal level of T cells specific to heat shock proteins, suggesting that the same phenomenon may also contribute to the disease in humans. The researchers’ studies thus far suggest that the effect is not specific to a particular strain of bacteria; rather, exposure to a combination of bacteria can generate T cells that target heat shock proteins.
One question the researchers plan to study further is whether other components of the immune system may be involved in the autoimmune process that gives rise to glaucoma. They are also investigating the possibility that this phenomenon may underlie other neurodegenerative disorders, and looking for ways to treat such disorders by blocking the autoimmune response.
“What we learn from the eye can be applied to the brain diseases, and may eventually help develop new methods of treatment and diagnosis,” Dong Feng Chen says.
MITnews.mit.edu/2018/glaucoma-autoimmune-disease-0810
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
New research from BRC has found a way to predict rejection of a kidney transplant before it happens, by monitoring the immune system of transplant patients.
The researchers have found that a signature combination of seven immune genes in blood samples can predict rejection earlier than current techniques. Monitoring these markers in transplant patients with regular blood tests could help doctors intervene before any damage to the organ occurs, and improve outcomes for patients.
A renal transplant offers the best treatment for patients whose kidneys have failed, with around 3,000 carried out annually in the UK. Acute rejection occurs when the body’s immune system begins to attack the donated organ. This is a common complication in the first year after the transplant, affecting around 2 in 10 patients. It can affect the lifespan of the transplanted organ.
Currently, acute rejection can only be confirmed by taking a biopsy of the transplanted organ. While acute rejection can be treated, this can only be done when the organ is already affected and damage has already occurred.
Once the new technique is validated further, it has the potential to offer clinicians the use of a simple blood test to predict rejection. Being able to intervene before the event will help prevent damage to patients, and extend the life of the transplanted organ.
Dr Paramit Chowdhury, a consultant nephrologist at Guy’s and St Thomas’ and author on the paper said: “This advance could make a huge difference to our ability to monitor kidney transplant patients and treat rejection earlier. It may also save some patients from an unnecessary biopsy. It is a first step in getting a better insight into the status of a patient’s immune system, allowing better tailoring of the patient’s anti-rejection treatment.
“A big challenge at the moment is that even the best transplanted organ has a limited lifespan of up to 30 years. By being able to pick up signs of rejection early, we might increase the lifespan of the organ and help patients have a better quality of life, for longer.”
The team recruited 455 patients who received a kidney transplant at Guy’s Hospital and followed these patients over the first year of their transplant, collecting regular blood and urine samples. Using these samples and analysing the data over time, they developed a signature combination of seven genes that differentiated patients who developed rejection from those who did not.
They then tested for the signature via a blood test in a separate cohort of patients, and validated that it predicted transplant rejection.
The team also identified a six gene signature for a less common form of complication. BK-virus nephropathy can look clinically similar to acute rejection, but requires a very different therapy – reducing immunosuppression. Being able to distinguish between these complications would mean clinicians can ensure that patients receive the most appropriate treatment.
Dr Maria Hernandez Fuentes, visiting senior lecturer at King’s College London and author on the study, said: “Biomarkers are naturally occurring genes or proteins that appear in the blood, which can tell us what is happening in the body. This is vital in determining the best course of treatment for patients. We were able to monitor the genes that were being expressed in transplant patients and map how these reflected their clinical outcomes.
National Institute for Health Research
Biomedical Research Centre at Guy’shttps://tinyurl.com/y4z9k2c8
Some variations in the gene LPHN3 –associated with the attention deficit / hyperactivity disorder (ADHD) in kids and adults- could favour likelihood to smoke, consume alcohol, cannabis and other addictive substances, according to an article.
The findings are based on the study of around 2,700 patients –children, adolescents and adults- from the United States, Colombia and Spain, and it will contribute to provide new genetic tools to improve prevention of addictive behaviours in people with ADHD.
ADHD is one of the most commons disorders in childhood and adolescence –it can linger until adulthood- and its traits are hyperactivity, impulsiveness, and attention deficit. One of the genes related to ADHD susceptibility is LPHN3, which codes the protein latrophilin 3, “a molecule related to the formation of synaptic connections between certain types of neurons, and therefore, a good candidate to set a relation with any psychiatric disorder”, notes the lecturer Bru Cormand, head of the Research Group on Neurogenetics of the Faculty of Biology of the UB.
The connection between LPHN3 and ADHD is one of the most studied regarding the etiology of the disorder. This gene, in addition, has an impact on the patients’ response to the medication, the degree of severity of the disease and disruptive behaviour. However, so far, the depth of the relation between the gene LPHN3 and substance addiction had not been explored.
In the new study, the experts applied an innovative statistical method (Recursive-partitioning Frameworks) which integrates clinical, demographic and genetic information on a specific disorder –in this case, ADHD- to predict another co-morbid disorder (which appears concurringly), such as addiction to tobacco, alcohol, cocaine, cannabis and marijuana, among others.
Conclusions note that, within the group of Spanish patients with ADHD, a specific variation of the LPHN3 gene increases by 40 % the risk of nicotine dependence. According to the experts, results are similar in the cases for alcohol and illegal drugs, which have been studied together in the research.
Not all those affected by ADHD show behaviours with an addictive profile over their lives. “We now know genetics play an important role in these behaviours. This helps us to prevent future risks in kids and adults with ADHD and to improve prevention strategies. However, ADHD genetics are diverse, there are many involved genes and these vary among the patients with the disorder”, notes Cormand.
75 % of ADHD has a genetic base and the remaining 25 % is related to environmental factors which can vary, according to the experts. Therefore, external factors can be relevant in the appearance of addictive behaviours in people with ADHD. For example, certain lifestyles or social interactions can play an important role.
“Also, cocaine and other addictive substances –warns Cormand- have a psychostimulant action similar to the one in the main pharmacological treatment for ADHD. This would explain why, in some cases, these are used by the affected people as self-medication for its apparently ‘beneficial’ effects”.
Psychological and pharmacological treatment and psychopedagogical intervention are the combined strategies that are most efficient in ADHD treatment. In the future, we will need new clinical studies to analyse the importance of genetics in ADHD susceptibility and addictive behaviours that can affect the patient’s health.
University of Barcelonahttps://tinyurl.com/y5qzsvv6
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