Category Archives: Gene Medicine

A new analysis of available data has convinced a panel genomic experts that nine genes previously believed to be associated with a rare, genetic heart conditionlong QT syndromewere an erroneously linked to the condition, as revealed in a new study funded by the National Human Genome Research Institute (NHGRI), a division of the National Institutes of Health (NIH).

Geneticists and heart specialists around the world had previously reported 17 genes to cause long QT syndrome. However, the Clinical Genome Resources (ClinGen) expert panel has critically reevaluated the scientific evidence for all 17 reported genes, and has concluded at least nine of the genes cannot be linked to the disease, and only three of the genes can be definitively associated with the most common form of the disease.

Long QT syndrome is caused by mutations in genes that regulate the hearts electrical activity. These mutations can cause the heart to have sudden, irregular heart rhythms, or arrhythmias. People with long QT syndrome can have arrythmias that are both unprovoked or as a result of stress and exercise. These arrythmias can be fatal.

Many people with long QT syndrome may be unaware they have the condition, unless they get an unrelated electrocardiogram, know their family history, and have undergone genetic testing.

Ever since the syndrome was described in 1957, researchers have engaged in a genetic race to identify the genes associated with it, which currently includes the 17 genes. By using such a standardized, evidence-based framework, the international ClinGen panel experts on long QT syndrome were able to classify the 17 genes into specific groups.

Three genes, KCNQ1, KCNH2 and SCN5A, had sufficient evidence to be implicated as definitive genetic causes for typical long QT syndrome. Four other genes had strong or definitive evidence supporting their role in causing atypical forms of long QT syndrome, particularly if they presented in the newborn period with associated heart block, seizures or delays in development.

The remaining ten genes were deemed to not have sufficient evidence to support a causal role in the syndrome. In fact, nine of these 10 remaining genes were placed in the limited or disputed category. The study authors suggest that these genes not be routinely tested in clinical settings when evaluating patients and families with long QT syndrome, because they lack sufficient scientific evidence as a cause for the condition.

This removal of genes from the testing list impacts genetic testing providers, who use research papers to determine which genes to include in their testing panels for diagnostic reporting to physicians. Published papers reporting gene-disease associations vary widely in their study design and strength of evidence to support their conclusions. Until recently, standard guidelines that can differentiate between genes found with strong and valid scientific approaches versus those with insufficient evidence did not exist. Clearly, this is a problematic approach, and led to several studies drawing early conclusions.

ClinGens expert panels include researchers, clinicians, and genetic counselors who apply an evidence-based framework in evaluating the available data from research papers to place gene-disease relationships into definitive, strong, moderate, limited, disputed, or refuted categories.

ClinGen is an impressive community effort. With over 1,000 researchers and clinicians from 30 countries volunteering their time and expertise, ClinGen is providing much needed clarity for the clinical genomics community regarding which gene-disease pairs have sufficient evidence to be used clinically, said Erin Ramos, Ph.D., project scientist for ClinGen and program director in the Division of Genomic Medicine at NHGRI.

Our study highlights the need to take a step back and to critically evaluate the level of evidence for all reported gene-disease associations, especially when applying genetic testing for diagnostic purposes in our patients. Testing genes with insufficient evidence to support disease causation only creates a risk of inappropriately interpreting the genetic information and leading to patient harm, says Michael Gollob, M.D., senior author of the paper and researcher at the Toronto General Hospital Research Institute.

Moreover, testing for genes not definitively associated with long QT syndrome can result in inappropriate and costly medical interventions such as implanting of a cardioverter-defibrillator.

This is not the first time a team at ClinGen has clarified published research for clinicians. The same team of researchers published a similar study in 2018, covering another heart condition called Brugada syndrome. In 2019, the American Society of Human Genetics considered the paper as one of the top 10 advances in genomic medicine.

ClinGen is an NHGRI-funded resource created to define the clinical relevance and validity of genes associated with various genetic disorders. It comprises more than 20 expert panels working on a variety of genetically influenced diseases, ensuring the reliability of gene-disease linkage. This work is also instrumental in determining which specific genes should be targeted for further study in precision medicine and research.

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Genes Previously Linked to Heart Condition Disputed - Clinical OMICs News

Information is the stuff of life. Not limited to DNA, information is found in most biomolecules in living cells. Here are some recent developments.

Certain forms of sugars (polysaccharides called chitosans) trigger the immune system of plants. Biologists at the University of Mnster are deciphering the sugar code. They describe the variables in chitosans that constitute a signaling system.

Chitosans consist of chains of different lengths of a simple sugar called glucosamine. Some of these sugar molecules carry an acetic acid molecule, others do not. Chitosans therefore differ in three factors: the chain length and the number and distribution of acetic acid residues along the sugar chain. For about twenty years, chemists have been able to produce chitosans of different chain lengths and with different amounts of acetic acid residues, and biologists have then investigated their biological activities. [Emphasis added.]

These polysaccharides, also found in animals, are perhaps the most versatile and functioning biopolymers, the scientists say. If they can learn to decipher this complex code, they might find ways to protect plants without the use of pesticides.

DNA is becoming known as a more of a team member in a society of biomolecules. In some ways, it is more a patient than a doctor. It gets operated on by numerous machines that alter its message. One of the most important doctors that operates on RNA transcripts is the spliceosome, says a review article in The Scientist about alternative splicing. This complex molecular machine can multiply the messages in the coding regions of DNA by cutting out introns and stitching coded parts called exons together in different ways.

The process of alternative splicing, which had first been observed 26 years before the Human Genome Project was finished, allows a cell to generate different RNAs, and ultimately different proteins, from the same gene. Since its discovery, it has become clear that alternative splicing is common and that the phenomenon helps explain how limited numbers of genes can encode organisms of staggering complexity. While fewer than 40 percent of the genes in a fruit fly undergo alternative splicing, more than 90 percent of genes are alternatively spliced in humans.

Astoundingly, some genes can be alternatively spliced to generate up to 38,000 different transcript isoforms, and each of the proteins they produce has a unique function.

The discovery of splicing seemed bizarre from an evolutionary perspective, the authors say, recalling obsolete ideas about junk DNA. It seemed weird and wasteful that introns were being cut out of transcripts by the spliceosome. Then, the ENCODE project found that the vast majority of non-coding DNA was transcribed, giving these seemingly nonfunctional elements an essential role in gene expression, as evidence emerged over the next few years that there are sequences housed within introns that can help or hinder splicing activity.

This article is a good reminder that evolutionary assumptions hinder science. Once biochemists ridded themselves of the evolutionary notion of leftover junk in the genetic code, a race was on to understand the role of alternative splicing.

Understanding the story behind each protein in our bodies has turned out to be far more complex than reading our DNA. Although the basic splicing mechanism was uncovered more than 40 years ago, working out the interplay between splicing and physiology continues to fascinate us. We hope that advanced knowledge of how alternative splicing is regulated and the functional role of each protein isoform during development and disease will lay the groundwork for the success of future translational therapies.

Another discovery that is opening doors to research opportunities comes from the University of Chicago. Darwin-free, they announce a fundamental pathway likely to open up completely new directions of research and inquiry. Biologists knew about how methyl tags on RNA transcripts regulate the ways they are translated. Now, Professor Chuan He and colleagues have found that some RNAs, dubbed carRNAs, dont get translated at all. Instead, they controlled how DNA itself was stored and transcribed.

This has major implications in basic biology, He said. It directly affects gene transcriptions, and not just a few of them. It could induce global chromatin change and affects transcription of 6,000 genes in the cell line we studied.

Dr. He is excited about the breakthrough. The conceptual change in how RNA regulates DNA offers an enormous opportunity to guide medical treatments and promote health. Take a look at this design-friendly quote:

The human body is among the most complex pieces of machinery to exist. Every time you so much as scratch your nose, youre using more intricate engineering than any rocket ship or supercomputer ever designed. Its taken us centuries to deconstruct how this works, and each time someone discovers a new mechanism, a few more mysteries of human health make sense and new treatments become available.

Remember the evolutionary myth that jumping genes were parasites from our evolutionary past that learned how to evade the immune system? A discovery at the Washington University School of Medicine changes that tune, saying, Jumping genes help stabilize DNA folding patterns. These long-misunderstood genes thought by some evolutionists to be sources of novel genetic traits actually function to provide genomic stability.

Jumping genes bits of DNA that can move from one spot in the genome to another are well-known for increasing genetic diversity over the long course of evolution. Now, new research at Washington University School of Medicine in St. Louis indicates that such genes, also called transposable elements, play another, more surprising role: stabilizing the 3D folding patterns of the DNA molecule inside the cells nucleus.

It appears that by moving around, these genes can preserve the structure of DNA while not altering its function. (Note: the evolution they speak of appears to be microevolution, which is not controversial; hear Jonathan Wells discuss this on ID the Future.)

According to the researchers, this redundancy makes the genome more resilient. In providing both novelty and stability, jumping genes may help the mammalian genome strike a vital balance allowing animals the flexibility to adapt to a changing climate, for example, while preserving biological functions required for life.

Lead author Ting Wang says this gives insight into why coding regions between different animals vary in structure.

Our study changes how we interpret genetic variation in the noncoding regions of the DNA, Wang said. For example, large surveys of genomes from many people have identified a lot of variations in noncoding regions that dont seem to have any effect on gene regulation, which has been puzzling. But it makes more sense in light of our new understanding of transposable elements while the local sequence can change, but the function stays the same.

So while evolutionists had expected junk and simplicity, Wang says the opposite has occurred. We have uncovered another layer of complexity in the genome sequence that was not known before. Now, more discoveries are likely to flow from intelligent designs expectation that a closer look reveals more complexity.

In another recent podcast at ID the Future honoring the late Phillip E. Johnson, Paul Nelson likened a graph of mounting discoveries about life to a sharply rising mountain range. Darwin proposed his theory on the flatlands, unaware of the peaks his theory would have to explain. In the last fifty years, scientists have encountered mountain after mountain of complexity in life that evolutionary theory never anticipated back out there on the flatlands. We cant see the top of the mountains yet, but we know that were still not there, and we wont be for a long, long time, Nelson says. As we witness scientists continuing up the mountains, we anticipate with awe more wonders of design that will likely come to light in the next decade.

Image: Interior of a cell, courtesy of Illustra Media.

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Surprises in Cell Codes Reveal Information Goes Far Beyond DNA - Discovery Institute

Some of the prominent players operating in the precision medicine software market include 2bPrecise, Syapse, Inc., IBM Corporation

PUNE, India, Jan. 27, 2020 /PRNewswire/ -- Precision medicine is a prototype in healthcare which provides the customization of healthcare with medical decisions, practices, treatments, and products for patients in person. It states about right therapeutic approach for the right patient at the right time. The use of precision medicine is to identify which treatment approach is effective for patients on the basis of genetic, environment, and lifestyle factors. Precision medicine software allows the healthcare professionals (HCPs) to provide personalized treatment plans to patients based on their genetic content. It gives a wide range of applications in both the clinical and diagnostic areas and it combines genetic and clinical data to cater targeted patient care, which is increasing the demand of precision medicine software market.

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The global precision medicine software market is experiencing lucrative growth owing to the increase in the number of patients suffering from chronic diseases such as cancer, heart diseases, and diabetes. For instance, as per the data presented by International Agency for Research on Cancer (IARC), in 2018, the cancer burden was 18.1 million new cases and 9.6 million deaths across the world. One in five men and one in six women around the globe develop cancer during their lifetime, and one in eight men and one in 11 women die from the disease.

Koninklijke Philips N.V. (Philips Healthcare), a multinational electronics company focusing on healthcare, offers precision medicine platform, namely, IntelliSpace. It enables end-to-end oncology care or cancer management. The platform unifies and streamlines oncology care throughout the patient journey from molecular diagnostics to therapy recommendations. IntelliSpace, a precision medicine oncology solution integrates information over different clinical domains such as pathology, electronic health record (EHR) systems, radiology, and genomics. It consolidates all key patient and medical data in one location to represent a clear, comprehensible view of patient status in its disease and enable data driven clinical decision support, which in turn is propelling the precision medicine software market.

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Precision medicine with the integration of artificial intelligence (AI) will go to the next level with more accuracy and prediction of outcome for patients. Its major benefit for precision medicine is that it predicts outcomes as well as enables healthcare professionals to predict patient's probability of having diseases in the future, thus driving the demand of precision medicine software market. Oracle, an American multinational computer technology corporation offers precision medicine software that enables researchers, clinicians, and molecular pathologists to work together. The software addresses data aggregation, normalization and workflow issues, knowledge exchange which restricts timely creation of patient molecular profiles and it also enables spectrum testing from gene panels through whole genome sequencing, and integration with electronic health record systems for seamless clinical workflow.

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The detailed research study provides qualitative and quantitative analysis of the global precision medicine software market. The precision medicine software market has been analyzed from demand as well as supply side. The demand side analysis covers market revenue across regions and further across all the major countries. The supply side analysis covers the major market players and their regional and global presence and strategies. The geographical analysis done emphasizes on each of the major countries across North America, Europe, Asia Pacific, Middle East & Africa and Latin America.

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Global Precision Medicine Software Market

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Global Precision Medicine Software Market is Expected to Grow at CAGR 12.3% from 2019 to 2027 Owing to the Increase in the Number of People who are...

Image: Professor Chris Lord andDr Stephen Pettitt next to the olaparib display in the Science Museum's medicine galleries

The Science Museum's new 24 millionmedicine galleriesshowcases pioneering research from The Institute of Cancer Research, London, as part of its story of modern medicine.

The new galleries, which have transformed the first floor of the world-famous museum, explore humanity's relationship with medicine and health through more than 500 years of history.

Included in the exhibition are extraordinary medical artefacts from the collections of Henry Wellcome and the Science Museum Group, including the world's first MRI scanner, Fleming's penicillin mould, a professional pianist's prosthetic arm and robotic surgery equipment.

Science MuseumLatesare adults-only, after-hours theme nights that take place in the museum on the last Wednesday of every month. Tonight's (Wednesday 29 January) Lates event isMedicine Lates.

Follow #smLates on Twitter

The museum chose to showcase the ICR's pioneering research underpinning the development of targeted drug olaparib, which has transformed the lives of tens of thousands of women with breastand ovariancancers.

Olaparib's origins lie in ICR research into the BRCA genes in the 1990s, when our scientists tracked down the BRCA2 gene.

A decade after the identification of BRCA2, ICR researchers found that targeting a DNA repair protein called PARP was a potential way to kill cancer cells with a faulty BRCA gene. This helped lead to the development of olaparib, and other so-called PARP inhibitors.

The gallery features plates which replicate the original ICR experiment to successfully show that olaparib specifically kills cancer cells with defects in their BRCA genes, while leaving healthy cells unaffected.

You can see these in the Medicine and Bodies gallery, which explores how the search to understand more about the human body has transformed medicine.

Displayed alongside Crick and Watson's molecular DNA model, the plates represent how understanding the genetic basis of cancer has transformed our ability to treat it through the creation of targeted therapies.

Professor Chris Lord,Deputy Head of the Breast Cancer Now Toby Robins Research CentreandDivision of Breast Cancer Researchat the ICR (pictured above), said:

"The fact that the Science Museum have chosen to highlight PARP inhibitors in their new gallery is a real testament to how cancer research can genuinely lead to improvements in the treatment of the disease. We are immensely proud of this, as are the other labs across the world who also contributed to these discoveries."

"Despite PARP inhibitors now being highlighted in Science Museum, this is not the end for us we are still working very hard at the ICR to think about how we can improve the effectiveness of these drugs and to make sure that each patient receives the best possible treatment approach."

Daisy Henesy, the ICRs Public Engagement Officer, said:

"It's a thrill to see the ICR's research showcased alongside other huge advances in modern medicine, and richly deserved.

"I urge everyone to visit the new Science Museum galleries and have a look for yourself and don't forget to tweet us with any pictures @ICR_Londonand let us know what you think!"

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ICR research showcased in major new Science Museum gallery documenting history of medicine - The Institute of Cancer Research

HAMBURG, Germany and BALTIMORE, Jan. 28, 2020 /PRNewswire/ -- Pathologist Dr. Vincente Peg of the Vall dHebron University Hospital (Barcelona Spain) and colleagues have presented a correlation between the clearance of circulating tumor DNA (ctDNA) in HER2-positive or triple-negative breast cancer patients undergoing neoadjuvant treatment with a clinical/pathologic complete response at the American Association for Cancer Research (AACR) Advances in Liquid Biopsies conference held in Miami, Florida (USA), January 13-16, 2020. The researchers utilized both a SureSeq NGS cancer gene enrichment panel (Oxford Gene Technology, a Sysmex Group Company) for identifying lead mutations from breast cancer FFPE tissue, and Sysmex Inostics' SafeSEQ personalized liquid biopsy platform for patient-specific longitudinal analysis of plasma ctDNA.

Neoadjuvant therapy to reduce tumor size prior to surgical resection is common in the treatment of early stage breast cancer. However, there exists an unmet clinical need to distinguish those patients with residual disease after Neoadjuvant Therapy (NAT) from those who achieved complete response in order to better understand which patients are appropriately suited for surgery. Researchers from Vall dHebron deployed SureSeq NGS testing to identify driver mutations in breast cancer biopsy tissue of 29 patients with early stage disease. The mutations detected with SureSeq were subsequently followed in the plasma of patients with the SafeSEQ ultrasensitive personalized ctDNA platform to complement radiographic assessment and provide more detailed information on an individual's response to NAT.

Of 29 Stage II and Stage III triple-negative and HER2-positivebreast cancer patients examined in the study, 20 (69%) had TP53 or PIK3CA tissue mutations identified by SureSeq with 17 out of 20 (85%) patients having detectable mutations with SafeSEQ in plasma samples prior to initiation of NAT. Longitudinal plasma analysis conducted at treatment mid-point and post-treatment immediately prior to surgery demonstrated the absence of ctDNA following NAT was observed in all patients (12/12) showing a complete clinical response. However, ctDNA was detected in 3 out of 5 (60%) of patients who did not achieve complete clinical response suggesting that ctDNA testing - alongside of imaging - is an important clinical parameter to consider when determining complete response to neoadjuvant treatment.

"This study addresses the unmet need to de-escalate surgery in patients with no sign of disease." Dr. Vicente Peg commented. "How can we avoid surgically removing something that is just not there? Circulating tumor DNA by itself is able to detect 85% of patients that achieve pathologic complete response; however, when combined with imaging we can identify 100% of patients. These findings are an important first step to showing that we can accurately identify those patients who may avoid unnecessary surgery."

Reference:Ciriaco, N., Zamora, E. and Peg, V. et al. AACR Advances in Liquid Biopsy Conference 2020 Poster session B January 15, 2020. Clearance of ctDNA in triple-negative and HER2-positive breast cancer patients during neoadjuvant treatment is correlated with pathological complete responses, Poster B63.

About Sysmex Inostics

Sysmex Inostics, a subsidiary of Sysmex Corporation, is a molecular diagnostic company that is a pioneer in blood-based cell-free tumor DNA (ctDNA) mutation detection in oncology utilizing highly sensitive technologies such as OncoBEAM (digital PCR) and SafeSEQ (NGS).These technologies were initially developed by experts at the Johns Hopkins School of Medicine over a decade ago and this deep expertise in ctDNA analysis extends to the core of Sysmex Inostics' capabilities for technology development and implementation.

With more than 10 years of experience in liquid biopsy, Sysmex Inostics is a trusted partner to leading pharmaceutical companies, advancing their efforts to bring the most effective personalized cancer therapies to global markets, from discovery through companion diagnostics.

Sysmex Inostics' OncoBEAM and SafeSEQ services are readily available to support clinical trials and research in oncology. In addition, OncoBEAM tests are available through a CLIA-certified laboratory for routine clinical analysis as well as distributed kit products in the EU and Asia Pacific.

Sysmex Inostics' headquarters and GCP Service Laboratory are located in Hamburg Germany; Sysmex Inostics' CLIA-certified and GCP Clinical Laboratory is located in Baltimore, Maryland. For more information refer towww.sysmex-inostics.comor emailinfo@sysmex-inostics.com.

Contact: Sysmex InosticsPress ReleasePhone: +49-(0)-40-3259070Mail: info@sysmex-Inostics.com

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Sysmex Inostics and Oxford Gene Technology Plasma and Tissue Sequencing Show Clearance of ctDNA Correlates With Pathologic Complete Response in Breast...

The rate of new mutations in the human genome appear to be consistent across diverse populations, except onethe Old Order Amish of Lancaster, Pennsylvania. This group has a lower rate of developing new mutations, according to a study published January 21 in PNAS.The lower mutation rate does not appear to have a genetic component, pointing to a possible role for environmental factors in modifying how fast human genomes accrue new mutations.

It really looks like environmental differences might actually [have] the most significant effect on the number of mutations that you pass on to your offspring, rather than . . . there being some sort of gene causing mutations, says Aylwyn Scally, a geneticist at the University of Cambridge who was not involved in the work. In a larger study than this one, researchers might be better able to detect a genetic contribution if there is one, he says. But still its surprising that it hasnt jumped out, and instead theres this curious effect thats bolstered by their finding about the Amish. Maybe different environments are actually the biggest factor.

Mutation rates are a source of genetic variation within populations. Knowing more about these rates in humans can help researchers better understand disease and evolution. Before this study, mutation rates had really only been looked at in Europeans, and so we wanted to be able to look in a much broader, diverse population, evolutionary geneticist Timothy OConnor of the University of Maryland, a coauthor on the new paper, tells The Scientist.

To this end, he and his colleagues leveraged a dataset of whole genomes from more than 1,400 parent-child trios from the National Heart, Lung, and Blood Institutes TOPMed (Trans-Omics for Precision Medicine) program. The team found that the rate of de novo mutations was similar across populations of African, Latino, and European ancestry. That finding was intriguing because previous work had suggested that populations with high levels of genetic diversity, such as those of African descent, would have higher mutation rates.

Even more unexpected was the mutation rate detected in the 59 Amish families in the cohort. These Amish families are of European descent but have been genetically isolated from other populations since the 1700s and all descended from about 700 individual founders. They had a seven-percent-lower mutation rate compared with the other populations.

We were pretty surprised, says OConnor. Initially the team thought the lower mutation rate had to be an artifact of the sequencing or analysis. We did basically everything we could to try and figure out what kind of artifact would be causing it, and we couldnt find one.

The research team next tried to pinpoint what caused the Amish to have a lower incidence of new mutations. OConnor and his colleagues determined that the lower mutation rates were not heritable, which led the team to speculate that environmental factorssuch as the typical Amish diet and limits on technologymay contribute.

The findings are novel in that the reduced mutation rate hasnt been previously shown with so much sequencing data, says Heather Wheeler, a geneticist at Loyola University Chicago who was not involved in the study. The caveat is that it was still just in one group, and there were only 59 families in the Amish population, she notes. If this is a real effectthe clean-living hypothesis they proposewe definitely want to see it validated in other populations that have similar environments to the Amish.

M.D. Kessler et al., De novo mutations across 1,465 diverse genomes reveal mutational insights and reductions in the Amish founder population,PNAS,doi:10.1073/pnas.1902766117, 2020.

Abby Olena is a freelance journalist based in Alabama. Find her on Twitter@abbyolena.

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Human Mutation Rates Steady Across GroupsExcept in the Amish - The Scientist