Category Archives: Epigenetics

Do species really exist? Are genes destiny? Do only the fittest survive? Can we shape or stop evolution? New insights into nature are providing surprising answers, and a glorious new picture of lifes complexity

By Michael Le Page , Colin Barras , Richard Webb , Kate Douglas and Carrie Arnold

Our modern conception of evolution started with Charles Darwin and his idea of natural selection survival of the fittest to explain why certain individuals thrive while others fail to leave a legacy. Then came genetics to explain the underlying mechanism: changes in organisms caused by random mutations of genes.

Now this powerful picture is changing once more, as discoveries in genetics, epigenetics, developmental biology and other fields lend a new complexity and richness to our greatest theory of nature. Find out more in this special feature.

The principle of genetic plasticity

IN 1990, an international group of scientists embarked on one of the most ambitious research projects ever undertaken. They would sequence the entire human genome, determining the order of the 3.3 billion base pairs that code for the genes that make the proteins that each of us are built from. There was huge excitement at the prospect of decoding the blueprint of humanity. Given the complexity of our species, our genome was expected to contain at least 100,000 genes. What makes us human would finally be laid bare.

It didnt quite work out like that. The Human Genome Project was a resounding success, publishing its results in 2003, two years ahead of target. However, it revealed that humans only have around 22,000 genes, which is about the same number as other mammals. Meanwhile, the blueprint itself turned out to be encrypted in ways we are still trying to crack.

The same thing is true of us that is true of every species: our DNA can be expressed in myriad different ways

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Evolution is evolving: 13 ways we must rethink the theory of nature - New Scientist

Ischemic retinopathies, including glaucoma and diabetic retinopathy, are major causes of visual morbidity and blindness. New research from Louisiana State University Health Sciences Center in New Orleans shows that an epigenetic therapy reduces retinal injury from acute ischemia, not only in the animals that receive the treatment, but also in their untreated first-generation offspring.In a study published in the journal Investigative Ophthalmology & Visual Science, scientists treated male and female adult mice with one hour of mild-to-moderate systemic hypoxia three times per week for 16 weeks prior to mating.1 When their first-generation offspring reached adulthood, the response of their retina to transient, acute ischemic injury was functionally documented with scotopic electroretinography. Compared to age- and generation-matched controls, the ischemia-induced impairments in the retinas response to light in the mice derived from parents that received the epigenetic hypoxia treatment was reduced by 40-50%.

We knew from our previous work that a single exposure to systemic hypoxia would protect the adult retina from ischemia occurring one to two days thereafter, and that multiple doses over two weeks would extend that window of protection to two months, says senior author Dr Jeff Gidday.2,3 Gidday undertook the present study with the hope of showing that the duration of the induced, injury-resilient phenotype could be extended further, perhaps even into the next generation, if treatments continued for a much longer period of time.

As with most diseases, the pathologic mechanisms involved are diverse; activating innate, counter-responses to these injury mechanisms is the conceptual basis for epigenetics-based therapeutic strategies, like intermittent hypoxia. Gidday and his team contend that systemic hypoxia triggers changes in gene expression, but that the duration of the change is largely proportional to the frequency of this epigenetic stimulus. With prolonged treatment, even germ cells become reprogrammed, resulting in progeny that, as adults, exhibit this same inducible injury-resilient phenotype in the absence of treatment.

"We exposed mice to nonharmful hypoxia to trigger these adaptive changes," says first-author Jarrod Harman, a doctoral student in Dr Gidday's lab. But there are many epigenetic stimuli that might very well cause similar changes in gene expression, including exercise, and other 'positive' stressors. Not all stress is bad for you." These findings represent a converse example of the increase in disease susceptibility and incidence that is fairly well established to occur in progeny derived from parents repeatedly exposed to adverse, harmful stressors. To date, some rodent studies have shown that environmental enrichment can enhance baseline memory metrics in first-generation offspring, but the authors believe this is the first study to demonstrate, in mammals, that changes in the parental environment (in this case, intermittent exposure to whole-body hypoxia) can actually protect progeny against tissue injury.

The researchers also extensively analyzed the injury-resilient retinal phenotype using mass spectrometry to gain insights into the underlying mechanisms of neuroprotection. By comparing the protein profiles between mice derived from treated parents and mice derived from control parents, and then performing bioinformatic analyses of these hundreds of differentially expressed proteins, they identified dozens of biochemical pathways and networks that define the injury-resilient state. This included the reversal of a number of ischemia-induced changes in the expression of proteins and even protein subunits involved in the photoreceptor visual transduction pathway, which is responsible for the electroretinographic response to light that the authors measured as their functional metric of injury resilience. As examples, parental treatment abrogated the ischemia-induced reduction in the expression of rhodopsin by 2.5 fold, and enhanced the expression of the phosphodiesterase 6 -subunit, and several proteins (e.g., guanylate cyclase activator 1A), responsible for generating the dark current. Given the complexity of this intergenerational epigenetic response, using this big-data approach to illuminate the neuroprotective phenotype provides us and others a molecular foundation upon which more targeted, causal experiments can now be logically designed, Harman says.

Overall, the findings add to our understanding of the heritability of disease in this case, the heritability of disease resilience. "The direct inheritance of an induced, beneficial phenotype is what Lamarck famously proposed in 1809, the year Darwin was born," says Gidday. "Here we are, almost 200 years later, finding evidence to support this theory, despite it being largely displaced for the last 150 years by Darwin's Theory of Natural Selection. More than likely, both mechanisms are operative as a way to enhance both short- and long-term reproductive fitness."

References:

1. Harman JC, Guidry JJ, Gidday JM. Intermittent hypoxia promotes functional neuroprotection from retinal ischemia in untreated first-generation offspring: Proteomic mechanistic insights. Invest Ophthalmol Vis Sci (2020). doi:https://doi.org/10.1167/iovs.61.11.15.

2. Zhu Y, Ohlemiller KK, McMahan BK, Gidday JM. Mouse models of retinal ischemic tolerance. Invest Ophthalmol Vis Sci. (2002);43(6):1903-1911.

3. Zhu Y, Zhang Y, Ojwang BA, Brantley MA Jr, Gidday JM. Long-term tolerance to retinal ischemia by repetitive hypoxic preconditioning: role of HIF-1alpha and heme oxygenase-1. Invest Ophthalmol Vis Sci. 2007;48(4):1735-1743. doi:10.1167/iovs.06-1037.

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Epigenetic Therapy in Parents Protects Offspring From Ischemic Injury in Mouse Study - Technology Networks

Epigenetics-based instruments market is expected to register a substantial CAGR in the forecast period of 2019-2026. The report contains data from the base year of 2018 and the historic year of 2017. This rise in market value can be attributed to the various innovations and advancements of technologies associated with epigenetics.

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Few of the major competitors currently working in the global epigenetics-based instruments market arePacific Biosciences of California, Inc.; 10x Genomics; Illumina, Inc.; Merck KGaA; QIAGEN; Eisai Co., Ltd.; Novartis AG; Diagenode s.a.; Zymo Research; Active Motif, Inc.; Thermo Fisher Scientific Inc.; Agilent Technologies, Inc.; Bio-Rad Laboratories, Inc.; Bio-Techne among others.

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Global Epigenetics-Based Instruments Market Current Trends And Efficient Techniques, Forecast 2026|QIAGEN; Eisai Co., Ltd.; Novartis AG; Diagenode sa;...

Newswise Luis M. Tuesta, Ph.D., assistant professor in the Department of Psychiatry and Behavioral Sciences at the University of Miami Miller School of Medicine, has been awarded the Avenir Award from the National Institute on Drug Abuse, part of the National Institutes of Health, to study the epigenetic mechanisms of microglial activation and their role in shaping the behavioral course of opioid use disorder. The goal is to find new therapeutic targets to prevent opioid relapse and achieve long-term abstinence.

Dr. Tuesta and the Miller School will receive $2.3 million over five years from the NIH. He is one of four researchers in the country to receive the award grant in 2020. Dr. Tuesta joined the Universitys medical faculty in 2019 following a postdoctoral fellowship at Harvard Medical School.

A Prestigious Grant

This is one of the very best and most prestigious grants that a young researcher can receive, said Claes Wahlestedt, M.D., Ph.D., associate dean for therapeutic innovation at the Miller School. As a former chair of the NIH Avenir Award Committee, Dr. Wahlestedt recognizes the distinct honor of receiving this competitive award.

Dr. Tuesta explained his labs novel approach to understanding opioid addiction.

Throughout the history of addiction research, the neuron has usually played the protagonist role, he said. We are now setting our sights on the brains supporting cast of cells and how these can shape drug craving and relapse.

Namely, he and his lab are studying microglia, the resident immune cell of the brain.

Opioids can hijack the very tools that microglia use for sounding the alarm in case of a physical, chemical or biological injury, Dr. Tuesta explained. This artificial state of alarm can lead to neuroinflammation and shape the way we crave for opioids, ultimately leading to relapse. We believe epigenetic regulation in microglia plays a fundamental role in orchestrating this chain of events.

Epigenetics refers to factors that determine how genes are expressed without involving changes in the DNA sequence itself. Dr. Tuestas team will explore how microglial genes become open and closed for business across various phases of opioid addiction, and how specific epigenetic remodelers can contribute to this regulation.

Exploring New Therapeutic Avenues

Results from these studies have the potential not just to broaden our understanding of the epigenetic mechanisms underlying opioid use disorder, but also to push the field of addiction epigenetics beyond the neuron and explore a cell type that could yield exciting and completely different therapeutic avenues for the treatment of this devastating disease.

Ideally, a treatment drug would reverse changes in microglia brought on by opioids and curb the intense craving associated with opioid abstinence and withdrawal. Such an approach could help reduce the likelihood of relapse in recovering individuals.

Ultimately, we want to manipulate the root of the craving with a drug to change the behavioral course of addiction, Dr. Tuesta said.

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University of Miami Miller School Researcher Wins NIH Avenir Award to Pursue Innovative Opioid Addiction Research - Newswise

SALT LAKE CITY, Sept. 9, 2020 /PRNewswire/ --Inherent Biosciences, a biotechnology company headquartered in Salt Lake City, UT, today announced a $255,959 award from the National Science Foundation (NSF) to study epigenetic biomarkers to predict patient response to SARS-CoV2 (COVID-19) infection. The Small Business Innovation Research (SBIR) Phase I project aims to develop an on-site, clinical test to screen incoming patients potentially infected with COVID-19 and prioritize hospital resources and personnel based on a predicted infection severity and treatment response.

The variation in symptoms and outcomes for COVID-19 progression makes it challenging for health care workers to triage patients accurately. The development of a DNA methylation-based test to predict the severity of COVID-19 infection has tremendous potential for managing current and future pandemics.

"NSF is proud to support the technology of the future by thinking beyond incremental developments and funding the most creative, impactful ideas across all markets and areas of science and engineering," said Andrea Belz, Division Director of the Division of Industrial Innovation and Partnerships at NSF. "With the support of our research funds, any deep technology startup or small business can guide basic science into meaningful solutions that address tremendous needs."

Andy Olson, Co-founder and CEO of Inherent Biosciences, remarked: "We're thrilled to announce this award, which will enable us to expand our discovery and commercialization pipeline into the area of infectious disease - a critical area as witnessed by the COVID-19 pandemic we're living through."

The award provides support for Inherent to generate a comprehensive dataset of white blood cell DNA methylation patterns, health history, and clinical data for patients infected with COVID-19. The company then uses artificial intelligence (AI) and machine learning to identify DNA methylation biomarkers predictive of disease severity and treatment response.

Kristin Brogaard, Ph.D., Co-founder and COO of the company, and Principal Investigator for the project added: "Our focus is translating epigenetic discoveries, specifically DNA methylation biomarkers, from research discoveries into commercial products that benefit consumers, patients and health care providers."

Inherent has already translated one epigenetic discovery into a commercial product. The company's first product called "Path" (PathFertility.com) is for couples trying to conceive. Path is marketed directly to consumers as a general wellness sperm DNA test related to maintaining or encouraging a general state of health, specifically male reproductive health.

About Inherent Biosciences- Inherent Biosciences, Inc. is a molecular diagnostics company at the intersection of epigenetics and AI. Inherent believes that guesswork and trial-and-error medicine lead to severe pain and suffering. Inherent's vision is to revolutionize trial and error medicine and restore hope. The company does this by discovering what is inherent in our biology about the unexplained and translating discoveries into personal insights that inform actions. Learn more at http://www.inherentbio.comor connect on LinkedIn.

Contact: Inherent Biosciences, Inc.

Andy Olson, CEO

Phone: (509) 496-1204

Email: andy@inherentbio.com

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Inherent Biosciences Wins $256K NSF Grant to Predict COVID-19 Infection Severity and Treatment Response - KPVI News 6

A detailed synopsis of the epigenetics market has been presented in this research report. The synopsis has been charted out keeping in mind certain vital parameters such as global trends, industry insights, growth drivers, industry ecosystem analysis, and market segmentation. Details about the various companies constituting he competitive landscape of market as well as the regional bifurcation of this industry from a global standpoint is outlined in the study, in addition to the impact of the regulatory frame of reference worldwide.

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Market segmentation as per the Product landscape: Enzymes, Instruments and Consumables, Kits, Reagents, Bioinformatic tools, etc.

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Market segmentation as per the Application landscape: Oncology, Immunology, Cardiovascular diseases, Developmental biology, etc.

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Market segmentation as per the Technology landscape: Histone Modification, DNA Methylation, Others, etc.

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The epigenetics market research document is an extensive collection of pivotal insights pertaining to the industry. In a nutshell, the epigenetics market study aims to educate potential investors about the market scenario and future prospects. The report also endorses details about the industry pitfalls and challenges as well as the industry impact forces.

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Epigenetics Market Is Predicted to Witness A Massive Growth Up To 2026 - Fractovia News

Epigenetics is the study of chemical features that attach to genes and affect their activity. Mammals share similar life stages, yet little was known about whether specific epigenetic changes linked to these life stages look the same for different animals. A new study, in part supported by NIA, used epigenetics to compare aging of dogs and humans. Such epigenetic changes may help researchers better understand human aging processes. Findings updated the previous one dog year equal to seven human years formula and were recently published in Cell Systems.

Researchers from the University of California (UC), San Diego, National Human Genome Research Institute (part of the National Institutes of Health), Sanford Burnham Prebys Medical Discovery Institute in San Diego, University of Pittsburgh School of Medicine, and UC Davis looked at DNA methylation a common type of epigenetic change where methyl groups (small molecules) attach to and turn off or silence a particular gene. Methylation patterns change over time in a consistent way across humans, which some believe can be used as an epigenetic clock to predict age. To help understand whether the epigenetic clocks in other animals differ from humans, the researchers studied the lifespan methylation of both dogs and humans. Domesticated, or pet, dogs are animals similar in their environment, level of health care, and aging patterns to humans, providing a good model for comparison.

DNA Methylation data were collected from blood samples of 104 Labrador retrievers (puppies to 16 years of age) and compared to DNA methylation patterns of 320 humans (one to 103 years of age). Researchers found similar DNA methylation patterns between the dogs and humans, especially in the early and late life stages. Changes in DNA methylation across shared developmental genes were key to lining up dog and human DNA methylation patterns. Researchers used the analyzed patterns to relate the epigenetic clock of humans with dogs and created a new formula to calculate dog-to-human age. In this calculation, similar life stages matched to estimate an 8-week-old puppy as about the age of a 9-month-old baby, and a 12-year-old senior Labrador as about the age of a 70-year-old adult.

By comparing DNA methylation patterns, this study demonstrates the use of epigenetics to translate age and aging between species. Such translation may be a helpful tool for understanding aging and studying healthy aging interventions. Next steps include testing the formula with other dog breeds, and further exploring epigenetic changes in developmental genes as they relate to aging.

This research was supported in part by NIA grant P01AG031862.

Reference: Wang T, et al. Quantitative translation of dog-to-human aging by conserved remodeling of the DNA methylome. Cell Systems. 2020;11(2):176-185.e6. doi: 10.1016/j.cels.2020.06.006.

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Epigenetics study updates the dog-to-human age formula with implications for cross-species comparison to help understand human aging processes -...

Yes, even your metabolism has a memory and it can hold a grudge for years. In people with diabetes, periods of high blood sugar can negatively impact their health years later, even if they get their blood sugar under control. While this metabolic memory phenomenon has been known for years, why it happens is poorly understood.

Rama Natarajan, Ph.D., Professor and Chair of the Department of Diabetes Complications & Metabolism at City of Hope, turned to our epigenome for the answer.

Weve shown the first link between DNA methylation in blood and stems cells, blood sugar history, and future development of complications, said Natarajan. This highlights the importance of good glycemic control to prevent long-term complications.

The history of metabolic memory

We now know high blood sugar can lead to a variety of complications, including eye disease, kidney disease, nerve problems, heart disease, and stroke. But the relationship between strict blood sugar control and complication risk wasnt well understood before the 1980s.

Back in 1983, the Diabetes Control and Complications Trial (DCCT) began tracking complications in 1,441 participants with type 1 diabetes. Researchers compared the occurrence of long-term complications between participants who tightly regulated their blood glucose levels to those who followed less strict standard regulation.

After 10 years, the difference was striking the risk of diabetic complications was reduced in participants who tightly regulated their blood sugar but not in those following standard regulation. In other words, a person with higher blood sugar had a higher risk of complications.

To continue following the DCCT patients, the Epidemiology of Diabetes Interventions and Complications (EDIC) follow-up trial began at the end of DCCT in 1993 and is ongoing. At the end of DCCT, all participants were encouraged to adopt strict blood sugar regulation; many in the standard regulation group did.

Despite blood sugar regulation being very similar in all the patients (as measured by hemoglobin A1c, called HbA1c), differences persisted between the two original intervention groups. The phenomenon of long-term effects from high or variable blood sugar control is called metabolic memory (or the legacy effect in type 2 diabetes).

Complications resulted from total high blood sugar exposure it didnt matter whether the person was exposed to slightly elevated levels over a long time or high levels over a short time.

So, what caused the sweet sugar molecule to become so destructive?

Sugary destruction

Extra sugar in your blood can interact with your cells, DNA, and proteins, adding itself onto things it shouldnt be on through a process called glycation. In fact, HbA1c can be thought of as sugar-coated red blood cells.

The sugar-coated molecules cant function as well, if at all, and the damage begins a self-perpetuating cycle. Not only do these damaged molecules stop working, they can also accumulate in the skin, eyes, and other organs, causing damage. Build-up of sugar-coated molecules can trigger the creation of harmful free radicals, causing oxidative stress and feeding a destructive cycle.

Although sugar can directly modify molecules, it can also trigger other epigenetic modifications. These modifications can control how genes are expressed, changing protein levels in cells.

There hasnt been a strong genetic association with diabetic complications very few genetic mutations have been strongly linked to complications, Natarajan explained. But we knew the epigenome is what makes identical twins different and can have implications into why one gets diabetes or cancer and the other doesnt. So, we turned our focus to epigenetics.

Epigenetics and diabetes

Natarajan sought to explain the long-term sugary destruction wrought by high blood sugar by searching the epigenome. Her lab specifically looks for one type of modification called DNA methylation, where a tiny molecule called a methyl group is added onto DNA.

Epigenetics is the coating on top of genetics that can be altered by environmental influences, Natarajan said. We started focusing on the role of epigenetics in developing diabetes and its complications because we know that lifestyles, improper diet, lack of exercise, and even viruses can affect epigenetics.

Natarajans lab began collaborating with the DCCT trial group, analyzing data collected through the trial for epigenetic clues to explain the metabolic memory of complications. They found more modifications associated with active genes on proteins called histones that are wrapped by DNA in participants with regular blood sugar control compared to the strict controllers. Even more interesting was that many epigenetic DNA methylation variations between the two groups persisted through at least 17 years of follow-up in the EDIC study.

These changes were in important genes related to complications, showing something about persistent epigenetic programming in peripheral blood cells, commented Natarajan. Previous high blood sugar episodes could be a key factor in why these genes were continually misbehaving.

Now, Natarajans lab illuminated even more links between epigenetic changes, blood sugar history, and metabolic memory in their recent Nature Metabolism paper. Persistent epigenetic modifications of a few key genes were detected in participants with previously less regulated blood sugar who developed either retinopathy or nephropathy. They showed that DNA methylation is a key link between a patients HbA1c history, metabolic memory, and development of future complications.

Many HbA1c-associated modifications were in stem cells and the blood cells they create. Even though blood cells are turned over relatively quickly, stem cells stick around for a long-time, so changes in stem cells can have long-term consequences.

The important thing we found was the connection to stem cells, explained Natarajan. Were asking how these changes alter inflammatory gene expression and how we can interrupt those pathways.

Sugar-modified genes arent so sweet

Natarajans lab sorted through all the modified genes to find the most common modifications in participants with less strict blood sugar control. The most commonly modified gene coded for thioredoxin-interacting protein (TxNIP).

TxNIP is not a new protein, but the discovery that its DNA methylation is altered by different glycemic control is new, Natarajan added.

Thioredoxin-interacting protein is known to be highly regulated in certain pancreas cells, called beta cells, that release insulin. The plot thickened when high blood sugar was found to increase TxNIP protein production. Even more interesting, high TxNIP protein levels make beta-cells dysfunctional, ultimately leading to their untimely death. So, high blood sugar triggers more TxNIP to be produced, possibly through epigenetic modifications of the TxNIP gene, which ultimately leads to the death of insulin-producing beta cells.

Showing that the TxNIP gene can be epigenetically modified for years and years suggests that it could be one of the culprits causing long-term problems in diabetes, Natarajan said.

The proteins that TxNIP interacts with, called thioredoxins, protect against oxidative stress. TxNIP can bind to and inactivate thioredoxin to increase oxidative stress by increasing reactive oxygen species (ROS). In mouse cells in a dish, high glucose exposure triggered increased ROS levels mediated by TxNIP, leading to oxidative stress. Oxidative stress can trigger cell and organ damage, so this could be one mechanism explaining diabetes-induced damage.

Her lab also found epigenetic changes in other genes related to inflammation and inflammation-related processes.

Next steps and clinical implications

Natarajans lab is continuing to study the link between blood sugar history, epigenetics, and other complications of diabetes. They are also expanding their scope, searching the entire genome for more epigenetic modifications linked with past blood sugar maintenance.

This study also lays the groundwork for further studies with meaningful clinical implications, including developing epigenetic biomarkers for diabetic complications. In the future, Natarajan says a simple blood test looking at key epigenetic modifications, along with HbA1c history, could be used to predict future risk of retinopathy, nephropathy, and neuropathy. This would allow the doctor to figure out who should have early and more aggressive treatment to mitigate complication risk.

While these studies were done in type 1 diabetes patients, other studies in type 2 diabetes patients have shown similar epigenetic modifications after history of higher blood sugar levels.

Turning knowledge into potential drugs

What about doing something about the epigenetic modifications can we remove them? As a matter of fact, yes!

There is an interesting new type of experimental drug on the horizon called epigenetic editing. The hot new technology CRISPR isnt just for cutting out chunks of DNA or controlling genes it can also be used to insert or remove epigenetic modifications. While this technology is still experimental and in early preclinical animal studies, the potential is very exciting.

A CRISPR/enzyme pair can be used the CRISPR genetic material can hunt down the genetic spot you want to change; and the attached enzyme can snip or add certain molecules to the DNA, effectively removing or creating an epigenetic modification, thereby activating or silencing the targeted gene.

Enzymes such as methyltransferase or demethylase can add or remove methyl groups from genes. Because they just change what is on the gene or histone wrapped around it (not the genetic sequence itself), the gene itself isnt tampered with, meaning there could be less genetic complications associated with CRISPR epigenetic editing.

This is a futuristic thing, Natarajan concluded. The combination of genetics and epigenetics is going to be the future of personalized medicine.

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Can High Blood Sugar Haunt People with Diabetes Even After it is Under Control? - BioSpace

The links between methionine consumption, epigenetic patterns, and T-cell exhaustion were recently uncovered by scientists based at the University of Michigan. According to these scientists, who were led by Weiping Zou, M.D., Ph.D., targeting cancer methionine signaling could provide an immunotherapeutic approach.

Tumor cells compete with T cells for methionine, an amino acid that T cells need to maintain their histone patterns. Unfortunately, T cells consistently lose. When their histone patterns suffer, the T cells become dysfunctional, lose their fighting spirit, and let tumors grow. Could this discouraging chain of events be interrupted? Perhaps, if the right immunotherapeutic approach can be developed.

Details of the scientists work appeared September 2 in the journalNature, in an article titled, Cancer SLC43A2 alters T cell methionine metabolism and histone methylation. The article describes how tumor cells greedily consume methionine, denying it to CD8+T cells, which endure lower intracellular levels not only of methionine, but of the methyl donorS-adenosylmethionine (SAM).

The implications of SAM deficiency are dire. It results in reduced dimethylation at lysine 79 of histone H3 (H3K79me2) and, consequently, impaired expression of STAT5, a protein that signals T cells to sustain antitumor immunity.

As the scientists teased out these details, they considered a key question: How is it that tumor cells outcompete T cells for methionine? The answer to this question, the scientists knew, could point to new immunotherapeutic approaches.

The scientists determined that tumor cells outcompete T cells for methionine via SLC43A2, a major methionine transporter. Given that SLC43A2 is highly expressed on multiple human and mouse tumor cells with different genetic backgrounds, abnormal tumor SLC43A2 and its related methionine metabolism are unlikely to be driven by shared key oncogenes, the authors of the Naturearticle noted. Inhibition of tumor SLC43A2 can normalize methionine metabolism in effector T cells and rescue their function, and it can also improve spontaneous and checkpoint blockade-induced antitumor immunity in preclinical models.

Previous research had considered a systemic approach to starve tumor cells of methionine, with the idea that the tumor cells are addicted to it. But the current study shows why that approach may be a double-edged sword.

You have competition between tumor cells and T cells for methionine, said Zou. The T cells also need it. If you starve the tumor cells of methionine, the T cells dont get it either. You want to selectively delete the methionine for the tumor cells and not for the T cells.

In fact, the study found that supplementing methionine actually restored T-cell function. High enough levels of methionine meant there was enough for both tumor cells and T cells.

Genetic and biochemical inhibition of tumor SLC43A2 restored H3K79me2 in T cells, thereby boosting spontaneous and checkpoint-induced tumor immunity, the scientists reported. Moreover, methionine supplementation improved the expression of H3K79me2 and STAT5 in T cells, and this was accompanied by increased T cell immunity in tumor-bearing mice and patients with colon cancer. Clinically, tumor SLC43A2 correlated negatively with T cell histone methylation and functional gene signatures.

Tumor cells have more of the transporters that deliver methionine. Impairing those transporters, the researchers found, resulted in healthier T cells because the T cells were able to compete for methionine.

There are still a lot of mechanistic details we have not worked out, particularly the detailed metabolic pathways of methionine metabolism, Zou noted. We also need to understand how metabolism pathways may be different from tumor cells and T cells. We hope to find a target that is relatively specific to tumor cells so that we do not harm the T cells but impact the tumor.

In the meantime, Zou is working with drug discovery experts to identify a small molecule inhibitor that targets methionine in tumor cells.

Read more from the original source:
Researchers Link Epigenetics, T Cell Exhaustion, and Methionine to Tumor Growth - Clinical OMICs News

Fort Collins, Colorado The Epigenetics Market research report offers insightful information on the Epigenetics market for the base year 2019 and is forecast between 2020 and 2027. Market value, market share, market size, and sales have been estimated based on product types, application prospects, and regional industry segmentation. Important industry segments were analyzed for the global and regional markets.

The effects of the COVID-19 pandemic have been observed across all sectors of all industries. The economic landscape has changed dynamically due to the crisis, and a change in requirements and trends has also been observed. The report studies the impact of COVID-19 on the market and analyzes key changes in trends and growth patterns. It also includes an estimate of the current and future impact of COVID-19 on overall industry growth.

Epigenetics market garnered a revenue of USD 7.4 billion in the year 2019 globally and has been foreseen to yield USD 30.1 billion by the year 2027 at a compound annual growth (CAGR) of 18.9% over the forecast period.

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The report has a complete analysis of the Epigenetics Market on a global as well as regional level. The forecast has been presented in terms of value and price for the 8 year period from 2020 to 2027. The report provides an in-depth study of market drivers and restraints on a global level, and provides an impact analysis of these market drivers and restraints on the relationship of supply and demand for the Epigenetics Market throughout the forecast period.

The report provides an in-depth analysis of the major market players along with their business overview, expansion plans, and strategies. The main actors examined in the report are:

F. Hoffmann-La Roche Ltd

The Epigenetics Market Report offers a deeper understanding and a comprehensive overview of the Epigenetics division. Porters Five Forces Analysis and SWOT Analysis have been addressed in the report to provide insightful data on the competitive landscape. The study also covers the market analysis and provides an in-depth analysis of the application segment based on the market size, growth rate and trends.

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The research report is an investigative study that provides a conclusive overview of the Epigenetics business division through in-depth market segmentation into key applications, types, and regions. These segments are analyzed based on current, emerging and future trends. Regional segmentation provides current and demand estimates for the Epigenetics industry in key regions in North America, Europe, Asia Pacific, Latin America, and the Middle East and Africa.

Epigenetics Market Segmentation:

Epigenetics Market, By Technology (2016-2027)

Epigenetics Market, By Application (2016-2027)

Epigenetics Market, By Product (2016-2027)

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Epigenetics Market is Thriving Worldwide 2020-2027 | Top Companies Qiagen, Novartis AG, Active Motif, Merck Sharp & Dohme Corp, Thermo Fisher...