StemCell Therapy

LentiGlobin, Bluebird Bios investigational gene therapy for sickle cell disease (SCD), continues to show promising results in SCD patients participating in the companys Phase 1/2 HGB-206 clinical trial, according to the latest study data.

The new findings which included data from additional patients treated in the trial, updated data from those previously reported, and exploratory analyses were presented at the 61st American Society of Hematology (ASH) Annual Meeting and Exposition, held Dec. 6-10 in Orlando, Fla.

LentiGlobinisa gene therapy that has been developed to increase the levels of hemoglobin the protein that transports oxygen in the blood in people with SCD.

The therapy works by delivering functional copies of a modified form of the beta-globin gene (A-T87Q-globin gene) into patients red blood cell precursors, known as hematopoietic stem cells, or HSCs. Once these precursors differentiate, their red blood cells start producing a modified version of hemoglobin, called HbAT87Q.

By boosting the production of this anti-sickling form of the protein, LentiGlobin reduces the proportion of defective hemoglobin in patients red blood cells. That, in turn, reduces the sickling and destruction of these red blood cells and other complications associated with SCD.

The safety and efficacy of LentiGlobin is currently being evaluated in three groups identified as A-C of SCD patients participating in Bluebirds ongoing open-label, Phase 1/2 HGB-206 trial (NCT02140554).

Those in group A were treated per the original trial protocol. Meanwhile, those in groups B and C received an enhanced treatment protocol, approved in 2016, that is designed to increase the therapys efficiency. In groups A and B, patients HSCs were extracted from the bone marrow, while in group C, they were extracted from the blood.

As of the data cutoff date of August 26, 2019, seven participants in group A, two in group B, and 17 in group C had been treated with LentiGlobin. According to new data presented at the meeting, only two patients from group A required regular blood transfusions after the treatment.

In addition, the updated findings revealed that the levels of anti-sickling HbAT87Q remained stable in all participants from groups A and B over a post-treatment follow-up period of three years. Similarly, levels of total hemoglobin also were found to have remained stable in both patient groups over a two-year follow-up.

At the trial participants last visit, the median levels of anti-sickling HbAT87Q were 0.9 g/dL among those from group A, and 3.6 g/dL and 7.1 g/dL in the two patients from group B. The median levels of total hemoglobin were 9.0 g/dL among patients from group A, and 11.3 g/dL and 13.0 g/dL among those from group B.

Normal levels of hemoglobin in the blood range from 12.5 to 17.5 g/dL.

Among 12 patients from group C who were followed for at least six months, the median levels of anti-sickling HbAT87Q made up at least 40% of their total hemoglobin. At their last visit, the levels of anti-sickling HbAT87Q ranged from 2.7 to 9.0 g/dL, and the levels of total hemoglobin from 9.3 to 15.2 g/dL.

In groups A and B, LentiGlobin reduced the frequency of painful vaso-occlusive crises (VOCs) and acute chest syndrome (ACS) in the two years following treatment.

Nine patients from group C who were followed for at least six months had experienced four or more VOCs or ACS episodes in the two years prior to receiving LentiGlobin. Treatment with the gene therapy led to a reduction of 99% in the frequency of annual VOCs and ACS. In this group, there were no reports of ACS or severe VOCs for up to 21 months following treatment.

Moreover, among those from group C, LentiGlobin reduced the levels of different markers of red blood cells destruction, including reticulocytes, lactate dehydrogenase (LDH), and bilirubin.

LentiGlobins safety profile was consistent with previous data. No serious adverse events related to treatment were reported during the study. Only one mild, non-serious event of hot flush was found to be related to LentiGlobin. That event was rapidly resolved and did not require treatment.

Exploratory analyses were performed in a sub-group of patients from all three groups. In 12 participants who had been followed for at least six months, more than 70% of the individuals red blood cells were found to contain the anti-sickling HbAT87Q at the last study visit, these analyses showed. Moreover, in four of these patients, nearly all their red blood cells (90%) were positive for HbAT87Q.

In addition, exploratory analyses revealed that participants red blood cells were less prone to sickling following treatment with LentiGlobin.

At ASH, the growing body of data from our clinical studies of LentiGlobin for SCD reflects results from 26 treated patients with up to four years of follow-up, David Davidson, MD, Bluebird Bios chief medical officer, said in a press release.

We continue to observe patients treated in Group C producing high levels of gene-therapy derived anti-sickling hemoglobin, HbAT87Q, accounting for at least 40% of total hemoglobin in those with six or more months of follow-up, and exploratory assays show that HbAT87Q is present in most red blood cells of treated patients, Davidson said.

The robust production of HbAT87Q was associated with substantial reductions of sickle hemoglobin, HbS, as well as improvement in key markers of hemolysis [red blood cells destruction]. Most importantly, patients in Group C have not experienced any episodes of acute chest syndrome or serious vaso-occlusive crises following LentiGlobin for SCD treatment, he added.

The company is recruiting participants with transfusion-dependent -thalassemia (TDT) for a Phase 3 trial (NCT03207009) testing LentiGlobin. Moreover, according to the companys pipeline, there is a Phase 2/3 trial planned in sickle cell disease for this gene therapy.

Joana is currently completing her PhD in Biomedicine and Clinical Research at Universidade de Lisboa. She also holds a BSc in Biology and an MSc in Evolutionary and Developmental Biology from Universidade de Lisboa. Her work has been focused on the impact of non-canonical Wnt signaling in the collective behavior of endothelial cells cells that make up the lining of blood vessels found in the umbilical cord of newborns.

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Margarida graduated with a BS in Health Sciences from the University of Lisbon and a MSc in Biotechnology from Instituto Superior Tcnico (IST-UL). She worked as a molecular biologist research associate at a Cambridge UK-based biotech company that discovers and develops therapeutic, fully human monoclonal antibodies.

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LentiGlobin Gene Therapy Continues to Show Promising Results in SCD, Updated Trial Data Shows - Sickle Cell Anemia News

Autologous stem cell therapy market segment is anticipated to witness around 10% growth throughout the forecast timeframe. Autologous stem cell therapy has high compatibility with patients immune system and showcases strong efficacy. Additionally, it eliminates the need for finding donor and reduces the overall cost of treatment. Aforementioned advantages offered by autologous stem cell therapy will augment its demand thereby, escalating segment growth.

Oncology segment held over 37% revenue in 2018. Increasing prevalence of cancer globally will increase the demand for advanced stem cell Therapy. Metastatic cancer cells are difficult to destroy utilizing conventional methods. Radiations and chemotherapy cannot eradicate the disease completely and also results in several complications. Stem cells have unique properties such as secretion of bioactive factors and migration towards cancer cells promotes tumor targeting that are proven to be effective in treatment of cancer. Aforementioned factors will escalate the segmental growth.Rising government initiatives for promoting stem cell therapy in developed as well as developing countries will propel industry growth. Increasing government spending on research activities aimed at development of stem cell therapy for treatment of life-threatening diseases such as cancer. The government ensures that laboratories, research and academic centers are well-equipped with necessary equipment and advanced devices for facilitating the stem cell therapy research processes. Aforementioned factors are expected to boost the stem cell therapy market growth.

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Increasing efforts undertaken by companies for improving efficacy of stem cell therapy will fuel industry growth. Stem cells possess totipotency that enables them to transform into any differentiated cell. Stem cells play pivotal role in treatment of chronic diseases such as cancer, cardiovascular diseases and degenerative disorders. 0Currently, hematopoietic, embryonic and mesenchymal cells are being researched as they have the ability to cure several complications. Companies commercialize these stem cell products for providing effective therapy that should prove beneficial for the industry growth. However, ethical issues associated with stem cell therapy may affect industry growth to some extent.

Hospitals segment was valued around USD 4 billion in 2018. Significant growth is attributed to increasing prevalence of chronic diseases. Annually, large number of patients prefer stem cell therapy offered at hospitals as a treatment option to avoid complications caused due to invasive methods. Hospitals have dedicated resources allocated for providing uncompromised care to patients that speeds up the recovery process. Moreover, hospitals affiliated with government authorities receives enough funding and have the ability to provide superior quality stem cell therapy. Above mentioned factors will augment patients preference towards hospitals that will exceed segment growth.

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Asia Pacific stem cell therapy market held around 20% revenue in 2018. Substantial revenue share can be attributed to the increasing awareness regarding availability of stem cell therapies. Moreover, government encourages scientists and researchers to carry out studies and thesis on stem cell therapies in order to develop innovative solutions for treating chronic diseases. Also, several developing countries in the region have witnessed industry growth opportunities as government provide funds to establish stem cell centers. For instance, in Singapore JTC Corporation has established Biopolis, that is a biomedical research center of stem cell science. Such government initiatives in Asian countries will positively impact regional market growth.

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Prominent industry players operational in stem cell therapy market are Astellas Pharma Inc, Cellectis, Celyad, Novadip Biosciences, Gamida Cell, Capricor Therapeutics, Cellular Dynamics, CESCA Therapeutics, DiscGenics, OxStem, Mesoblast Ltd, ReNeuron Group and Takeda Pharmaceuticals. Industry players implement various strategies such as collaboration, acquisition, merger, product launch to sustain in the market. For instance, in February 2018, Astellas acquired Universal Cells so that they can utilize proprietary technology to manufacture pluripotent stem cells. This strategy will help Astellas to develop innovative solutions that will provide competitive advantage to company.

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Global Stem Cell Therapy Market 2019-2025 Analyzed by Business Growth, Development Factors, Applications, and Future Prospects - Technology Magazine

We can already edit genes in human embryos. We can even do it in a way to pass the edits down generations, fundamentally changing a familys genetic makeup.

Doing it well, however, is far more difficult.

Its impossible to talk about human germline genome editing without bringing up the CRISPR baby fiasco. Over a year ago, a rogue Chinese scientist performed an edit on fertilized human embryos that, in theory, makes them resistant to HIV infection. Two twin girls were born, and both had multiple unplanned edits in their genome with unknown health consequencesconsequences that may be passed on to their offspring.

The brash attempt at making scientific history clearly shows that, ethics and morality issues aside, when it comes to germline editingthat is, performing gene edits in egg, sperm, or the embryowere simply technologically not there. Make no mistake: CRISPR may one day wipe out devastating genetic diseases throughout entire family lines, or even the human race. But to harness its power responsibly, there are plenty of technical challenges we need to master first.

This week, Rebecca Lea and Dr. Kathy Niakan at the Human Embryo and Stem Cell Laboratory at the Francis Crick Institute in London, UK, laid out those challenges in a sweeping articlein Nature. CRISPR as a gene editor is getting more specific and efficient by the day, they explained. However, for it to gradually move into germline editing, we also need to understand how the tool tangos with cells during early human development.

The data, they argue, will not only let us zoom into the creation of human life. It will also help inform the debate about potential safe and effective clinical uses of this technology, and truly unlock the doors to the human genome for good.

Correcting dangerous genetic mutations is one reason to pursue germline editing, but CRISPRing human embryos can also unveil insights into the very first stages of human embryo development. Research shows that trying to understand how human embryos form by studying mice might not be the best route, especially when it comes to using those results to tackle infertility and other medical problems. With CRISPR, we have insight into these early stages that were previously completely unattainable. We might only solve infertility issues, but perhaps also allow same-sex couples to have genetic children in the future.

Another argument is that couples already screen for life-threatening mutations during IVF, and using CRISPR on top of that is unnecessary. Not true, the authors argued. When both parents carry a similar mutation that robs them of the ability to have a healthy child, CRISPRnot selection during IVFis the answer. Ultimately, providing more options for patients empowers them to make the choice that is best for their family and circumstances, they said.

This is where it gets complicated.

The big one: were still trying to tease out how CRISPR works in cells that form the embryo, in hopes that we can cut down on potential mistakes.

Let me explain: all cells in the body have a cell cycle, somewhat analogous to a persons life cycle. Many checkpoint life events happen along the way. The cell could decide to divide and have kids, so to speak, or temporarily halt its cycle and stop its own aging. During a cycle, the cells DNA dramatically changes in number and packaging in preparation for its next stage in life.

The problem? The way CRISPR works heavily depends on the cell cycle. Although dubbed an editor, CRISPR actually vandalizes the genome, creating breaks in the DNA strands. What we call gene editing is the cells DNA repair system kicking into high gear, trying to patch up the mess CRISPR left behind. Adult cells that cant be repaired stop their own life cycle at a checkpoint for the greater good. In embryos, however, cells arent nearly as altruistic. Their checkpoints arent fully developed, so they might continue to develop even with severe mutations. Zooming back to the full picture, it means that the resulting early-stage embryo may keep accumulating damage, until it fails in the mothers womb.

To get around this, scientists have tried other ways to push an embryo into accepting a healthy DNA template after a CRISPR snip, which in theory would cut down on unwanted mutations. One idea is injecting the CRISPR machinery at a specific time into fertilized eggs, so it catches the early-stage embryo at just the right time to reduce DNA breaks in both strands. While theoretically possible, the process is kind of like a person trying to jump from a high-speed train into a specific cabin on a rapidly rotating Ferris wheel while blindfolded.

But science is making progress. Although we dont have a detailed movie of cell cycles in human embryos yet, multiple labs are beginning to piece one together, with hopes itll eventually help take off the blindfold when injecting CRISPR. Others are looking into adding CRISPR to sperm before fertilization as an alternative.

At the same time, scientists are also trying to characterize the entire scope of mutations caused by CRISPR. Its not just adding, swapping, or deleting specific letters in genes. Rather, the range of mutations is more complex, including large swaths of genetic rearrangements, unintended cuts relatively far from targeted spots, and other dramatic DNA lesions following CRISPR action. Its perhaps not surprising that the edits in CRISPR babies didnt work as intended.

Base editors, which swap one genetic letter for another, might be a better approach compared to the classic hack-and-paste, the authors said. So far, however, the tools havent yet been validated in embryosnot even those from mice.

Finally, for the edit to make a difference to the child, the embryo has to develop normally inside a womb into a baby. But success rates for assisted reproductive technologies are already fairly low. Add in a dose of genetic editing tool that cuts into an already-sensitive genomic landscape, and it becomes incredibly hard to maintain the health of the edited embryo.

Putting it all together, there is simply not enough data at present to understand the capability of early[embryos] to repair DNA, the authors said.

Far from it. Although theres much we dont yet understand, we do have an impressive range of tools to predict and evaluate mutations in human embryos. Exactly how to determine whether a gene-edited embryo is healthy remains up for debatefor example, is five unexpected mutations considered ok? What about 500 or 5,000?

That said, just having tools to diagnose the genetic health of an embryo from a tiny bit of DNA is already extremely useful, especially if we as a society decide to move into germline editing as a treatment.

With machine learning making an ever-larger splash in computational biology, these predictive tools will only become more accurate. Add to that ever-more-effective CRISPR variations, and were on the right trackas long as any potential applications of embryo editing only come after in-depth public and policy discussions and fit a number of strict ethical and safety criteria, the authors said.

In response to the CRISPR baby scandal, multiple governments and the World Health Organization have all drafted new guidelines or legislation to tap on the brakes. The technology isnt mature enough for clinical use, the authors said, and much more work is needednot just to further improve CRISPR tools, but especially for understanding how it works in human embryos.

Ultimately, were talking about potentially engineering the future of the human race. Tiptoeing, rather than stumbling ahead, is the least we can do. One must ensure that the outcome will be the birth of healthy, disease-free children, without any potential long-term complications, the authors concluded.

Image Credit: Image by marian anbu juwan from Pixabay

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How Far Are We from (Accurately and Safely) Editing Human Embryos? - Singularity Hub

A highly effective vaccine to prevent hepatitis B virus (HBV) infection has been available for nearly 40 years, yet millions of people worldwide continue to become infected with the liver-attacking virus and more than 600,000 die from its complications each year, according to the U.S. Centers for Disease Control and Prevention. A new strategic plan from the National Institutes of Health outlines efforts to intensify ongoing HBV research with the goals of developing a cure and improving scientific understanding of the virus while creating improved strategies for screening and treating patients.

HBV is transmitted through sex, contact with infected blood or bodily fluids, or from an infected mother to her baby, and can result in either an acute infection that resolves or a chronic infection. Chronic HBV infection can lead to serious health issues including cirrhosis (scarring of the liver), liver failure or liver cancer. Approximately 80% to 90% of infants infected during the first year of life will develop chronic infection, while only 5% of people infected as adults will become chronically infected. Between 850,000 and 2 million people in the United States have chronic hepatitis B; globally, that number is 257 million, according to the World Health Organization.

Although treatments are available to control HBV infection, they must be taken for years if not for life. Additionally, high medication costs, the need for continuous disease monitoring and adhering to treatment regimens present significant burdens for people with chronic hepatitis B. Even among those treated for chronic hepatitis B, the risk of developing cirrhosis and liver cancer remains elevated.

Scientific discoveries within the past decade suggest that a hepatitis B cure is possible. The new NIH plan defines a hepatitis B cure as a sustained loss of a specific protein on the surface of HBV called hepatitis B virus surface antigen preferably with antibodies against the antigen and undetectable viral DNA after completion of a finite course of treatment. Ideally, a hepatitis B cure would also reduce a persons risk of liver failure and liver cancer. To effectively address the global public health challenge posed by HBV, a curative treatment will need to complement better approaches to screening, follow-up care, and vaccination coverage.

The Strategic Plan for Trans-NIH Research to Cure Hepatitis B focuses on three key research areas. The first priority calls for a better understanding of hepatitis B biology, including the viral and host factors that lead to disease, immunity, reactivation and transmission, as well as the impact of co-infections with other hepatitis viruses and HIV. An improved understanding of these factors and the HBV lifecycle is essential to developing a cure.

The second priority emphasizes the development and sharing of tools and resources to support fundamental research and product development. This includes standardizing and sharing reagents and assays; improving and creating new animal models to study the progression of human liver disease and mother-to-child transmission; and establishing biomarkers for disease progression and response to therapy.

The third priority calls for the creation of strategies to cure and prevent hepatitis B infection. A cure could include approaches to blocking viral replication, stimulating the anti-HBV immune responses or eliminating HBV-infected cells. However, achieving a cure requires strengthening existing public health efforts for promoting hepatitis screening, ensuring that high-risk and underserved populations have access to vaccination, and prioritizing follow-up to care and adherence to treatment, according to the plan.

The strategic plan builds on NIHs ongoing hepatitis B research portfolio and the U.S. National Viral Hepatitis Action Plan. NIH sought input from academia, patient advocacy organizations, private and nonprofit companies, government organizations, and clinical trial networks funded by the NIH in the development of this strategic plan.

Reference

Ortinau et al. (2019) Identification of Functionally Distinct Mx1+SMA+ Periosteal Skeletal Stem Cells. Cell Stem Cell. DOI: https://doi.org/10.1016/j.stem.2019.11.003

This article has been republished from the following materials. Note: material may have been edited for length and content. For further information, please contact the cited source.

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Strategic Plan To Cure Hepatitis B in the Making - Technology Networks

Myelodysplastic syndrome (MDS) is a blood disorder caused due to the production of abnormal blood cells in bone marrow. Bone marrow failure leads to drop in the number of healthy blood cells in the body. In MDS, bone marrow does not produce healthy red blood cells, white blood cells, and/or platelets. Symptoms of MDS in the beginning are no specific than causes of pancytopenia i.e., deficiency of RBC, WBC and platelets. Therefore, the final diagnosis of MDS is done after examination of the cells of bone marrow.

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Bone marrow sample is taken from inside of a bone (usually the hip bone) and examined with a microscope using special stains to look for abnormal and immature cells. According to the American Cancer Society, over 13,000 new cases of MDS occur in the U.S. each year. According to the National Organization for Rare Disorders, 30% of patients with MDS can develop a form of blood cancer known as acute myeloid leukemia. Majority of patients diagnosed with MDS are aged between 65 and 70; however, MDS can affect people of any age and the risk of developing MDS increases with age.

The global myelodysplastic syndrome treatment market is driven by rise in the global geriatric population as MDS is most commonly found in this population and remains an incurable disease. Moreover, significant progress has been made in the diagnosis of MDS with the help of sequencing technologies. Chromosomal abnormalities can be identified in MDS patients with these technologies. These are useful for both diagnosis and prognosis in MDS patients. For instance, patients with chromosome 5q deletions are more likely to respond to lenalidomide. No new drugs have been approved for MDS by the U.S. Food and Drug Administration since 2006. Current available therapies can be efficacious, but are generally not curative. Some of the challenges in developing new treatments are the complexity and heterogeneity of MDS as a disease.

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The global myelodysplastic syndrome treatment market can be segmented based on type of treatment and region. In terms of type of treatment, the market can be classified into supportive therapy, growth factors, chemotherapy (including hypomethylating agents), and stem cell transplant. Cytarabine, azacitidine, decitabine, and lenalidomide are the major drugs used during chemotherapy.

Stem cell transplant is the only cure for MDS; however, majority of patients are not treated with stem cell transplant due to various factors such as high treatment cost, transplant-related deaths, and relapse rate at five years (as high as 40%). The chemotherapy segment is expected to hold major share of the global myelodysplastic syndrome treatment market due to larger application and less complications than other therapies such as stem cell transplant.

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Geographically, the global myelodysplastic syndrome treatment market can be segmented into North America, Europe, Asia Pacific, Latin America, Africa, and Middle East. North America is projected to dominate the global myelodysplastic syndrome market during the forecast period due to factors such as the rise in aging population and growing awareness about the disease among the population coupled with unmet medical needs in this region.

Key players operating in the global myelodysplastic syndrome treatment market are Celgene Corporation, Otsuka Holdings Co., Ltd., Sandoz, Inc., Dr. Reddys Laboratories, Inc., Accord Healthcare Ltd., Mylan N.V., and Pfizer, Inc.

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Myelodysplastic Syndrome Treatment Market: Research Analysis by Basic Information, Manufacturing Base, Sales Area and Regions - Drnewsindustry

THURSDAY at noon on "The Source" An estimated14%of Bexar County's population lives with Type 2 diabetes. This preventable disease typically presents later in life, but is increasingly contracted by youn peoplewho can experience earlier, more advanced complications such as blindness, amputations and even death.

Of the more than30 millionAmerican adults with diabetes, approximately90%live with Type 2, which is managed with diet, exercise and insulin.Approximately half a million Texans are still undiagnosed.

Risk factors include poor diet, obesity, sedentary lifestyle and prediabetes. Children diagnosed with Type 2 diabetes often have a family history with the disease.

According to the Centers for Disease Control and Prevention, nearly 1 in 5 adolescents are living with prediabetes, defined as having blood sugar levels higher than normal but not yet at the threshold for an official Type 2 diabetes diagnosis.

Is there a public health strategy to combat the epidemic of Type 2 diabetes in Bexar County? Who is most at risk and what's being done to break the cycle?

What are the potential short and long term effects of Type 2 diabetes? Can it be reversed with healthier living? What does responsible treatment entail and how do individuals without health insurance manage?

What is to blame for the rising rates of Type 2 and prediabetes in young people? Could earlier identification and treatment help mitigate the disease?

The Texas Diabetes Institute is recruiting for diabetes-related clinical trials. Interested listeners can call 210-358-7200 for more information.

Guests:

"The Source" is a live call-in program airing Mondays through Thursdays from 12-1 p.m. Leave a message before the program at (210) 615-8982. During the live show, call 210-614-8980, email thesource@tpr.org or tweet @TPRSource.

*Audio for this interview will be available by 3:30 p.m. on Thursday, December 12.

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GREENVILLE A new year is a great time to learn how to improve your health by increments with a free six-week Healthy U workshop for adults living with diabetes or pre-diabetes 2-4:30 p.m. on Fridays, January 10 through February 14 at Family Health (Conference Room), 5735 Meeker Road, Greenville. The workshop is open to adults of any age living with diabetes, pre-diabetes, and/or their caregivers.

Workshops need a minimum number of participants in order to take place. Register by calling Jane Urlage at (937) 547-2319, ext. 1229 or emailing jurlage@familyhealthservices.org. Sign up now to celebrate a healthier Valentines Day.

Healthy U is an evidence-based, interactive, small group workshop proven to improve quality of life and reduce health care expenses by increasing self-confidence and providing new skills to better manage symptoms and feel healthier. Participants explore new ways to address challenges common to anyone with diabetes. This workshop is different from clinical diabetes programs, and instead focuses on common problems like chronic pain, nutrition, exercise, medication use, emotions, and communicating with doctors and family. Participants develop skills and coping strategies to manage symptoms through setting achievable goals, problem-solving, decision-making, social support, and more.

Everyone who completes the course receives the companion textbook, Living a Healthy Life with Chronic Conditions, and a relaxation CD.

Workshops are supported by the Area Agency on Aging, PSA 2. The Agency on Aging helps older adults of west central Ohio remain in their homes with independence and dignity. We are an independent, private, nonprofit corporation that plans and funds services for older persons in Champaign, Clark, Darke, Greene, Logan, Miami, Montgomery, Preble, and Shelby Counties.

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Resolve to take charge of diabetes - The Daily Advocate

(Reuters Health) - People whose mothers had diabetes during pregnancy may be at increased risk of developing cardiovascular disease by early adulthood, a recent study suggests.

The analysis followed more than 2.4 million babies born in Denmark for up to four decades, including nearly 55,000 whose mothers had diabetes during pregnancy. During the study period, cardiovascular disease developed before age 40 in 1,153 people whose mothers had diabetes while pregnant and 91,311 whose mothers did not.

When mothers had diabetes during pregnancy, their offspring were 29% more likely to develop cardiovascular disease, researchers report in The BMJ.

Preventing, screening and treating diabetes in women of childbearing age may be important not only for improving health of the women but also for reducing long-term cardiovascular disease risks in their offspring, said study leader Yongfu Yu of Aarhus University in Denmark.

We also need to monitor cardiovascular disease risks in offspring of diabetic mothers and investigate possible life-course interventions that may reduce the occurrence of cardiovascular disease, Yu said by email.

A total of 26,272 infants were born to mothers who had gestational diabetes, which develops during pregnancy and usually disappears after the pregnancy is over.

Another 22,055 babies were exposed to their mothers type 1 diabetes, which typically develops in childhood or young adulthood when the pancreas cant produce insulin.

And 6,537 infants were exposed to maternal type 2 diabetes, which is linked to overweight and aging and happens when the body cant properly use insulin to convert blood sugar into energy.

Gestational diabetes was associated with a 19% higher risk of cardiovascular disease in early adulthood for the children, while exposure to maternal type 1 or type 2 diabetes was tied to a 34% greater risk of cardiovascular disease for the young adult children.

The study wasnt designed to determine whether maternal diabetes causes cardiovascular disease or hastens its development in offspring.

The children exposed in utero to maternal diabetes were also more likely to have parents with a history of cardiovascular disease, and to have higher rates as adults of obesity, high blood pressure, high cholesterol, chronic kidney disease - and diabetes, which is itself a powerful risk factor for heart disease.

Yu noted that pregnant women with diabetes have more glucose, or sugars, in the placenta, which may lead developing babies to produce more insulin and have higher levels of blood sugar while theyre in the womb. That, in turn, could potentially lead to changes in blood vessel function later in life that contribute to cardiovascular disease.

We have known for a while that children born to women with diabetes, including both diabetes before pregnancy as well as gestational diabetes, have a higher rate of important complications early in life including macrosomia (babies that are too large sometimes resulting in difficult deliveries), a higher rate of congenital malformations, more frequent admission to NICU because of babies having difficulties regulating their own blood sugar levels, to name a few, said Dr. Jorge Chavarro of the Harvard T.H. Chan School of Public Health in Boston.

These babies are known to have higher risks for being overweight or obese in childhood, and recent work has also suggested theyre at higher risk of cardiovascular and metabolic diseases as adults based on risk factors like levels of sugar and fats in the blood, said Chavarro, who wasnt involved in the study. This new study, he said by email, provides evidence that maternal diabetes can also result in a higher frequency of clinically relevant cardiovascular events during the first four decades of life.

SOURCE: bit.ly/2PBOV8h The BMJ, online December 4, 2019.

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Maternal diabetes in pregnancy tied to heart disease in adult kids - Reuters

Earlier on Monday, new Sanofi CEO Paul Hudson baited the hook on his upcoming strategy presentation Tuesday with a tell-tale deal to buy Synthorx for $2.5 billion. That fits squarely with hints that hes pointing the company to a bigger future in oncology, which also squares with a major industry tilt.

In a big reveal later in the day, though, Hudson offered a slate of stunners on his plans to surgically dissect and reassemble the portfoloio, saying that the company is dropping cardio and diabetes research which covers two of its biggest franchise arenas. Sanofi missed the boat on developing new diabetes drugs, and now its pulling out entirely. As part of the pullback, its dropping efpeglenatide, their once-weekly GLP-1 injection for diabetes.

To be out of cardiovascular and diabetes is not easy for a company like ours with an incredibly proud history, Hudson said on a call with reporters, according to the Wall Street Journal. As tough a choice as that is, were making that choice.

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For sale: Long-acting PhIII GLP-1 diabetes drug that's way behind rivals, now spurned by Sanofi - Endpoints News

STOCKHOLM, Dec. 12, 2019 /PRNewswire/ -- Diamyd Medical announces that a new analysis based on data from more than 530 individual patients from previous phase III and II trials in Europe and US with the diabetes vaccine Diamyd has identified genetically defined subgroups of type 1 diabetes patients that show a positive and statistically significant dose-dependent treatment response.

In the analysis, patients who were positive for certain HLA genotypes and treated with the highest number of doses of Diamyd (three and four subcutaneous injections) experienced a statistically significant treatment effect of approximately 60% compared to placebo at 15 months from baseline. Also, when treatments with low number and high number dose regimens (two, three and four subcutaneous doses) were combined, a statistically significant treatment effect of approximately 40% was seen.

"This has great significance for Diamyd Medical, type 1 diabetes research and the antigen-specific immunotherapy field in general", says Mark Atkinson, Professor and Board member of Diamyd Medical. "These results support the notion that you can identify patients that will have a much higher likelihood to respond to a GAD-based therapy based on a well-known and scientifically plausible genetic profile. This finding has implications for both disease prevention as well as intervention trials in type 1 diabetes. I am encouraged that we are poised to advance a safe, specific and efficious treatment that has the potential to signifcantly change the course of this disease."

"The importance of today's announcement cannot be understated," says Ulf Hannelius, CEO of Diamyd Medical. "This finding strengthens the likelihood of success for the diabetes vaccine Diamyd and will be taken into account in the analysis of the ongoing DIAGNODE-2 trial. Notably, in the phase IIb trial DIAGNODE-2 we are advancing intralymphatic administration of Diamyd which we forsee to be even more efficacious than the subcutaneous route used in previous trials."

Professor Johnny Ludvigsson, Principal Investigator for the analysed Swedish Phase II and European Phase III trials and for the ongoing Phase IIb trial DIAGNODE-2 trial underlines the importance of these findings: "This may be a break through step towards understanding how personalized medicine for autoimmune diseases will evolve. It is a great achievment to for the first time be able to identify a large cohort of patients that experience a significant effect of autoantigen-specific treatment."

The analysis is based on data from more than 530 patients from three previously published trials: a European phase III trial, a Swedish phase II trial and a US phase II trial. The group showing the strongest response to the GAD-specific immunotherapy Diamyd represented approximately 25% of the total number of patients involved in the analysis. Also, a more broadly defined responder subgroup, representing approximately 50% of the total number of patients, showed a statistically significant treatment response. The results will be submitted as an abstract to a scientific conference and are based on a collaborative effort between Diamdy Medical, academic researchers and clinicians.

About Diamyd Medical

Diamyd Medical develops the diabetes vaccine Diamyd, as an antigen-specific immunotherapy for the preservation of endogenous insulin production. Diamyd has demonstrated good safety in trials encompassing more than 1,000 patients as well as effect in some pre-specified subgroups. Besides the Company's own European Phase IIb trial DIAGNODE-2 where the diabetes vaccine is administered directly into a lymph node, two investigator initiated clinical trials are ongoing with Diamyd. Diamyd Medical also develops the GABA-based investigational drug Remygen for regeneration of endogenous insulin production. An investigator-initiated Remygen trial in patients living with type 1 diabetes for more than five years is ongoing at Uppsala University Hospital. Diamyd Medical is one of the major shareholders in the stem cell company NextCell Pharma AB and has holdings in the medtech company Companion Medical, Inc., San Diego, USA.

Diamyd Medical's B-share is traded on Nasdaq First North Growth Market under the ticker DMYD B. FNCA Sweden AB is the Company's Certified Adviser; phone: +46 8-528 00 399, e-mail: info@fnca.se.

CONTACT:

For further information, please contact: Ulf Hannelius, President and CEOPhone: +46 736 35 42 41E-mail: ulf.hannelius@diamyd.com

This information was brought to you by Cision http://news.cision.com

https://news.cision.com/diamyd-medical-ab/r/significant-effect-of-diamyd--in-type-1-diabetes-shown-in-a-new-comprehensive-analysis-of-previous-p,c2989690

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Significant Effect of Diamyd in Type 1 Diabetes Shown in a New Comprehensive Analysis of Previous Phase III and Phase II Trials - PRNewswire

A study discovered that diabetes may have an adverse impact on the labor market due to work absence, unemployment, and disability pension. Danish national registers were queried to identify patients with type 1 (n=431) and type 2 (n=4,047) diabetes between 1994 and 2011; patients with diabetes were compared with non-diabetic controls (n=101,295). The authors employed multi-state Cox proportional hazards analyses to calculate hazards ratios (HRs) with 95% confidence intervals (CIs) for transitions between work, sickness absence, unemployment, and disability pension. Compared with non-diabetics, those in both diabetes cohorts were significantly more likely to sustain sickness absence (type 1 diabetes women, HR, 1.34; 95% CI, 1.12-1.62; type 1 diabetes men, HR, 1.43; 95% CI, 1.01-2.03 vs. type 2 diabetes women, HR, 1.46; 95% CI, 1.35-1.58; type 2 diabetes men, HR, 1.64; 95% CI, 1.46-1.85). Unemployment HRs were higher among males with type 1 diabetes (1.25; 95% CI, 1.01-1.53) and both sexes with type 2 diabetes (women, 1.09; 95% CI, 1.03-1.16; men, 1.17; 95% CI, 1.08-1.27). Between the sexes, both diabetes cohorts had higher HRs of disability pension (type 1 diabetes women, HR, 1.90; 95% CI, 1.46-2.46; type 2 diabetes men, HR, 2.09; 95% CI, 1.38-3.18 vs. type 2 diabetes women, HR, 1.78; 95% CI, 1.62-1.96; type 2 diabetes men, HR, 2.11; 95% CI, 1.86-2.40). Women with type 2 diabetes were the only patients less likely to return to work from sickness absence (HR, 0.91; 95% CI, 0.86-0.98) or unemployment (HR, 0.89; 95% CI, 0.85-0.94). HRs for diabetes in terms of unemployment, sickness absence while unemployed, and disability pension were much higher for men compared with women. The study authors called for future research to take into account comorbidity and social gradient.

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The Effect of Diabetes on the Labor Market - DocWire News

Maternal diabetes before or during pregnancy is associated with increased risks of metabolic syndromeand congenital heart disease in offspring. Research has shown that the children of mothers with elevated blood sugar that is shy of level that would categorize them as havingof gestational diabetes are, nonetheless,more likely to be obese. But less is known about the associations between prenatal exposure to maternal diabetesand early-onset CVD in infants. So researchers from Aarhus University Hospital, Denmark, and University of California, Los Angeles, looked at data from nearly 2.5 million births to find out more. They reported their results on Dec. 4, 2019, on the BMJ website,

During up to 40 years of follow-up, 1,153 offspring of mothers with diabetes were diagnosed with CVD, as were 91,311 children of mothers without diabetes. The offspring of mothers with diabetes had a 29% increased overall rate of early-onset CVD.

Children of mothers with diabetes were also more likely to have diabetes, hypertension, hypercholesterolemia, and chronic kidney diseases, and to be obese. The rates of specific types of CVD were increased for heart failure, and close to doubled for hypertensive disease, deep vein thrombosis, and pulmonary embolism. A mother with diabetes and CVD herself also nearly doubled the offsprings chances of early-onset CVD.

The diabetic intrauterine environment could have a programming effect on the development of CVD in children, the researchers say. They note that during pregnancies complicated by diabetes, large amounts of maternal glucose freely cross the placenta, which could lead to increased secretion of fetal insulin. Exposure to hyperinsulinemia and hyperglycemia could have long-lasting effects, they say, and result in changes in vascular function. Their findings underscore the importance of screening for diabetes risks, especially in pregnant women, to avoid multigenerational hits to heart health.

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Mothers With Diabetes, Kids With Heart Disease - P&T Community

Studies have evaluated the adverse impacts of non-adherence to medication among adults with type 2 diabetes, including poor outcomes and increased healthcare costs. However, data are limited on adolescent patients. The Treatment Options for Type 2 Diabetes in Adolescents and Youth (TODAY) study examined whether additional oral medications or insulin impacted adherence to primary study medication. The TODAY study included 699 patients aged 10 to 17 years who were recently diagnosed with type 2 diabetes. Patients were classified as adherent (80% taken by pill count) or non-adherent (<80%); adherence rates were compared by patients who did and did not have additional medications. At 36 months, just less than half of patients (46.3%) were taking additional oral medications, and 31.9% were on insulin. Study medication adherence did not differ with additional oral medications: zero additional medications prescribed, 55.1%; one, 67.1%; and two or more, 56.7% (P=0.16). Female patients taking oral contraceptives had higher 36-month adherence (65.2% vs. 55.8%; P=0.0054), and patients on insulin had lower 36-month adherence (39.7% vs. 59.3%; P<0.0001). Patients with depression at baseline had lower adherence (P=0.008). The researchers called for future studies to explore potentially modifiable risk factors associated with medication adherence.

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The Effect of Adding Medications to Type 2 Diabetes Regimen on Adherence in Adolescents - DocWire News

Two piglets recently born in China look like average swine on the outside, but on the inside, they are (a very small) part monkey.

A team of researchers generated the pig-primate creatures by injecting monkey stem cells into fertilized pig embryos and then implanting them into surrogate sows, according to a piece by New Scientist. Two of the resulting piglets developed into interspecies animals known as chimeras, meaning that they contained DNA from two distinct individuals in this case, a pig and a monkey.

"This is the first report of full-term pig-monkey chimeras," co-author Tang Hai, a researcher at the State Key Laboratory of Stem Cell and Reproductive Biology in Beijing, told New Scientist. Eventually, Hai and his colleagues aim to grow human organs in animals for use in transplant procedures. For now, the team plans to stick with monkey cells, as developing human-animal chimeras presents a slew of "ethical issues," the authors noted in a report published Nov. 28 in the journal Protein & Cell.

To create pig-primate chimeras, Hai and his co-authors first grew cells from cynomolgus monkeys (Macaca fascicularis) in lab dishes. The team then altered the cells' DNA by inserting instructions to build a fluorescent protein, which caused the cells to glow a bright green. These luminescent cells gave rise to equally radiant embryonic stem cells, which the researchers then injected into prepared pig embryos. These glowing spots allowed the researchers to track the monkey cells as the embryos grew into piglets.

Related: The 9 Most Interesting Transplants

In total, 4,000 embryos received an injection of monkey cells and were implanted in surrogate sows. The pigs bore 10 piglets as a result of the procedure, but only two of the offspring grew both pig and monkey cells. By scanning for spots of fluorescent green, the team found monkey cells scattered throughout multiple organs, including the heart, liver, spleen, lungs and skin.

In each organ, between one in 1,000 and one in 10,000 cells turned out to be a monkey cells in other words, the interspecies chimeras were more than 99% pig.

Although low, the ratio of monkey to pig cells still outnumbered the maximum amount of human cells ever grown in a human-animal chimera. In 2017, scientists created human-pig chimeras that grew only one human cell for every 100,000 pig cells. The interspecies embryos were only allowed to develop for a month for ethical reasons, including the concern that humans cells might grow in the chimera's brain and grant the animal human-like consciousness, according to New Scientist.

Despite these ethical qualms, the same team of researchers went on to create human-monkey chimeras earlier this year, according to a July report from the Spanish newspaper El Pas. The results of the controversial experiment have not yet been reported, but the scientists said that no human-primate embryos were allowed to develop for more than a few weeks, the paper reported.

Hai and his co-authors may have avoided the ethical issues involved with human-animal chimeras, but one expert wasn't impressed with their interspecies piglets. Stem-cell biologist Paul Knoepfler of the University of California, Davis, told New Scientist that the low ratio of monkey to pig cells seems "fairly discouraging." Additionally, the two chimeras and all eight other piglets died shortly after being born, he noted.

The exact reason for the piglets' death remains "unclear," Hai told New Scientist, but he said that he suspects the deaths are linked to the in vitro fertilization (IVF) procedure rather than the injection of monkey DNA. Other scientists have also found that IVF doesn't consistently work in pigs, according to a 2019 report in the journal Theriogenology.

In the immediate future, Hai and his colleagues aim to increase the proportion of monkey cells to pig cells in future chimeras, and eventually, grow entire monkey organs in their pigs, Hai told New Scientist. In their paper, the authors noted that their work in pigs could help "pave the way" toward the "ultimate goal of human organ reconstruction in a large animal."

Originally published on Live Science.

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First Pig-Monkey Chimeras Were Just Created in China - Livescience.com

This article highlights some of the most recent drug target discoveries that could be used to develop and design a treatment for pancreatic cancer.

Scientists investigating pancreatic cancer have identified new targets which, with further research, could be the basis for developing future therapies. Listed below are five of the most recent target discoveries, in order of their journal publication dates, with the newest first.

Scientists at the Queen Mary University of London, UK and Zhengzhou University, China have developed a personalised vaccine system that may be able to delay the onset of pancreatic cancer.

Cells taken from mice, mutated chemically into pancreatic cancer cells and then infected with Adenovirus (AdV) as a prime or Vaccinia virus (VV) as a boost, create a vaccine product. The virus kills the cancerous cells in such a way that their antigens are released and are therefore able to prime the immune system to prevent pancreatic cancer returning.

Injection of the virus-infected cells into mice destined to develop pancreatic cancer doubled their survival rate, compared to their unvaccinated counterparts. The vaccine also delayed the onset of the condition in these mice.

Using cells from the recipient of the vaccine enables the immune system to respond to the exact antigens seen in tumour cells of the individual, resulting in a vaccine regime tailored to them.

Through this international collaboration, we have made progress towards the development of a prophylactic cancer vaccine against pancreatic cancer, said Professor Yaohe Wang, leader of the study, from Queen Mary University of London and the Sino-British Research Centre at Zhengzhou University in China.

Researchers at Sanford Burnham Prebys Medical Discovery Institute in the US have identified that a combination of two anti-cancer compounds, already approved for use to treat other cancers, shrank pancreatic tumours in mice.

Our study identifies a potential treatment combination that can immediately be tested against these aggressive tumours. We are already meeting with oncologists at Oregon Health & Science University, US to discuss how to advance this discovery into clinical evaluation, explained Dr Zeev Ronai, a professor in Sanford Burnham Prebys Tumor Initiation and Maintenance Program, also senior author of the study.

Scientists used L-asparaginase to starve pancreatic tumours of asparagine, an amino acid required by cells for protein synthesis. However, the tumour cells did not die, instead switching on a stress response pathway whereby they could produce asparagine themselves. Scientists then used an MEK inhibitor to block the stress response pathway, causing the pancreatic tumour to shrink.

L-asparaginase is already US Food and Drug Administration (FDA) approved to treat leukaemias and similarly the MEK inhibitor is approved for the treatment of solid tumours, including melanoma skin cancer.

This research lays the basis for the inhibition of pancreatic tumour growth by a combined synergistic attack based on asparagine restriction and MAPK signalling inhibition, says Dr Eytan Ruppin, chief of the Cancer Data Science Library at the National Cancer Institute (NCI) and co-author of the study.

Scientists from the Max Planck Institute for Biology of Ageing, Germany have identified that YME1L, a protease in the membrane of mitochondria, is activated when a cell uses glycolysis to produce energy anaerobically.

scientists were able to reduce tumour growth by switching off the glycolysis signalling pathway in the mitochondria

Cells adapt to oxygen deficiency by switching their energy supply to glycolysis, which ferments sugar without oxygen. This switch is often necessary in old age, as the cells in the body become poorly supplied with oxygen and nutrients.

Cancer cells can also face this problem; prior to angiogenesis, tumours are poorly perfused and so the tissue is deprived of oxygen. Oxidative stress in tumours drives the switch-on of multiple pathways. This includes the glycolysis pathway that alters the behaviour of the mitochondria to provide tumour cells with energy despite being starved of oxygen.

Scientists found that the YME1L protease is activated during the conversion to glycolysis. YME1L appears altered and breaks down various proteins in the organelles, preventing the formation of new mitochondria and causing the remaining organelles to change their metabolism. This process eventually stops as YME1L begins to degrade itself at high activity.

Researchers examined cancer cells originating from patients with pancreatic tumours and were able to reduce tumour growth by switching off the glycolysis signalling pathway in the mitochondria, with reproducible results both in the petri dish and in pancreatic tumours in mice.

There is currently no treatment available for pancreatic cancer. I believe that this protease can be a very interesting therapeutic target because we have seen that the signalling pathway is also active in human patients with pancreatic cancer, explained Thomas Langer, the Max Planck Director, continuing: However, there are no known substances that have an effect on this protease.

Researchers at the Crick Institute have identified cancer stem cells as a driver of pancreatic cancer growth. These cells can metastasise and differentiate into different tumour types to continue the spread of cancer.

Cancer stem cells appear at all stages of cancer growth so being able to identify where they are present could be vital in both targeting cancer and developing new treatments, according to the researchers. Analysis of gene expression in the cancer stem cells identified a protein, CD9, is present on tumour surfaces during development and when it is more established. This protein could therefore be used as a marker to help locate these cells.

A further development of the study established that this protein is not just a marker of cancer stem cells, but also promotes their malignant behaviour. By altering the amount of CD9 in tumour cells in mice, researchers found that reduced levels of this protein caused smaller tumours to form and increasing levels of CD9 created more aggressive cells able to form large tumours quickly.

These cells are vital to pancreatic cancer and if even just a few of them survive chemotherapy, the cancer is able to bounce back. We need to find effective ways to remove these cells and so stop them from fuelling cancer growth. However, we need more experiments to validate the importance of CD9 in human pancreatic cancer, says Victoria Wang, lead author and member of the Adult Stem Cell Laboratory at the Crick Institute.

A look into cancer stem cell metabolism also revealed CD9 increases the rate tumour cells take up glutamine, an amino acid which helps provide energy for cancer growth.

Now we know this protein is both linked to cancer stem cells and helps cancer growth, this could guide the development of new treatments that are targeted at the protein and so cut off the supply of glutamine to cancer stem cells, effectively starving the cancer, says Axel Behrens, corresponding author and group leader in the Adult Stem Cell Laboratory at the Crick Institute.

Scientists at Tel Aviv University, Israel have found that PJ34, a small molecule, causes human pancreatic cancer cells to self-destruct. The researchers tested PJ34 on xenografts (transplants) of human pancreatic tumours in mice.

this mechanism also exists in other types of cancer and therefore the treatment could be valuable for use on those resistant to current therapies

The mice were treated with a molecule called PJ34, which is permeable in the cell membrane but affects human cancer cells exclusively. This molecule causes an anomaly during the duplication of human cancer cells, provoking their rapid cell death. Thus, cell multiplication itself resulted in cell death in the treated cancer cells, explains Professor Malca Cohen-Armon, project lead at Tel Aviv Universitys Sackler Faculty of Medicine.

The treatment consisted of daily PJ34 injections for 14 days and four weeks later there was a relative drop of 90 percent in the number of cancer cells within the tumours of the mice. Cohen-Armon also noted there were no adverse side-effects observed in the mice.

This mechanism similarly exists in other types of cancer and therefore the treatment could be valuable for use on those resistant to current therapies. The molecule PJ34 is being tested in pre-clinical trials according to FDA regulations before clinical trials begin.

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Five recent drug target discoveries for pancreatic cancer - Drug Target Review

NEW YORK--(BUSINESS WIRE)--CurePSP, the foundation for prime of life neurodegeneration, has issued four Venture Grants totaling $300,000 for research in progressive supranuclear palsy (PSP) and the related disease, corticobasal degeneration (CBD). The studies will investigate the mechanisms of toxic tau protein aggregation in the brain.

Tau is a normal brain protein that, when folded on itself in an abnormal way, forms clumps called neurofibrillary tangles that are toxic to some types of brain cells. In the cases of PSP and CBD, the brain cells involved are important in the control of movement, behavior, and thinking. Unlike many other disorders of tau aggregation, PSP and CBD are pure tauopathies, which means that no other proteins are clumping along with tau. This makes these disorders good subjects for studying the pathology involved in many other and often more common neurodegenerative conditions, including Alzheimers disease, which afflicts some six million people in the U.S. alone.

Lawrence I Golbe, MD, CurePSP Director of Scientific Affairs, said, We are pleased to be able to fund these talented investigators whose studies will advance our understanding of the key role that tau protein aggregation plays in neurodegeneration.

The grants will fund the following studies:

Lukasz Joachimiak, The University of Texas Southwestern Medical Center, Dallas

The Mary Jane Semcer Legacy Study

Structural basis for tau strain conformation in CBD and PSP

In the brain, the tau protein can form an altered shape that clumps together in an aggregated form. This study will isolate the tau protein from healthy PSP and CBD patient brain tissues. Specialized research tools will be applied to determine how the abnormally folded shape of tau differs from the tau from healthy brains. Understanding the fine details of how the tau protein changes from a normal shape to the different bad forms found in disease will provide the blueprint for designing new methods to detect and prevent these devastating diseases in patients.

David Butler, Neural Stem Cell Institute, Rensselaer, NY

Bifunctional intrabodies to lower tau

The goal of this project is to develop therapeutic agents that will prevent tau accumulation and associated death of brain cells with novel antibody-based reagents (termed intrabodies). Intrabodies are antibodies expressed within brain cells, while antibodies produced by the immune system or administered by vein do not penetrate brain cells. These antibodies are highly selective for tau, and they have been engineered to target tau for degradation using the cells normal clearing process. The studys central hypothesis is that targeted degradation of tau protein will reduce the amount of tau available to misfold and thus reduce cell death.

J. Mark Cooper, University Hospital, London

The influence of TRIM11 on tau, aggregation, release, and propagation

This study will investigate the effects of a protein known as TRIM11 on toxic tau protein aggregation in the brain. TRIM11 is believed to play a role in regulating the levels of some proteins within the cell, in particular proteins that may form aggregates. To identify how changes to TRIM11 may influence PSP, the study will use models of brain cells grown in the laboratory to focus on how changes to TRIM11 influence tau protein regulation, in particular, its tendency to aggregate. These findings may help to identify potential therapeutic targets to modify PSP disease progression.

K. Matthew Scaglione, Duke University, Durham, NC

Small-molecule regulation of a protein quality-control E3 to treat PSP

The protein Hsc70, or CHIP, accelerates the removal of tau from the brain. This project intends to identify compounds that stimulate CHIP functions. One important such function is as an E3 enzyme, which is an important part of one of the brain cells garbage disposal mechanisms called the ubiquitin-proteasome system (UPS). E3 allows the UPS to recognize specific proteins for appropriate disposal. Finding new compounds to stimulate this function is an important first step toward developing small (that is, orally dosable) molecules to slow or prevent the progression of PSP and CBD.

CurePSPs Venture Grants program provides seed funding for early-career investigators who want to test their innovative ideas. Grant applications are reviewed by CurePSPs eminent international Scientific Advisory Board (SAB) chaired by Dr. Golbe. CurePSPs Venture Grants program is one of the few sources of funding for early stage research into PSP and CBD.

About CurePSP

CurePSP is the nonprofit organization for prime of life neurodegenerative diseases, a spectrum of fatal brain disorders that often strike during a person's most productive and rewarding years. Since it was founded in 1990, CurePSP has funded more than 180 research studies and is a leading source of support and advocacy for patients, families, and other caregivers and education and information for doctors and allied healthcare professionals. CurePSP is based in New York City. Please visit http://www.curepsp.org for more information.

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CurePSP Funds Four Venture Grants for the Study of Neurodegenerative Diseases - Business Wire

KENILWORTH, N.J.--(BUSINESS WIRE)--Merck (NYSE: MRK), known as MSD outside the United States and Canada, announced that KEYTRUDA, Mercks anti-PD-1 therapy, showed improvements in overall survival (OS), progression-free survival (PFS) and objective response rate (ORR) as monotherapy for the first-line treatment of patients with metastatic nonsquamous non-small cell lung cancer (NSCLC) whose tumors expressed PD-L1 (tumor proportion score [TPS] 1%), regardless of KRAS mutational status. These findings, which are based on an exploratory analysis of the pivotal Phase 3 KEYNOTE-042 trial, were presented today in a proffered paper presentation (Abstract #LBA4) at the European Society for Medical Oncology (ESMO) Immuno-Oncology Congress 2019 in Geneva, Switzerland.

KRAS mutations occur in approximately 20% of people with non-small cell lung cancer, and some previous studies have suggested that these mutations are associated with a poorer response to treatment, said Dr. Jonathan Cheng, vice president, oncology clinical research, Merck Research Laboratories. It was therefore encouraging to see in this exploratory analysis that KEYTRUDA monotherapy was associated with a survival benefit in certain patients with metastatic nonsquamous non-small cell lung cancer, regardless of KRAS mutational status.

The objective of the exploratory analysis was to assess the prevalence of KRAS mutations and their association with efficacy in the KEYNOTE-042 trial. Of the 1,274 untreated patients with metastatic nonsquamous NSCLC whose tumors expressed PD-L1 (TPS 1%) enrolled in KEYNOTE-042, 301 patients had KRAS evaluable data (n=232 without any KRAS mutation; n=69 with any KRAS mutation, including n=29 with the KRAS G12C mutation). Tissue tumor mutational burden (tTMB) and KRAS mutational status were determined by whole-exome sequencing (WES) of tumor tissue and matched normal DNA (blood). Patients were randomized 1:1 to receive KEYTRUDA 200 mg intravenously every three weeks (Q3W) (n=637) or investigators choice of chemotherapy (pemetrexed or paclitaxel) (n=637). Treatment continued until progression of disease or unacceptable toxicity. The primary endpoint was OS with a TPS of 50%, 20% and 1%, which were assessed sequentially. The secondary endpoints were PFS and ORR.

Findings from this exploratory analysis showed that KEYTRUDA monotherapy was associated with improved clinical outcomes, regardless of KRAS mutational status, in patients with metastatic nonsquamous NSCLC versus chemotherapy. In this analysis, KEYTRUDA reduced the risk of death by 58% (HR=0.42 [95% CI, 0.22-0.81]) in patients with any KRAS mutation and by 72% (HR=0.28 [95% CI, 0.09-0.86]) in patients with the KRAS G12C mutation compared to chemotherapy. The safety profile of KEYTRUDA was consistent with what has been seen in previously reported studies among patients with metastatic NSCLC.

Additional efficacy results from this exploratory analysis showed:

With Any KRASMutation

With KRAS G12CMutation

Without Any KRAS Mutation

KEYTRUDA Mono-therapy

(N = 30)

Chemo-therapy

(N = 39)

KEYTRUDA Mono-therapy(N = 12)

Chemo-therapy(N = 17)

KEYTRUDA Mono-therapy

(N = 127)

Chemo-therapy(N = 105)

OS, median, mo(95% CI)

28 (23-NR)

11 (7-25)

NR (23-NR)

8 (5-NR)

15 (12-24)

12 (11-18)

OS, HR(95% CI)

0.42 (0.22-0.81)

0.28 (0.09-0.86)

0.86 (0.63-1.18)

ORR, %(95% CI)

56.7

18.0

66.7

23.5

29.1

21.0

PFS, median, mo(95% CI)

12 (8-NR)

6 (4-9)

15 (10-NR)

6 (4-8)

6 (4-7)

6 (6-8)

PFS, HR(95% CI)

0.51 (0.29-0.87)

0.27 (0.10-0.71)

1.00 (0.75-1.34)

Data from an exploratory analysis of KEYNOTE-189 (Abstract #LBA5), which evaluated KRAS mutations and their association with efficacy outcomes for KEYTRUDA in combination with pemetrexed and platinum chemotherapy, were also presented in a mini-oral session today at the ESMO Immuno-Oncology Congress 2019. KEYNOTE-189 was conducted in collaboration with Eli Lilly and Company, the makers of pemetrexed (ALIMTA).

About Lung Cancer

Lung cancer, which forms in the tissues of the lungs, usually within cells lining the air passages, is the leading cause of cancer death worldwide. Each year, more people die of lung cancer than die of colon and breast cancers combined. The two main types of lung cancer are non-small cell and small cell. Non-small cell lung cancer (NSCLC) is the most common type of lung cancer, accounting for about 85% of all cases. Small cell lung cancer (SCLC) accounts for about 10 to 15% of all lung cancers. Lung cancer can also be characterized by the presence of different biomarkers, including PD-L1, KRAS, ALK, EGFR and ROS1. KRAS mutations occur in about 20% of NSCLC cases. Between 2008 and 2014, the five-year survival rate for patients diagnosed in the U.S. with advanced NSCLC was only 5%.

About KEYTRUDA (pembrolizumab) Injection, 100mg

KEYTRUDA is an anti-PD-1 therapy that works by increasing the ability of the bodys immune system to help detect and fight tumor cells. KEYTRUDA is a humanized monoclonal antibody that blocks the interaction between PD-1 and its ligands, PD-L1 and PD-L2, thereby activating T lymphocytes which may affect both tumor cells and healthy cells.

Merck has the industrys largest immuno-oncology clinical research program. There are currently more than 1,000 trials studying KEYTRUDA across a wide variety of cancers and treatment settings. The KEYTRUDA clinical program seeks to understand the role of KEYTRUDA across cancers and the factors that may predict a patients likelihood of benefitting from treatment with KEYTRUDA, including exploring several different biomarkers.

Selected KEYTRUDA (pembrolizumab) Indications

Melanoma

KEYTRUDA is indicated for the treatment of patients with unresectable or metastatic melanoma.

KEYTRUDA is indicated for the adjuvant treatment of patients with melanoma with involvement of lymph node(s) following complete resection.

Non-Small Cell Lung Cancer

KEYTRUDA, in combination with pemetrexed and platinum chemotherapy, is indicated for the first-line treatment of patients with metastatic nonsquamous non-small cell lung cancer (NSCLC), with no EGFR or ALK genomic tumor aberrations.

KEYTRUDA, in combination with carboplatin and either paclitaxel or paclitaxel protein-bound, is indicated for the first-line treatment of patients with metastatic squamous NSCLC.

KEYTRUDA, as a single agent, is indicated for the first-line treatment of patients with NSCLC expressing PD-L1 [tumor proportion score (TPS) 1%] as determined by an FDA-approved test, with no EGFR or ALK genomic tumor aberrations, and is stage III where patients are not candidates for surgical resection or definitive chemoradiation, or metastatic.

KEYTRUDA, as a single agent, is indicated for the treatment of patients with metastatic NSCLC whose tumors express PD-L1 (TPS 1%) as determined by an FDA-approved test, with disease progression on or after platinum-containing chemotherapy. Patients with EGFR or ALK genomic tumor aberrations should have disease progression on FDA-approved therapy for these aberrations prior to receiving KEYTRUDA.

Small Cell Lung Cancer

KEYTRUDA is indicated for the treatment of patients with metastatic small cell lung cancer (SCLC) with disease progression on or after platinum-based chemotherapy and at least one other prior line of therapy. This indication is approved under accelerated approval based on tumor response rate and durability of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in confirmatory trials.

Head and Neck Squamous Cell Cancer

KEYTRUDA, in combination with platinum and fluorouracil (FU), is indicated for the first-line treatment of patients with metastatic or with unresectable, recurrent head and neck squamous cell carcinoma (HNSCC).

KEYTRUDA, as a single agent, is indicated for the first-line treatment of patients with metastatic or with unresectable, recurrent HNSCC whose tumors express PD-L1 [combined positive score (CPS) 1] as determined by an FDA-approved test.

KEYTRUDA, as a single agent, is indicated for the treatment of patients with recurrent or metastatic HNSCC with disease progression on or after platinum-containing chemotherapy.

Classical Hodgkin Lymphoma

KEYTRUDA is indicated for the treatment of adult and pediatric patients with refractory classical Hodgkin lymphoma (cHL), or who have relapsed after 3 or more prior lines of therapy. This indication is approved under accelerated approval based on tumor response rate and durability of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in the confirmatory trials.

Primary Mediastinal Large B-Cell Lymphoma

KEYTRUDA is indicated for the treatment of adult and pediatric patients with refractory primary mediastinal large B-cell lymphoma (PMBCL), or who have relapsed after 2 or more prior lines of therapy. This indication is approved under accelerated approval based on tumor response rate and durability of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in confirmatory trials. KEYTRUDA is not recommended for the treatment of patients with PMBCL who require urgent cytoreductive therapy.

Urothelial Carcinoma

KEYTRUDA is indicated for the treatment of patients with locally advanced or metastatic urothelial carcinoma (mUC) who are not eligible for cisplatin-containing chemotherapy and whose tumors express PD-L1 [CPS 10] as determined by an FDA-approved test, or in patients who are not eligible for any platinum-containing chemotherapy regardless of PD-L1 status. This indication is approved under accelerated approval based on tumor response rate and duration of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in the confirmatory trials.

KEYTRUDA is indicated for the treatment of patients with locally advanced or metastatic urothelial carcinoma (mUC) who have disease progression during or following platinum-containing chemotherapy or within 12 months of neoadjuvant or adjuvant treatment with platinum-containing chemotherapy.

Microsatellite Instability-High (MSI-H) Cancer

KEYTRUDA is indicated for the treatment of adult and pediatric patients with unresectable or metastatic microsatellite instability-high (MSI-H) or mismatch repair deficient (dMMR).

This indication is approved under accelerated approval based on tumor response rate and durability of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in the confirmatory trials. The safety and effectiveness of KEYTRUDA in pediatric patients with MSI-H central nervous system cancers have not been established.

Gastric Cancer

KEYTRUDA is indicated for the treatment of patients with recurrent locally advanced or metastatic gastric or gastroesophageal junction (GEJ) adenocarcinoma whose tumors express PD-L1 (CPS 1) as determined by an FDA-approved test, with disease progression on or after two or more prior lines of therapy including fluoropyrimidine- and platinum-containing chemotherapy and if appropriate, HER2/neu-targeted therapy. This indication is approved under accelerated approval based on tumor response rate and durability of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in the confirmatory trials.

Esophageal Cancer

KEYTRUDA is indicated for the treatment of patients with recurrent locally advanced or metastatic squamous cell carcinoma of the esophagus whose tumors express PD-L1 (CPS 10) as determined by an FDA-approved test, with disease progression after one or more prior lines of systemic therapy.

Cervical Cancer

KEYTRUDA is indicated for the treatment of patients with recurrent or metastatic cervical cancer with disease progression on or after chemotherapy whose tumors express PD-L1 (CPS 1) as determined by an FDA-approved test. This indication is approved under accelerated approval based on tumor response rate and durability of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in the confirmatory trials.

Hepatocellular Carcinoma

KEYTRUDA is indicated for the treatment of patients with hepatocellular carcinoma (HCC) who have been previously treated with sorafenib. This indication is approved under accelerated approval based on tumor response rate and durability of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in the confirmatory trials.

Merkel Cell Carcinoma

KEYTRUDA is indicated for the treatment of adult and pediatric patients with recurrent locally advanced or metastatic Merkel cell carcinoma. This indication is approved under accelerated approval based on tumor response rate and durability of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in the confirmatory trials.

Renal Cell Carcinoma

KEYTRUDA, in combination with axitinib, is indicated for the first-line treatment of patients with advanced renal cell carcinoma (RCC).

Selected Important Safety Information for KEYTRUDA

Immune-Mediated Pneumonitis

KEYTRUDA can cause immune-mediated pneumonitis, including fatal cases. Pneumonitis occurred in 3.4% (94/2799) of patients with various cancers receiving KEYTRUDA, including Grade 1 (0.8%), 2 (1.3%), 3 (0.9%), 4 (0.3%), and 5 (0.1%). Pneumonitis occurred in 8.2% (65/790) of NSCLC patients receiving KEYTRUDA as a single agent, including Grades 3-4 in 3.2% of patients, and occurred more frequently in patients with a history of prior thoracic radiation (17%) compared to those without (7.7%). Pneumonitis occurred in 6% (18/300) of HNSCC patients receiving KEYTRUDA as a single agent, including Grades 3-5 in 1.6% of patients, and occurred in 5.4% (15/276) of patients receiving KEYTRUDA in combination with platinum and FU as first-line therapy for advanced disease, including Grade 3-5 in 1.5% of patients.

Monitor patients for signs and symptoms of pneumonitis. Evaluate suspected pneumonitis with radiographic imaging. Administer corticosteroids for Grade 2 or greater pneumonitis. Withhold KEYTRUDA for Grade 2; permanently discontinue KEYTRUDA for Grade 3 or 4 or recurrent Grade 2 pneumonitis.

Immune-Mediated Colitis

KEYTRUDA can cause immune-mediated colitis. Colitis occurred in 1.7% (48/2799) of patients receiving KEYTRUDA, including Grade 2 (0.4%), 3 (1.1%), and 4 (<0.1%). Monitor patients for signs and symptoms of colitis. Administer corticosteroids for Grade 2 or greater colitis. Withhold KEYTRUDA for Grade 2 or 3; permanently discontinue KEYTRUDA for Grade 4 colitis.

Immune-Mediated Hepatitis (KEYTRUDA) and Hepatotoxicity (KEYTRUDA in Combination With Axitinib)

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Data from Exploratory Analysis Show Merck's KEYTRUDA (pembrolizumab) Improved Overall Survival as Monotherapy for the First-Line Treatment of...

On Wednesday, Dec. 11, 2018, Baylor University announced that Lady, one of the Universitys two American Black Bear mascots, is undergoing an innovative, noninvasive radiation treatment for a benign mass, or thymoma, in her chest. The asymptomatic tumor was found during a routine wellness examination with veterinarians at Texas A&M College of Veterinary Medicine & Biomedical Sciences.

Lady has received treatment at Texas A&M Veterinary Medical Teaching Hospital with a low-dose TomoTherapy System, a state-of-the-art treatment system that targets tumors while minimizing exposure of radiation to surrounding healthy tissues and causing fewer side effects compared to conventional forms of radiation therapy. Veterinarians continue to closely monitor the tumor, which has not grown since it was discovered. Lady is resting comfortably at her campus home the Bill and Eva Williams Bear Habitat along with her older sister, Joy.

Additional Media Resources

Dec. 11, 2019 Letter to the Baylor Family from President Linda A. Livingstone, Ph.D.

Dec. 11, 2019 News Release: Baylor Bear Mascot Lady Undergoing Treatment for Benign Thymoma

2019 Bear Mascot Program Fact Sheet about the program, daily and medical/health care, and Ladys diagnosis and treatment.

Photos, b-roll and video interview clips: https://baylor.box.com/v/BaylorBearsMascots

Thisfolder includes photos and b-roll of Lady and Joy in the Bill and Eva Williams Bear Habitat on campus, at their off-campus enrichment facility and at Texas A&M Veterinary Medical Teaching Hospital, where Lady is being treated. In addition, the folder includes interview clips with J. Jill Heatley, DVM, zoological medicine specialist at Texas A&M College of Veterinary Medicine & Biomedical Sciences. Please credit the photos to Matthew Minard/Baylor University and the video courtesy of Baylor University.

Baylor Bear Program website: http://www.baylor.edu/bear

See the article here:
2019 Baylor Bear Mascots | Media and Public Relations - Baylor University

Veterinary Medicine Market Overview:

The Veterinary Medicine Market is expected to grow at a significant pace, reports Verified Market Research. Its latest research report, titled [Veterinary Medicine Market Size and Forecast to 2026, Breakdown Data by Manufacturers, Key Regions, Types and Application], offers a unique point of view about the global market. Analysts believe that the changing consumption patterns are expected to have a great influence on the overall market. For a brief overview of the Veterinary Medicine Market, the research report provides an executive summary. It explains the various factors that form an important element of the market. It includes the definition and the scope of the market with a detailed explanation of the market drivers, opportunities, restraints, and threats.

Request a Sample Copy of this report @ https://www.verifiedmarketresearch.com/download-sample/?rid=21894&utm_source=DNI&utm_medium=005

Key Players Mentioned in the Veterinary Medicine Market Research Report:

Veterinary Medicine Market: Segmentation

Segmental analysis is one of the key sections of this report. The authors of the report have segregated the Veterinary Medicine market into product type, application, end user, and region. All the segments are studied on the basis of their CAGR, market share, and growth potential. In the regional analysis, the report highlights the regional markets having high growth potential. This clear and thorough assessment of the segments would help the players to focus on revenue generating areas of the Veterinary Medicine market.

Veterinary Medicine Market: Regional Segmentation

For a deeper understanding, the research report includes geographical segmentation of the Veterinary Medicine Market. It provides an evaluation of the volatility of the political scenarios and amends likely to be made to the regulatory structures. This assessment gives an accurate analysis of the regional-wise growth of the Veterinary Medicine Market.

Veterinary Medicine Market: Research Methodology

The research methodologies used by the analysts play an integral role in the way the publication has been collated. Analysts have used primary and secondary research methodologies to create a comprehensive analysis. For an accurate and precise analysis of the Veterinary Medicine Market, analysts have bottom-up and top-down approaches.

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Table of Content

1 Introduction of Veterinary Medicine Market

1.1 Overview of the Market 1.2 Scope of Report 1.3 Assumptions

2 Executive Summary

3 Research Methodology of Verified Market Research

3.1 Data Mining 3.2 Validation 3.3 Primary Interviews 3.4 List of Data Sources

4 Veterinary Medicine Market Outlook

4.1 Overview 4.2 Market Dynamics 4.2.1 Drivers 4.2.2 Restraints 4.2.3 Opportunities 4.3 Porters Five Force Model 4.4 Value Chain Analysis

5 Veterinary Medicine Market, By Deployment Model

5.1 Overview

6 Veterinary Medicine Market, By Solution 6.1 Overview

7 Veterinary Medicine Market, By Vertical

7.1 Overview

8 Veterinary Medicine Market, By Geography 8.1 Overview 8.2 North America 8.2.1 U.S. 8.2.2 Canada 8.2.3 Mexico 8.3 Europe 8.3.1 Germany 8.3.2 U.K. 8.3.3 France 8.3.4 Rest of Europe 8.4 Asia Pacific 8.4.1 China 8.4.2 Japan 8.4.3 India 8.4.4 Rest of Asia Pacific 8.5 Rest of the World 8.5.1 Latin America 8.5.2 Middle East

9 Veterinary Medicine Market Competitive Landscape

9.1 Overview 9.2 Company Market Ranking 9.3 Key Development Strategies

10 Company Profiles

10.1.1 Overview 10.1.2 Financial Performance 10.1.3 Product Outlook 10.1.4 Key Developments

11 Appendix

11.1 Related Research

Complete Report is Available @ https://www.verifiedmarketresearch.com/product/Veterinary-Medicine-Market/?utm_source=DNI&utm_medium=005

We also offer customization on reports based on specific client requirement:

1-Free country level analysis forany 5 countries of your choice.

2-Free Competitive analysis of any market players.

3-Free 40 analyst hours to cover any other data points

About Us:

Verified Market Research has been providing Research Reports, with up to date information, and in-depth analysis, for several years now, to individuals and companies alike that are looking for accurate Research Data. Our aim is to save your Time and Resources, providing you with the required Research Data, so you can only concentrate on Progress and Growth. Our Data includes research from various industries, along with all necessary statistics like Market Trends, or Forecasts from reliable sources.

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Veterinary Medicine Market Size 2019 Focuses on Top Companies, Research Methodology, Drivers and Forecast to 2026 - Drnewsindustry

The CSU Employee Appreciation Board had the privilege of recognizing the College of Veterinary Medicine and Biomedical Sciences Finance and Research Office for their exemplary service on Oct. 21.

Nominated by Dana Schwartz, the group continuously goes above and beyond by assisting with tasks and providing customer service beyond their normal scope of duties. When an accountant in the Veterinary Teaching Hospital suddenly left, an employee in the Finance and Research Office offered to take on PCard reallocation for the VTH during the stressful year-end time frame.

In another instance, when a complicated research training grant was awarded to a department outside of CVMBS, this group volunteered to take over the administration of it because of their expertise on these types of awards and the outside department was unfamiliar with it.

Schwartz also shared another example of how this group embodies the true spirit of customer service. The Dish Network office was previously located where the finance office is now, and they still get people coming in wanting help with Dish issues. Recently, a gentleman in his 80s who couldnt get his TV to work came in. One of the employees helped him call the number on the bill to help get it fixed.

This group deserved to be recognized for making CSU a great place to work, and ultimately giving individuals positive experiences with CSU, Schwaartz said. The CSUEAB agrees! Congratulations on a job well done!

To nominate a department or office, visit the EAB website.

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CVMBS Finance and Research Office recognized by the Employee Appreciation Board - Source