BOSTON and LAUSANNE, Switzerland, Sept. 02, 2022 (GLOBE NEWSWIRE) -- SOPHiA GENETICS SA (Nasdaq: SOPH), a cloud-native software company in the healthcare space, announced today Chief Executive Officer, Dr. Jurgi Camblong and Chief Financial Officer, Ross Muken will participate in a fireside chat at the 20th Annual Morgan Stanley Global Healthcare Conference on Monday, September 12, 2022, at 8:45 a.m. EDT.

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SOPHiA GENETICS to Participate in Fireside Chat at 20th Annual Morgan Stanley Global Healthcare Conference

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MELBOURNE, Australia, Sept. 02, 2022 (GLOBE NEWSWIRE) -- Genetic Technologies Limited (ASX: GTG; NASDAQ: GENE, “Company”, “GTG”, “GENE”), a global leader in guideline driven genomics-based tests in health, wellness and serious disease, is pleased to report excellent commercial progress in the USA strategic operations with the following updates:

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Genetic Technologies Provides Update on US Operations and Payer Engagement

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SEATTLE, Sept. 02, 2022 (GLOBE NEWSWIRE) -- Adaptive Biotechnologies Corporation (“Adaptive Biotechnologies”) (Nasdaq: ADPT), a commercial stage biotechnology company that aims to translate the genetics of the adaptive immune system into clinical products to diagnose and treat disease, today announced it will be participating in the upcoming Morgan Stanley Global Healthcare Conference in New York, NY.

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Adaptive Biotechnologies to Participate in the Morgan Stanley Global Healthcare Conference

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SAN DIEGO, Sept. 02, 2022 (GLOBE NEWSWIRE) -- Crinetics Pharmaceuticals (Nasdaq: CRNX) today announced that Monica R. Gadelha, MD, PhD, professor of endocrinology at the Medical School of the Universidade Federal do Rio de Janeiro and a principal investigator in the Phase 2 ACROBAT program, will be presenting data from a planned two-year interim analysis from the ACROBAT Advance open label extension (OLE) study at the 35th Brazilian Congress of Endocrinology and Metabolism (CBEM) being held in São Paulo, Brazil from September 3-7, 2022.

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New Long-Term Safety and Efficacy Data for Investigational Compound Paltusotine to be Presented at the Brazilian Congress of Endocrinology and...

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SAN DIEGO, Sept. 02, 2022 (GLOBE NEWSWIRE) -- Fate Therapeutics, Inc. (the “Company” or “Fate Therapeutics”) (NASDAQ: FATE), a clinical-stage biopharmaceutical company dedicated to the development of programmed cellular immunotherapies for patients with cancer, today announced that the Company will participate in the following upcoming investor conferences:

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Fate Therapeutics to Participate at Upcoming September Investor Conferences

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WESTLAKE VILLAGE, Calif., Sept. 02, 2022 (GLOBE NEWSWIRE) -- Arcutis Biotherapeutics, Inc. (Nasdaq: ARQT), an early-stage commercial company focused on developing meaningful innovations in immuno-dermatology, today announced that Neha Krishnamohan has been appointed to the Arcutis Board of Directors and as a member of the audit committee. Following the appointment, the Board will be composed of 10 directors.

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Arcutis Announces Appointment of Neha Krishnamohan to Board of Directors

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HAYWARD, Calif., Sept. 02, 2022 (GLOBE NEWSWIRE) -- Benitec Biopharma Inc. (NASDAQ: BNTC) (“Benitec” or “the Company”), a development-stage, gene therapy-focused, biotechnology company developing novel genetic medicines based on its proprietary DNA-directed RNA interference ("ddRNAi") platform, today announced financial results for its Fiscal Year ended June 30, 2022. The Company has filed its annual report on Form 10-K for the quarter ended June 30, 2022, with the U.S. Securities and Exchange Commission.

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Benitec Biopharma Releases Full Year 2022 Financial Results and Provides Operational Update

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CAMBRIDGE, Mass., Sept. 02, 2022 (GLOBE NEWSWIRE) -- Immuneering Corporation (Nasdaq: IMRX), a biopharmaceutical company using translational bioinformatics to advance a pipeline of product candidates designed to benefit large populations of patients with cancer and other diseases, today announced it submitted an Investigational New Drug (IND) application to the U.S. Food and Drug Administration (FDA). The IND application supports a Phase 1/2a clinical trial of IMM-1-104, an oral once daily small molecule in development for the treatment of advanced RAS mutant solid tumors. In contrast to the narrow approach of targeting specific mutations such as KRAS-G12C, IMM-1-104 is a third generation MEK inhibitor designed for broad pan-RAS activity as well as activity in other MAPK-activated tumors. Based on preclinical data to date, IMM-1-104 has demonstrated robust single-agent anti-tumor activity across a broad range of in vitro and in vivo tumor models driven by MAPK pathway activation events. This includes animal models of KRAS mutant pancreatic cancer, NRAS mutant melanoma, KRAS mutant colorectal cancer, and KRAS mutant lung cancer, regardless of the specific mutation upstream of MEK that drives activation of the MAPK pathway, and all while maintaining a well-tolerated safety profile in such models.

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Immuneering Announces Submission of IND Application to the FDA for Phase 1/2a Trial of IMM-1-104 to Treat Advanced Solid Tumors with RAS Mutations

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ORION CORPORATION STOCK EXCHANGE RELEASE – OTHER INFORMATION DISCLOSED ACCORDING TO THE RULES OF THE EXCHANGE2 SEPTEMBER 2022 at 17.30 EEST

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Prosecutor appealed the district court's decision to dismiss the charges pressed against a member of Orion's Board of Directors for a suspected...

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Company also retains B2i Digital to enhance engagement with the investor community

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Todos Medical Announce Kingcarlx as Brand Ambassador for the Tollovid #TolloUp Lifestyle Campaign

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COPENHAGEN, Denmark, September 2, 2022 – Bavarian Nordic A/S (OMX: BAVA) announced today the dosing of the first subject in the Phase 3 clinical trial of ABNCoV2, a VLP-based, non-adjuvanted COVID-19 booster vaccine candidate.

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Bavarian Nordic Announces Initiation of a Global Phase 3 Clinical Trial of its COVID-19 Booster Vaccine Candidate

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Montrouge, France, September 2, 2022

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DBV Technologies to Present at Upcoming Investor Conferences

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Leuven, BELGIUM, Boston, MA, US – September 2, 2022 – CET 10:30PM – Oxurion NV (Euronext Brussels: OXUR) a biopharmaceutical company developing next generation standard of care ophthalmic therapies, with clinical stage assets in vascular retinal disorders, announced today that it has amended its mandatory convertible bonds issuance and subscription agreement announced on April 6, 2021 (“funding program”) with the Negma Group, a financial institution focused on supporting growth and capturing value through a multi-strategy approach. The proceeds will be devoted to Oxurion’s KALAHARI Phase 2, Part B clinical trial. The trial is currently underway and is evaluating THR-149, its novel therapeutic for second line therapy, against market leader aflibercept in the treatment of diabetic macular edema (DME) for the 40-50% of DME patients that get suboptimal response to standard of care anti-VEGF therapy, with top-line data expected mid next year.

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Oxurion Announces Amendment to Funding Program with Negma Group for EUR 6 Million in Funding

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How do bone marrow transplants work, and what conditions do they treat?

A bone marrow transplant is actually a misnomer, as these procedures transplant stem cells, not the actual bones. Specifically, these procedures use hematopoietic stem cells (HSC), also known as blood-forming stem cells, to potentially cure an ever-expanding number of diseases.

There are three main cell types found inside a persons blood based on their function:

red blood cells: these cells carry oxygen throughout the body

platelets: these cells help form clots to stop bleeding

white blood cells: these cells lead the charge in fighting infections (also known as the immune system)

Each of these cell types, despite their different functions, shapes, sizes and lifespan, arise from the same source the hematopoietic stem cell, which constantly replenish each cell type. HSCs reside almost exclusively deep inside our bones in the center of the hard, protective shelter of calcium and other minerals. So, the marrow (soft, middle portion of our bones) can be thought of as the factory that supply each person with the blood cells needed to overcome infections, trauma, and to live a healthy, long life.

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When we perform a transplant, we are actually either using a patients own stem cells (autologous transplant) or stem cells from another human (allogeneic transplant), leading to the more appropriate name of hematopoietic stem cell transplant (HSCT). These transplants are most commonly used to treat and cure cancer.

Autologous transplants are used in the treatment of many types of solid tumors (such as brain tumors, germ cell tumors, neuroblastoma), where the tumor can only be effectively destroyed by giving very high doses of chemotherapy that also damage the patients own HSCs. Before giving a patient those high doses of chemotherapy, we collect his or her own HSCs with a process very similar to dialysis (we remove stem cells from their blood), and then freeze and store them in a specialized lab.

After the patient receives that high dose of chemotherapy, the treatment team then thaws the stem cells and infuses them back into the patient via a specialized catheter placed in his or her veins. The stem cells quickly return home and find the bone marrow space, and within 10 to 21 days, they will start making new white blood cells and platelets, followed by red blood cells.

Allogeneic transplants are performed for many types of leukemias or bone marrow failure syndromes (such as aplastic anemia or Fanconi anemia) where the patients own stem cells are broken and need to be replaced by a healthy humans stem cells. However, many other non-malignant conditions (not cancer) can be effectively cured with this procedure, as conditions that result from defects of different blood cell types (red blood cells, white blood cells or platelets) are corrected when the factory is replaced with a healthy donors stem cells.

This is an exciting time in the field of transplant, as we are now able to offer cures for many childhood diseases that historically are chronic and/or life-threatening. HSCT is now being offered to patients with sickle cell disease/thalassemia (red blood cells are defective), along with many conditions that are now called inborn errors of immunity (white blood cells are defective).

Among the more than 500 different genetic conditions that damage white blood cells include severe combined immunodeficiency (SCID), hemophagocytic lymphohistiocytosis (HLH), chronic granulomatous disease (CGD), and severe congenital neutropenia (SCN). Not only are the numbers of conditions potentially cured with HSCT rapidly growing, but the success rates and ability to prevent and treat complications of this procedure are improving exponentially as well. We are looking forward to offering these procedures to more children here at UVa Childrens.

To learn more about Dr. Roehrs and the care he provides, visit uvahealth.com/findadoctor/profile/philip-a-roehrs.

Dr. Philip Roehrs is the clinical director for pediatric stem cell transplant and cellular therapy at UVa Childrens and UVa Health.

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Ask the Expert: How do bone marrow transplants work, and what conditions do they treat? - The Daily Progress

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City of Hope recently shared significant news at the 24th Annual AIDS Conference about a patient treated in 2019 whose HIV has been in remission. The man had been living with HIV for 31 years before coming to City of Hope with another grave diagnosisacute myeloid leukemia.One of the best hopes for long-term remission of acute myeloid leukemia (AML) is a stem cell transplant, and City of Hope has one of the nations leading transplant programs, having performed more than 17,000 transplants since 1976. In addition, the institution is at the forefront of using transplants to treat older adults with blood cancers, including increasing efficacy and safety in those over 60 and those with comorbidities, like the then 63-year-old City of Hope patient with HIV. The research was presented by Jana K. Dickter, M.D., City of Hope associate clinical professor in the Division of Infectious Diseases.

City of Hope hematologist Ahmed Aribi, M.D., assistant professor in the Division of Leukemia, prepared the patient for an allogeneic blood stem cell transplant with a chemotherapy-based, reduced-intensity regimen developed for treatment of older patients with blood cancers. Reduced-intensity chemotherapy makes the transplant more tolerable for older patients and reduces the potential for transplant-related complications from the procedure.

Aribi and his team worked with City of Hopes Unrelated Donor BMT Program directed by Monzr M. Al Malki, M.D. to find a donor who was a perfect match for the patient and had the rare genetic mutation, homozygous CCR5 Delta 32, which is found in just 1 to 2% of the general population.

People who have this mutation have a resistance to acquiring HIV. CCR5 is a receptor on CD4+ immune cells, and most strains of HIV use that receptor to enter and attack the immune system. But the CCR5 mutation blocks that pathway, which stops HIV from replicating.

After this successful transplant for both AML and HIV, the patient has been in remission for HIV since stopping ART in March 2021. While this outcome has happened in three other patients, the City of Hope patient was both the oldest to undergo a transplant with HIV and leukemia and go into remission for both. He had also lived with HIV the longest 31 years.

The City of Hope patient is another major advancement. It demonstrates that research and clinical care developed and led at City of Hope are changing the meaning of an HIV diagnosis for patients across the United States and the world, said John Zaia, M.D., director of City of Hopes Center for Gene Therapy, Aaron D. Miller and Edith Miller Chair for Gene Therapy and a leader in HIV research. City of Hope remains at the forefront of clinical research that changes peoples lives for the better.

When I was diagnosed with HIV in 1988, like many others, I thought it was a death sentence. I never thought I would live to see the day that I no longer have HIV. City of Hope made that possible, and I am beyond grateful. The City of Hope patient

The story above is one significant example of several important advances being made at City of Hope in the care of people with HIV. When many centers still treated patients with low-intensity, noncurative treatment approaches for HIV-related lymphoma, City of Hope challenged that paradigm by demonstrating that autologous transplantation could be used to cure patients who would otherwise die.

More recently, City of Hope is leveraging its leadership in CAR T cell therapya groundbreaking treatment currently used to rally the bodys natural defenses against cancer and exploring its potential in tandem with another advance, City of Hopes vaccine for cytomegalovirus (CMV).

In a proof-of-concept study, funded by theCalifornia Institute for Regenerative Medicine, lab models demonstrated that the combination therapy could recognize and eliminate HIV without serious toxicity to cells in the virus host. In cultured human cells, the CAR T cells killed cells tagged with the gp120 protein, and kept killing them, without significant signs of risking damage to healthy cells. In a mouse model for HIV/AIDS, high doses of the dual-action CAR T cells followed by the CMV vaccine were successful in controlling HIV, and even nestled into the bone marrow, indicating potential for treatment to keep working over the long term.

In addition to achieving breakthrough outcomes in cancer and HIV, City of Hope has been recognized as the seventh "Best Hospital" for cancer in the nation according to U.S. News & World Report's 2022-23 Best Hospitals: Specialty Ranking. This marks the first time the cancer treatment center has cracked the top 10 of the U.S. News & World Report annual rankings and the 16th consecutive year it has been distinguished as one of the nation's elite cancer hospitals. It was also rated as high performing in four cancer surgery specialties: lung, colon, prostate and ovarian cancers.

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From optimized stem cell transplants to CAR T cell therapy: Advancing options for cancer, HIV and more - City of Hope

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So far, Bcells havent gotten the same attentionindeed, genetically engineered versions have never been tested in a human. Thats partly because engineering B cells is not that easy, says Xin Luo, a professor at Virginia Tech who in 2009 demonstrated how to generate B cells that have an added gene.

That early work, carried out at Caltech, explored whether the cells could be directed to make antibodies against HIV, perhaps becoming a new form of vaccination.

While that idea didnt pan out, now biotech companies like Immusoft, Be Biopharma, and Walking Fish Therapeutics want to harness the cells as molecular factories to treat serious rare diseases. These cells are powerhouses for secreting protein, so thats something they want to take advantage of, says Luo.

Immusoft licensed the Caltech technology and got an early investment from Peter Thiels biotech fund, Breakout Labs. Company founder Matthew Scholz, a software developer, boldly predicted in 2015 that a trial could start immediately. However, the technology the company terms immune-system programming didnt turn out to be as straightforward as coding a computer.

Ainsworth says Immusoft had to first spend several years working out reliable ways to add genes to B cells. Instead of using viruses or gene editing to make genetic changes, the company now employs a transposona molecule that likes to cut and paste DNA segments.

It also took time to convince the FDA to allow the trial. Thats because its known that if added DNA ends up near cancer-promoting genes, it can sometimes turn them on.

The FDA is concerned if you are doing this in a B cell, could you develop a leukemia situation? That is something that they are going to watch pretty closely, says Paul Orchard, the doctor at the University of Minnesota who will be recruiting patients and carrying out the study.

The first human test could resolve some open questions about the technology. One is whether the enhanced cells will take up long-term residence inside peoples bone marrow, where B cells typically live. In theory, the cells could survive decadeseven the entire life of the patient. Another question is whether theyll make enough of the missing enzyme to help stall MPS, which is a progressive disease.

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A new gene therapy based on antibody cells is about to be tested in humans - MIT Technology Review

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North America Market Comprises Of 53.1% Market Share Due To Rising Number Of Spine-Related Disorders

Fact.MR A Market Research and Competitive Intelligence Provider: Theglobal bone grafts and substitutes marketreached a valuation ofUS$ 3.06 Bnin 2020. Moreover, sales of bone grafts and substitutes are slated to rise at a CAGR of4.9%to reachUS$ 4.44 Bnby the end of 2028.

Bone grafts and substitutes (BGS) are rapidly used common materials used mainly to replace missing bones or mend fractures. Moreover, it is commonly being used in the hip, foot, and ankle surgeries, as well as fractures and musculoskeletal injuries. Moreover, the primary goal of using bone grafts and substitutes is to aid in the healing of fractures and bone injuries, as well as to replace natural bone.

Moreover, surge in demand for synthetics and xenografts, rise in usage of bone graft substitutes in regenerative medicines, and the surge in the number of illnesses that necessitate their usage would propel the market for bone grafts and substitutes forward.

In addition to this, continuous R&D initiatives to upgrade product offerings are one of the most common trends in the market. This rise in R&D initiatives is driven by surge in need for bone graft substitutes for bone-related occurrences fractures and trauma. Researchers from across the globe are putting in efforts to find new ways to use bone grafts in regenerative medicines.

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Bone grafts manufacturers are constantly investing in the development of new products with improved bioactivity, biocompatibility, and mechanical qualities. Companies have a varied product portfolio that is technologically advanced, as well as a larger global presence. Key players in the market are putting emphasis on innovative products in various orthopedic application areas.

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Bone Growth Stimulator Market - Bone growth stimulator market was nearly worthUS$ 1.8Bn in 2020 and is anticipated to expand1.6xover the forecast period, anticipated to reach a valuation ofUS$ 3Bn by 2031. In the short-run, bone growth stimulators revenue is likely to topUS$ 1.9Bn by 2022.

Bone Marrow Processing Systems Market - A bone marrow processing system is a functionally closed, sterile system designed for automatically isolating and concentrating stem cells derived from donated bone marrow aspirate.

Bone Broth Protein Powder Market - Bone broth protein powder supports a healthy gut, skin hydration, immune system, joint health, and flexibility and physical functioning of the body and thus is a significant attraction for health enthusiast and sportspersons. The market for bone broth protein powder is anticipated to increase over the forecast years owing to its restorative and healing properties.

Bone Meal Supplement Market - The demand for bone meal supplement is anticipated to increase over the forecast year due to increasing application of bone meal supplements in animal feed and fertilizers. The bone meal supplement is obtained from crushed and coarsely ground animal bones and waste from slaughterhouses.

Bone Biopsy Systems Market - The global bone biopsy systems market is set to enjoy a valuation of US$ 227.6 million in 2022 and expand at a CAGR of 6% to reach US$ 408.9 million by the end of 2032. Sales of bone biopsy systems accounted for more than 30% of the global bone biopsy market at the end of 2021.

Antibiotic-loaded Bone Cement Market - Infections are among the major issues encountered during various orthopedic surgeries, and antibiotic-loaded bone cement is commonly used to avoid any sorts of medical predicaments. To ensure the safety of patients undergoing orthopedic surgeries, the demand for antibiotic-loaded bone cement is increasing across the healthcare industry.

Injectable Bone Graft Substitutes Market - Growing instances of bone defects among individuals has fuelled demand for the bone grafting techniques in the healthcare industry. As the need to conduct trauma and orthopedic surgeries persist, manufacturers are developing a range of bone grafts or bone graft substitutes to stimulate insufficient or impaired bone regeneration.

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Bone Grafts And Substitutes Market Is Expected To Witness An Impressive CAGR Of 4.9% Due To Rise In Usage Of Bone Grafts And Substitutes For Healing...

Bone Marrow Stem Cells Comments Off on Bone Grafts And Substitutes Market Is Expected To Witness An Impressive CAGR Of 4.9% Due To Rise In Usage Of Bone Grafts And Substitutes For Healing… | September 3rd, 2022

By Giles Campion, EVP, head of R&D and chief medical officer, Silence Therapeutics

siRNA is a gene-silencing technology with great potential for treating a wide range of rare diseases, as I discussed in my previous article, but its promise doesnt end there. In this last article in the series, I examine siRNAs potential for treating not-so-rare and even quite common diseases.

Unlike rare diseases, which are often caused by pathological genetic mutations, common diseases may be associated with genetic variants that are not pathological and therefore do not dysregulate a biological process. For example, variants of the LPA or PCSK9 gene can increase a persons risk of cardiovascular disease by affecting cholesterol levels, but these variants do not directly cause cardiovascular disease by disrupting a fundamental biological process. This contrasts with, for example, mutations in the HBB gene that cause beta thalassemia and disrupt the mechanisms that protect the body from toxic iron buildup.

Nevertheless, the approach to treating rare and common diseases with siRNA therapies is similar: silence a gene that has little or no effect on phenotypes outside the disease, thereby maximizing safety. This is an important factor in rare diseases, which often begin early in life and require lifelong treatment. But it is equally important in common chronic diseases, such as hyperlipidemia, in which a patient has abnormally high levels of fats in the blood, where patients may live for decades before they experience any overt symptoms from their condition and are not likely to tolerate a therapy with even minor side effects that interfere with their quality of life.

At the forefront of common conditions being targeted by gene silencing is elevated lipoprotein (a), or Lp(a), a cholesterol-rich particle closely related to the well-known cardiovascular risk factor LDL. High levels of Lp(a) are associated with high risk of cardiovascular events, such as heart attacks and strokes; low levels of Lp(a) are associated with a low risk of these events.

Unlike other types of cholesterol-carrying particles, Lp(a) levels are not significantly modifiable by lifestyle factors; levels are genetically determined by the variant of the LPA gene, which encodes apolipoprotein (a) a major protein component of Lp(a) that a person has. Because these variants are not pathological mutations, the person may not experience disease symptoms for years and may even be unaware of their elevated Lp(a) levels. Yet the condition is common: One in five people have high levels of Lp(a), defined as 50 mg/dl or 120 nmol/L. Other cholesterol-reducing medicines, such as statins, have no effect on Lp(a) and can even increase levels; currently there are no approved Lp(a)-reducing therapies.

However, assessments of human genetic databases, such as the UK Biobank, have revealed that cardiovascular risk is the only phenotype associated with Lp(a) levels. Some individuals have zero levels of Lp(a), and the only known phenotype in them is a much-reduced incidence of cardiovascular events. This indicates that silencing LPA with a properly designed siRNA therapy, such as Silences clinical-stage asset SLN360, could reduce the risk of cardiovascular disease in people with elevated Lp(a) while minimizing the risk of any unwanted or unexpected side effects.

The PCSK9 gene is another example of an siRNA target for the common condition of hyperlipidemia. The PCSK9 protein negatively regulates the cellular uptake of low-density lipoprotein-cholesterol (LDL-C) in the bloodstream by reducing the number of LDL receptors on the surface of cells. This means that high levels of PCSK9 decrease cellular uptake of LDL-C, leaving more of it in circulation.

High LDL-C levels in blood are associated with coronary artery disease (CAD). While not entirely determined by genetics, as Lp(a) levels are, some variants of the PCSK9 gene are associated with low levels of LDL-C and a reduced incidence of cardiovascular disease. Similar to the LPA gene, this suggests that silencing PCSK9 with an siRNA could reduce LDL-C levels in the blood to treat hyperlipidemia and reduce the risk of CAD. Indeed, the siRNA therapy inclisiran, which silences PCSK9, was approved by the European Union in December 2020 and in the United States in December 2021 for use in people with atherosclerotic cardiovascular disease (ASCVD), ASCVD risk equivalents, and heterozygous familial hypercholesterolemia (HeFH), in conjunction with lifestyle changes and other cholesterol-lowering medicines.

An important feature of siRNA therapies in the treatment of common chronic conditions such as elevated Lp(a) and elevated LDL-C is that they have long-lasting effects, and thus they require less frequent dosing than statins and other small molecule drugs, which must be taken daily. This in turn should increase patients compliance with the therapeutic regimen and thereby improve outcomes. In fact, a 2018 retrospective study found that hyperlipidemia patients who were prescribed the right intensity (level) of statin treatment and complied 100% with their therapy had a 40% lower risk of cardiovascular events than patients who received low-intensity statin treatment and had 5% compliance.1The study concluded that an optimal therapy could reduce the risk of cardiovascular events by 30% in three years.

Though published before any siRNA therapy was approved for hyperlipidemia, the studys implications are clear: Therapeutic intensity and patient compliance are important factors in saving peoples lives. With siRNA therapies, the intensity is known, and the compliance issues are likely to be less of an issue compared with oral drugs. This is just one aspect of siRNA that makes it as well-suited for treating common diseases as rare diseases.

siRNA also has the potential to improve outcomes in hematopoietic stem cell transplantation (HSCT). Though not a disease per se, HCST is a procedure commonly used to treat a range of blood cancers and, with increasing frequency, certain autoimmune disorders.

HCST involves ablating the existing bone marrow to make way for a healthy stem cell graft to repopulate the marrow. This ablation shifts an enormous load of dead iron-laden blood cells into the circulation. Retrospective studies suggest this acute release of toxic iron from ablated cells can adversely affect the survival of the stem cell graft and increase the risk of potentially lethal infections in HSCT patients.

As in the rare disease examples I mentioned previously, silencing TMPRSS6 with an siRNA could increase hepcidin to reduce iron levels in HSCT patients, potentially improving their survival and engraftment outcomes.

I am passionate about RNA technology and the benefits that targeted, precision siRNA medicines can bring to patients with rare diseases and not-so-rare diseases who need new therapeutic options. As both a physician and drug developer, I find it rewarding and exciting to witness this technology finally coming into its own, with the promise of delivering even greater benefits in the coming years.

Reference

About The Author:

Giles Campion, MD, joined Silence Therapeutics as head of R&D and chief medical officer in 2019 and was appointed as an executive director in 2020. He is an expert in translational medicine and an experienced biotech and pharmaceutical professional across many therapeutic areas, most recently in orphan neuromuscular disorders. He has held senior global R&D roles in several large pharma, diagnostics, and biotech companies, including as group vice president of the neuromuscular franchise at BioMarin Pharmaceutical Inc., and chief medical officer and senior vice president of R&D at Prosensa. He is also a co-founder of PepGen Ltd. He earned his bachelors and doctorate degrees in medicine from the University of Bristol and is listed on the General Medical Council (UK) Specialist Register (Rheumatology).

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The Promise Of Gene Silencing To Treat Not-So-Rare Diseases - BioProcess Online

Bone Marrow Stem Cells Comments Off on The Promise Of Gene Silencing To Treat Not-So-Rare Diseases – BioProcess Online | September 3rd, 2022

Pluripotent embyronic cell group giving rise to diverse cell lineages

Neural crest cells are a temporary group of cells unique to vertebrates that arise from the embryonic ectoderm germ layer, and in turn give rise to a diverse cell lineageincluding melanocytes, craniofacial cartilage and bone, smooth muscle, peripheral and enteric neurons and glia.[1][2]

After gastrulation, neural crest cells are specified at the border of the neural plate and the non-neural ectoderm. During neurulation, the borders of the neural plate, also known as the neural folds, converge at the dorsal midline to form the neural tube.[3] Subsequently, neural crest cells from the roof plate of the neural tube undergo an epithelial to mesenchymal transition, delaminating from the neuroepithelium and migrating through the periphery where they differentiate into varied cell types.[1] The emergence of neural crest was important in vertebrate evolution because many of its structural derivatives are defining features of the vertebrate clade.[4]

Underlying the development of neural crest is a gene regulatory network, described as a set of interacting signals, transcription factors, and downstream effector genes that confer cell characteristics such as multipotency and migratory capabilities.[5] Understanding the molecular mechanisms of neural crest formation is important for our knowledge of human disease because of its contributions to multiple cell lineages. Abnormalities in neural crest development cause neurocristopathies, which include conditions such as frontonasal dysplasia, WaardenburgShah syndrome, and DiGeorge syndrome.[1]

Therefore, defining the mechanisms of neural crest development may reveal key insights into vertebrate evolution and neurocristopathies.

Neural crest was first described in the chick embryo by Wilhelm His Sr. in 1868 as "the cord in between" (Zwischenstrang) because of its origin between the neural plate and non-neural ectoderm.[1] He named the tissue ganglionic crest since its final destination was each lateral side of the neural tube where it differentiated into spinal ganglia.[6] During the first half of the 20th century the majority of research on neural crest was done using amphibian embryos which was reviewed by Hrstadius (1950) in a well known monograph.[7]

Cell labeling techniques advanced the field of neural crest because they allowed researchers to visualize the migration of the tissue throughout the developing embryos. In the 1960s Weston and Chibon utilized radioisotopic labeling of the nucleus with tritiated thymidine in chick and amphibian embryo respectively. However, this method suffers from drawbacks of stability, since every time the labeled cell divides the signal is diluted. Modern cell labeling techniques such as rhodamine-lysinated dextran and the vital dye diI have also been developed to transiently mark neural crest lineages.[6]

The quail-chick marking system, devised by Nicole Le Douarin in 1969, was another instrumental technique used to track neural crest cells.[8][9] Chimeras, generated through transplantation, enabled researchers to distinguish neural crest cells of one species from the surrounding tissue of another species. With this technique, generations of scientists were able to reliably mark and study the ontogeny of neural crest cells.

A molecular cascade of events is involved in establishing the migratory and multipotent characteristics of neural crest cells. This gene regulatory network can be subdivided into the following four sub-networks described below.

First, extracellular signaling molecules, secreted from the adjacent epidermis and underlying mesoderm such as Wnts, BMPs and Fgfs separate the non-neural ectoderm (epidermis) from the neural plate during neural induction.[1][4]

Wnt signaling has been demonstrated in neural crest induction in several species through gain-of-function and loss-of-function experiments. In coherence with this observation, the promoter region of slug (a neural crest specific gene) contains a binding site for transcription factors involved in the activation of Wnt-dependent target genes, suggestive of a direct role of Wnt signaling in neural crest specification.[10]

The current role of BMP in neural crest formation is associated with the induction of the neural plate. BMP antagonists diffusing from the ectoderm generates a gradient of BMP activity. In this manner, the neural crest lineage forms from intermediate levels of BMP signaling required for the development of the neural plate (low BMP) and epidermis (high BMP).[1]

Fgf from the paraxial mesoderm has been suggested as a source of neural crest inductive signal. Researchers have demonstrated that the expression of dominate-negative Fgf receptor in ectoderm explants blocks neural crest induction when recombined with paraxial mesoderm.[11] The understanding of the role of BMP, Wnt, and Fgf pathways on neural crest specifier expression remains incomplete.

Signaling events that establish the neural plate border lead to the expression of a set of transcription factors delineated here as neural plate border specifiers. These molecules include Zic factors, Pax3/7, Dlx5, Msx1/2 which may mediate the influence of Wnts, BMPs, and Fgfs. These genes are expressed broadly at the neural plate border region and precede the expression of bona fide neural crest markers.[4]

Experimental evidence places these transcription factors upstream of neural crest specifiers. For example, in Xenopus Msx1 is necessary and sufficient for the expression of Slug, Snail, and FoxD3.[12] Furthermore, Pax3 is essential for FoxD3 expression in mouse embryos.[13]

Following the expression of neural plate border specifiers is a collection of genes including Slug/Snail, FoxD3, Sox10, Sox9, AP-2 and c-Myc. This suite of genes, designated here as neural crest specifiers, are activated in emergent neural crest cells. At least in Xenopus, every neural crest specifier is necessary and/or sufficient for the expression of all other specifiers, demonstrating the existence of extensive cross-regulation.[4] Moreover, this model organism was instrumental in the elucidation of the role of the Hedgehog signaling pathway in the specification of the neural crest, with the transcription factor Gli2 playing a key role.[14]

Outside of the tightly regulated network of neural crest specifiers are two other transcription factors Twist and Id. Twist, a bHLH transcription factor, is required for mesenchyme differentiation of the pharyngeal arch structures.[15] Id is a direct target of c-Myc and is known to be important for the maintenance of neural crest stem cells.[16]

Finally, neural crest specifiers turn on the expression of effector genes, which confer certain properties such as migration and multipotency. Two neural crest effectors, Rho GTPases and cadherins, function in delamination by regulating cell morphology and adhesive properties. Sox9 and Sox10 regulate neural crest differentiation by activating many cell-type-specific effectors including Mitf, P0, Cx32, Trp and cKit.[4]

The migration of neural crest cells involves a highly coordinated cascade of events that begins with closure of the dorsal neural tube.

After fusion of the neural fold to create the neural tube, cells originally located in the neural plate border become neural crest cells.[17] For migration to begin, neural crest cells must undergo a process called delamination that involves a full or partial epithelial-mesenchymal transition (EMT).[18] Delamination is defined as the separation of tissue into different populations, in this case neural crest cells separating from the surrounding tissue.[19] Conversely, EMT is a series of events coordinating a change from an epithelial to mesenchymal phenotype.[18] For example, delamination in chick embryos is triggered by a BMP/Wnt cascade that induces the expression of EMT promoting transcription factors such as SNAI2 and FoxD3.[19] Although all neural crest cells undergo EMT, the timing of delamination occurs at different stages in different organisms: in Xenopus laevis embryos there is a massive delamination that occurs when the neural plate is not entirely fused, whereas delamination in the chick embryo occurs during fusion of the neural fold.[19]

Prior to delamination, presumptive neural crest cells are initially anchored to neighboring cells by tight junction proteins such as occludin and cell adhesion molecules such as NCAM and N-Cadherin.[20] Dorsally expressed BMPs initiate delamination by inducing the expression of the zinc finger protein transcription factors snail, slug, and twist.[17] These factors play a direct role in inducing the epithelial-mesenchymal transition by reducing expression of occludin and N-Cadherin in addition to promoting modification of NCAMs with polysialic acid residues to decrease adhesiveness.[17][21] Neural crest cells also begin expressing proteases capable of degrading cadherins such as ADAM10[22] and secreting matrix metalloproteinases (MMPs) that degrade the overlying basal lamina of the neural tube to allow neural crest cells to escape.[20] Additionally, neural crest cells begin expressing integrins that associate with extracellular matrix proteins, including collagen, fibronectin, and laminin, during migration.[23] Once the basal lamina becomes permeable the neural crest cells can begin migrating throughout the embryo.

Neural crest cell migration occurs in a rostral to caudal direction without the need of a neuronal scaffold such as along a radial glial cell. For this reason the crest cell migration process is termed free migration. Instead of scaffolding on progenitor cells, neural crest migration is the result of repulsive guidance via EphB/EphrinB and semaphorin/neuropilin signaling, interactions with the extracellular matrix, and contact inhibition with one another.[17] While Ephrin and Eph proteins have the capacity to undergo bi-directional signaling, neural crest cell repulsion employs predominantly forward signaling to initiate a response within the receptor bearing neural crest cell.[23] Burgeoning neural crest cells express EphB, a receptor tyrosine kinase, which binds the EphrinB transmembrane ligand expressed in the caudal half of each somite. When these two domains interact it causes receptor tyrosine phosphorylation, activation of rhoGTPases, and eventual cytoskeletal rearrangements within the crest cells inducing them to repel. This phenomenon allows neural crest cells to funnel through the rostral portion of each somite.[17]

Semaphorin-neuropilin repulsive signaling works synergistically with EphB signaling to guide neural crest cells down the rostral half of somites in mice. In chick embryos, semaphorin acts in the cephalic region to guide neural crest cells through the pharyngeal arches. On top of repulsive repulsive signaling, neural crest cells express 1and 4 integrins which allows for binding and guided interaction with collagen, laminin, and fibronectin of the extracellular matrix as they travel. Additionally, crest cells have intrinsic contact inhibition with one another while freely invading tissues of different origin such as mesoderm.[17] Neural crest cells that migrate through the rostral half of somites differentiate into sensory and sympathetic neurons of the peripheral nervous system. The other main route neural crest cells take is dorsolaterally between the epidermis and the dermamyotome. Cells migrating through this path differentiate into pigment cells of the dermis. Further neural crest cell differentiation and specification into their final cell type is biased by their spatiotemporal subjection to morphogenic cues such as BMP, Wnt, FGF, Hox, and Notch.[20]

Neurocristopathies result from the abnormal specification, migration, differentiation or death of neural crest cells throughout embryonic development.[24][25] This group of diseases comprises a wide spectrum of congenital malformations affecting many newborns. Additionally, they arise because of genetic defects affecting the formation of neural crest and because of the action of Teratogens [26]

Waardenburg's syndrome is a neurocristopathy that results from defective neural crest cell migration. The condition's main characteristics include piebaldism and congenital deafness. In the case of piebaldism, the colorless skin areas are caused by a total absence of neural crest-derived pigment-producing melanocytes.[27] There are four different types of Waardenburg's syndrome, each with distinct genetic and physiological features. Types I and II are distinguished based on whether or not family members of the affected individual have dystopia canthorum.[28] Type III gives rise to upper limb abnormalities. Lastly, type IV is also known as Waardenburg-Shah syndrome, and afflicted individuals display both Waardenburg's syndrome and Hirschsprung's disease.[29] Types I and III are inherited in an autosomal dominant fashion,[27] while II and IV exhibit an autosomal recessive pattern of inheritance. Overall, Waardenburg's syndrome is rare, with an incidence of ~ 2/100,000 people in the United States. All races and sexes are equally affected.[27] There is no current cure or treatment for Waardenburg's syndrome.

Also implicated in defects related to neural crest cell development and migration is Hirschsprung's disease (HD or HSCR), characterized by a lack of innervation in regions of the intestine. This lack of innervation can lead to further physiological abnormalities like an enlarged colon (megacolon), obstruction of the bowels, or even slowed growth. In healthy development, neural crest cells migrate into the gut and form the enteric ganglia. Genes playing a role in the healthy migration of these neural crest cells to the gut include RET, GDNF, GFR, EDN3, and EDNRB. RET, a receptor tyrosine kinase (RTK), forms a complex with GDNF and GFR. EDN3 and EDNRB are then implicated in the same signaling network. When this signaling is disrupted in mice, aganglionosis, or the lack of these enteric ganglia occurs.[30]

Prenatal alcohol exposure (PAE) is among the most common causes of developmental defects.[31] Depending on the extent of the exposure and the severity of the resulting abnormalities, patients are diagnosed within a continuum of disorders broadly labeled Fetal Alcohol Spectrum Disorder (FASD). Severe FASD can impair neural crest migration, as evidenced by characteristic craniofacial abnormalities including short palpebral fissures, an elongated upper lip, and a smoothened philtrum. However, due to the promiscuous nature of ethanol binding, the mechanisms by which these abnormalities arise is still unclear. Cell culture explants of neural crest cells as well as in vivo developing zebrafish embryos exposed to ethanol show a decreased number of migratory cells and decreased distances travelled by migrating neural crest cells. The mechanisms behind these changes are not well understood, but evidence suggests PAE can increase apoptosis due to increased cytosolic calcium levels caused by IP3-mediated release of calcium from intracellular stores. It has also been proposed that the decreased viability of ethanol-exposed neural crest cells is caused by increased oxidative stress. Despite these, and other advances much remains to be discovered about how ethanol affects neural crest development. For example, it appears that ethanol differentially affects certain neural crest cells over others; that is, while craniofacial abnormalities are common in PAE, neural crest-derived pigment cells appear to be minimally affected.[32]

DiGeorge syndrome is associated with deletions or translocations of a small segment in the human chromosome 22. This deletion may disrupt rostral neural crest cell migration or development. Some defects observed are linked to the pharyngeal pouch system, which receives contribution from rostral migratory crest cells. The symptoms of DiGeorge syndrome include congenital heart defects, facial defects, and some neurological and learning disabilities. Patients with 22q11 deletions have also been reported to have higher incidence of schizophrenia and bipolar disorder.[33]

Treacher Collins Syndrome (TCS) results from the compromised development of the first and second pharyngeal arches during the early embryonic stage, which ultimately leads to mid and lower face abnormalities. TCS is caused by the missense mutation of the TCOF1 gene, which causes neural crest cells to undergo apoptosis during embryogenesis. Although mutations of the TCOF1 gene are among the best characterized in their role in TCS, mutations in POLR1C and POLR1D genes have also been linked to the pathogenesis of TCS.[34]

Neural crest cells originating from different positions along the anterior-posterior axis develop into various tissues. These regions of neural crest can be divided into four main functional domains, which include the cranial neural crest, trunk neural crest, vagal and sacral neural crest, and cardiac neural crest.

Cranial neural crest migrates dorsolaterally to form the craniofacial mesenchyme that differentiates into various cranial ganglia and craniofacial cartilages and bones.[21] These cells enter the pharyngeal pouches and arches where they contribute to the thymus, bones of the middle ear and jaw and the odontoblasts of the tooth primordia.[35]

Trunk neural crest gives rise two populations of cells.[36] One group of cells fated to become melanocytes migrates dorsolaterally into the ectoderm towards the ventral midline. A second group of cells migrates ventrolaterally through the anterior portion of each sclerotome. The cells that stay in the sclerotome form the dorsal root ganglia, whereas those that continue more ventrally form the sympathetic ganglia, adrenal medulla, and the nerves surrounding the aorta.[35]

The vagal and sacral neural crest cells develop into the ganglia of the enteric nervous system and the parasympathetic ganglia.[35]

Cardiac neural crest develops into melanocytes, cartilage, connective tissue and neurons of some pharyngeal arches. Also, this domain gives rise to regions of the heart such as the musculo-connective tissue of the large arteries, and part of the septum, which divides the pulmonary circulation from the aorta.[35]The semilunar valves of the heart are associated with neural crest cells according to new research.[37]

Several structures that distinguish the vertebrates from other chordates are formed from the derivatives of neural crest cells. In their "New head" theory, Gans and Northcut argue that the presence of neural crest was the basis for vertebrate specific features, such as sensory ganglia and cranial skeleton. Furthermore, the appearance of these features was pivotal in vertebrate evolution because it enabled a predatory lifestyle.[38][39]

However, considering the neural crest a vertebrate innovation does not mean that it arose de novo. Instead, new structures often arise through modification of existing developmental regulatory programs. For example, regulatory programs may be changed by the co-option of new upstream regulators or by the employment of new downstream gene targets, thus placing existing networks in a novel context.[40][41] This idea is supported by in situ hybridization data that shows the conservation of the neural plate border specifiers in protochordates, which suggest that part of the neural crest precursor network was present in a common ancestor to the chordates.[5] In some non-vertebrate chordates such as tunicates a lineage of cells (melanocytes) has been identified, which are similar to neural crest cells in vertebrates. This implies that a rudimentary neural crest existed in a common ancestor of vertebrates and tunicates.[42]

Ectomesenchyme (also known as mesectoderm):[43] odontoblasts, dental papillae, the chondrocranium (nasal capsule, Meckel's cartilage, scleral ossicles, quadrate, articular, hyoid and columella), tracheal and laryngeal cartilage, the dermatocranium (membranous bones), dorsal fins and the turtle plastron (lower vertebrates), pericytes and smooth muscle of branchial arteries and veins, tendons of ocular and masticatory muscles, connective tissue of head and neck glands (pituitary, salivary, lachrymal, thymus, thyroid) dermis and adipose tissue of calvaria, ventral neck and face

Endocrine cells:chromaffin cells of the adrenal medulla, glomus cells type I/II.

Peripheral nervous system:Sensory neurons and glia of the dorsal root ganglia, cephalic ganglia (VII and in part, V, IX, and X), Rohon-Beard cells, some Merkel cells in the whisker,[44][45] Satellite glial cells of all autonomic and sensory ganglia, Schwann cells of all peripheral nerves.

Enteric cells:Enterochromaffin cells.[46]

Melanocytes and iris muscle and pigment cells, and even associated with some tumors (such as melanotic neuroectodermal tumor of infancy).

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Rise In Number Of CROS In Various Regions Such As Europe Is Expected To Fuel The Growth Of Induced Pluripotent Stem Cell Market At An Impressive CAGR...

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