All posts by medical

Cell Biology

Organoids, iPSCs, and advanced cell models: Advancing discovery from basic research to drug discovery – Science Magazine

Various in vitro cell culture assays have been used for decades to evaluate disease pathology and uncover potential therapeutic treatments. Despite many successes with these models, they have critical shortcomings. Growing evidence suggests that models providing more predictive and translational observations are desperately needed. Researchers are now moving from reductionist, 2D monoculture assay models to more complex 3D cell models, such as organoids and induced pluripotent stem cell (iPSC) cultures, in order to better evaluate the dynamic interactions between cells in an environment more closely emulating that of the in vivo milieu, and to assess patient-specific phenotypic effects following drug treatment. Effective, well-characterized, advanced cell models hold promise for improving our understanding of disease pathology and progression, and are critical for the identification of novel therapeutic targets.

During this roundtable webinar, the speakers will:

This webinar will last for approximately 60 minutes.

STEMCELL TechnologiesCambridge, UK

Dr. Simmini is an R&D scientist in the gastrointestinal biology group at STEMCELL Technologies. His group focuses on developing products that support the generation of 3D gastrointestinal organoid cultures both from human primary tissue and human induced pluripotent stem cells. Prior to joining STEMCELL Technologies in 2016, he obtained his Ph.D. in stem cells, developmental biology, and cancer at the University of Utrecht in The Netherlands. During that time, he conducted research with the group of Jacqueline Deschamps at the Hubrecht Institute in Utrecht, where he investigated the molecular mechanisms controlled by transcription factor CDX2 in adult mouse intestinal stem cells and during embryonic development. In 2015, he began postdoctoral research, joining the group of Jan Paul Medema and Louis Vermeulen at the Amsterdam Medical Centre in Amsterdam, where he investigated mechanisms regulating intestinal stem cell proliferation and differentiation in colorectal cancer. He is currently involved in several Horizon 2020 European Research Council projects in different roles: researcher within the INTENS (INtestinal Tissue ENgineering Solution) consortium; partner in the SINERGIA (Advanced technologieS for drug dIscovery and precisioN mEdicine: in vitRo modellinG human physiology and diseAse) project; and supervisor and member of the executive board of the Organovir-ETN (Organoids for Virus Research-European Training Network) grant.

Wellcome Sanger InstituteCambridge, UK

As a staff scientist at the Wellcome Sanger Institute, Dr.Hale undertakes basic research projects into hostbacterial interactions while also teaching relevant skills to students and visiting scientists. Her projects include growing and differentiating human induced pluripotent stem cells to either a macrophage-like lineage or as intestinal 3D organoids, then utilizing them to investigate pathogen interactions. The main techniques used are flow cytometry, confocal imaging, high-throughput Cellomics assays, Luminex cytokine assays, and cell culture. The pathogens have varied over the years, but have included Salmonella, Klebsiella, enteropathogenic Escherichia coli (EPEC), Chlamydia, and Leishmania.

UK Dementia Research InstituteCambridge, UK

Dr. Avezov received his Ph.D. in cell research and immunology from the George S. Wise Faculty of Life Sciences at Tel Aviv University in 2010. He conducted his postdoctoral work at the University of Cambridge Wellcome-MRC Institute of Metabolic Science and the Cambridge Institute for Medical Research until 2017 with David Ron, FRS. Quantitative cell biology in the context of human disease has been at the core of Dr. Avezovs research. Working at the interface of biomedical research, physics, and mathematical sciences, he developed the cross-disciplinary expertise for probing intracellular chemical and physical processes in real time. This enabled discoveries of unexpected features of the endoplasmic reticulum (ER), such as an active ER luminal transport mechanism. These findings provide insights into the roles of the ER and its morpho-regulation in neuronal (patho)physiology. Dr. Avezov is currently a UK Dementia Research Institute Group Leader running an interdisciplinary program that seeks to understand early contributions of fundamental cellular processes ranging from ER transport to neurodegeneration.

Science/AAASWashington, D.C.

Dr. Oberst did her undergraduate training at the University of Maryland, College Park, and her Ph.D. in Tumor Biology at Georgetown University, Washington D.C. She combined her interests in science and writing by pursuing an M.A. in Journalism from the Philip Merrill College of Journalism at the University of Maryland, College Park. Dr. Oberst joined Science/AAAS in 2016 as the Assistant Editor for Custom Publishing. Before then she worked at Nature magazine, the Howard Hughes Medical Institute, The Endocrine Society, and the National Institutes of Mental Health.

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Organoids, iPSCs, and advanced cell models: Advancing discovery from basic research to drug discovery - Science Magazine

Cell Biology

‘Cells At Work!’ Will Teach You About Biology, With Gratuitous Violence and an Overload of Cuteness – /FILM

(Welcome toAni-time Ani-where, a regular column dedicated to helping the uninitiated understand and appreciate the world of anime.)

Whenever a piece of entertainment tries to be educational, it usually suffers from one of two things: either it shoves a bunch of facts down your throat to the point where it becomes overwhelming and dull, or it dumbs down the story to appeal to kids or complete newbies to a degree that it alienates the rest of its audience.

Cells at Work! is different. This is an anime that takes the edutaining from Magic School Bus, the anthropomorphized cuteness of Inside Out, and the horror and gory violence of the Anatomy Park episode of Rick and Morty. The premise: we follow the inside of the human body, where cells are depicted as humans really dedicated to their jobs. Our main character is a red blood cell that always gets lost on her way to deliver boxes of oxygen to different locations, and a white blood cell thats really good at slaughtering bacteria (and absolutely loves to kill them). Its a godsend for nerds studying biology, and it basically confirms my belief that deep down, were all anime inside an incredibly violent anime where cells are constantly on the edge of a gruesome and traumatic demise. Ahead of its second season, which is coming later this year, lets revisit an anime thats literally a story about you. Yes, you!

The first thing to note is that Cells at Work! really, really commits to its concept. It reimagines our bodies as a huge metropolis and every tiny cell as a person, which results in incredibly crowded open spaces, a lot of diverse landscapes, and unfathomable amounts of death and destruction.

The cast of the show is huge, and the characterizations are very creative, from macrophages as hardworking cleaning workers (and occasionally brutal and jovial mass murderers), to T-cells as nave young boys without battle experience, to white blood cells as elite combat units and red blood cells as food delivery people. Then theres the shows secret weapon: the platelets, imagined as cute little kindergarteners. Forget about Baby Yoda platelets are not only real, they keep you from bleeding out whenever you get a paper cut, and they are precious babies.

Anime fans may recognize the animation in Cells at Work! as being made by the same studio that gave us Jojos Bizarre Adventure (yes, there are indeed Jojo references in the show). The show includes many, many scenes of gratuitous and colorful anime violence thats not only visually stunning, but they make you appreciate the work your body does in keeping you alive while you spend your time reading this article. All pathogens look like monsters under a microscope, but Cells at Work! blows them out of proportion and imagines a wide variety of creatures that range from kind of cute to outright disturbing, as is the case of a virus looking like a pink hat that takes over cells and turns them into zombies, or a parasite that is depicted as a full-on kaiju.

And it is in this juxtaposition of cuteness and hyper-violence and horror that Cells at Work! thrives. The show has a very tongue-in-cheek tone throughout, fully acknowledging and diving into the ridiculousness of its premise and energetically playing with it. Not only does it manage to teach you about the different cells in your body and how different pathogens affect you, but it does so through goofy comedy that hides the gruesome seriousness of what its portraying, resulting in one of the most entertaining anime in recent years.

By presenting the smallest areas of the human body as massive cities, every single problem becomes an apocalyptic-level catastrophe. A sneeze becomes a rocked being launched into the sky, a cut becomes a nuclear blast that opens a huge hole in the ground, making every small event feel incredibly important. This serves to both educate you on how your body works and reacts to pathogens and to caution about how to prevent things like heatstrokes. It might make you actually care about what happens inside you and maybe even inspire you to take better care of yourself.

Theres no better example of this than episode 7, which deals with cancer. As controversial with some audiences as it was popular with other audiences and even doctors, the episode is perhaps the most somber of the season. Cells at Work! takes the horrible disease and characterizes it as a tragic boy who saw his entire family hunted down by white cells just for being born different, and grew to despise all cells as a result. Though some took issue with how sympathetic the cancer cell seemed to be, the show doesnt try to say anything positive about the disease, but gives the character a tragic backstory in order to reflect the real tragedy that is cancer itself. Cells at Work! may have a very goofy sense of humor, but it isnt afraid to slow down and reflect on how serious some of the threats to the human body really are, as it challenges the notion of what edutainment can be.

Cells at Work! does what Osmosis Jones tried and failed to do: it makes you learn new things without it getting in the way of a fun and cute story of cells going about their day. The show manages to take all the action, blood, and cute little creatures typical in anime and mixes them with actual microbiology lessons.

Whether youre here to learn some basics about how cells work and how pathogens affect the body, or just in it for some very violent, visually inventive action (and also those platelets), Cells at Work! has something for you.

Watch This If You Like: The Magic School Bus, Osmosis Jones, Dr. Stone.

Cells At Work is now streaming on Netflix.

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'Cells At Work!' Will Teach You About Biology, With Gratuitous Violence and an Overload of Cuteness - /FILM

Cell Biology

How do cells regulate proteins that are on the outside of their membranes? – Medical News Bulletin

Scientists investigate how cells regulatethe proteins that are on the outside of their membranes. This research couldprovide important clues to help develop treatments for Alzheimers disease.

Proteins are the complex molecules that play a critical role in cell biology. They are made up of a chain of amino acids that fold up to form a 3D structure and shape. Each protein has a unique structure that determines its function. Think of proteins like tools, hammers and screwdrivers have different shapes but they are each designed to perform a very specific task. Proteins are made in the cell and sometimes they dont fold correctly or their structural integrity is damaged due to stresses like high temperatures and oxidative stress. This can be dangerous as the abnormal proteins can aggregate and cause damage in the cell. This can lead to a range of illnesses called protein deposition diseases such as Alzheimers disease, Huntingtons disease, and Parkinsons disease. In the case of Alzheimers disease, beta-amyloid peptides are toxic because they stick together and form aggregates. These are often secreted outside the cell and the aggregates then stick to extracellular molecules and form plaques.

Protein quality control systems

In healthy cells, there are protein quality control systems in place to make sure proteins fold correctly. One of these systems uses chaperones, these are proteins whose sole job is to ensure that other proteins are the correct shape. If the target proteins are incorrectly folded one of two things happens, either the chaperone uses energy (in the form of ATP) to refold the protein or the entire protein is degraded.

What happens to the proteins that are secreted and function outside of the cell?

Not all proteins are designed to workwithin the cell. These proteins can be susceptible to damage from stressorssuch as pathological conditions, shear stress, and acidosis and alkalosis (incorrectpH). So what happens when these proteins undergo structural changes? Somechaperone proteins are also secreted, such as clusterin. The problem is thatthere is a thousand times less ATP (energy) outside the cell, meaning that thesechaperones cant refold misfolded proteins. The exact mechanism of how thechaperons work outside the cell is not well understood.

How does clusterin work?

In a recently published article in the Journal of Cell Biology, scientists fromJapan wanted to know how clusterin worked. They speculated that clusterinworked by binding to misfolded proteins and bringing them into contact with thecell. The cell would then engulf the clusterin and misfolded protein complexand degrade it.

New internalisation test developed

The first question the researchers askedwas if clusterin that is bound to a misfolded protein would be able to getinside the cell. They wanted to know if these proteins would be broken downinside a cell structure called the lysosome. Lysosomes are another proteinquality control system and they are responsible for degrading proteins with anacidic environment and digestive enzymes.

The scientists designed a newinternalisation test to help them answer these questions. They used geneticengineering to attach two fluorescent proteins to clusterin (one green and theother red). The red fluorescent protein is resistant to acidic conditions anddigestive enzymes. So if the scientists saw red under the microscope they couldconclude clusterin was indeed internalised and degraded but if they saw onlygreen they could conclude that the clusterin was internalised but not degraded.The scientists combine their internalisation assay with flow cytometry andfluorescent microscopy to show that the Clusterin-misfolded protein complex waspreferentially internalised and degraded with a lysosome. The team used variouscell types (kidney, ovary, lung, bone, liver, and colon) to test their assayand showed this internalisation occurred generally. They then went to show thatthe beta-amyloid peptide was able to bind to clusterin and was subsequentlydegraded in human embryonic kidney cells.

What is the clusterin receptor?

The scientists wanted to know if there wasa receptor on the cell surface that bound to clusterin and triggered theinternalisation of this complex. The team used a genome-wide CRISPR screen tofind out which genes were important for clusterin uptake. They identified 20different genes important for uptake of clusterin and many of them wereimplicated in heparan sulphate (HS) synthesis. To test if HS was the receptorfor clusterin the scientists used genetic engineering to prevent the expressionof various genes involved in the HS pathway. They found that when these geneswere knocked out there was reduced uptake of the clusterin-misfolded proteincomplex. When they restored the gene expression they found this restoredcomplex uptake. This data showed that HS pathway disruption preventedinternalisation of only the clusterin complex and not of endocytosis ingeneral. The scientists then used a pull-down assay to confirm that clusterindirectly binds to HS. These data strongly suggested that HS is the receptor forthe uptake of clusterin-misfolded protein complexes. The group went on to show that HS was theclusterin receptor independent of the misfolded proteins bound. They testedbeta-amyloid peptide and a variety of misfolded red blood cell proteins.

The researchers were able to show anentirely novel mechanism for regulating extracellular proteins called thechaperone- and receptor-mediated extracellular protein degradation (CRED)pathway. Although this is an exciting discovery the involvement of the pathwayin Alzheimers disease requires further investigation. The tests onbeta-amyloid peptides were conducted in kidney cells and not neuronal celllines. There was also no investigation into whether or not this mechanism worksin animals. It seems unlikely that increasing clusterin expression will resultin a treatment for Alzheimers disease as overexpression of this protein hasbeen linked to cancer pathogenesis. The work present is an excitingcontribution to our basic understanding of protein regulation outside the celland is promising progress toward understanding many of the protein depositiondiseases.

Written by Tarryn Bourhill MSc, PhD Candidate.

References:

1 Yerbury, J. J., Stewart, E. M.,Wyatt, A. R. & Wilson, M. R. Quality control of protein folding inextracellular space. EMBO reports 6, 1131-1136 (2005).

2 Jones, S. E.& Jomary, C. Clusterin. Theinternational journal of biochemistry & cell biology 34, 427-431 (2002).

3 Nuutinen, T.,Suuronen, T., Kauppinen, A. & Salminen, A. Clusterin: a forgotten player inAlzheimers disease. Brain researchreviews 61, 89-104 (2009).

4 Wyatt, A. R.,Yerbury, J. J., Ecroyd, H. & Wilson, M. R. Extracellular chaperones andproteostasis. Annual review ofbiochemistry 82, 295-322 (2013).

5 Itakura, E., Chiba, M., Murata, T. & Matsuura, A. Heparan sulfate is a clearance receptor for aberrant extracellular proteins. Journal of Cell Biology 219 (2020).

Image byKonstantin KolosovfromPixabay

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How do cells regulate proteins that are on the outside of their membranes? - Medical News Bulletin

Cell Biology

Dr Lisa Crawford: The research matters because today’s treatment for myeloma might not be as effective tomorrow – Belfast Telegraph

Fundraising will support the work of leading local researcher in myeloma, Dr Lisa Crawford, who is a lecturer based at the Centre for Cancer Research and Cell Biology at Queens University Belfast.

r Crawford is pioneering new research into enhancing treatments for myeloma and to fund it Leukaemia and Lymphoma NI has launched the MyMATTERS (Myeloma Metabolic Manipulation To Enhance Response) appeal to raise the 100,000 needed. The charity strongly believes in prioritising research that will support the future needs which an increasing older population will require. It is estimated that by 2039, the population aged 65 and over will have increased by 74% and the population aged 85 and over will have increased by 157%.

The research aims to study metabolism within myeloma cells to identify ways to improve existing treatments making them last longer as well as improving the quality of life for thousands of people living with myeloma today and tomorrow.

With over 10 years experience in researching myeloma, Dr Crawford and her team aim to understand how metabolism works to help myeloma cells survive and from this research it will help identify ways to enhance existing treatments.

Dr Crawford feels passionately about finding answers to questions that could make such a huge difference for our loved ones, in Northern Ireland and across the world.

Speaking about the urgency of the research, she says: Myeloma may be more treatable, but it is still incurable. My research matters because todays treatment for myeloma might not be as effective tomorrow. This research is vital as existing treatments for myeloma are initially successful in treating the disease but patients often develop resistance and stop responding to treatment.

No two patients are the same and a one size fits all approach to treatment will not work.

New therapeutic strategies to tackle drug resistance and disease relapse are urgently needed for the growing elderly population that will develop myeloma over the next 10 years. More effective treatments will increase quality of life, adding life to years as well as years to life.

Experts indicate that myeloma is projected to rise by 11% in the UK by 2035.

New, enhanced and effective treatments will increase survival rates as well as improve the quality of care for the ageing population.

This is incredibly important as the Northern Ireland ageing population is set to increase and myeloma is a type of blood cancer normally prevalent in people over the age of 60.

Investing over 650,000 this year in local cancer research, Leukaemia and Lymphoma NI is the only charity in Northern Ireland solely dedicated to fighting leukaemia, lymphoma, myeloma and other related conditions.

To help fund MyMATTERS and world class life-enhancing research in Belfast, local people, communities and businesses are urged to get involved.

For more information on how you can help support MyMATTERS, visit llni.co.uk

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Dr Lisa Crawford: The research matters because today's treatment for myeloma might not be as effective tomorrow - Belfast Telegraph

Cell Biology

AXT adds new range of microscopes suited to in situ incubator applications – News-Medical.net

Mar 3 2020

AXT Pty Ltd is pleased to add the Etaluma range of Lumascopes to their life science portfolio. These compact high-resolution inverted microscopes provide live cell imaging capabilities and have been designed to operate inside standard CO2 incubators.

The Etaluma LS720 Lumascope for live cell imaging within an incubator.

The Lumascope range of microscopes is designed specifically for the examination and analysis of live cell morphology, viability and growth. Etaluma has designed the Lumascope from the ground up. By starting with the application, they are able to avoid redundant features seen in traditional inverted microscopes and instead focus on a custom design for a specific need.

Etalumas range of microscopes represents a new concept in digital fluorescence microscopy, which forms the backbone of life science imaging. Capable of produce high-quality multichannel images of both fixed and live samples, they feature zero pixel shift filters, high-resolution camera sensors and modern LED light sources.

With manual or automated options, they accommodate microplates, flasks, dishes, custom labware as well as slides which can be examined in situ inside incubators, biological safety cabinets and other environmentally controlled workstations.

Chris Shumate, CEO of Etaluma said:

We are excited to be working with the AXT team who have an excellent reputation and footprint in the life science microscopy market. We have every confidence that they will grow our market share in Australia and New Zealand."

Etaluma's range of microscopes will make an excellent addition to our product range and support our strategy to bring technologies that enable better live cell imaging to market. Their products are unrivalled on a cost to performance basis. We look forward to showing the capabilities of the Lumascopes to our customers."

Richard Trett, AXTs Managing Director

Etalumas range of live cell imaging microscopes will complement AXTs existing range of cell biology solutions.

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AXT adds new range of microscopes suited to in situ incubator applications - News-Medical.net

Cell Biology

Fate Therapeutics Reports Fourth Quarter 2019 Financial Results and Operational Progress with 2020 Outlook – Yahoo Finance

Reported Initial Clinical Data from FT500 Phase 1 Study in Advanced Solid Tumors, Supporting Safety and Tolerability of Multi-dose Treatment Paradigm for Off-the-shelf, iPSC-derived NK Cells

First Patients Treated with FT516, the First-ever Engineered iPSC-derived Cellular Immunotherapy, for AML and for B-cell Lymphoma in Combination with Rituximab

Initiated Enrollment of First-in-human Clinical Trial of FT596, the First-ever Cellular Immunotherapy Engineered with Three Active Anti-tumor Modalities

Ended Quarter with $261 Million in Cash, Cash Equivalents and Marketable Securities

SAN DIEGO, March 02, 2020 (GLOBE NEWSWIRE) -- Fate Therapeutics, Inc. (FATE), a clinical-stage biopharmaceutical company dedicated to the development of programmed cellular immunotherapies for cancer and immune disorders, today reported business highlights and financial results for the fourth quarter ended December 31, 2019.

In 2019, we made tremendous progress in pioneering the clinical development of off-the-shelf, iPSC-derived cancer immunotherapy. Our FT500 program demonstrated that multiple doses of iPSC-derived NK cells can be delivered off-the-shelf to a patient in a safe manner without patient matching. Additionally, our FT516 program provided initial clinical evidence that engineered iPSC-derived NK cells may confer anti-tumor activity and deliver clinically meaningful benefit to patients. We also showed the unmatched scalability of our proprietary iPSC product platform, having manufactured hundreds of cryopreserved, infusion-ready doses of our iPSC-derived NK cell product candidates at a low cost per dose in our new GMP manufacturing facility, said Scott Wolchko, President and Chief Executive Officer of Fate Therapeutics. In 2020, we look forward to additional clinical data from our FT500 and FT516 programs, and initial clinical data from FT596, our ground-breaking iPSC-derived CAR NK cell product candidate for the treatment of B-cell malignancies designed to overcome many of the limitations inherent in current CAR T-cell immunotherapies. We also expect to begin clinical investigation of our off-the-shelf, iPSC-derived NK cell programs in multiple myeloma with planned IND submissions for FT538, the first-ever CRISPR-edited, iPSC-derived cell therapy, and for FT576, our multi-antigen targeted, CAR-BCMA product candidate. Finally, under our collaboration with Memorial Sloan Kettering, we strive to be the first group in the world to bring off-the-shelf, iPSC-derived CAR T-cell therapy to patients.

Clinical Programs

Preclinical Pipeline

Fourth Quarter 2019 Financial Results

Today's Conference Call and Webcast

The Company will conduct a conference call today, Monday, March 2, 2020 at 5:00 p.m. ET to review financial and operating results for the quarter ended December 31, 2019. In order to participate in the conference call, please dial 877-303-6229 (domestic) or 631-291-4833 (international) and refer to conference ID 9879730. The live webcast can be accessed under "Events & Presentations" in the Investors & Media section of the Company's website at http://www.fatetherapeutics.com. The archived webcast will be available on the Company's website beginning approximately two hours after the event.

About Fate Therapeutics iPSC Product PlatformThe Companys proprietary induced pluripotent stem cell (iPSC) product platform enables mass production of off-the-shelf, engineered, homogeneous cell products that can be administered with multiple doses to deliver more effective pharmacologic activity, including in combination with cycles of other cancer treatments. Human iPSCs possess the unique dual properties of unlimited self-renewal and differentiation potential into all cell types of the body. The Companys first-of-kind approach involves engineering human iPSCs in a one-time genetic modification event and selecting a single engineered iPSC for maintenance as a clonal master iPSC line. Analogous to master cell lines used to manufacture biopharmaceutical drug products such as monoclonal antibodies, clonal master iPSC lines are a renewable source for manufacturing cell therapy products which are well-defined and uniform in composition, can be mass produced at significant scale in a cost-effective manner, and can be delivered off-the-shelf for patient treatment. As a result, the Companys platform is uniquely capable of overcoming numerous limitations associated with the production of cell therapies using patient- or donor-sourced cells, which is logistically complex and expensive and is subject to batch-to-batch and cell-to-cell variability that can affect clinical safety and efficacy. Fate Therapeutics iPSC product platform is supported by an intellectual property portfolio of over 300 issued patents and 150 pending patent applications.

Story continues

About FT500

FT500 is an investigational, universal, off-the-shelf natural killer (NK) cell cancer immunotherapy derived from a clonal master induced pluripotent stem cell (iPSC) line. The product candidate is being investigated in an open-label, multi-dose Phase 1 clinical trial for the treatment of advanced solid tumors (NCT03841110). The study is designed to assess the safety and tolerability of three once-weekly doses of FT500 as a monotherapy and in combination with one of three FDA-approved immune checkpoint inhibitor (ICI) therapies nivolumab, pembrolizumab or atezolizumab in patients that have failed prior ICI therapy. Despite the clinical benefit conferred by approved ICI therapy against a variety of tumor types, these therapies are not curative and, in most cases, patients either fail to respond or their disease progresses on these agents. One common mechanism of resistance to ICI therapy is associated with loss-of-function mutations in genes critical for antigen presentation. A potential strategy to overcome resistance is through the administration of allogeneic NK cells, which have the inherent capability to recognize and directly kill tumor cells with these mutations.

About FT516

FT516 is an investigational, universal, off-the-shelf natural killer (NK) cell cancer immunotherapy derived from a clonal master induced pluripotent stem cell (iPSC) line engineered to express a novel high-affinity 158V, non-cleavable CD16 (hnCD16) Fc receptor, which has been modified to prevent its down-regulation and to enhance its binding to tumor-targeting antibodies. CD16 mediates antibody-dependent cellular cytotoxicity (ADCC), a potent anti-tumor mechanism by which NK cells recognize, bind and kill antibody-coated cancer cells. ADCC is dependent on NK cells maintaining stable and effective expression of CD16, which has been shown to undergo considerable down-regulation in cancer patients. In addition, CD16 occurs in two variants, 158V or 158F, that elicit high or low binding affinity, respectively, to the Fc domain of IgG1 antibodies. Numerous clinical studies with FDA-approved tumor-targeting antibodies, including rituximab, trastuzumab and cetuximab, have demonstrated that patients homozygous for the 158V variant, which is present in only about 15% of patients, have improved clinical outcomes. FT516 is being investigated in an open-label, multi-dose Phase 1 clinical trial as a monotherapy for the treatment of acute myeloid leukemia and in combination with CD20-directed monoclonal antibodies for the treatment of advanced B-cell lymphoma (NCT04023071). Additionally, the FDA has allowed investigation of FT516 in an open-label, multi-dose Phase 1 clinical trial in combination with monoclonal antibody therapy, including PDL1-, PD1-, EGFR- and HER2-targeting therapeutic antibodies, across a broad range of solid tumors.

About FT596FT596 is an investigational, universal, off-the-shelf natural killer (NK) cell cancer immunotherapy derived from a clonal master induced pluripotent stem cell (iPSC) line engineered with three anti-tumor functional modalities: a proprietary chimeric antigen receptor (CAR) optimized for NK cell biology, which contains a NKG2D transmembrane domain, a 2B4 co-stimulatory domain and a CD3-zeta signaling domain, that targets B-cell antigen CD19; a novel high-affinity 158V, non-cleavable CD16 (hnCD16) Fc receptor, which has been modified to prevent its down-regulation and to enhance its binding to tumor-targeting antibodies; and an IL-15 receptor fusion (IL-15RF) that promotes enhanced NK cell activity. In preclinical studies of FT596, the Company has demonstrated that dual activation of the CAR19 and hnCD16 targeting receptors, in combination with IL-15RF signaling, convey synergistic anti-tumor activity. Increased degranulation and cytokine release were observed upon dual receptor activation in lymphoma cancer cells as compared to activation of each receptor alone, indicating that multi-antigen engagement may elicit a deeper and more durable response. Additionally, in a humanized mouse model of lymphoma, FT596 in combination with the anti-CD20 monoclonal antibody rituximab showed enhanced killing of tumor cells in vivo as compared to rituximab alone. FT596 is being investigated in an open-label Phase 1 clinical trial as a monotherapy, and in combination with rituximab, for the treatment of advanced B-cell lymphoma and in combination with obinutuzumab for the treatment of chronic lymphocytic leukemia (NCT04245722).

About Fate Therapeutics, Inc.Fate Therapeutics is a clinical-stage biopharmaceutical company dedicated to the development of first-in-class cellular immunotherapies for cancer and immune disorders. The Company has established a leadership position in the clinical development and manufacture of universal, off-the-shelf cell products using its proprietary induced pluripotent stem cell (iPSC) product platform. The Companys immuno-oncology product candidates include natural killer (NK) cell and T-cell cancer immunotherapies, which are designed to synergize with well-established cancer therapies, including immune checkpoint inhibitors and monoclonal antibodies, and to target tumor-associated antigens with chimeric antigen receptors (CARs). The Companys immuno-regulatory product candidates include ProTmune, a pharmacologically modulated, donor cell graft that is currently being evaluated in a Phase 2 clinical trial for the prevention of graft-versus-host disease, and a myeloid-derived suppressor cell immunotherapy for promoting immune tolerance in patients with immune disorders. Fate Therapeutics is headquartered in San Diego, CA. For more information, please visit http://www.fatetherapeutics.com.

Forward-Looking Statements

This release contains "forward-looking statements" within the meaning of the Private Securities Litigation Reform Act of 1995 including statements regarding the Companys results of operations, financial condition and sufficiency of its cash and cash equivalents to fund its operations, as well as statements regarding the advancement of and plans related to its product candidates, clinical studies and preclinical research and development programs, the Companys progress, plans and timelines for the manufacture and clinical investigation of its product candidates, the timing for the Companys receipt of data from its clinical trials and preclinical studies, the Companys development and regulatory strategy, and the therapeutic and market potential of the Companys product candidates. These and any other forward-looking statements in this release are based on management's current expectations of future events and are subject to a number of risks and uncertainties that could cause actual results to differ materially and adversely from those set forth in or implied by such forward-looking statements. These risks and uncertainties include, but are not limited to, the risk that results observed in prior studies of the Companys product candidates, including preclinical studies and clinical trials, will not be observed in ongoing or future studies involving these product candidates, the risk of a delay or difficulties in the manufacturing of the Companys product candidates or in the initiation of, or enrollment of patients in, any clinical studies, the risk that the Company may cease or delay preclinical or clinical development of any of its product candidates for a variety of reasons (including requirements that may be imposed by regulatory authorities on the initiation or conduct of clinical trials or to support regulatory approval, difficulties or delays in patient enrollment in current and planned clinical trials, difficulties in manufacturing or supplying the Companys product candidates for clinical testing, and any adverse events or other negative results that may be observed during preclinical or clinical development), and the risk that the Companys expenditures may exceed current expectations for a variety of reasons. For a discussion of other risks and uncertainties, and other important factors, any of which could cause the Companys actual results to differ from those contained in the forward-looking statements, see the risks and uncertainties detailed in the Companys periodic filings with the Securities and Exchange Commission, including but not limited to the Companys most recently filed periodic report, and from time to time in the Companys press releases and other investor communications.Fate Therapeutics is providing the information in this release as of this date and does not undertake any obligation to update any forward-looking statements contained in this release as a result of new information, future events or otherwise.

Availability of Other Information about Fate Therapeutics, Inc.

Investors and others should note that the Company routinely communicates with investors and the public using its website (www.fatetherapeutics.com) and its investor relations website (ir.fatetherapeutics.com) including, without limitation, through the posting of investor presentations, SEC filings, press releases, public conference calls and webcasts on these websites. The information posted on these websites could be deemed to be material information. As a result, investors, the media, and others interested in Fate Therapeutics are encouraged to review this information on a regular basis. The contents of the Companys website, or any other website that may be accessed from the Companys website, shall not be deemed incorporated by reference in any filing under the Securities Act of 1933, as amended.

Condensed Consolidated Statements of Operations and Comprehensive Loss(in thousands, except share and per share data)(unaudited)

Condensed Consolidated Balance Sheets(in thousands)(unaudited)

Contact:Christina TartagliaStern Investor Relations, Inc.212.362.1200christina@sternir.com

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Fate Therapeutics Reports Fourth Quarter 2019 Financial Results and Operational Progress with 2020 Outlook - Yahoo Finance

Neuroscience

Neuroscience: Overview, history, major branches

Neuroscientists focus on the brain and its impact on behavior and cognitive functions, or how people think.

They also investigate what happens to the nervous system when people have neurological, psychiatric, and neurodevelopmental disorders.

A neuroscientist can specialize in a wide range of fields, from neuroanatomy to neuropsychology. Research in this field can improve our understanding of both the brain and the body, how they work, and the health issues that affect them.

Neuroscience is an interdisciplinary science that works closely with other disciplines, such as mathematics, linguistics, engineering, computer science, chemistry, philosophy, psychology, and medicine.

Neuroscientists study the cellular, functional, behavioral, evolutionary, computational, molecular, cellular, and medical aspects of the nervous system. There are various fields that focus on different aspects, but they often overlap.

Researchers might look into brain activity in people with ailments such as Alzheimers disease. Tools used include MRI scans and computerized 3-D models. They may do experiments using cell and tissue samples.

The findings may lead to the development of new medications. Some neuroscientists are involved in treating patients.

Neuroscience affects many, if not all, human functions, but it also contributes to a better understanding of a wide range of common conditions.

These include:

A greater understanding of neurological factors can help in developing medications and other strategies to treat and prevent these and many other health issues.

The ancient Egyptians thought the seat of intelligence was in the heart. Because of this belief, during the mummification process, they would remove the brain but leave the heart in the body.

The ancient Greeks were among the first people to study the brain. They attempted to understand the role of the brain and how it worked and to explain neural disorders.

According to an article in Scientific American, Aristotle, the Greek philosopher, had a theory that the brain was a blood-cooling mechanism.

Pierre Paul Broca (1824-1880) was a French physician, surgeon, and anatomist. He worked with patients who had brain damage. He concluded that different regions in the brain were involved in specific functions.

The part of the brain known as Brocas area is responsible for some speech and other functions. Damage to this area during a stroke can lead to Brocas aphasia, when a person can no longer produce accurate or coherent speech.

In the 19th century, von Hemholtz, a German physician and physicist, measured the speed at which nerve cells produced electrical impulses.

During 1873, Gamillo Golgi, an Italian physician, pathologist, and scientist, used silver chromate salt to see what neurons looked like.

Early in the 20th century, Santiago Ramn y Cajal, a Spanish pathologist, histologist, and neuroscientist, hypothesized that the neurons are independent nerve cell units.

In 1906, Golgi and Cajal jointly received the Nobel Prize in Physiology or Medicine for their work and categorization of neurons in the brain.

Since the 1950s, research and practice in modern neurology have made great strides, leading to developments in the treatment of stroke, cardiovascular disease, multiple sclerosis (MS) and other conditions.

Scientific developments have enabled neuroscientists to study the nervous systems structure, functions, development, abnormalities, and ways it can be altered.

Some major branches of neuroscience can be broadly categorized in the following disciplines:

Affective neuroscience: Research looks at how neurons behave in relation to emotions.

Behavioral neuroscience: This is the study of how the brain affects behavior.

Clinical neuroscience: Medical specialists, such as neurologists and psychiatrists, look at the disorders of the nervous system from basic neuroscience findings to find ways to treat and prevent them. They also look for ways to rehabilitate those who have undergone neurological damage. Clinical neuroscientists consider mental illnesses as brain disorders.

Cognitive neuroscience: This looks at how the brain forms and controls thoughts, and the neural factors that underlie those processes. During research, scientists measure brain activity while people carry out tasks. This field combines neuroscience with the cognitive sciences of psychology and psychiatry.

Computational neuroscience: Scientists try to understand how brains compute. They use computers to simulate and model brain functions, and applying techniques from mathematics, physics, and other computational fields to study brain function.

Cultural neuroscience: This field looks at the interaction between cultural factors and are genomic, neural, and psychological processes. It is a new discipline that may help explain variations in health measures between different populations. Findings may also help scientists to avoid cultural bias when designing experiments.

Developmental neuroscience: This looks at how the brain and the nervous system grow and change, from conception through adulthood. Information gathered helps scientists understand more about how the neurological systems develop and evolve. It enables them to describe and understand a range of developmental disorders. It also offers clues about how and when neurological tissues regenerate.

Molecular and cellular neuroscience: Scientists look at the role of individual molecules, genes, and proteins in the functioning of nerves and the nervous system at a molecular and cellular level.

Neuroengineering: Researchers use engineering techniques to better understand, replace, repair, or improve neural systems.

Neuroimaging: This is a branch of medical imaging that concentrates on the brain. Neuroimaging is used to diagnose disease and assess the health of the brain. It can also be useful in the study of the brain, how it works, and how different activities affect the brain.

Neuroinformatics: This field involves collaboration between computer scientists and neuroscientists. Experts develop effective ways to collect, analyze, share, and publish data.

Neurolinguistics: Specialists investigate how the brain enables us to acquire, store, understand, and express language. It helps speech therapists develop strategies to help children with speech difficulties or people who wish to regain their speech after, for example, a stroke.

Neurophysiology: This looks at how the brain and its functions relate to different parts of the body, and the role of the nervous system, from the subcellular level to whole organs. It helps scientists understand how human thought works and provides insight into disorders relating to the nervous system.

Neuroscience is a new and important field with implications for every aspect of how people move, think, and behave. In 2007, it was estimated that abnormal neurological conditions were thought to affect up to 1 billion people worldwide.

People who join this profession need to have an interest in science and math. Most neuroscientists start out by completing a bachelors degree in neuroscience before then pursuing a PhD.

Those who wish to do clinical work and treat patients must also train first as a Medical Doctor (MD) and complete a medical residency. They must also pass the United States Medical Licensing Examination.

They may then take a postdoctoral fellowship, for example, in a lab, to get further training before applying for a job.

According to the United States Bureau of Labor Statistics, the median annual salary of a medical scientist, including neuroscientists, in 2016 was $80,530. Salaries ranged from a low of $57,000 to a high of $116,840.

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Neuroscience: Overview, history, major branches

Neuroscience

Duck flies to Capitol Hill as one of top undergrad researchers in U.S. – AroundtheO

Research matters, and scientists can do more to make their important work accessible to the public. Those are the messages UO biology major Rennie Kendrick takes to Congress this April.

The Stamps Scholar from Portland was chosen among 60 of the nations top undergraduate researchers to participate in Posters on the Hill, a Washington, D.C. event showcasing innovative student work and demonstrating the value of federal investments in undergraduate research.

Its exciting, said the Clark Honors College senior. It will be great for members of Congress to see whats happening at the undergraduate level. Its important to fund and encourage this research, because discoveries have been made by undergraduates important discoveries.

Sponsored by the Council on Undergraduate Research, the annual event highlights student research for members of Congress, congressional staffers and federal government officials. A national panel of experts in their respective fields selects the finalists, and Kendrick is the second UO student to attend since the university joined the council in 2014.

The Undergraduate Research Opportunity Program and Vice President for Research and Innovation are helping fund her trip.

Kendrick will be presenting a poster on memory and innovative thinking, the subject of her honors thesis. Her plans include meeting with members of Oregons congressional delegation. Assistant professor Dasa Zeithamova-Demircan is helping Kendrick with the project, part of their work in the UOs Brain and Memory Lab.

The research is novel and complex. But Kendrick is planning a straightforward presentation.

There seems to be a growing misunderstanding about science for the general public, as well as the politicians who make decisions and allocate resources, she said. As scientists, we need to be able to communicate.

Kendricks fascination with science started early. After learning about birds in the third grade, she wanted to be an ornithologist. For Christmas, shed ask for research-related gifts, such as her treasured weather measurement kit.

Kendrick first learned about neuroscience while preparing for the eighth-grade science fair. She started her project on memory the summer before school had even started, submitting her idea to the Institutional Review Board so she could conduct experiments with people.

When youre an eighth-grader, you cant do much with human subjects, she recalled. But I got my approval. And I checked out every neuroscience book they had at the library. I just could not get enough of it. I knew about psychology and biology, then they fused together in my mind. I realized there was an entire biology to how we memorize things and have memories. That blew my mind. From then on, I have wanted to be a neuroscientist.

Kendrick excelled at Portlands Grant High School, where she ran track and cross country, participated in the state championship cross country team, was part of the 2016 state girls 6A champion 4x400 meter relay squad and qualified for state in the 1,500- and 3,000-meter events. She also served as managing editor of Grant Magazine, participated in Grants award-winning Constitution Team which has competed in the We the People national finals sang in the Royal Blues chamber choir, and volunteered in a behavioral neuroscience lab at Oregon Health and Science University-Portland Veterans Affairs Medical Center, where she was a 2017 Portland Veterans Affairs research fellow.

She chose the UO because she was offered a Stamps Scholarship, the universitys most prestigious and generous scholarship. Granted by the UO and the Strive Foundation, it is awarded to just 10 incoming freshmen each year, five residents and five nonresidents.

Kendrick joined the UOs track and cross-country teams as a walk-on during her first year and continued until injuries ongoing stress fractures that sporadically kept her from competing forced her to step down this year.

Those were tough lessons, she said. You put so much time into something and tomorrow you could be on crutches. Thats a good analogy for research, because you can put years into a project and find that its a null result. You have to be OK with saddling up again and putting effort into something, even if you know it could all go wrong at the drop of a hat. Its a nonlinear progression sometimes, but you have to keep in mind you are still making progress.

Over the years, Kendrick has been able to participate in research opportunities and make the most of her undergraduate experience thanks to support from UO organizations such as the Undergraduate Research Opportunity Program, the Office of the Vice President for Research and Innovation, the Center for Undergraduate Research and Engagement and the Office of Distinguished Scholarships.

Kendrick and another student are collaborating with professor Alice Barkan on a genetics research project and Kendrick was a 2019 Peter ODay Research Fellow. She currently works in the UOs Brain and Memory Lab, as well as the McCormick Lab at the Institute of Neuroscience. She also teaches a supplemental instruction course for business calculus and tutors students in biology, math and chemistry.

After graduating this spring, Kendrick heads to the University of British Columbia, where shell be working in a lab studying mechanisms of fear memory formation. She hopes to someday join the faculty at a college or university, combining her top three interests: research, teaching and writing.

By Ed Dorsch, University Communications

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Duck flies to Capitol Hill as one of top undergrad researchers in U.S. - AroundtheO

Neuroscience

Too Much Excitation: The Neural Basis of Sensory Hypersensitivity – Technology Networks

Many people with autism spectrum disorders are highly sensitive to light, noise, and other sensory input. A new study in mice reveals a neural circuit that appears to underlie this hypersensitivity, offering a possible strategy for developing new treatments.MIT and Brown University neuroscientists found that mice lacking a protein called Shank3, which has been previously linked with autism, were more sensitive to a touch on their whiskers than genetically normal mice. These Shank3-deficient mice also had overactive excitatory neurons in a region of the brain called the somatosensory cortex, which the researchers believe accounts for their over-reactivity.

There are currently no treatments for sensory hypersensitivity, but the researchers believe that uncovering the cellular basis of this sensitivity may help scientists to develop potential treatments.

We hope our studies can point us to the right direction for the next generation of treatment development, says Guoping Feng, the James W. and Patricia Poitras Professor of Neuroscience at MIT and a member of MITs McGovern Institute for Brain Research.

Feng and Christopher Moore, a professor of neuroscience at Brown University, are the senior authors of the paper. McGovern Institute research scientist Qian Chen and Brown postdoc Christopher Deister are the lead authors of the study.Too much excitationThe Shank3 protein is important for the function of synapses connections that allow neurons to communicate with each other. Feng has previously shown that mice lacking the Shank3 gene display many traits associated with autism, including avoidance of social interaction, and compulsive, repetitive behavior.

In the new study, Feng and his colleagues set out to study whether these mice also show sensory hypersensitivity. For mice, one of the most important sources of sensory input is the whiskers, which help them to navigate and to maintain their balance, among other functions.

The researchers developed a way to measure the mices sensitivity to slight deflections of their whiskers, and then trained the mutant Shank3 mice and normal (wild-type) mice to display behaviors that signaled when they felt a touch to their whiskers. They found that mice that were missing Shank3 accurately reported very slight deflections that were not noticed by the normal mice.

They are very sensitive to weak sensory input, which barely can be detected by wild-type mice, Feng says. That is a direct indication that they have sensory over-reactivity.

Once they had established that the mutant mice experienced sensory hypersensitivity, the researchers set out to analyze the underlying neural activity. To do that, they used an imaging technique that can measure calcium levels, which indicate neural activity, in specific cell types.

They found that when the mices whiskers were touched, excitatory neurons in the somatosensory cortex were overactive. This was somewhat surprising because when Shank3 is missing, synaptic activity should drop. That led the researchers to hypothesize that the root of the problem was low levels of Shank3 in the inhibitory neurons that normally turn down the activity of excitatory neurons. Under that hypothesis, diminishing those inhibitory neurons activity would allow excitatory neurons to go unchecked, leading to sensory hypersensitivity.

To test this idea, the researchers genetically engineered mice so that they could turn off Shank3 expression exclusively in inhibitory neurons of the somatosensory cortex. As they had suspected, they found that in these mice, excitatory neurons were overactive, even though those neurons had normal levels of Shank3.

If you only delete Shank3 in the inhibitory neurons in the somatosensory cortex, and the rest of the brain and the body is normal, you see a similar phenomenon where you have hyperactive excitatory neurons and increased sensory sensitivity in these mice, Feng says.Reversing hypersensitivityThe results suggest that reestablishing normal levels of neuron activity could reverse this kind of hypersensitivity, Feng says.

That gives us a cellular target for how in the future we could potentially modulate the inhibitory neuron activity level, which might be beneficial to correct this sensory abnormality, he says.

Many other studies in mice have linked defects in inhibitory neurons to neurological disorders, including Fragile X syndrome and Rett syndrome, as well as autism.

Our study is one of several that provide a direct and causative link between inhibitory defects and sensory abnormality, in this model at least, Feng says. It provides further evidence to support inhibitory neuron defects as one of the key mechanisms in models of autism spectrum disorders.

He now plans to study the timing of when these impairments arise during an animals development, which could help to guide the development of possible treatments. There are existing drugs that can turn down excitatory neurons, but these drugs have a sedative effect if used throughout the brain, so more targeted treatments could be a better option, Feng says.

We dont have a clear target yet, but we have a clear cellular phenomenon to help guide us, he says. We are still far away from developing a treatment, but were happy that we have identified defects that point in which direction we should go.ReferenceThijssen et al. (2020) Diagnostic value of plasma phosphorylated tau181 in Alzheimers disease and frontotemporal lobar degeneration. Nature Medicine. DOI: https://doi.org/10.1038/s41591-020-0762-2

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Neuroscience

Immersion Neuroscience Reveals What Folks Really Love with a Little Help From PR Mavens at Bob Gold & Associates – Broadcasting & Cable

Immersion Neuroscience, the worlds most advanced predictive software company unlocking neuroscience to measure what people love, has selected Bob Gold & Associates, a nationally recognized boutique public relations and marketing agency, as its public relations agency of record to help launch its new cloud-based audience prediction platform. The Immersion platform helps companies identify, quantify and predict what live or taped events, training, and entertainment motivate audiences to action so that companies can significantly improve their ability to connect with consumers and increase ROI.

"With more than two decades of research, weve developed an entirely new way to understand how the brain values content, and how to predict what content will drive actions with high accuracy," said Paul J. Zak, Ph.D., Founder of Immersion. We coined the term immersion to denote a measurable neurologic state, and today, Immersion offers an easy to use and powerful tool that allows any company to analyze content and predict how audiences will respond. And it doesn't take a neuroscientist to know that Bob Gold & Associates, with their unparalleled expertise and a proven track record, is the right company to help get our story told.

Immersions proprietary solution and software is the world's most accurate way to measure the brain's unconscious emotional responses to virtually any type of content whether its video, music, live events, training, educational resources and more. Developed by distinguished research scientists, Immersions simple to use and scalable predictive SaaS platform democratizes neuroscience so that anyone can measure what people love at scale.

Life doesnt happen inside a lab, Zak added. Until now, companies could only measure what people in the real world said they liked not how their brains were truly valuing an experience. Immersion is able to measure what folks truly, viscerally love, anywhere, anytime and in real time.

The Immersion platform infers when the brain values an experience in real-time with a small wearable sensor that can be used anywhere. Unlike traditional neuroscience technologies that use expensive, immobile and delicate lab equipment and require highly trained professionals to collect and analyze the data, Immersion takes multiple measures of brain activity and puts them into an easy to understand 0-10 measure collected every second. Immersions clients use the platform anywhere, anytime and at scale, empowering companies to predict future behavior and market outcomes with 90% or better accuracy.

"Immersion is a revolutionary company. With their unique cloud-based solution, measuring brain activity is no longer confined to a laboratory with expensive instruments," said Bob Gold, CEO of Bob Gold & Associates. "There are billions of dollars being spent in original programming, half of which never connects with audiences. Today for every network and streaming service, hits are everything. Immersion has proven, with peer-reviewed publications and blinded studies, its ability to identify hit shows, movies, songs and so much more.

Because its built in the cloud, and not in a lab, Immersions software is portable and effortlessly scalable, enabling clients to leverage the power of neuroscience on the fly, anywhere in the world. And while other companies can take months to compile results, Immersions software provides an immediate assessment, unlocking the power of neuroscience for anyone without the need for extensive training.

In one study, for example, two measures from the platform peak immersion, and frustration were enough to predict the top-rated unscripted TV shows with 84% accuracy.

Many leading global brands are already utilizing Immersion in countless ways. This includes shaping content and business decisions by predicting hit TV shows and movies, chart-topping songs, sales bumps, TV ratings, viral content, what has the highest impact at live events, and even HR and corporate training, all by accurately identifying what is truly valued by audience members brains.

For more about Bob Gold & Associates, visit http://www.bobgoldpr.com.

To learn more about Immersion, visit http://www.getimmersion.com.

For more information, contact:

Bob Gold & Associates

310-320-2010

immersion@bobgoldpr.com

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Immersion Neuroscience Reveals What Folks Really Love with a Little Help From PR Mavens at Bob Gold & Associates - Broadcasting & Cable