Gladstone Institutes unveils redesigned website to bring biomedical research closer to the public. 4 hours ago 5 PROTECT YOUR DNA WITH QUANTUM TECHNOLOGY Gladstone Institutes, the independent nonprofit biomedical research organization based in San Francisco, has announced the launch of a newly redesigned website at gladstone.org. The overhaul is intended to serve as a modernized, accessible digital gateway to the institute's work, bringing its biomedical research closer to three audiences at once: the general public, the scientific community, and the key partners who help translate laboratory discoveries into new therapies. Rather than a cosmetic refresh, the redesign reorganizes the entire online experience around the way Gladstone actually conducts science, foregrounding its disease areas and enabling technologies as the primary routes through which visitors can explore the institute's output. The new platform was developed in partnership with KNI (Kurt Noble, Inc.), an award-winning full-service digital and design agency based in San Francisco. According to the announcement, the collaboration reflects Gladstone's broader commitment to driving innovation and leveraging science to overcome disease. The resulting digital experience is built on a clean, intuitive architecture with interactive elements designed to streamline how visitors navigate the institute's discoveries. For an organization whose research spans cardiology, neurology, infectious diseases, and immunology for cancer and autoimmune conditions, that architectural clarity matters: the site functions as a map of a large, multidisciplinary research enterprise, guiding users from broad disease categories down to individual researchers, publications, and scientific topics. A central highlight of the redesigned site is its clear emphasis on Gladstone's core disease and technology areas. This structure is intended to make complex scientific concepts and multidisciplinary research more inviting for patients, the public, and the wider scientific community. Instead of forcing lay readers to decode laboratory jargon or institutional department names, the site invites them to begin with the disease or health challenge they care about and then discover the tools, model systems, and technologies that underpin progress against it. The technology section, in turn, highlights the platforms that enable breakthroughs and accelerate their translation into new therapies, giving visitors a view of the methodological engine room behind the institute's disease-focused mission. The redesign also introduces a revamped News and Insights page, conceived as a central hub for the latest developments, breakthroughs, and stories emerging from Gladstone. Complementing it is an enhanced search function intended to ensure seamless discovery of researchers, publications, and scientific topics across the site. In practical terms, this means that a journalist looking for an expert, a patient seeking plain-language explanations of a disease area, a prospective collaborator scanning recent publications, or a donor evaluating the institute's portfolio can all arrive at the same domain and find tailored paths to the information they need. The unified search and reorganized content architecture are the technical backbone of that flexibility. Anna-Marie Rooney, vice president of communications at Gladstone, framed the redesign as an extension of the institute's scientific identity. "Our goal with this redesign was to create an online experience as innovative and forward-thinking as the research taking place inside our labs every day," she said in the announcement. "By reorganizing our site around disease areas and implementing enhanced design and search elements, we're opening our doors wider to the public, making our science accessible and engaging for everyone who visits." The statement underscores a deliberate communications strategy: treating the website not as a static brochure but as an active interface between working scientists and the audiences who fund, follow, and ultimately benefit from their work. The new site also serves as the showcase for Gladstone's updated and refined brand. "As users explore our new website, they will also uncover Gladstone's updated and refined brand," Rooney said. "Drawing inspiration from the complexity of human biology and the hard work of our scientists, our brand showcases unique microscopy images, intricate textures and shapes, and memorable photographs that will take our audience on a tour of our research and our culture." The visual language, built from actual scientific imagery such as microscopy, ties the institute's aesthetic identity directly to its research practice, so that the look and feel of the site communicates the same mechanistic curiosity that drives the laboratories themselves. Understanding the significance of the redesign requires understanding the scale and character of the organization behind it. Gladstone is dedicated to disease-focused discovery research, with a workforce of more than 600 biologists, chemists, engineers, and data scientists who bring a deep mechanistic understanding of how the human body works and what goes wrong in disease. That mechanistic orientation, the effort to explain disease at the level of molecules, cells, and systems rather than symptoms alone, is what allows discoveries in one domain to inform another, and it is the logic the new website's disease-and-technology structure is designed to mirror. Artificial intelligence and data science occupy a distinctive position in that enterprise. According to the institute, its expertise in AI and data science is integrated into all research areas, accelerating discoveries across cardiology, neurology, infectious diseases, and immunology for cancer and autoimmune diseases. This cross-cutting computational capability is one reason a single institutional website can plausibly be organized around disease areas: the same data-driven methods and technological platforms recur across therapeutic domains, connecting researchers who might otherwise work in parallel silos. The redesigned technology section gives this infrastructure a public face, presenting the tools and approaches that speed the path from fundamental insight to therapeutic candidate. The institute's research scope, as described in the announcement, spans cardiovascular diseases, neurological conditions, immunotherapy for cancer and autoimmune diseases, and infectious diseases. By pairing these disease focuses with explicit attention to enabling technologies, the new website signals how modern biomedical research is actually organized: breakthroughs increasingly emerge from the intersection of biology with engineering, computation, and large-scale data analysis. For visitors, the site makes those intersections visible, showing not only what Gladstone studies but how its scientists study it, and how discoveries in one area can be translated into new approaches for treating or preventing disease in another. With the launch, Gladstone joins a growing number of research institutions treating their digital presence as core scientific infrastructure rather than communications afterthought. The redesigned gladstone.org, with its disease-centered navigation, technology showcases, revamped News and Insights hub, improved search, and biology-inspired brand identity, is now live and open to the public. For an organization that describes its mission as steering toward a new world of cures and prevention for currently intractable diseases, the new platform represents an invitation: a public-facing window into the laboratories where more than 600 scientists are working to understand, treat, and ultimately overcome some of medicine's most persistent challenges. Subject of Research: Redesign of the Gladstone Institutes website to improve public access to biomedical research Article Title: Gladstone Institutes launches redesigned website, bringing cutting-edge bomedical research into focus Article References: Gladstone Institutes launches redesigned website, bringing cutting-edge bomedical research into focus. (n.d.). Original publication DOI: Not provided Keywords: Gladstone Institutes, website redesign, biomedical research, digital platform, artificial intelligence, data science, cardiovascular disease, neurology, infectious diseases, immunology, science communication, San Francisco * homepage * biology * Gladstone Institutes unveils redesigned website to bring biomedical research closer to the public.

New toolkit turns macrophages into better cancer fighters. A team of scientists from Gladstone and UCSF developed a new method to genetically edit myeloid cells, immune cells that act as the body's first responders. For more than a decade, scientists have used CRISPR gene editing to study the DNA sequences that control human T cells and to reprogram their functions, including massive efforts to develop improved living cancer drugs known as CAR-T therapies. But T cells are only one branch of the human immune system. Myeloid cells - a group of immune cells that include monocytes, macrophages, and dendritic cells - have remained largely off-limits to this kind of engineering, even though these cells are often the first responders to infection, injury, and tumors. Now, researchers at Gladstone Institutes and UC San Francisco (UCSF), along with collaborators at several other institutions, have developed a toolkit to deploy CRISPR in myeloid cells. Their approach, described in Nature Biotechnology, uses virus-like particles - empty viral shells repurposed as delivery vehicles - to carry gene-editing machinery into the immune cells. "We had a realization that we weren't really tapping into this whole other arm of the immune system to help fight some of the most difficult diseases out there," says Julia Carnevale, MD, an affiliate investigator at Gladstone, an assistant professor of hematology and oncology at UCSF, and co-senior author of the study. "We wanted to unlock the power of these other cells." Carnevale and her colleagues identified a gene that acts as a brake on inflammation - removing this gene could help cells be better at fighting cancer cells. Using the new toolkit, the team screened thousands of genes inside living human macrophages and identified a gene that acts as a brake on inflammation. Removing that brake from re-engineered macrophages made the cells dramatically better at fighting cancer cells. "We now have a whole toolbox of CRISPR perturbations we can make in myeloid cells, which took us a decade to build up in T cells," adds Alex Marson, MD, PhD, director of the Gladstone-UCSF Institute of Genomic Immunology and co-senior author of the study. "Beyond our initial observations with these tools in macrophages, this is an important technology resource for the field." A better delivery system. Myeloid cells have been notoriously difficult to engineer. The standard method for getting CRISPR gene editing machinery into cells, called electroporation, uses a jolt of electricity to poke temporary holes in a cell's outer membrane. It works well in T cells, but in monocytes, macrophages, and dendritic cells, it renders them unresponsive - likely because the cells are so sensitive to stress as a function of their job. "The old way of editing works well to edit genes, but the surprise was that, for myeloid cells, it left the cells dysfunctional," Marson says. As they searched for genes that control inflammation in myeloid cells, the research team co-led by Marson combined different technologies to create a new system that allowed them to test thousands of genes at once. In the new work, Marson and Carnevale's labs turned to virus-like particles that can carry proteins, including gene editing machinery, into a cell through their infection mechanism. Beyond simply deleting genes, the team showed they could use the new system to make targeted single-letter DNA changes (called base editing), silence genes without deleting their sequences, and even insert large new stretches of DNA. "This system can allow us achieve high editing efficiency, and also use the same platform for base editing and epigenetic silencing," says Hyuncheol Jung, PhD, co-first author of the study and a postdoctoral scholar in the Carnevale and Marson labs. "So instead of building a new delivery method for every kind of edit we want to make, we have one flexible toolkit that can do all of them in these cells." An inflammatory brake. To search in an unbiased way for genes that control inflammation in myeloid cells, the team needed to be able to test thousands of genes at once and trace which gene had been disabled in which cell. That required a second delivery tool: a modified virus that could both carry genetic instructions into each cell and permanently record which instruction it had received. That's where the researchers hit a new obstacle. Myeloid cells carry a built-in defense that normally blocks viruses from writing anything into their DNA. To overcome this, the team borrowed a trick from HIV; they used a protein that disables the immune defense. Paired with their virus-like-particle delivery, this combined system, called SLICeVLP, let them test the effect of removing thousands of different genes, one at a time, from living macrophages. The two first authors of the study, Hyuncheol Jung (left) and Pascal Devant (right), helped develop a toolkit that can now be used by many scientists studying myeloid cell biology in the lab. Running multiple separate screens, the researchers looked for genes that control different facets of immune activation in macrophages. The same gene rose to the top across multiple screens: TNFAIP3, which encodes a protein called A20. A20 was already known from mouse studies to act as a brake that keeps macrophages from becoming overly inflammatory, but there had been no way to target that brake directly in human macrophages. Now, for the first time, the researchers had an easy way to test whether disabling A20 could be useful therapeutically. They began with CAR-macrophages - macrophages that have been engineered with cancer-targeting receptors, similar in concept to the CAR-T cells. Then, they used their system to remove the TNFAIP3 gene encoding A20. The edited cells became more inflammatory, significantly better at killing cancer cells, and more resistant to the immune-suppressing signals that tumors produce to shut down the immune system. "Our screens helped us prioritize certain genes over others as potential targets," says Pascal Devant, PhD, co-first author of the study and a postdoctoral scholar in Marson's lab. "The question is always: what's a gene you'd actually want to target in a therapy?" Toward the future. The new myeloid gene editing system isn't yet ready to test in human therapeutics - the scientists found some small unintended genetic changes in cells edited with the base editing machinery, for instance. But they see the tool as the beginning of a new era of exploring myeloid cell biology in the lab. "We've had a lot of interest from people studying anything from neurobiology to atherosclerosis of the cardiovascular system," Marson says. "This toolset can help a lot of scientists probe these cells in whole new ways, in the context of whatever disease they're studying, from cancer to autoinflammatory and infectious diseases." The researchers are continuing to fine-tune the editing toolset, as well as scale it up to make more genetic edits and in more myeloid cell types. "We're excited to see what people do with this technology," Carnevale says. For Media Julie Langelier Associate Director, Communications 415.734.5000 Email About the Study The paper, "Virus-like particles enable targeted gene engineering and pooled CRISPR screening in primary human myeloid cells," was published in the journal Nature Biotechnology on August 17, 2026. In addition to Carnevale, Marson, Devant, and Jung, authors are Mineto Ota, Emma Dann, Ronghui Zhu, Chandrima Modak, Ana Vasquez-Ibarra, Zachary Steinhart, Jae Hyun J. Lee, Vincent Allain, Brian R. Shy, Justin Eyquem, and Jennifer A. Doudna of Gladstone; Carter Ching, Luis Sandoval, Jae Hyung Jung, Esha Urs, Peixin Amy Chen, and Luke A. Gilbert of UC San Francisco; Jonathan K. Pritchard of Stanford University; Jennifer R. Hamilton (now at Azalea Therapeutics), Wayne Ngo, Da Xu, and James K. Nuñez of UC Berkeley; Meirui An and David R. Liu of the Broad Institute of MIT and Harvard; and Takuya Tada and Nathaniel R. Landau of NYU Grossman School of Medicine. The work was supported by the National Institutes of Health (grants DA046100, AI122390, R35GM155044, K08CA252605, DP2CA311215, U54AI170792, P01AI55393, R01DK129364, and R01CA276368), the Laboratory for Genomics Research, the Bakar Fellows Program, the Weill Neurohub Fellows Program, the Astellas Foundation for Research on Metabolic Disorder, the Chugai Foundation for Innovative Drug Discovery Science, the Parker Institute for Cancer Immunotherapy, the Burroughs Wellcome Fund, the Damon Runyon Cancer Research Foundation, the CRISPR Cures for Cancer Initiative; the Lydia Preisler Shorenstein Donor Advised Fund, the Pascarella Scholars Fund, the Simons Foundation, K. Jordan, the Jane Coffin Childs Fund for Medical Research, the National Research Foundation of Korea Postdoctoral Overseas Training Program (RS-2023-00242661), the Chan Zuckerberg Initiative Foundation (CZIF2025-011112), the Silicon Valley Community Foundation, and the Weill Cancer Hub West. About Gladstone Institutes Gladstone Institutes is an independent, nonprofit life science research organization that uses visionary science and technology to overcome disease. Established in 1979, it is located in the epicenter of biomedical and technological innovation, in the Mission Bay neighborhood of San Francisco. Gladstone has created a research model that disrupts how science is done, funds big ideas, and attracts the brightest minds.