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GEN – Genetic Engineering and Biotechnology NewsHomeBlog
Bone Marrow-on-a-Chip Model Offers New Window Into Immune Cell Development and Behavior
Uduak Thomas-
September 11, 2026
0With support from the National Institutes of Health, a team of scientists have developed a laboratory model that reveals how antibody-producing plasma cells migrate, mature, and survive in human bone marrow. According to its developers, the platform combines a lymph node that mimics an organoid with a tissue chip that mimics bone marrow, and supports studies into the key stages of plasma cell development. Full details of the work are published in a newScience Advancesstudy titled “Ex VivoBone Marrow Subniches Influence the Fate of Human Antibody-Secreting Cells.”
The work was done by scientists from Georgia Tech and Vanderbilt University. The human lymphoid organoid was developed by a team led by Ankur Singh, PhD, a professor of bioengineering and director of the Center for Immunoengineering at Georgia Tech. They developed it by isolating B cells from human tonsil tissue and blood sources and growing them in an environment similar to lymphoid tissue. They used inactivated influenza virus to overcome challenges associated with culturing B cells and getting to transform into antibody secreting plasma cells.
Meanwhile, scientists in the lab of Krishnendu Roy, PhD, dean of engineering and professor of biomedical engineering at Vanderbilt University, designed a microfluidics-based vascularized microenvironment for the bone marrow chip that mimics the conditions found in human bone marrow. Essentially, they tried to “mimic the structure, fundamental biological functions, and spatial microenvironments” of human bone marrow in order “to ask questions about human organ-like behavior in this more simplified model,” Roy explained.
As explained by the developers, the final model is assembled within a three-by-five stack of 96-well plastic plates, that are each less than half-an-inch thick. It features multiple channels that are coated with a gel-like material similar to bone marrow with nutrients and growth factors to support plasma cell function and maintenance. Its layers correspond to an area at the outer edge of the bone marrow cavity, known as the endosteal subniche, where plasma cells are stored. The model also replicates an area deeper inside the center of the bone marrow, the perivascular subniche, which surrounds a network of blood vessels, where plasma cells proliferate and are activated.
“It is nearly impossible to achieve high imaging resolution of plasma cells in living human bone marrow,” Singh said. Though it is possible to “do some level of imaging in the bone marrow of a mouse” which is where some previous efforts have been focused.
Now with this new model, scientists will be able to run new types of experiments. “A fundamental question [that] our study addresses [is] why it is that when B cells are ready to make antibodies, they relocate from lymph nodes, the spleen, and other organs and enter and take up residence in bone marrow,” Singh said. “Another is a question of the role that the environment of bone marrow plays in orienting those cells and responses to reinfection.”
Furthermore, the model can be seeded with cells from unique patient populations to study things like the effects of aging on plasma cell function. It could also be used to study cells from people with autoimmune or allergic diseases to understand how autoimmunity or allergy-promoting plasma cells are produced and maintained. Other studies could focus on addressing questions such as why B cells show a stop-and-go pattern of movement and whether it is part of a migration pattern in the bone marrow.
CloudScope Enables Continuous Remote Monitoring of Brain Activity in Freely Moving Mice
Julianna LeMieux, PhD-
September 11, 2026
0In order to understand and characterize preclinical models of diseases of the central nervous system (CNS), it is critical to be able to conduct continuous neuroimaging of multiple physiological variables—neuronal activity, blood flow, blood volume, oxygenation, and cellular dynamics—within the CNS microenvironment. This continuous multimodality neuroimaging capability is known as neurosurveillance.
However, a long-standing challenge in neuroscience and neuropathology has been how to continuously observe biological processes that unfold over hours, days, and even weeks in the brain.
Now, researchers at Johns Hopkins Medicine have demonstrated a new approach to brain imaging that enables continuous monitoring of brain activity and the physiologic changes associated with neurological disease progression for more than 24 hours in freely moving mouse models. The cloud-based miniaturized microscope, CloudScope, operates autonomously and allows scientists to access live imaging data remotely from anywhere in the world, creating new opportunities to study diseases as they develop over time.
The study demonstrates the ability to remotely capture and analyze changes in brain activity, blood flow, blood vessel remodeling, oxygenation and cellular behavior over extended periods, providing a more holistic picture of brain disease progression than conventional imaging approaches.
This work is published inNature Methodsin the paper, “A cloud-based miniscope for neurosurveillance of brain health and disease in freely behaving animals.”
“We started with a fundamental question: If we wanted to image a seizure or brain tumor formation continuously in a preclinical or animal model over 24 hours or longer, how would we do that?” says Arvind Pathak, PhD, professor of radiology, oncology, and biomedical and electrical engineering at Johns Hopkins. “The consequence of us working through this question and its associated challenges is what resulted in this innovation.”
Using this approach, the team captured spontaneous seizures occurring several hours after a drug-induced seizure in mice, events that would have been missed using conventional short-term imaging methods. In separate studies of brain cancer, researchers were able to characterize the behavior of individual cancer cells and observe dynamic changes in the brain’s microenvironment as the disease progressed. These findings suggest that continuous monitoring may reveal critical biological events that occur outside the limited observation windows typically used in laboratory research.
“Most central nervous system diseases develop over hours, days or even weeks. Yet modern imaging tools are designed to continuously probe only a small fraction of this time window,” says Janaka Senarathna, PhD, assistant professor of radiology at Johns Hopkins. “We developed a device to break this time barrier.”
In addition to advancing neuroimaging research, the investigators have also demonstrated a promising application involving artificial intelligence. By combining the first-ever 24-hour brain imaging dataset with video recordings of the lab animals’ behavior, the team successfully trained an AI framework to predict whether an animal was minimally mobile, moderately active, or running based solely on neuronal activity measurements made with the device. The researchers believe this approach could help scientists better understand the neurological effects of conditions such as stroke or Parkinson’s disease and potentially reveal new insights into the relationship between brain activity and behavior. Additionally, researchers say the device enables time-shared imaging from anywhere in the world, and it creates a pathway to reduce animal use while enabling neuroscientific and neuropathological insights. Lastly, CloudScope’s architecture enables “time-shared” imaging, which potentially reduces animal use.
To explore the effect of disease on different brain regions, the team plans to continue expanding the platform’s capabilities, such as imaging larger regions of the animals’ brains and leveraging AI to accelerate brain imaging and cancer cell tracking.
Transcenta Therapeutics and WuXi Biologics Team Up to Accelerate Commercialization of HiCB Technology
John Sterling-
September 11, 2026
0Transcenta Therapeutics says it will grant WuXi Biologics and its affiliates a non-exclusive license to certain technologies relating to Transcenta’s intensified continuous bioprocessing (HiCB) platform and ExcelPro cell culture media.
Transcenta will receive an upfront payment of $1.5 million and will be eligible for milestone payments upon the achievement of specified conditions. Through this collaboration, WuXi Biologics will become Transcenta’s strategic partner for CMC development and supporting molecules across Transcenta’s development pipeline.
A Transcenta spokesperson explained that the HiCB platform integrates intensified continuous perfusion upstream processing with hybrid continuous downstream purification, enabling a step-change in productivity, achieving an increase in productivity compared with conventional fed-batch processes.
HiCB can significantly reduce cost of goods, lower capital investment, and enable agile production, claims the company official, while providing a solution for improving recovering yield and product quality for complex biologics.
Transcenta, headquartered in Suzhou, China, is a clinical-stage biopharmaceutical company with expertise in biologics discovery, translational research, clinical, and process development. The company develops a pipeline of over ten therapeutic antibody candidates spanning oncology, bone, and kidney disorders.
Samsung Biologics Signs $262 Million Manufacturing Agreement with European Pharma Firm
John Sterling-
September 11, 2026
0Samsung Biologics reported that it has inked a $262 million manufacturing agreement with an unnamed European pharmaceutical company. The deal includes manufacturing commitments, which will be conducted at Samsung Biologics’ Songdo manufacturing site in South Korea extending through 2033.
A Samsung Biologics’ spokesperson stated that the company’s cumulative contract value surpasses $21.9 billion following the latest agreement.
The company currently operates 845 kL of manufacturing capacity across Korea and the U.S., including 785 kL in Songdo and 60 kL at its Rockville, MD site. Acquired in March 2026, the Rockville facility established Samsung Biologics’ first manufacturing presence in the U.S., expanding the company’s global production network. Officials at Samsung Biologics say the company is also strengthening its regional presence through offices in NJ, Boston, Tokyo, and Amsterdam.
Samsung has secured land for Bio Campus III, establishing the foundation for its next phase of long-term capacity and capability expansion. The planned campus is expected to support dedicated R&D and manufacturing programs for next-generation therapeutics while the company continues to evaluate additional capacity investments in line with long-term market demand and client requirements.
Alongside capacity expansion, Samsung Biologics announced that it is pursuing opportunities to broaden its portfolio and address an increasingly diverse range of therapeutic modalities. The company has announced an all-cash offer to acquire PolyPeptide Group, which is expected to expand Samsung Biologics’ capabilities into peptide-based therapeutics and further diversify its global manufacturing network, subject to the completion of the proposed transaction.
Cancer Treatment Genetic Effects in Healthy Cells May Reveal Clues to Side Effects and Resistance
Sophia Ktori-
September 11, 2026
0The results of a study by scientists at Wellcome Sanger Institute, University of Cambridge, University College London, and collaborators indicate that cancer treatments, including chemotherapy and radiotherapy, give a growth advantage to cells with particular genetic changes in healthy tissue. The team used DNA sequencing to map mutations in normal esophagus tissue from esophageal cancer patients who had received either chemotherapy, chemotherapy and radiotherapy, or no treatment before surgery.
The results showed that different cancer treatments changed the landscape of mutations in normal tissue. In particular, combined treatment using chemotherapy and radiotherapy led to significantly more normal cells with cancer-related mutations in these patients. The team suggests that sequencing normal tissue from cancer patients receiving treatment could show how our genes regulate our tissue’s response to drugs, including side effects.
Research co-lead Phil Jones, FRS, a professor of cancer development at the University of Cambridge and a senior group leader at the Wellcome Sanger Institute, said: “Our bodies are a Darwinian battleground, where cells are constantly evolving, expanding and fighting for space in our normal tissues. If you change the rules of this competition by introducing a drug, different genetic mutations are going to enable cells to win or lose. We were surprised to find that only a few weeks of cancer treatment can drastically change decades of evolution in our cells. By looking at normal tissues, we can begin to uncover how drugs work in the body, in order to make more effective treatments with fewer side effects in the future.”
Jones is co-senior and co-corresponding author of the researchers’ published paper inNature Genetics, titled “Cancer treatment alters mutant selection in normal esophagus,” in which they stated, “Sequencing normal epithelia reveals treatment-specific selection of mutations and may identify genes implicated in cellular responses to therapy.”
Over time, all cells in the body acquire genetic changes, known as somatic mutations. While the majority of these do not affect how the cell functions, some make cells fitter, so they outcompete their neighbors. Sometimes, combinations of these mutations cause uncontrollable growth leading to cancer and the formation of tumors.
By middle age, the human esophagus has evolved into a patchwork of mutated cells. “Aging epithelial tissues, including the esophagus, are colonized by somatic mutant clones under strong competitive selection,” the authors wrote. “Mutant clones with increased fitness expand, collide and compete for space in the tissue, with only the fittest mutations surviving.” However, as the authors also pointed out, “The effect of cancer treatment on mutant selection in normal epithelium is unknown.”
By age 60 to 70 years almost all of the cells in the esophagus will be mutated. While the majority of these mutations do not lead to cancer, if tumors do form they can be hard to treat, as often symptoms appear when the cancer has started to spread.
Around 9,500 people are diagnosed with esophageal cancer in the U.K. each year, with almost half of new cases in people aged 75 and over. It is treated with surgery, chemotherapy, radiotherapy, a combination of the two—chemoradiotherapy—and immunotherapy. “We hypothesized that anticancer treatment may alter the selection of mutant clones in the already densely mutated normal esophagus,” the team commented.
For their newly reported study the Sanger Institute researchers and their collaborators set out to understand the effects of cancer treatments on normal cells, and whether chemotherapy and radiotherapy treatments give some mutant cells an advantage. The team used DNA sequencing to analyze normal cells from the esophageal lining—esophageal epithelium—that had been removed from 70 patients after treatment for esophageal cancer. The patients had either received combination chemotherapy, chemoradiotherapy, or no treatment before surgery. “The presence of normal esophagus within the surgically excised tissue gave us the opportunity to test if the mutational landscape of the normal esophageal epithelia was altered by cancer treatment using duplex, whole-genome (WGS) and targeted DNA sequencing,” they further explained.
The investigators found significant differences in genetic mutations in the cells from the patients, depending on the treatment they had received. In patients who received chemoradiotherapy, there were significantly more clones, with mutations inTP53—a vital tumor suppressor gene known as the “guardian of the genome”—and inPPM1D,a gene that makes an enzyme that manages cell stress andTP53function.
Among patients who had received combination chemotherapy there was an increase in normal cells carrying mutations associated with resistance to the chemotherapy drug 5-fluorouracil (5-FU). The increased resilience to 5-FU in a patient’s healthy cells during cancer treatment leads to protection from life-threatening toxicities.
“These findings demonstrate that the mutational landscape of a normal epithelium that has evolved over decades may be altered dramatically in just a few weeks under the selective pressure of anticancer treatment,” they noted. “This leads to the selective expansion of preexisting mutant clones in certain treatment groups.”
Chemotherapy drugs usually leave tell-tale patterns of mutations, known as mutational signatures, in the genomes of normal tissues. Despite seeing changes in mutant cell fitness following treatments, the team found no mutational signatures associated with the chemotherapies. “The absence of a chemotherapy mutational signature in both NanoSeq and whole-genome samples of normal epithelium is notable,” they stated.
Cancer treatments can cause severe side effects in normal tissues, which may result in reducing treatment dose. The researchers suggest that their findings begin to uncover the genes and protein domains that make normal cells sensitive or resistant to treatment. The results could help shape cancer treatment in the future to help reduce damage to normal tissues. The study findings might also help inform the development of targeted treatments that destroy cancer cells while leaving normal tissue unharmed.
By identifying the mutant cells in normal tissue that are selected for by cancer treatment, the study may also provide a catalogue of potential genetic targets that modify how our cells respond to treatment, and lead to further research into how tumors become drug resistant. “… mutants in normal tissues providein vivoevidence of actionable targets for mitigating normal tissue toxicity and may inform strategies for overcoming drug resistance in tumors,” the scientists stated.
For the next steps, the team is conducting a pilot study to investigate these effects in other tissues, taking cheek swabs, blood and urine samples from patients before and after having treatment for skin, head and neck cancers. The researchers are investigating on a larger scale, whether there is further evidence of genetic mutations in normal cells that are being selected for by cancer treatment.
Commenting on the study Hayley Brown, research information manager at Cancer Research UK, said, “People with esophageal cancer often need intensive treatment, but we still have much to learn about how these therapies affect the rest of the body. Cancer treatments can be incredibly effective, but they can also affect healthy tissues. This study gives us an unusual opportunity to see how healthy cells change during treatment, helping us understand what happens elsewhere in the body, not just in the tumor. The more we learn about these changes, the better chance researchers have of finding ways to reduce the impact of treatment on patients without making it less effective against cancer.”
PD-L2 Blockade May Reduce Harmful Aging Cell Buildup
Savannah Wiegel-
September 10, 2026
0A protein better known for its role in immune checkpoint signaling may help harmful aging cells, or senescent cells, remain hidden from the immune system, allowing them to accumulate in tissues and contribute to age-related dysfunction, according to a new study from Cedars-Sinai Health Sciences University investigators.
The study is titled “Blocking PD-L2 prevents senescent cell accumulation and age-related dysfunction.” The findings, published inCell Metabolism, point to programmed cell death ligand 2, or PD-L2, as a possible target for therapies designed to help clear senescent cells, as well as a potential blood marker for tracking their presence. Senescent cells are damaged cells that stop dividing but do not die. Instead, they can persist in tissues, where they release inflammatory factors and disrupt the function of nearby cells. Their buildup has been linked to metabolic dysfunction, impaired physical fitness, and other health problems associated with aging.
“Our findings suggest that PD-L2 may help aging cells stay in the body when they would normally be removed by the immune system,” said Selim Chaib, PhD, research assistant professor of medicine at Cedars-Sinai and first and co-corresponding author of the study.
Immune checkpoint proteins have been studied extensively in cancer, where they can help tumor cells escape immune attack. In the new study, the researchers examined whether a similar process might allow senescent cells to evade immune clearance during aging. They found that PD-L2 was increased in isolated senescent human cells and rose with age in some human tissues. Circulating soluble PD-L2 also increased with aging and declined after senolytic treatment in humans, according to the study’s highlights.
The team then tested the effects of removing or blocking PD-L2 in mice. Older mice lacking PD-L2 accumulated fewer senescent cells than older wild-type mice. They also showed greater insulin sensitivity and grip strength, two measures tied to metabolic function and physical fitness. In aged wild-type mice, anti-PD-L2 therapy restored insulin sensitivity and increased physical strength.
Together, the results suggest that PD-L2 may act as an immune checkpoint on senescent cells, helping them avoid removal and promoting their persistence during aging. The work also adds to the growing interest in senescence-targeted approaches, including senolytics, that aim to reduce the burden of dysfunctional cells rather than treating one age-related disease pathway at a time.
“If we can find a way to block this protein, we may be able to help the immune system get rid of these cells and potentially improve health problems linked with aging,” said James Kirkland, MD, PhD, director of the Center for Advanced Gerotherapeutics and senior author of the study.
The authors cautioned that more research is needed to determine whether blocking PD-L2 can safely produce health benefits in people.
What 25 Years of Research Have Revealed About 9/11’s Long-Term Health Effects
Uduak Thomas-
September 10, 2026
0Since the attacks on the World Trade Center in New York City, at the Pentagon in Arlington, Virginia, and near Shanksville, Pennsylvania on September 11, 2001, scientists and clinicians have learned much about the enduring effects of exposure to environmental toxins and hazardous materials. A perspective paper, published today inJAMA, highlights some insights from long-term follow-up of people with 9/11-related health effects, lessons learned in terms of care delivery and clinical understanding, as well as some implications for future disaster responses.
The perspective paper, titled “Twenty-Five Years After 9/11—Lessons From the World Trade Center Health Program,” is authored by scientists and clinicians affiliated with the World Trade Center Health Program (WTC Health Program), National Institute for Occupational Safety and Health, which is part of the U.S. Centers for Disease Control and Prevention.
It begins by highlighting some of the health effects experienced by the cohort including the fact that “many affected individuals have experienced multimorbidity” and developed multiple conditions such as “cancer, respiratory disease, gastroesophageal reflux disease, and mental disorders.” Some of these conditions developed years post-exposure “underscoring the importance of sustained clinical monitoring and research.”
Other findings from their analysis indicate that people in the cohort have a higher prevalence of both chronic conditions and poorer health-related quality of life compared to the general population. They noted that this “multimorbidity contributes to increased disability, more complex clinical management, and higher health care utilization and cost.” However, “access to no-cost care for covered conditions may improve survival, illustrating the interplay between exposure-related risk and access to care.” Elsewhere in the paper, multimorbidity is also listed as a “defining feature of care” as this population ages, although to be clear, not all their conditions are related to 9/11 exposures. The data also suggests that “integrated systems combining surveillance, clinical care, exposure assessment, and research may improve their chronic disease management.”
Insights from the program have also shaped the patient health management strategies adopted by the program over time and expanded the list of covered conditions. As part of the study, the scientists assessed the effectiveness of the WTC Health Program in helping patients manage their conditions and improve their health outcomes. According to numbers reported in the paper, as of June 2026, more than 154,000 responders and survivors have enrolled in the program. Eligibility is based on documented occupational or environmental 9/11 exposure, and clinical coverage is limited to specific conditions described on the program’s website.
Their analysis of program data indicates that its efforts have been largely effective. Specifically, the scientists reported “strong performance in preventative care and chronic disease management” with screening rates for some cancers “exceeding national benchmarks.” They also found that “responders with cancer who participate in the WTC Health Program experienced 26% to 64% lower mortality rates compared with the New York State general population across multiple cancer types.” They further observed a lower smoking prevalence, about four percent, in the cohort compared to the U.S. adult prevalence of 9.1%, which “may reflect the availability and uptake of smoking cessation and related WTC Health Program services.”
The data for chronic disease management efforts was similarly positive. For people with chronic respiratory disease, “program data indicate high levels of guideline-concordant asthma management, with most members achieving an appropriate balance between controller and rescue medications,” the scientists wrote.
Overall, there are lessons from the program that could inform future disaster response initiatives and improve public health preparedness programs among other benefits. “First, the health effects of large-scale environmental and occupational exposures may unfold over decades, requiring sustained investment in monitoring and care,” the scientists wrote. The evidence also shows that “integrated systems that link surveillance, research, and clinical care are essential for identifying and responding to emerging health risks” and “access to care at no out-of-pocket cost can help mitigate the long-term health effects of large-scale environmental exposure and support overall member well-being,” they said.
Chronic Interferon Exposure Linked to Immunosuppression in Cancer
Sophia Ktori-
September 10, 2026
0As soon as a cancer cell appears, the immune system jumps into action—and interferons (IFNs) are among the first responders. Interferons are pro-inflammatory cytokines, or signaling proteins, that recruit specialized immune cells, such as like T cells or B cells to destroy the cancer. This is a critical, powerful step in the body’s fight against cancer, but chronic exposure to interferons can turn them from ally to enemy.
A Salk Institute team has now discovered a novel pathway that links chronic interferon II (IFN-II) exposure to mitochondrial dysfunction that ultimately causes immunosuppression. By explaining how interferon II turns from “good” to “bad,” the foundational insights provide a path to future therapies that combat immunotherapy resistance.
“Why interferons, which are initially anti-cancer, can become pro-cancer has been a big question in the field,” says senior author Gerald Shadel, PhD, professor and holder of the Audrey Geisel Chair in Biomedical Science at Salk. “Our study reveals a major reason for why interferons transition from ‘good’ to ‘bad,’ as well as how we can prevent this switch for therapeutic advantage moving forward.”
Shadel is senior and corresponding author of the researchers’ published paper inScience,titled “Chronic type II interferon promotes tumor growth through mitochondrial RNA–induced type I interferon and prostaglandin synthesis.”
Cancer biology and, in turn, cancer treatment have come a long way in the last few decades. Most people recognize this progress in breakthroughs like immunotherapy—a treatment strategy first deployed in 2011 that leverages the body’s own immune cells to fight cancer and revolutionized the treatment landscape. However, progress doesn’t mean all the questions have been answered.
One of those questions is why interferons that recruit the immune system to attack cancer cells can, when they linger too long, start helping the tumor grow rather than shrink. “Interferons (IFNs) are proinflammatory cytokines that promote immune cell engagement to eliminate malignant cells,” the authors wrote. “Paradoxically, chronic interferon signaling can also activate anti-inflammatory mechanisms that allow cancer cells to evade the immune system.”
Shadel’s lab has been studying interferons for a while, and for his team, the context is always mitochondria. The Shadel lab first discovered that mitochondria invoke interferon responses through the release of mitochondrial genetic material (mtDNA) into the rest of the cell. The lab’s research seeks to uncover the ways mitochondrial dysfunction can lead to inflammation, aging, and pathology.
“For this study, we turned our focus around,” Shadel explained. “Instead of asking how mitochondria affect interferons, we asked how interferons affect mitochondria. And cancer is a powerful system to ask this question in, since interferons are so essential to the body’s cancer response.”
To determine how interferons affect mitochondria the team first exposed melanoma cells to interferon I or interferon II for either acute or chronic periods. Little happened to the mitochondria on acute exposure, but chronic exposure led to measurable changes in their energetic function. The researchers then transferred these melanoma cells to a mouse model, finding that chronic interferon II exposure unexpectedly enhanced tumor growth.
The team next worked to decipher the cellular mechanisms behind the enhanced tumor growth. They found interferon II causes mitochondrial genetic material (mtRNA) to leave the mitochondria, where the rest of the cell perceives it as an invader and produces interferon I to respond. “We show that chronic type II interferon (IFN-II) exposure distinctively induced tumor growth by activating a type I interferon (IFN-I) response mediated by release of double-stranded mitochondrial RNA (ds-mtRNA) into the cytoplasm,” they noted.
Interferons I and II then work together to boost levels of the enzyme cyclooxygenase 2, which increases the synthesis of the bioactive lipid prostaglandin E2 (PGE2). “These IFN-II and IFN-I signals then synergize to up-regulate COX2-dependent PGE2 synthesis, an immunosuppressive pathway implicated in cancer progression and chemo-, immuno-, and targeted therapy resistance,” the team continued.
If prostaglandin E2is causing immunosuppression, the team asked, what then happens if the melanoma cells are incapable of synthesizing PGE2?
Anti-PD1 immunotherapies are among the most widely used immunotherapies. They work by blocking a signal that cancer cells use to keep immune cells from attacking the tumor. But tumors can also suppress the immune system through other pathways, allowing them to continue growing despite anti-PD1 treatment.
“Chronic interferon exposure is a major factor in immunotherapy resistance,” says first author Melissa Johnson, a graduate student researcher in Shadel’s lab. “We wondered whether cancer cells that have become resistant to anti-PD1 therapy were upregulating the immunosuppressive mitochondria-centered pathway we identified, and whether that pathway is a viable target for combating immunotherapy resistance.”
The researchers blocked the synthesis of prostaglandin E2in mouse melanoma cells. They found that eliminating this signal restored the immune system’s ability to see and fight the cancer cells. Blocking prostaglandin E2also reversed resistance to anti-PD1 immunotherapies. In nine of 10 mice evaluated the tumors completely regressed and didn’t return, even though they were previously resistant to immunotherapy.” Elimination of PGE2synthesis in immunotherapy-resistant melanoma cells restored their responsiveness to anti-PD1 treatment, indicating that this covert mtRNA-IFN-prostaglandin pathway could be a therapeutic target to combat immunotherapy resistance,” the team concluded.
The findings demonstrate potential for clinical translation in the future, offering a potential way to sustain the immune system’s attack on cancer and hope in cases of immunotherapy resistance. “Our study enriches our understanding of how the immune system attacks cancer cells but can also be stymied by other factors in the tumor environment,” said Shadel, “and also conveys the importance of integrating mitochondrial signaling functions into cancer studies.”
Manus and UT Austin Advance Biomanufacturing Product Recovery Through BioMADE Program
John Sterling-
September 10, 2026
0Manus, The BioAlternatives Company®, and the University of Texas at Austin say they have completed aBioMADE-sponsored program to make industrial yeast fermentation more efficient and sustainable.
The project, carried out with Hal Alper, PhD, and the Alper Lab in UT Austin’s McKetta department of chemical engineering, engineered yeast to disrupt their own cell walls at the end of fermentation. This programmed lysis approach simplifies downstream processing by reducing reliance on energy-intensive mechanical disruption and removes the need for hazardous solvent-based extraction, according to the researchers.
The result, they add, is lower production costs and improved sustainability across a broad range of bioalternative products that accumulate inside cells, including lipids, proteins, vitamins, pigments, biosurfactants, and polysaccharides.
Reduced mechanical separation energy requirements
The team said they demonstrated the technology up to pilot scale (300 liters) for two industrially relevant yeasts. InYarrowia lipolytica, engineered strains enabled a reduction in mechanical separation energy requirements by more than 50 percent. InSaccharomyces cerevisiae, the team achieved autolysis in a relevant production strain. They pointed out that the work advanced the technology from laboratory demonstration to integrated pilot operation.
“Downstream processing is one of the largest hidden costs in biomanufacturing, and it heavily influences whether a bioalternative can compete on price. By engineering yeast to disrupt their own cell walls, we reduce cost, energy, and complexity, which widens the range of products that can be made economically and sustainably at scale,” says Christine Santos, PhD, chief technology officer, Manus. By cutting processing intensity and improving recovery, these advances strengthen the case for domestic biomanufacturing.
“This work uniquely combined academic and industrial settings to take bench-scale discoveries and more rapidly translate them to higher technology readiness,” adds Alper. “This technology finally helps to address the challenge of producing cheaper intracellular products that traditionally require high-cost separations and more laborious process steps.”
The scientists note that the technology has broad application across many products that are made and accumulate inside microbial cells. By cutting processing intensity and improving recovery, these advances strengthen the case for domestic biomanufacturing built on abundant, low-cost American feedstocks.
Data Integrity as the Foundation for AI
Kathy Vuksanaj-
September 10, 2026
0Artificial intelligence is advancing quickly into laboratory operations, which is why thinking about the quality and integrity of the supporting data early on is important. In regulated environments, that means understanding where the data came from, how it changes, and how AI-generated insights or recommendations can be traced, reviewed, trusted, and ultimately defended.
In thisGENpodcast, LabVantage’s Gary Stimson digs into what it takes to build a data foundation for trustworthy AI. The discussion covers concepts like data lineage, traceability, explainability and governance, and the importance of audit-ready laboratory operations. It also looks at the role of intended use, ongoing monitoring, and human review in deploying AI responsibly.
Podcast Guest:
Principal Architect, Head of AI Technologies
LabVantage Solutions
Produced with support from:
Bone Marrow-on-a-Chip Model Offers New Window Into Immune Cell Development and Behavior
By reproducing elements of human bone marrow on a chip, scientists have created a new tool that will help them gain new insights into how immune cells develop and function.
Read moreArtificial IntelligenceCloudScope Enables Continuous Remote Monitoring of Brain Activity in Freely Moving Mice
Johns Hopkins researchers developed CloudScope, a cloud-based microscope enabling continuous, remote brain imaging in freely moving mice, revealing disease progression, seizures, cellular changes and behavior over extended periods.
Read moreBioprocessingTranscenta Therapeutics and WuXi Biologics Team Up to Accelerate Commercialization of HiCB Technology
Transcenta, headquartered in China and with a pipeline of over ten therapeutic antibody candidates, is a clinical-stage biopharmaceutical company with expertise in biologics discovery, translational research, clinical, and process development.
Read moreBioprocessingSamsung Biologics Signs $262 Million Manufacturing Agreement with European Pharma Firm
Alongside decisions involving capacity expansion, officials at Samsung Biologics announced that the company is pursuing opportunities to broaden its portfolio and address an increasingly diverse range of therapeutic modalities.
Read moreCancerCancer Treatment Genetic Effects in Healthy Cells May Reveal Clues to Side Effects and Resistance
Researchers used DNA sequencing to map mutations in normal tissue from cancer patients undergoing different types of treatment. They found significant differences in the genetic mutations in healthy tissue, depending on whether the patients received radiotherapy, chemotherapy, or chemoradiation.
Read moreNewsPD-L2 Blockade May Reduce Harmful Aging Cell Buildup
Blocking PD-L2 reduced senescent cell accumulation in aged mice and improved measures tied to metabolic function and physical strength.
Read moreCancerWhat 25 Years of Research Have Revealed About 9/11’s Long-Term Health Effects
Twenty-five years after 9/11, long-term monitoring of responders and survivors continues to reveal the complex health consequences of exposure to environmental toxins and hazardous materials.
Read moreCancerChronic Interferon Exposure Linked to Immunosuppression in Cancer
A preclinical study uncovered a novel pathway that links chronic IFN-II exposure to mitochondrial dysfunction and ultimately immunosuppression in cancer, creating foundational insights that may point to future therapies that combat immunotherapy resistance.
Read moreBioprocessingManus and UT Austin Advance Biomanufacturing Product Recovery Through BioMADE Program
A new study showed that a programmed lysis approach cut mechanical separation energy by over 50 percent at pilot scale, widening the range of bioalternatives that can compete pricewise.
Read moreGENcastData Integrity as the Foundation for AI
In this sponsored podcast, LabVantage’s Gary Stimson digs into what it takes to build a data foundation for trustworthy AI.
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