Background and aimSocial workers regularly encounter clients affected by substance use disorders (SUD), yet training in evidence-based assessment and interventions remains limited. In Sweden, municipal social workers have statutory responsibility for SUD assessment, intervention planning and client follow-up which underscores the need for targeted professional education. This study aimed to: (i) describe social workers’ baseline self-assessed competence in evidence-based practices for SUD and its associations with demographic and professional characteristics, and; (ii) examine knowledge gains associated with completion of an evidence-based educational intervention.MethodsA non-randomized pre–post design included 173 municipal social workers recruited from 64 municipalities across five cohorts (2021–2023). Baseline self-assessed competence was analyzed using ordinal logistic regression, and knowledge gains were assessed using module-specific pre–post items with paired t-tests with Cohen’s d.ResultsBaseline competence was rated as low to moderate, with professional experience predicting higher perceived competence. Substantial baseline knowledge gaps were observed, particularly in evidence-based psychosocial interventions and use of digital technology in assessment and planning of treatment. Knowledge increased significantly across all modules after training completion (d = 0.26–1.41). The largest knowledge gains were for modules on use of technology in the assessment and treatment-planning, biopsychosocial interventions, research-informed use of the assessment tool Addiction Severity Index (ASI), and the professional role in assessment and care planning. Score variability decreased across several modules.ConclusionCompletion of an immersive, online, evidence-based training was associated with meaningful improvements in social workers’ knowledge related to substance use assessment, intervention planning, and use of technology. Although causal inference is limited by the non-randomized single-group pre–post design, the findings support the potential of scalable educational interventions to address competence gaps in substance use services even in organizations with high caseloads, workforce turnover, and limited training opportunities.
<![CDATA[Check out new phase 2 dose-ranging study data evaluating alixorexton in patients with narcolepsy type 2. ]]>
Digital Platform to Provide Health Data Feedback for Neurorehabilitation Patients: User-Centered Development and Proof-of-Concept Usability Study
Background: An increasing amount of digital health data are being collected across rehabilitation settings, but their integration into routine clinical practice remains limited, despite its potential to motivate patients or inform clinical decision-making. Specifically, effective visualization and communication of assessment outcomes to both patients and health care practitioners (HCPs) represent a key gap in the neurorehabilitation practice. Objective: This study describes the development and evaluation of RehaLink (author ND, ETH Zürich), a proof-of-concept mobile app that delivers structured, interpretable feedback from conventional and technology-based assessments to neurorehabilitation patients and HCPs. Methods: The app was developed through a 3-step iterative co-design process involving 17 inpatients with multiple sclerosis and 15 HCPs from a single rehabilitation center. The app integrates a full battery of conventional assessments routinely conducted at the clinic, as well as digital health metrics from the Virtual Peg Insertion Test, a validated technology-based assessment of upper limb function, as a proof of concept for integrating technology-based assessment data into clinical workflows. Three structured feedback sessions were conducted, in which participants evaluated feedback types, visualization formats, and app usability using Likert-scale ratings, preference rankings, open-ended questions, and the System Usability Scale. Data were analyzed using descriptive statistics and directed content analysis. Results: Across all 3 sessions, progress bars and color-coded indicators were consistently preferred over text-heavy or abstract formats by both patients and HCPs. A persistent set of competing demands was observed, with participants requesting both visual simplicity and access to absolute values and normative comparisons. HCPs tended to underestimate patients’ preference for informative visualizations. The perceived value of structured feedback increased over the course of the study; patients’ median ratings rose from 4.0 to 5.0 and HCPs’ from 4.0 to 4.5 on a 5-point Likert scale. The resulting mobile app prototype demonstrated high usability, with patients achieving a mean System Usability Scale score of 93.6 (mean 6.4; best imaginable) and HCPs 80.9 (SD 8.1; good), according to established benchmarks. Conclusions: These findings demonstrate the feasibility and value of a co-designed digital feedback tool for neurorehabilitation. By combining conventional and technology-based assessment outcomes in an accessible, user-centered format, the app has the potential to enhance patient engagement, support clinical decision-making, and advance the implementation of value-based, personalized care.
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The Feasibility of an App-Based Worksite Health Promotion Program to Improve Mental Well-Being and Work-Related Vitality in University Hospital Workers: Process and Preliminary Effect Evaluation Study
Background: University hospital employees face role-specific stressors that can impair mental well-being and work-related vitality. While worksite health promotion programs show potential for improving mental well-being by targeting lifestyle behaviors, most target single professions or hospital subunits, and evidence for mental well-being and work-related vitality remains mixed. Mobile apps offer unique advantages for delivering such worksite health promotion programs hospital-wide. However, accessible interventions tailored to a diverse workforce are lacking. Objective: This study aimed to investigate the feasibility of an app-based worksite health promotion program (the Recharge360 program [The Recharge Company]) targeting multiple lifestyle behaviors, including a team-based competition element, for improving mental well-being and work-related vitality of hospital employees over a 5-month follow-up period by evaluating two objectives: (1) the implementation process of the program, and (2) the preliminary effects of the program on mental well-being and work-related vitality. Methods: We included 532 employees (mean age 43, SD 12 y; n=482, 91% women; n=480, 90% highly educated) from a university hospital in Amsterdam, the Netherlands. The study had a single-arm, longitudinal pretest-posttest design lasting 5 months, during which employees participated in the 5-day Recharge360 program (Recharge week) 3 times—in weeks 1, 9, and 17. At baseline (T0) and after each Recharge week (T1-T3), we assessed mental well-being, work ability, need for recovery, and task performance. The process was evaluated by assessing recruitment, attrition, and survey completion rates, and the degree of participation. Preliminary effects were evaluated by linear mixed model regression analyses to assess changes in mental well-being and work-related vitality between baseline and follow-up. Results: Recruitment appeared feasible, but attrition rates were high (up to 70% in the final Recharge week), and the degree of participation decreased over time. We showed statistically significant, albeit small, increases in well-being at T3 (unstandardized β coefficient=2.08, 95% CI 0.33-3.84), with progressively larger improvements in the analyses among those who started at least 1, 2, and all 3 Recharge weeks (unstandardized β coefficient=3.27, 95% CI 1.09-5.45). Results for work-related vitality were mixed. The need for recovery remained unchanged, task performance increased slightly at T3 (unstandardized β coefficient=0.16, 95% CI 0.07-0.24). Work ability showed a small, but statistically significant, decline across follow-up (unstandardized β coefficient=−0.46, 95% CI −0.64 to −0.29). Conclusions: This app-based worksite health promotion program might be feasible to implement in a university hospital setting and shows potential to slightly improve mental well-being, but primarily for a selective group of highly educated, health-conscious women. While these findings support further investigation in a randomized controlled trial in similar university hospital settings, they also highlight the need for more participatory study designs to improve the tailoring of program components and engagement of underrepresented groups, as well as for a supportive culture and population-based approaches at the organizational level.
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Personalized Cartilage Graft Developed for Life-Threatening Infant Airway Narrowing
A study led by researchers at Children’s Hospital of Philadelphia (CHOP) demonstrated a new method of using decellularized cartilage with patient-specific cells to help enlarge the pediatric airways narrowed as a result of severe subglottic stenosis (SGS). The condition is a narrowing of the airway below the vocal cords and above the trachea, and affects an estimated 20,000 infants per year.
Researchers demonstrated in a preclinical model that this new method of airway reconstruction was faster, more effective, and able to overcome issues, such as donor site morbidity, insufficient tissue volume and delayed timeline, associated with the current standard grafts used for laryngotracheal reconstruction (LTR).
Riccardo Gottardi, PhD, assistant professor with the Perelman School of Medicine at the University of Pennsylvania and leader of the Bioengineering and Biomaterials (Bio2) lab, and Ian Jacobs, MD, medical director of the Center for Pediatric Airway Disorders in the Division of Otolaryngology (ENT) at CHOP, co-led the research, which is reported in Nature Communications, in a paper titled “A translational approach to airway reconstruction leveraging decellularized meniscus and cartilage progenitor cells.” In their paper the team said, “This technology has the potential to revolutionize the field of pediatric LTR.”
Severe subglottic stenosis (SGS) develops in children almost exclusively as a response to intubation, and affects nearly 1.5% of the over 200,000 infants in intensive care units each year in the United States, the authors explained. The most severe cases require laryngotracheal reconstruction (LTR), an open airway surgery that is used to enlarge the airway by implanting cartilage taken from a rib cage. While LTR is used to successfully treat thousands of children with subglottic stenosis, in many cases, young children often lack enough costal cartilage—the cartilage connecting our ribs to the sternum—for these grafts.
As a result, operations often need to be delayed, leaving the child attached to a tracheostomy tube until they are older and grown enough to supply sufficiently sized cartilage for an effective LTR, and there is a higher risk of needing follow-up surgery because the airway is at risk of narrowing again. “In adults, LTR has a 90% success rate with low rates of revision,” the team stated. “However, in children, success rates significantly drop, and the incidence of restenosis requiring revision surgery increases to over 24%.”
To improve this process and reduce the risk of these potential complications, Gottardi and Jacobs and colleagues have been looking at tissue engineering a laryngotracheal graft. Tissue engineering, the team wrote, could provide “an ideal alternative to autologous cartilage grafts to alleviate unnecessary comorbidities as well as reduce surgical time.” However, the complexity of the trachea prevents the use of conventional cartilage engineering techniques for this procedure.
“We needed something that could be equivalent to a piece of cartilage, integrate well with the surrounding tissue, be well tolerated by the patient, behave like native tissues and regrow and be part of the airway,” Gottardi said. “This required quite a bit of creative thinking because of the additional challenges in children who are so small and still growing.”
To overcome the limitations of existing methods, the researchers, led by former Gottardi lab member Paul Gehret, PhD, created a first-of-its-kind scaffold based on porcine meniscal cartilage decellularization (MEND – MENiscus Decellularization). They realized that if the cells, elastin, and blood vessels present in the meniscus are “digested” away, the meniscal cartilage becomes amenable to recellularization and integration while being less likely to provoke an immune response. In their paper the researchers explained, “Building on the strengths of previous decellularized therapies, we established an innovative approach that leverages the selective enzymatic removal of the elastin fibers and blood vessels uniquely present in the fibro-elastic cartilage of the meniscus to create microchannels, which support cellular invasion while substantially preserving native structure.”
Using ear-derived cartilage progenitor cells (eCPCs), which can mature into cartilage-producing chondrocytes, the researchers demonstrated that MEND can be recellularized after the removal of elastin and blood vessels and suitable for implantation in less than a month. “Notably, porcine menisci, such as those used in this study, are a highly abundant cartilage source, being easily available as a waste product of the food industry, which can ensure no shortage of material for surgeons to shape into an ideal implant,” the team noted.
Importantly, the new method needed to work in a clinically relevant timeframe. In a real-world scenario, clinicians may only have one or two months to be able to perform the procedure when it can still benefit the patient. Harvesting seed cells within days and creating a scaffold within three to four weeks is significantly less time than the six months that was typically needed for engineered cartilage. “Here we demonstrate that MEND can be fully recellularized in three days with ear-derived cartilage progenitor cells and reaches structural and functional maturation suitable for implant within three weeks of chondrogenic differentiation, a time frame compatible with clinical translation,” the authors stated.
They validated their technology in a preclinical rabbit in vivo model, and demonstrated better performance than costal cartilage, the standard of care, with no instances of adverse events reported. “Our results demonstrate airway expansion, graft reepithelialization, neocartilage formation, and integration with adjacent native laryngotracheal cartilage at three months,” the team stated. “Notably, MEND implants perform better in all outcomes than autologous costal cartilage, the standard of care.”
These findings will be further validated prior to proposing the procedure for patients suffering from severe subglottic stenosis. “These results demonstrate the feasibility of our translational tissue engineering approach to laryngotracheal reconstruction and could overcome the autograft-associated limitations in pediatric patients, decreasing the need for invasive revision surgery,” the investigators concluded.
“This research shows really promising data that suggests this novel approach could overcome the autograft-associated limitations we sometimes encounter when attempting laryngotracheal reconstruction in infants,” Jacobs said. “With more research, we expect this could decrease the need for invasive surgery, and we may be able to apply the technology to other conditions that require a cartilage graft.”
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OLE Identified as a Potential Alzheimer’s Therapy Targeting Microglia
A research collaboration between investigators from the Spanish National Research Council (CSIC), the Miguel Hernández University of Elche (UMH), and the École Polytechnique Fédérale de Lausanne (EPFL) has identified a molecule that may could be a new approach to treating Alzheimer’s disease (AD) by restoring the protective functions of microglia, immune cells found in the brain. The findings, published in Cell Death & Disease, said the molecule N-oleoyl-Leucine (OLE), which is derived from the Alzheimer’s disease-associated gene PM20D1, was shown to reduce amyloid pathology, improve cognition, and promote neuroprotection.
“One of the most significant findings is that we have identified a molecule capable of restoring microglia’s protective function,” said senior author José Vicente Sánchez Mut, PhD, principal investigator at the Functional Epi-Genomics of Aging and Alzheimer’s Disease laboratory at the Institute for Neurosciences, a joint CSIC-UMH center. “In Alzheimer’s disease, these cells become progressively impaired. Our results suggest that this process can be reversed, pointing to new therapeutic and research avenues to counteract the disease.”
In recent years, there has been a surge of research into microglia’s role in AD. As the researchers noted, genetic risk variants associated with AD are enriched in regions that regulate microglial function, and microglial gene-expression programs have been shown to be altered during disease progression. As the disease advances, microglia proliferate and accumulate around amyloid plaques, but lose their ability to maintain tissue homeostasis and clear amyloid beta (Aβ). At the same time these immune cells take on inflammatory and neurotoxic characteristics.
PM20D1 has been identified recently as a risk gene in the development of AD. It is a quantitative trait locus associated not only with Alzheimer’s disease but also with diabetes, obesity, and other disorders. People exhibiting lower PM20D1 expression have a higher risk of developing metabolic disorders and Alzheimer’s disease. Other prior research studies also showed that PM20D1 overexpression in mouse models reduced amyloid levels and cognitive deficits, making it a potentially fruitful area for additional study.
PM20D1 encodes a secreted enzyme that regulates the conjugation of fatty acids with amino acids, generating compounds known as N-acyl amino acids (NAAA). OLE is one of these amino acids and was selected for further investigation because PM20D1 activity in living organisms appears to favor its production and because OLE levels are strongly correlated with PM20D1 expression in both humans and mice.
“There is increasing evidence of microglia participation in Alzheimer’s disease (AD), which incentives their modulation to intercept the disease,” the researchers wrote. “Here, we describe a new mechanism by which the recently AD-associated Peptidase M20 Domain Containing 1 (PM20D1) instructs microglia to tackle AD.”
To evaluate OLE’s therapeutic potential, the team first tested it in genetically engineered Caenorhabditis elegans worms that produce beta-amyloid, where they showed that OLE treatment reduced protein aggregation and improved mobility. The researchers then administered OLE to APP/PS1 mouse models of AD for three months. Again, the mice demonstrated better performance in memory tests and showed reductions in amyloid plaque burden.
A cellular analyses found that microglia were the cells most responsive to OLE treatment.
“Single-cell analysis allowed us to determine that microglia were the cells that responded most strongly to the treatment,” said first author Victoria Pozzi, PhD, a postdoctoral researcher working in the Sánchez Mut lab. “From there, we observed that the compound helped these cells move toward beta-amyloid plaques and better contain the damage associated with the disease.”
The study also found that OLE increased Aβ chemotaxis and clearance in cultured microglia. In neuronal cultures exposed to Alzheimer’s-related stressors, OLE enhanced cell survival, indicating that the molecule may have direct neuroprotective effects in addition to its effects on immune cells.
The team believes OLE may function as a disease-modifying therapy by altering microglial behavior and reducing amyloid-associated damage, but because OLE was administered systemically in their experiments, more work is needed to determine whether its primary effects occur in microglia or whether it acts independently on multiple cell types. They also plan to investigate whether other N-acyl amino acids have therapeutic potential and whether OLE can influence tau pathology and neurodegeneration.
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AI Discovers Two New Antibiotics for Drug-Resistant Gonorrhea
Scientists have developed a deep learning model that could significantly accelerate the discovery of novel antibiotic compounds. In a study published today in Science Translational Medicine, the AI algorithm was able to identify two compounds effective against gonorrhea infections, each operating through mechanisms unlike those of any antibiotics in use today.
“Faced with the threat of untreatable gonorrhea, new antibiotics are urgently needed,” writes James J. Collins, PhD, professor of medical engineering and science at the Broad Institute of MIT and Harvard. “Our work establishes a much-needed hit discovery tool to address the growing crisis of antimicrobial resistance for this pathogen.”
According to the CDC and WHO, gonorrhea is one of the most urgent antibiotic-resistant threats worldwide. When left untreated, this sexually transmitted infection can lead to serious health complications. Yet treatment is becoming increasingly challenging as strains of Neisseria gonorrhoeae continue to develop resistance to existing antibiotics.
“Previous first-line therapies for gonorrhea—including penicillin, tetracycline, ciprofloxacin, cefixime, and azithromycin among others—are no longer recommended because of excessively high resistance rates in circulating strains,” says Collins. “The last remaining first-line monotherapy, ceftriaxone, is at risk of becoming obsolete, with resistance rates of over 10% in parts of the world.”
Traditional antibiotic discovery relies on high-throughput screening methods that search large chemical libraries for promising compounds. However, this approach cannot keep pace with the fast expansion of chemical space, which today englobes over 75 billion compounds.
To overcome this limitation, Collins and colleagues turned to deep learning algorithms capable of making large-scale screening significantly more time- and cost-efficient. They selected a predictive graph neural network (GNN), a model that represents molecules as graphs and can virtually screen thousands of molecules per second. Compared to large language models, the GNN more accurately identified molecules with activity against gonorrhea that were structurally different from both the training data and existing antibiotics.
To train the model, the team screened 38,650 small molecules with diverse structures and identified those capable of inhibiting the growth of N. gonorrhoeae. The model was then able to virtually screen through nearly six million compounds, which led to identification of 83 antibiotic candidates with confirmed activity against N. gonorrhoeae.
Among them, two compounds stood out for having distinct structures from existing antibiotics, known as MP20 and A1. In mice and an organ-on-a-chip model of vaginal gonorrhea infection, both molecules rapidly and selectively killed the bacteria without inducing drug resistance.
Proteomics analyses revealed the mechanism of action of each antibiotic candidate. MP20 was found to disrupt the bacterial membrane and damage DNA, while A1 targeted an enzyme essential for the synthesis of the bacterial cell wall.
“There is a critical need to fill the trickling antimicrobial development pipeline with promising antibiotic candidates, especially ones with distinct mechanisms of action,” says Collins. “We have shown that these compounds can retain potency against even the most highly resistant strains of N. gonorrhoeae, exhibit selective killing toward bacteria, and act through orthogonal mechanisms from those of existing first-line antibiotics.”
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GLP-1 Drugs Reduce Crime-Linked Behavior
GLP-1 drugs could act upon impulsive behavior that leads to violence and criminal acts, research suggests.
The study adds to evidence suggesting that these drugs could have benefits outside their widely used action on diabetes and obesity.
Specifically, it suggests that GLP-1 drugs could act upon impulse control and stress-reward systems in the brain relating to substance and alcohol misuse.
The findings appear in the journal Criminology.
“As GLP-1 medications become increasingly widespread, understanding their broader behavioral effects becomes an important public health and criminological question that requires careful study,” said researcher Daniel Semenza, PhD, from Rutgers University.
Recent research has suggested that GLP-1 receptor agonists (RAs) such as exenatide, liraglutide, semaglutide, and dulaglutide have benefits beyond glycemic control and weight loss.
These include reducing the risk of multiple psychiatric and neurocognitive conditions and improving impulse control.
Semenza and Christopher Thomas, also from Rutgers, examined the relationship between the use of GLP-1 drugs and violent behavior using recent survey data from 821 U.S. adults in a 2025 nationally representative survey who had used these medications at some point in their lives. Of these, 597 were current users and 224 were former users.
Given established connections between aggression, alcohol use, and impulsivity, they also investigated whether current GLP-1 use was associated with a lower risk of violence by moderating the associations of impulsivity and alcohol use with violent crime.
The team found that impulsivity and alcohol use were strongly associated with committing violent crime. Each standard deviation increase in impulsivity was associated with a 1.9-fold increase in violence, and each unit increase in an alcohol use index was associated with a 1.8-fold increase.
However, current GLP-1 receptor agonist use was associated with significantly weaker associations between either impulsivity or alcohol use and violent crime compared with former GLP-1 drug use, attenuating these by approximately 62% and 52%, respectively.
This meant that even when users of GLP-1 receptor agonists drank alcohol or acted impulsively, it would be less likely to lead to violent crime.
The relationship was particularly strong relating to impulsivity and less so with alcohol use.
“Understanding the neurobiological mechanisms by which GLP-1 receptor signaling may moderate impulsivity-related risk pathways represents an important research opportunity,” the researchers concluded.
“Given the rapidly expanding use of GLP-1 receptor agonists throughout the United States and the rest of the world, this pattern of reduced violence risk warrants ongoing attention from both researchers and policymakers.”
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NIH diversity programs doubled undergraduates’ odds of getting a Ph.D., 20-year study finds
The path to becoming a scientist is long and twisting, making it difficult to assess whether programs intended to help those careers along are successful.
But on Wednesday, the results of one such study are being published after 20 years of research. The paper in the journal Science Advances found that two diversity-oriented programs supported by the National Institutes of Health doubled the odds that an undergraduate student would earn a Ph.D.
Macrophage EGFR Activity Linked to Immune Suppression, Tumor Growth in Colorectal Cancer
Researchers at the Medical University of Vienna have identified a new role played by epidermal growth factor receptor (EGFR) signaling in metastatic colorectal cancer (mCRC), finding that its activity in myeloid immune cells helps shape the tumor microenvironment and influences tumor growth. The study, published in Cell Death & Differentiation, indicates that EGFR signaling does not affect only cancer cells but contributes to how immune cells regulate anti-tumor responses.
“Our results show that EGFR in myeloid cells is a key regulator of the tumor-promoting immune landscape,” said senior author Maria Sibilia, PhD, a professor of tumor biology and director of the Center for Cancer Research at Medical University of Vienna.
Metastatic colorectal is a leading cause of cancer-related deaths worldwide. EGFR-blocking antibody treatments are already part of standard first-line therapy for patients with wild-type KRAS/BRAF tumors, but not all patients respond to this form of treatment, and even among those that do respond, resistance frequently develops. The new findings help clarify why EGFR expression in tumor cells alone does not fully predict therapeutic outcomes and suggest that immune-cell signaling is an important factor in treatment response.
While, EGFR has been broadly studied as a tumor cell receptor, earlier research has suggested that EGFR-positive myeloid cells are associated with worse prognosis in CRC and hepatocellular carcinoma. Studies in mice had also shown that deleting EGFR in myeloid cells reduced tumor burden, while deleting it in tumor epithelial cells had limited effect. However, the contribution of immune-cell EGFR signaling on the response to anti-EGFR therapy has not been broadly studied or understood.
To address this, the Sibilia lab used genetically engineered mouse models of colorectal cancer with single-cell RNA sequencing, proteomic profiling, and combined it with analysis of patient-derived datasets. The team focused on tumor-associated myeloid cells, including macrophage subsets known to shape immune suppression within the tumor microenvironment. To allow direct comparison of outcomes, EGFR was selectively deleted in either myeloid cells or tumor epithelial cells in preclinical models.
Single-cell analyses showed that loss of EGFR in myeloid cells reduced populations of tumor-promoting macrophages, including Spp1+ and C1qc+ subsets, and altered signaling pathways linked to inflammation and immune regulation. Reduced activity in TGFβ, IFNγ, and JAK/STAT pathways was associated with decreased expression of immune checkpoint molecules and changes in myeloid–T cell communication. CD8+ T cells in EGFR-deficient tumors showed lower expression of exhaustion markers such as Pdcd1 and Havcr2, suggesting a shift in T cell functional state.
A key finding was the identification of thrombospondin-1 (THBS1) as a myeloid-derived ligand regulated by EGFR signaling. Further analysis confirmed that EGFR activity influences THBS1 expression in macrophages and patient data also showed that high expression of both EGFR and THBS1 correlated with poorer outcomes, and combined gene signatures were associated with reduced survival.
The researchers also noted that tumor-associated macrophages and other myeloid populations can shift between anti-tumor and tumor-promoting states, and that their role in EGFR-targeted therapy response had not been fully defined.
One conclusion drawn by the researchers based on their work is that myeloid EGFR signaling contributes to immunosuppression in mCRC and may affect treatment response to both targeted therapy and immunotherapy approaches. “These findings strongly suggest that targeting EGFR specifically in myeloid cells may be of great therapeutic benefit for patients with CRC,” the researchers wrote.
The data also indicate that therapeutic strategies that only address tumor cell EGFR likely don’t address the full landscape of its effects and may not indicate the extent of treatment response. Instead, the investigators suggested, modulation of EGFR signaling in immune cells, particularly macrophage populations, could improve the effectiveness of existing EGFR inhibitors and may enhance response to immune checkpoint blockade by reducing T cell exhaustion and checkpoint expression.
Building on this, the team will now investigate myeloid-specific EGFR inhibition strategies and explore targeted delivery methods, such as nanoparticles directed toward EGFR-positive macrophage populations. Additional work will also seek to validate THBS1 as a biomarker for patient stratification and to determine how targeting this pathway might be integrated with immunotherapy regimens.
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