PubMed Trending Research Digest — September 06, 2026

Automated digest · 97 articles · 15 research areas · September 06, 2026

Overview

Across this week’s papers, a dominant theme is immunology as a “systems” problem: therapies are being reframed around how immune cells are programmed by their microenvironments (e.g., fibroinflammatory stroma in hepatocellular carcinoma, senescence-driven immune activation in AML, and fibroblast-mediated suppression of cGAS–STING signaling in pancreatic cancer). Mechanistic work is increasingly paired with translational intent—such as PPARα activation to restore GSDME-dependent pyroptosis and sensitize HCC to PD-1 blockade, or senescence–TGF-β–SMAD–NET signaling as a target to prevent chemotherapy-driven metastatic “awakening.” Complement and inflammasome/PANoptosome biology also continue to expand as actionable nodes for modulating inflammatory cell death and neuroinflammation.

A second major thread links metabolism, microbiota, and inflammation to disease trajectories. Studies connect gut-derived metabolites (e.g., imidazole propionate in PSC; KRAS-driven tumor microbiome shifts in colorectal cancer) and exercise physiology (lactate/Gpr81 signaling) to immune function and clinical risk. In parallel, multiple papers emphasize immunometabolic regulators—such as itaconate as an inflammatory brake, mitochondrial dysfunction as an OXPHOS–immune trigger in heart failure, and lipid metabolism/epigenetic control in tumor-associated macrophages. Together, these results reinforce a growing view that controlling inflammatory outcomes often requires tuning metabolic inputs and inter-organ signaling.

Finally, the digest highlights accelerating “measurement and prediction” capabilities: AI/ML approaches for EEG and epilepsy decision support, imaging/radiomics for immune structure (TLS) in breast cancer, and biomarker frameworks spanning neurodegeneration (ALS protein signatures, ALS–FTD biotypic models) and cardiovascular risk (trajectory-based inflammatory–metabolic indices). Clinical and perioperative research also appears—ranging from device- and protocol-level strategies (ECCO2R, ROX-guided intubation, hemodynamic monitoring signals) to risk stratification and long-term outcomes—suggesting that better data integration is increasingly central to improving care.

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Neurodegeneration & neuroinflammation (including ALS/FTD/AD)

Protein Biomarkers in Risk and Prognosis of Amyotrophic Lateral Sclerosis.

This study profiled 363 proteins in plasma and cerebrospinal fluid (CSF) from 198 patients with amyotrophic lateral sclerosis (ALS) and 125 matched controls using Olink assays, and assessed associations with disease status, survival, functional decline, and longitudinal biomarker stability, with external validation in UK Biobank (UKB). It identified 125 proteins significantly associated with at least one ALS outcome and performed network/enrichment analyses to define risk and prognosis biomarker patterns. These plasma/CSF protein signatures could support earlier detection of ALS pathobiology and improve prognostic stratification for clinical trials and patient management.

Pan L, Hou C, Seitz C et al. · European journal of neurology · (2026) · View on PubMed ↗ · Free PDF ↗

Progress towards a biotypic biomarker profile for amyotrophic lateral sclerosis-frontotemporal spectrum disorders.

This article reviewed and advanced the concept of a biotypic biomarker profile for the amyotrophic lateral sclerosis–frontotemporal spectrum (ALS-FTSD), focusing on when silent pathobiology becomes detectable before clinical phenoconversion. It argues that ALS and FTD lie on a spectrum with shared genetic risk and pathology, and that an array of biomarkers is needed to map underlying disease activity years to decades before symptom onset. Scientifically, a biotypic biomarker framework could enable earlier and more precise timing of disease-modifying therapies across the ALS-FTSD continuum.

Strong MJ, Donison N, Al-Chalabi A et al. · Brain : a journal of neurology · (2026) · View on PubMed ↗ · Free PDF ↗

Breaking the autophagy-oxidative stress vicious cycle in Alzheimer’s disease: Lactiflorin unlocks P62 dual phosphorylation via ULK1 targeting.

This mechanistic preclinical study investigated how lactiflorin (LAC), a monoterpene glycoside from Paeonia lactiflora, modulates autophagy and oxidative stress in models of Alzheimer’s disease. The authors report that lactiflorin unlocks P62 dual phosphorylation by targeting ULK1, thereby breaking the autophagy–oxidative stress vicious cycle. Targeting the ULK1–P62 axis with lactiflorin could represent a therapeutic strategy to restore autophagy and reduce neurodegenerative stress pathways.

Zhang J, Chen X, Hu Z et al. · Journal of ethnopharmacology · (2026) · View on PubMed ↗

Identification of interleukin-11 as a comorbid risk factor for prostate cancer and Alzheimer’s disease using integrated bioinformatics and machine learning.

Using integrated bioinformatics and a two-tier machine learning pipeline on multi-cohort transcriptomic datasets (AD: GSE48350, GSE5281, GSE28146; PCa: TCGA-PRAD, DKFZ2018, MSKCC), this study investigated shared molecular drivers of prostate cancer and Alzheimer disease and tested interleukin-11 (IL11) as a functional comorbidity factor. IL11 emerged as a shared transcriptomic signal and was supported by machine-learning prioritization and downstream analyses (including differential expression, weighted gene co-expression network analysis, and validation steps) linking IL11-related pathways to both diseases. Identifying IL11 as a shared risk/comorbidity driver could enable new therapeutic targeting strategies for patients with overlapping susceptibility to PCa and AD.

Wang M, Qian Y, Huang E et al. · Frontiers in immunology · (2026) · View on PubMed ↗ · Free PDF ↗

Multilevel genomic, transcriptomic, and epidemiologic evidence linking diabetic retinopathy to Alzheimer disease.

This study combined two-sample Mendelian randomisation, Bayesian colocalisation, and summary-data-based MR to test whether genetically predicted diabetic retinopathy (DR) liability is causally associated with Alzheimer disease (AD) risk and to identify shared genomic loci and expression-mediated genes. The multi-omics approach provided evidence for genetic convergence between DR and AD and implicated shared neurovascular-metabolic regulatory pathways through colocalised loci and candidate genes. These findings support a biologically grounded link between DR and AD and may help prioritize molecular targets for preventing or treating AD in people with diabetes-related microvascular disease.

Li J, Liu Q, Ma Q et al. · Journal of global health · (2026) · View on PubMed ↗ · Free PDF ↗

Intraoperative hemodynamic patterns during hypotension prediction index-guided care: a high-resolution secondary analysis of the HYT trial.

In a high-resolution secondary analysis of the multicenter HYT trial, investigators studied 181 surgical patients to characterize how arterial pressure, preload-related physiology (stroke volume variation, SVV), and Hypotension Prediction Index (HPI)-derived hypotension risk signals co-occur over time. The signal analysis quantified temporal relationships between MAP drops (MAP <65 mmHg), SVV-defined preload dependence (SVV >13%), and algorithmic risk, describing patterns of coexistence during hypotension prediction and care. This work is significant because it helps explain why HPI reduces intraoperative hypotension yet may yield inconsistent patient-centered outcomes, guiding refinement of hemodynamic monitoring and prediction algorithms.

Ripollés-Melchor J, Espinosa ÁV, Aldecoa C et al. · Minerva anestesiologica · (2026) · View on PubMed ↗

The Crosstalk Between Diabetes and Alzheimer’s Disease: A Molecular Perspective.

This narrative molecular review synthesized evidence linking type 2 diabetes mellitus (T2DM) and Alzheimer disease (AD), framing AD as a “type 3 diabetes” concept driven by impaired brain insulin signaling and insulin resistance. It highlights shared mechanisms such as chronic neuroinflammation, oxidative stress, mitochondrial dysfunction, and dysregulated glucose metabolism, with particular emphasis on the PI3K/Akt pathway as a central node connecting insulin resistance to AD pathology. The review is significant because it supports diabetes-targeted molecular pathways as potential therapeutic avenues for AD prevention or treatment.

Catakli D, Ozen-Basoglu O, Tuncgovde EB et al. · Basic & clinical pharmacology & toxicology · (2026) · View on PubMed ↗ · Free PDF ↗

Priming of CD8+ T cells by peripheral dendritic cells exacerbates tau-mediated neurodegeneration.

This study investigated how peripheral dendritic cells prime CD8+ T cells that exacerbate tau-mediated neurodegeneration, using tauopathy mouse models with cDC1 deficiency and impaired antigen cross-presentation. Tauopathy mice lacking cDC1s or antigen cross-presentation were protected from neurodegeneration, showing reduced brain CD8+ T cell infiltration and glial activation with limited clonal expansion. The findings identify cDC1-mediated cross-presentation as a key step enabling pathogenic CD8+ T-cell priming in tauopathies, suggesting a potential immunomodulatory intervention point.

Hu H, Lin PB, Zeng C et al. · Nature neuroscience · (2026) · View on PubMed ↗ · Free PDF ↗

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Clinical trials, perioperative care, and health outcomes (non-oncology)

Comprehensive Risk Factor Control Attenuates Excess Cardiovascular Risk in Rheumatoid Arthritis: A Prospective Cohort Study.

This prospective cohort study in UK Biobank evaluated whether a nine-component joint risk factor control score (diet, smoking, physical activity, blood pressure, glycated hemoglobin, LDL-C, hsCRP, BMI, and estimated GFR) attenuates incident cardiovascular disease (CVD) in 4,426 rheumatoid arthritis (RA) patients versus 17,704 matched non-RA controls, including modification by genetic susceptibility. Joint risk factor control was associated with reduced excess CVD risk in RA, indicating that comprehensive management can blunt RA-related cardiovascular vulnerability. Clinically, the findings support aggressive, multi-domain risk factor control as a practical strategy to lower CVD events in RA patients, potentially guided by genetic risk.

Fan H, Zi X, Li T et al. · European journal of preventive cardiology · (2026) · View on PubMed ↗ · Free PDF ↗

Impact of an ROX index-guided intubation strategy on mortality in patients receiving high-flow nasal cannula: a target trial emulation.

Using a target trial emulation approach with MIMIC-IV electronic health record data, this study compared per-protocol outcomes of ROX index-guided intubation (intubation within 2 hours after ROX threshold crossing) versus usual care in adults who initiated high-flow nasal cannula (HFNC) within 7 days of ICU admission. The analysis estimated the effect of acting on the ROX index to guide intubation timing on mortality after HFNC initiation. If ROX-guided strategies reduce mortality, they would provide an actionable bedside decision rule to improve outcomes in patients at risk of HFNC failure.

Yamamoto R, Tohyama T, Han A et al. · Journal of intensive care · (2026) · View on PubMed ↗ · Free PDF ↗

Enhancing medical record management: effective implementation of operational standards at Wallaga University Comprehensive Specialized Hospital, 2025.

This quality improvement project implemented operational standards for medical record management at Wallaga University Comprehensive Specialized Hospital, targeting improved retrieval and tracking of patient records between 15 September and 10 December 2025. Using sequential plan-do-study-act (PDSA) cycles and staff training, the intervention aimed to raise the baseline record management performance from 35% to 90%. Improved medical record handling can reduce delays and inefficiencies, supporting faster access to information and better care delivery.

Bayisa G, Fite MB, Degefe A et al. · BMJ open quality · (2026) · View on PubMed ↗

An integrated lifestyle intervention for mitigation of adverse effects associated with androgen deprivation therapy for prostate cancer (STAMINA): a multicentre, randomised trial.

This multicentre, randomized trial (STAMINA) evaluated an integrated lifestyle intervention combining supervised exercise to mitigate adverse effects of androgen deprivation therapy (ADT) in men with prostate cancer across 15 UK NHS trusts. Participants on ADT were randomized to the STAMINA intervention versus behaviourally Optimised Usual Care, with primary focus on cancer-specific quality of life and fatigue. If effective, embedding structured exercise into ADT care could improve patient-centered outcomes and reduce treatment-related burden.

Bourke L, Rosario DJ, Reale S et al. · The Lancet. Oncology · (2026) · View on PubMed ↗

Unmet needs in the treatment of erectile dysfunction and a place for topical treatments in the therapeutic landscape.

This Delphi consensus initiative synthesized evidence and expert recommendations on unmet needs in erectile dysfunction (ED) treatment and the appropriate role of topical therapy, specifically the FDA-cleared topical agent MED3000 (Eroxon®), for men who may not respond to systemic phosphodiesterase type 5 inhibitors (PDE5is). The key outcome was a structured set of consensus statements guiding clinical decision-making about when and how to use topical Eroxon in the ED treatment landscape. Scientifically and clinically, it helps standardize care pathways for ED patients with inadequate response or preference against systemic PDE5 inhibition.

Brock GB, Yafi FA, Hellstrom WJG et al. · The journal of sexual medicine · (2026) · View on PubMed ↗

How I Treat Pediatric Hematology-Oncology Patients from Families Identifying as Jehovah’s Witnesses.

This article reviewed practical approaches for clinicians managing pediatric hematology-oncology patients from families identifying as Jehovah’s Witnesses, emphasizing ethical and clinical considerations around blood transfusion refusal. It highlighted that transfusion avoidance is not uniform and depends on patient/family conscience and interpretation of religious guidance, and it illustrates strategies through three clinical cases. The significance is improved, case-based decision-making that aligns hematology-oncology care with patient-centered ethics while maintaining safety in transfusion-averse settings.

Weaver MS, Takemoto C, Johnson LM · Blood · (2026) · View on PubMed ↗

Depressive Symptoms Trajectories Across the Transition to Cardiovascular Disease in Middle-Aged and Older Adults: A Multicohort Study.

This multicohort longitudinal study analyzed depressive symptom trajectories around incident cardiovascular disease (CVD) using data from the Health and Retirement Study (HRS), English Longitudinal Study of Ageing (ELSA), and China Health and Retirement Longitudinal Study (CHARLS). Depressive symptoms were tracked before and after CVD diagnosis across multinational aging populations to characterize how mental health changes during the transition to diagnosed CVD. The results are clinically significant for identifying when depressive symptoms emerge or worsen relative to CVD onset, informing timing of screening and integrated care.

Wang J, Wu Z, Zou X et al. · European journal of preventive cardiology · (2026) · View on PubMed ↗

Long-term hormone therapy for perimenopausal and postmenopausal women.

This updated Cochrane systematic review evaluated long-term hormone therapy (≥1 year) in perimenopausal and postmenopausal women, focusing on mortality, cardiovascular outcomes, cancer, gallbladder disease, fractures, and cognition. It synthesized evidence from randomized trials and related sources to determine the prolonged effects of hormone therapy on these clinically important endpoints. The review is significant for guiding risk–benefit decisions about extended hormone use in women transitioning through menopause.

Bofill Rodriguez M, Yong LN, Mirkov S et al. · The Cochrane database of systematic reviews · (2026) · View on PubMed ↗

Physical, Psychophysical and Psychological Predictors of Persistent or Recurrent Non-Specific Low Back Pain: A Systematic Review and Meta-Analysis.

This systematic review and meta-analysis assessed whether physical, psychophysical, or psychological predictors can forecast persistent or recurrent non-specific low back pain (LBP), using studies searched through January 2025. It evaluated predictors of pain intensity and disability with risk-of-bias assessment (QUIPS) and evidence certainty grading (GRADE). The findings are important for developing prognostic tools and targeting modifiable psychosocial or physical factors to reduce chronicity in non-specific LBP.

Wongwitwichote K, Yu CWG, Devecchi V et al. · European journal of pain (London, England) · (2026) · View on PubMed ↗

Volatile-Free Total Intravenous Anesthesia for Major Gynecologic Surgery in a Manifesting Female Carrier of Becker Muscular Dystrophy: A Case Report.

This case report described volatile-free total intravenous anesthesia for major gynecologic surgery in a manifesting female carrier of Becker muscular dystrophy due to a dystrophin (DMD) gene variant. The report addresses perioperative risk in dystrophinopathies, where succinylcholine and volatile anesthetics can be associated with hyperkalemia, rhabdomyolysis, and malignant hyperthermia-like reactions, and highlights the rarity of clinically manifest BMD in females. The clinical significance is that it provides practical perioperative guidance for anesthetic selection in a high-risk genetic neuromuscular condition.

Ibrahim H, Eletreby IM, Sabra BA et al. · Cureus · (2026) · View on PubMed ↗ · Free PDF ↗

Observed Weight Gain in Patients With Pulmonary Arterial Hypertension Treated With Sotatercept.

This single-center retrospective observational cohort study evaluated adult Group 1 pulmonary arterial hypertension (PAH) patients treated with sotatercept to characterize observed changes in body weight and body composition. Patients showed clinically notable total body weight gain that was reported as not attributable to fluid retention, suggesting a potential lean-mass or off-target body-composition effect. These findings are important for PAH management because excessive weight gain may worsen outcomes while increases in lean mass could improve exercise capacity, informing monitoring and future mechanistic studies of sotatercept.

Greene RA, Tat D, Sherman-Roe A et al. · Pulmonary circulation · (2026) · View on PubMed ↗ · Free PDF ↗

Endoscopic Sphincterotomy Prior to Biliary Stenting for Malignant Biliary Obstruction: A Systematic Review and Meta-Analysis of Randomized Controlled Trials.

This systematic review and meta-analysis of randomized controlled trials assessed whether endoscopic sphincterotomy (ES) performed prior to ERCP-guided biliary stenting improves outcomes in patients with unresectable malignant biliary obstruction (MBO), compared with biliary stenting without ES. The analysis focused on safety and effectiveness, particularly post-ERCP pancreatitis (PEP) risk and bleeding risk, and examined how effects might vary by MBO etiology and stent type. The results are clinically significant for optimizing ERCP procedural strategy in MBO by balancing pancreatitis prevention against procedure-related bleeding.

Meine SC, de Oliveira Amaral G, Tedesco MR et al. · Journal of gastroenterology and hepatology · (2026) · View on PubMed ↗ · Free PDF ↗

MRPL35 Suppresses Autophagy-Mediated Ferroptosis in Hepatocellular Carcinoma via the AMPK/mTOR Axis.

This preclinical study examined the role of mitochondrial ribosomal protein L35 (MRPL35) in hepatocellular carcinoma (HCC) by testing whether MRPL35 suppresses autophagy-mediated ferroptosis via the AMPK/mTOR signaling axis. MRPL35 was reported to modulate autophagy and ferroptosis-related phenotypes in HCC cells using RT-qPCR, western blotting, and functional assays (including proliferation/migration assays and flow cytometry-based measurements). These findings suggest MRPL35–AMPK/mTOR–autophagy–ferroptosis as a potential therapeutic vulnerability in HCC.

Xu Y, Xiao L, Shi Z et al. · Current cancer drug targets · (2026) · View on PubMed ↗

Global prevalence of multiple sclerosis surpasses 3 million: 2024 update of the Multiple Sclerosis International Federation Atlas of MS.

This epidemiological analysis updated the Multiple Sclerosis International Federation (MSIF) Atlas using country-submitted data to estimate global multiple sclerosis prevalence (including pediatric MS) and incidence, and to assess changes over time using 2013, 2020, and 2024 datasets. The update incorporated data from 133 countries (covering 93% of the global population) and reported that global MS prevalence surpasses 3 million. These findings are significant for health planning and resource allocation by providing the most current global burden estimates and trends for MS worldwide.

King R, Marrie RA, van der Mei I et al. · Multiple sclerosis (Houndmills, Basingstoke, England) · (2026) · View on PubMed ↗

2026 iCatCare consensus guidelines on the diagnosis and management of chronic kidney disease in cats.

This consensus guideline article provides veterinary recommendations for diagnosing and managing chronic kidney disease (CKD) in cats, aligned with the International Renal Interest Society (IRIS) staging system. It summarizes practical approaches for early diagnosis, staging, and medical and nutritional treatment, including optimizing the home and clinic environment to improve quality of life. These guidelines are clinically significant because they standardize CKD care in senior cats to slow progression and improve survival and welfare.

Taylor S, Finch N, Caney S et al. · Journal of feline medicine and surgery · (2026) · View on PubMed ↗ · Free PDF ↗

Safety and Glycemic Efficacy of Perioperative Liraglutide in Cardiac Surgery: A Systematic Review and Meta-Analysis of Randomized Controlled Trials.

This systematic review and meta-analysis evaluated randomized controlled trials in adults undergoing cardiac surgery comparing perioperative subcutaneous liraglutide (a GLP-1 receptor agonist) versus placebo or insulin-based usual care. The key finding was that liraglutide’s glucose-lowering effect is glucose-dependent, potentially separating glycemic efficacy from hypoglycemia risk compared with intravenous insulin strategies used for perioperative hyperglycemia. Clinically, this supports considering liraglutide as a safer perioperative glycemic-control alternative in cardiac surgery patients, pending the pooled RCT outcome data.

Gamal I, Elkasaby MH, Ewidat O et al. · Cardiology in review · (2026) · View on PubMed ↗

Percutaneous Coronary Intervention in Patients Undergoing Transcatheter Aortic Valve Implantation: A Systematic Review and Meta-Analysis With Reconstructed Individual Patient Data and GRADE Assessment.

This systematic review and meta-analysis reconstructed individual patient data from randomized trials to compare percutaneous coronary intervention (PCI) versus conservative management/deferral in transcatheter aortic valve implantation (TAVI/TAVR) candidates with coronary artery disease. The analysis synthesized trial-level and reconstructed time-to-event data to estimate pooled effects of PCI on clinical outcomes in this specific high-risk population. Scientifically and clinically, it aims to clarify whether routine PCI provides incremental benefit over deferral in TAVI patients with coexisting CAD.

Yassin MN, Elfeqi K, Abdelmaksoud A et al. · Cardiology in review · (2026) · View on PubMed ↗

Extracorporeal CO2 elimination for acute exacerbation of severe COPD requiring invasive mechanical ventilation: a randomized controlled trial (the X-COPD trial).

The X-COPD randomized controlled trial studied adults with acute hypercapnic respiratory failure due to acute exacerbation of COPD (AE-COPD) requiring invasive mechanical ventilation (IMV) who failed or were ineligible for extubation within 24 hours, comparing extracorporeal CO2 elimination (ECCO2R) to standard IMV. The key objective was to test whether ECCO2R-facilitated early extubation improves outcomes versus continuing IMV. If effective, this would provide a device-based strategy to reduce IMV-related complications and improve survival/disability outcomes in severe AE-COPD.

Karagiannidis C, Riera J, Blanco-Schweizer P et al. · Critical care (London, England) · (2026) · View on PubMed ↗ · Free PDF ↗

Functional coupling between MC4R and Kir7.1 contributes to clozapine-induced weight gain in female mice.

This study investigated the neural mechanism of clozapine-induced weight gain in female mice by testing functional coupling between the melanocortin 4 receptor (MC4R) and the Kir7.1 potassium channel. It found that clozapine promotes obesity through hyperphagia and that this effect requires MC4R–Kir7.1 functional coupling, identifying the axis as a downstream convergence node within clozapine’s polypharmacology. The significance is that it provides a tractable circuit-level target for mitigating clozapine-associated metabolic syndrome.

Li L, Hernandez CC, Gimenez LE et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Prognostic Value of pc-ASPECTS Before Endovascular Therapy in Posterior Circulation Stroke: A Systematic Review and Meta-Analysis.

This systematic review and meta-analysis evaluated the prognostic performance of posterior circulation Acute Stroke Prognosis Early CT Score (pc-ASPECTS; 0–10) measured before endovascular therapy (EVT) in patients with posterior circulation stroke, focusing on how performance varies by imaging modality (e.g., DWI, CTA source imaging). Across included studies, pc-ASPECTS was assessed for association with 90-day modified Rankin Scale (mRS) outcomes, and the analysis specifically addressed whether modality used to derive pc-ASPECTS changes prognostic accuracy. Clinically, clarifying modality-dependent prognostic validity can improve patient selection and risk stratification for EVT in vertebrobasilar stroke.

Elek A, Kıran F, Valizadeh P et al. · AJNR. American journal of neuroradiology · (2026) · View on PubMed ↗ · Free PDF ↗

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Autoimmunity, immune regulation, and tolerance

Evaluating the effect of age and comorbidity on dupilumab-dependent immunoglobulin E reduction in children with food allergy.

This retrospective analysis studied 44 children with food allergy receiving dupilumab to determine whether food-specific IgE (sIgE) decreases over time and whether longitudinal sIgE change depends on allergen type, race, sex, indication for therapy, or age at initiation. The key finding was that dupilumab-associated sIgE reductions occurred over time and were evaluated for differential effects across these patient and treatment characteristics. If confirmed prospectively, these data could help personalize dupilumab use in pediatric food allergy by anticipating which subgroups are most likely to achieve meaningful sIgE lowering.

Afzal SY, MacDougall MS, Lu D et al. · Allergy and asthma proceedings · (2026) · View on PubMed ↗

Lessons learned from clinical trials of thymic stromal lymphopoietin (TSLP) inhibition.

This article reviewed lessons from clinical trials targeting thymic stromal lymphopoietin (TSLP) inhibition in type 2 (T2) immune-mediated epithelial-driven diseases. It discusses the biology of TSLP in activating dendritic cells and promoting IL-4, IL-5, and IL-13 pathways, and frames the therapeutic rationale for tezepelumab, a monoclonal antibody that blocks TSLP. Synthesizing trial experience can guide future development and optimization of TSLP-targeted therapies across inflammatory conditions.

Corren J, Borish L, Brightling C et al. · The Journal of allergy and clinical immunology · (2026) · View on PubMed ↗

One mechanism, two diseases: Involvement of enzyme-substrate complexes in the pathogenesis of celiac disease and rheumatoid arthritis.

This review article analyzed shared immunopathogenic mechanisms in celiac disease and rheumatoid arthritis, focusing on HLA class II determinants, antibodies to deamidated/citrullinated peptides, and autoantibodies to the modifying enzymes transglutaminase 2 (TG2) and peptidyl arginine deiminase 2/4 (PAD2/PAD4). It highlights a unifying model in which enzyme–substrate complexes are pivotal for antigen generation and downstream T-cell/antibody responses in both diseases. The mechanistic synthesis provides a framework for designing more precise antigen- and enzyme-complex–targeted therapies across autoimmune conditions.

Sollid LM · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗

Human-inherited RORγT deficiency encompasses genetic heterogeneity, T cell deficiency, and clinical homogeneity.

The study characterized inherited RORγT deficiency by reporting five additional patients with mycobacterial disease and chronic mucocutaneous candidiasis who were homozygous for new loss-of-function variants in RORC (the gene encoding RORγT). Patients showed near-complete depletion of innate-like adaptive T cells, including mucosa-associated invariant T (MAIT) and invariant natural killer T (iNKT) cells, with clinical features that were largely homogeneous except for one patient receiving early prophylaxis. This expands the genetic heterogeneity of RORC/RORγT deficiency and clarifies the immunologic basis of susceptibility, supporting early prophylaxis strategies for affected individuals.

Fagniez I, Tsumura M, Guérin A et al. · The Journal of experimental medicine · (2026) · View on PubMed ↗

Tape Strip Transcriptomics Reveal Nemolizumab Effects on Pruritus, Hyperplasia, Inflammation, and Extracellular Matrix Markers in Patients With Moderate-to-Severe Atopic Dermatitis.

Using tape-strip transcriptomics from lesional and non-lesional skin, this study evaluated molecular effects of nemolizumab (an anti-IL-31Rα monoclonal antibody) in patients with moderate-to-severe atopic dermatitis enrolled in ARCADIA 1 and 2 trials. After 16 weeks, nemolizumab-treated patients showed transcriptomic changes consistent with reduced pruritus-associated signaling and improvements in epidermal hyperplasia, inflammation, and extracellular matrix marker expression compared with placebo. These results are clinically important because they provide mechanistic biomarkers for nemolizumab’s action and may help predict or monitor response in adolescents and adults receiving background topical corticosteroids ± calcineurin inhibitors.

Liu D, Duca ED, Delaleu N et al. · Allergy · (2026) · View on PubMed ↗ · Free PDF ↗

Vaccination considerations in autoimmune rheumatic diseases.

This narrative review synthesized evidence and practical guidance on vaccination strategies for patients with autoimmune rheumatic diseases (ARDs) who are at increased infection risk due to immune dysregulation and immunosuppressive therapies. The key message was that vaccination coverage is suboptimal and that optimizing timing, adherence, and vaccine selection—especially during outbreaks like COVID-19 and measles—is crucial for this population. Scientifically and clinically, it supports tailored vaccination approaches to reduce vaccine-preventable infections while accounting for treatment-related immunogenicity and immunosenescence.

Kapetanovic MC · Nature reviews. Rheumatology · (2026) · View on PubMed ↗

Targeting the FOXP3-T-bet interaction to restore Treg stability in IFN-γ-driven autoimmunity.

This study examined how the FOXP3V408M mutation affects FOXP3 transcriptional complex remodeling and Treg stability in IFN-γ-driven autoimmunity using FOXP3V408M IPEX patients and FOXP3V408M knock-in mice. The V408M mutation intrinsically impairs Treg-mediated control of Th1 inflammation, revealing a distinct pathogenic mechanism for this IPEX mutation. Targeting the FOXP3–T-bet interaction is proposed as a strategy to restore Treg stability and reduce Th1/IFN-γ–associated autoimmunity in FOXP3V408M disease.

Zhang W, Liu X, Gu Z et al. · Cellular & molecular immunology · (2026) · View on PubMed ↗

IL-17A-producing γδ T cells control pulmonary Mycobacterium abscessus infection in mice.

This study investigated the role of IL-17A–producing γδ T cells in pulmonary Mycobacterium abscessus infection using mouse infection models with and without functional IFN-γ–mediated immunity and with pulmonary fibrosis. IL-17A+ γδ T cells were essential for controlling infection by directly eliminating extracellular bacteria, with bactericidal activity mediated through granzyme B–dependent cytotoxic pathways. These findings support IL-17A+ γδ T cells as a potential immunotherapeutic target to enhance host defense against non-tuberculous mycobacteria.

Hu X, Lin S, Meng W et al. · Nature microbiology · (2026) · View on PubMed ↗

Role of complement and complement-targeted therapeutics in neurological diseases.

This review studied how complement biology and complement-targeted therapeutics contribute to neurological diseases in humans, focusing on complement-fixing pathogenic antibodies and broader complement dysfunction. It found that while approved complement-pathway drugs are largely concentrated in antibody-mediated disorders such as myasthenia gravis and neuromyelitis optica spectrum disorder, an expanding pipeline of emerging therapies targets additional complement mechanisms relevant to neuroinflammation. The work is significant because it frames complement as a central driver of both impaired clearance and autoimmune neurodegeneration, guiding therapeutic development beyond current antibody-centric indications.

Dalakas MC, Lünemann JD · Nature reviews. Neurology · (2026) · View on PubMed ↗

Immune reset after deep B-lineage depletion: remission is not reprogramming.

This viewpoint article studied the concept of “immune reset” after deep B-lineage depletion therapies, including CAR T cells and T-cell engagers, in refractory systemic autoimmune diseases. It concluded that durable remission alone does not prove immune reset, because immune reset would require evidence of elimination of autoreactive memory and reconstitution of a renewed, self-tolerant repertoire. The article is significant because it sets evidentiary standards for mechanistic claims about CAR-based therapies in autoimmune disease.

Scherlinger M, Avouac J, Tsokos GC · Annals of the rheumatic diseases · (2026) · View on PubMed ↗ · Free PDF ↗

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Hematologic malignancies (AML/MDS/myelofibrosis) therapeutics & outcomes

Recent advances in cell therapy for AML/MDS.

This review summarized recent advances and ongoing challenges in cell therapy for acute myeloid leukemia (AML) and myelodysplastic syndromes (MDS), focusing on why progress has lagged behind CAR-T success in CD19- and B-cell maturation antigen (BCMA)-targeted malignancies. It highlighted that identifying an optimal CAR-T target with clinically manageable on-target effects on normal myeloid cells remains a central barrier. The scientific significance is that better target selection and engineering strategies could unlock effective CAR-T or related cellular therapies for AML/MDS.

Yokoyama H · International journal of hematology · (2026) · View on PubMed ↗

Comparison of venetoclax and azacitidine versus a cytarabine-based treatment for patients with acute myeloid leukaemia in first relapse after chemotherapy. A real-world study of the DATAML-IPC-AURAML consortium.

This retrospective real-world study from the DATAML-IPC-AURAML consortium compared salvage therapy with intermediate/high-dose cytarabine (DAC) versus venetoclax plus azacitidine (VEN-AZA) in adults with acute myeloid leukemia (AML) in first relapse after achieving complete remission (CR1) following 7+3 or CPX351 induction. Both approaches produced similar CR2 rates (66.0% with I/HDAC vs 66.7% with VEN-AZA). These findings support VEN-AZA as an effective salvage option with comparable early response to cytarabine-based regimens in relapsed AML patients.

Dumas PY, Bertoli S, Bérard E et al. · British journal of haematology · (2026) · View on PubMed ↗

Closing the disease modification gap: Emerging therapies in myelofibrosis beyond JAK inhibition.

This review studied emerging therapies for myelofibrosis beyond JAK inhibition, focusing on strategies that target pathways other than JAK-STAT signaling in myeloproliferative neoplasms. It highlighted multiple investigational drug classes—such as BET inhibition (pelabresib), PIM kinase inhibition (TP-3654), telomerase inhibition (imetelstat), nuclear export inhibition (selinexor), LSD1 inhibition (bomedemstat), and MDM2 antagonism—as potential options to address JAK inhibitor resistance and toxicity. The review is clinically significant because it frames how next-generation agents may improve disease modification and outcomes for patients with myelofibrosis.

Aluri A, Kishtagari A · Seminars in hematology · (2026) · View on PubMed ↗ · Free PDF ↗

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Inflammation, immunometabolism, and metabolic-immune axes

UBE2N deficiency contributes to MASH development via p62-regulated mitophagy and PANoptosis.

This mechanistic study examined how UBE2N (a K63-ubiquitin–conjugating enzyme) influences metabolic dysfunction-associated steatohepatitis (MASH) by using THAP11-regulated UBE2N downregulation in human and mouse hepatocytes and hepatocyte-specific Ube2n deficiency models. It found that Ube2n deficiency worsened western diet-induced MASH and fibrosis via PANoptosis and impaired mitophagy, while UBE2N overexpression reversed pathology by promoting PARKIN-mediated K63-p62 signaling at lysine 420. These results position UBE2N–K63 ubiquitination–p62/PARKIN pathways as potential therapeutic targets to prevent or treat MASH progression.

Wang F, Lee J, Park JS et al. · Nature metabolism · (2026) · View on PubMed ↗

Inflammation as a therapeutic target to improve kidney and cardiovascular outcomes.

This narrative review synthesized evidence that inflammation is a therapeutic target linking chronic kidney disease (CKD) to adverse kidney and cardiovascular outcomes, emphasizing biomarkers such as high-sensitivity C-reactive protein (hsCRP). It describes CKD as a pro-inflammatory state with dysregulated inflammatory pathways and highlights how systemic and local inflammation contribute to kidney damage, atherosclerosis, and cardiac dysfunction. The significance is that anti-inflammatory strategies—potentially guided by inflammatory biomarkers—may improve both renal and cardiovascular outcomes in CKD.

Tuttle KR, Kanbay M, Alicic RZ et al. · Nature reviews. Nephrology · (2026) · View on PubMed ↗

Tissue mitochondrial activity dictates the macrophage pool size.

This study examined how tissue mitochondrial activity influences macrophage pool size by tracking uptake of parenchyma-released mitochondria by macrophages across organs with oxidative metabolism (heart, skeletal muscle, and brown adipose tissue). It found that macrophage numbers closely matched organ mitochondrial activity, with mitochondrial activity in myofibers regulating CSF1 availability to control macrophage abundance. These results link metabolic state to immune cell homeostasis, suggesting that manipulating mitochondrial activity or CSF1 signaling could tune tissue macrophage populations.

Pena-Couso L, Sicilia J, Vieto S et al. · Science immunology · (2026) · View on PubMed ↗

Impaired liver-muscle lactate metabolism causes sarcopenia via lactic acidosis in skeletal muscle in mice.

This mouse study investigated whether impaired liver–skeletal muscle lactate metabolism drives sarcopenia by causing lactic acidosis in skeletal muscle. Aged mice showed reduced systemic lactate tolerance due to impaired hepatic lactate processing, leading to lactate accumulation and intracellular acidification in skeletal muscle that caused sarcopenia; pharmacologic HIF activation or liver-specific HIF1α activation improved age-associated phenotypes. These findings suggest that targeting lactate handling or HIF1α signaling could be a therapeutic approach to prevent or treat sarcopenia.

Eguchi T, Hayashiji N, Tabata S et al. · Science advances · (2026) · View on PubMed ↗

Cardiomyocyte-intrinsic somatic mtDNA mutations induce an OXPHOS-dependent immune response and promote progressive heart failure.

The study used PolgiMut mice to induce proofreading-deficient mitochondrial DNA polymerase (POLG D257A) somatic mtDNA mutations specifically in cardiomyocytes and assessed resulting phenotypes in vivo. Cardiomyocyte-intrinsic mtDNA mutations triggered an OXPHOS-dependent immune response, causing progressive contractile dysfunction and worsening heart failure. These findings support a cell-intrinsic mechanism linking age-associated mtDNA mutations to inflammatory, OXPHOS-driven cardiac decline and suggest potential targets in mitochondrial metabolism–immune signaling for heart failure progression.

Bubb K, Rigoni G, Papadea P et al. · Science advances · (2026) · View on PubMed ↗

Longitudinal inflammatory-metabolic-adiposity burden and incident heart failure across cardiovascular-kidney-metabolic stages: a prospective cohort study.

This prospective cohort study followed 1,946 participants across cardiovascular-kidney-metabolic (CKM) stages to test whether longitudinal trajectories of a CTGW composite index—C-reactive protein × triglyceride-glucose index × waist-to-height ratio—predict incident heart failure. The key finding was that cumulative and trajectory-based inflammatory–metabolic–adiposity burden was associated with higher risk of incident heart failure, with effects modified by baseline CKM stage. These results support using longitudinal composite biomarker trajectories for risk prediction and for identifying high-risk CKM phenotypes for prevention of heart failure.

Dai F, Dai Y · Cardiovascular diabetology · (2026) · View on PubMed ↗ · Free PDF ↗

Evaluative performance of triglyceride-glucose-frailty index versus surrogate insulin resistance indices for advanced cardiovascular-kidney-metabolic syndrome, cardiometabolic multimorbidity, and mortality: the role of estimated glomerular filtration rate.

This analysis evaluated 11,228 adults (NHANES 2001–2018) to compare the triglyceride-glucose-frailty index (TyG-FI) against surrogate insulin resistance indices for associations with advanced CKM syndrome, cardiometabolic multimorbidity (CMM), and mortality, with attention to baseline estimated glomerular filtration rate (eGFR). The key finding was that TyG-FI provided stronger evaluative performance for advanced CKM/CMM and mortality risk than conventional metabolic markers, and that baseline kidney function (eGFR) influenced these relationships. Clinically, TyG-FI may improve identification of patients at highest risk of adverse cardiometabolic outcomes, especially when kidney function is considered.

Liu K, Zhang JY, He H et al. · Cardiovascular diabetology · (2026) · View on PubMed ↗ · Free PDF ↗

Genetic evidence supports the combined targeting of lipoprotein(a) and LDL cholesterol to reduce coronary artery disease risk.

This genetic association study used coding loss-of-function variants in LPA and PCSK9 and polygenic/genetic scores for Lp(a) and LDL-C levels to test whether combined lowering of lipoprotein(a) and LDL cholesterol provides additive coronary artery disease (CAD) risk reduction. In 408,039 UK Biobank participants, LPA or PCSK9 loss-of-function carriers had lower CAD risk than noncarriers, and individuals carrying both variants had even lower risk (OR 0.73), supporting additive benefit. These findings provide genetic evidence that simultaneously targeting Lp(a) and LDL-C could more effectively reduce CAD risk than targeting either alone.

Wang S, Tang Y, Sui Y et al. · Nature cardiovascular research · (2026) · View on PubMed ↗

BCL-2 inhibition at antiretroviral therapy initiation reduces the intact SIV reservoir in macaques.

This study tested whether BCL-2 inhibition at antiretroviral therapy (ART) initiation reduces the intact SIV reservoir in 24 rhesus macaques treated at 14 days post infection with ART alone or ART plus venetoclax (with or without CD8α depletion). Venetoclax treatment produced a rapid and sustained reduction of the intact SIV reservoir in blood and lymph nodes, with partially reduced apoptotic features among CD4+ T cells that persisted. The results support venetoclax as a strategy to shrink the intact viral reservoir when combined with early ART in primate models.

Wiche Salinas TR, Harper J, Deleage C et al. · Nature microbiology · (2026) · View on PubMed ↗ · Free PDF ↗

The inhibition of lactate/Gpr81 signalling driven by moderate-intensity continuous training protects against osteoarthritis.

This study tested whether inhibiting lactate/Gpr81 signaling explains the protective effects of moderate-intensity continuous training (MICT) against osteoarthritis, using mouse models with gut microbiota depletion and microbiota transplantation. MICT had greater therapeutic potential than high-intensity continuous training, but its benefits were abolished by gut microbiota depletion and were transferable by transplanting microbiota from MICT-treated mice. The work implicates lactate/Gpr81 signaling as a mechanistic link between exercise-modulated gut microbiota and reduced OA progression.

Sun P, Guo Y, Xue A et al. · Experimental & molecular medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Itaconate and its derivatives in human health and diseases.

This review studied itaconate and its derivatives in human health and disease, focusing on the IRG1/ACOD1–itaconate immunometabolic axis. It found that itaconate acts as an immunometabolic “brake” connecting the TCA cycle to immune signaling by modulating inflammatory tone and redox balance across conditions including infection, metabolic disorders, ischemia–reperfusion injury, neurodegeneration, and autoimmunity. The significance is that it consolidates mechanistic and therapeutic rationale for targeting itaconate pathways to regulate inflammation and tissue homeostasis.

Gu J, Zhang W, Zhang J et al. · Signal transduction and targeted therapy · (2026) · View on PubMed ↗ · Free PDF ↗

Mitochondrial calcium, a potential sensor for homeostatic synaptic plasticity.

This study investigated whether mitochondrial calcium can act as a sensor for homeostatic synaptic plasticity in the chick embryo spinal cord (either sex). It found evidence that perturbations affecting neuronal activity engage calcium-dependent compensatory mechanisms and that the sensing may occur within mitochondria rather than only in the cytoplasm. The results are significant because they propose a mitochondrial calcium-based mechanism for maintaining network stability after perturbations.

Pekala D, Safar M, Lampert M et al. · The Journal of neuroscience : the official journal of the Society for Neuroscience · (2026) · View on PubMed ↗ · Free PDF ↗

Piezo1 in intestinal epithelial cells plays a critical role in the mechanobiological positive feedback underlying intestinal fibrosis.

This study investigated whether the mechanosensitive ion channel Piezo1 in intestinal epithelial cells (IECs) drives intestinal fibrosis using DSS-induced fibrosis models, IBD patient samples, and IEC-specific Piezo1 knockout (Piezo1ΔIEC) mice. IEC Piezo1 promoted a mechanobiological positive-feedback program linked to altered mitochondrial oxidative phosphorylation (OXPHOS) and reactive oxygen species (ROS) signaling under stiffness-gradient conditions (1–10 kPa), thereby enhancing fibrotic progression. Scientifically, it identifies Piezo1 as a mechanotransduction node connecting tissue stiffening to pro-fibrotic epithelial-to-mesenchymal transition pathways, suggesting a potential therapeutic target for intestinal fibrosis in IBD.

Liu X, He R, Xu Z et al. · Journal of Crohn’s & colitis · (2026) · View on PubMed ↗

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Microbiome–immune interactions in disease

Gut microbiota-derived imidazole propionate promotes primary sclerosing cholangitis via p38 signalling.

This study investigated gut-liver mechanisms in primary sclerosing cholangitis (PSC) by testing whether the gut microbiota-derived metabolite imidazole propionate (ImP) drives disease, using human observational data and cholangiocyte experiments with pathway readouts. It showed that PSC patients have higher circulating ImP levels, high ImP predicts reduced survival, and ImP activates mTORC1 signaling in cholangiocytes. The clinical significance is that ImP could serve as a prognostic biomarker and a mechanistic target for interventions aimed at modulating gut-derived metabolites in PSC.

Molinaro A, Braadland PR, Carpino G et al. · Nature metabolism · (2026) · View on PubMed ↗ · Free PDF ↗

Bacteroides acidifaciens enriched by KRAS mutation promotes colorectal tumorigenesis.

This study profiled intratumoral microbiomes in KRAS-mutant colorectal cancer (CRC) patients and intestine-specific KRASG12D mice, and tested causality using isogenic CRC cells and mutant-KRAS mouse models. KRAS reshaped the tumor microbiome by enriching Bacteroides acidifaciens, which promoted CRC tumorigenesis and was associated with poor prognosis in KRAS-mutant patients. These findings identify a KRAS–microbiome interaction in which B. acidifaciens may be a therapeutic target or biomarker to modulate KRAS-driven CRC progression.

Jiao Y, Cheng CH, Gao X et al. · Cell host & microbe · (2026) · View on PubMed ↗

Chemotherapy Reawakens Dormant Disseminated Pancreatic Cancer Cells in the Liver by Promoting Senescent Hepatocyte-Induced Neutrophil Extracellular Traps.

The study used a dormancy-tracking system in human and mouse models to test how chemotherapy affects dormant disseminated pancreatic cancer cells (DTCs) in the liver, with attention to hepatocyte senescence and neutrophil extracellular trap (NET) formation. Chemotherapy induced hepatocyte senescence, leading to TGF-β secretion and SMAD-dependent NETosis that reactivated dormant DTCs and promoted metastatic recurrence. This identifies a senescence–TGF-β–SMAD–NET axis as a potential combination-therapy target to prevent chemotherapy-driven metastatic awakening in pancreatic ductal adenocarcinoma.

Shi S, Yan J, Zhang Y et al. · Cancer research · (2026) · View on PubMed ↗

Chronic Stress Promotes Gastric Cancer Metastasis by Inducing Microbiota-Associated Kynurenine Accumulation and Macrophage Remodeling.

This study used chronic restraint stress (CRS) in male mice to model how stress affects gastric cancer metastasis, combining single-cell transcriptomics of lung metastases with gut microbiota profiling and macrophage depletion experiments. CRS increased metastatic burden and reduced survival across lung and peritoneal dissemination models and increased tumor burden in an orthotopic gastric cancer model, while stress remodeled tumor-associated macrophages toward immunosuppressive states and enriched Lactobacillus reuteri with associated microbiota-linked kynurenine accumulation. These findings suggest a stress–microbiome–kynurenine–macrophage axis that could be targeted to reduce stress-enhanced metastatic progression in gastric cancer.

Zhao S, Song Z, Zhang J et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗ · Free PDF ↗

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Cancer immunotherapy & tumor microenvironment

Therapy induced senescence promotes immunogenicity in acute myeloid Leukemia through reduced EZH2 activity.

This study examined how therapy-induced senescence (TIS) affects immunogenicity in acute myeloid leukemia (AML) by using ex vivo chemotherapy-treated, therapy-naïve AML samples and assessing immune signaling and antigen presentation features. It found that TIS increased interferon signaling, upregulated HLA class I and II molecules, enhanced presentation of leukemia/senescence-associated peptides, and promoted stronger autologous CD4+ and CD8+ T-cell responses, associated with reduced EZH2 activity. These findings suggest that inducing senescence (or modulating EZH2) could be leveraged to enhance anti-leukemia immune recognition and potentially improve treatment responses in AML.

Gilioli D, Fusco S, Tavella T et al. · Nature communications · (2026) · View on PubMed ↗

The Evolution of Immunotherapy Revolution in Lung Cancer: A 20-Year Perspective.

This 20-year perspective review examined how lung cancer treatment evolved from cytotoxic chemotherapy to immune-based strategies, focusing on immune checkpoint inhibition across stages of disease. It highlights that advances in tumor immunology and antigen presentation enabled effective use of checkpoint inhibitors as monotherapy and in combination regimens, improving patient outcomes. The review synthesizes key breakthroughs and limitations to inform future clinical integration of immunotherapy in lung cancer.

Waissengrin B, Tagliamento M, Sankar K et al. · Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · (2026) · View on PubMed ↗

Evaluating the potential of candidate surrogate endpoints for overall survival in treatment-naive metastatic melanoma treated with anti-PD-1-based regimens with or without anti-CTLA-4 therapy.

Using individual-patient data from 1865 treatment-naive metastatic melanoma patients treated with first-line anti–PD-1 regimens (nivolumab alone or nivolumab plus ipilimumab) versus dacarbazine or immunotherapy, this study evaluated candidate overall survival (OS) surrogate endpoints. The analysis tested objective response rate (ORR), progression-free survival (PFS), and time to next treatment or death (TNTD) using a two-level meta-analytic framework. Identifying reliable OS surrogates could accelerate development and regulatory evaluation of anti–PD-1-based therapies in metastatic melanoma.

Squifflet P, Saad ED, Kurt M et al. · Journal for immunotherapy of cancer · (2026) · View on PubMed ↗

Hyperprogression Upon Cemiplimab Alone or With Short Course Chemotherapy in PD-L1 ≥ 50% Non-small Cell Lung Cancer: A Biomarker Guided Multicenter International Phase 2 Trial-HYPERBOLIC Study.

This multicenter phase 2 trial (HYPERBOLIC; NCT07274384) evaluated immune checkpoint inhibition with cemiplimab alone versus cemiplimab plus short-course platinum chemotherapy in advanced non-small cell lung cancer (NSCLC) patients with PD-L1 ≥50%, stratifying by risk of hyperprogressive disease (HPD) using baseline circulating CD10− low-density neutrophils (LDNs). The study was designed to test whether adding short-course chemotherapy mitigates HPD risk compared with cemiplimab monotherapy in this biomarker-defined population. If successful, this would support a biomarker-guided first-line regimen to prevent treatment-related hyperprogression in PD-L1–high NSCLC.

Mollica L, Tassi E, Copaloni A et al. · Clinical lung cancer · (2026) · View on PubMed ↗

Synthetic long peptide and DNA personalized cancer vaccines induce robust neoantigen-specific T cell responses in pancreatic cancer.

This work reported two phase 1 clinical trials in pancreatic ductal adenocarcinoma (PDAC) evaluating safety and immunogenicity of synthetic long peptide (SLP) and DNA personalized cancer vaccines (PCVs) administered after resection and adjuvant chemotherapy. Using tumor/normal whole-exome sequencing, RNA sequencing, and neoantigen prioritization (pVACtools), the vaccines were well tolerated and induced robust neoantigen-specific T cell responses measured by IFN-γ ELISpot and related assays. The clinical significance is that personalized neoantigen vaccination can generate functional T cell immunity in PDAC, supporting further development of vaccine-based immunotherapy strategies.

Zhang Perkins F, Zhang X, Yu YYL et al. · Science advances · (2026) · View on PubMed ↗

ACLY palmitoylation reprograms macrophages histone acetylation rewiring to repress hepatocellular carcinoma.

The study investigated how ATP-citrate lyase (ACLY) palmitoylation regulates macrophage chromatin remodeling in hepatocellular carcinoma (HCC), including analyses of tumor-associated macrophages (TAMs) from patients and functional experiments such as SCD1 knockout. Saturated fatty acid (especially palmitic acid) availability promoted ACLY-C893 palmitoylation, which reprogrammed macrophage histone acetylation to repress HCC progression, and SCD1 knockout increased PA and improved primary and metastatic tumor outcomes. These results connect lipid metabolism to epigenetic control in TAMs and suggest ACLY palmitoylation/PA handling as a therapeutic lever to modulate the HCC tumor microenvironment.

Zhao J, Xie D, Si J et al. · Cell reports · (2026) · View on PubMed ↗

CD55 organizes lipid raft-LCK signaling to potentiate NK-cell antitumor immunity.

This study examined how the complement regulatory protein CD55 functions in NK cells to organize lipid raft–LCK signaling and potentiate antitumor immunity, using tumor encounter models and mechanistic signaling assays. NK cells upregulated CD55 via an NKG2D–p65 transcriptional axis, and CD55 engaged tumor-expressed CD97 in trans to trigger lipid raft aggregation and LCK activation, acting as a primary signal initiator for cytotoxicity. Defining CD55–CD97 as a tumor-sensing axis suggests a new target to enhance NK-cell function in the tumor microenvironment.

Li L, Li Z, Liu Y et al. · Cell research · (2026) · View on PubMed ↗

Beyond cold to hot: oncolytic virotherapy as the next cornerstone of immuno-oncology.

This review analyzed next-generation oncolytic virotherapy beyond the “cold-to-hot” paradigm, focusing on limitations shared with immune checkpoint inhibitors related to reliance on pre-existing tumor-specific T cells (TSTs). It argues that next-generation oncolytic viruses can act as antigen-agnostic in situ cancer vaccines by intratumorally infecting tumors to drive immune reprogramming without requiring de novo generation of TSTs from pre-existing pools. The synthesis positions oncolytic virotherapy as a cornerstone immuno-oncology approach capable of overcoming the immunological ceiling of TST-dependent therapies.

Jia W, Zhao R, Kaufman HL et al. · Nature reviews. Clinical oncology · (2026) · View on PubMed ↗

CAFs shape the immunosuppressive microenvironment of pancreatic cancer through the Lin28b-STING Axis.

This study examined how Lin28b+ cancer-associated fibroblasts (CAFs) shape the pancreatic ductal adenocarcinoma immune microenvironment via the Lin28b–STING axis. It found that Lin28b directly binds STING mRNA to promote its degradation, suppressing cGAS–STING type I interferon signaling and thereby reducing dendritic cell antigen presentation and CD8+ T cell cytotoxic responses, while Lin28b loss activates cGAS–STING signaling. The results are significant because they identify a fibroblast-intrinsic post-transcriptional mechanism that can be therapeutically targeted to convert “cold” pancreatic tumors into more immunogenic states.

Fan M, Zhang Z, Xu W et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

PPARα activation overcomes fibroinflammatory liver microenvironment-associated anti-PD-1 resistance in hepatocellular carcinoma by mediating GSDME-dependent pyroptosis.

This study investigated how the fibroinflammatory liver microenvironment (FILM) affects response to PD-1 blockade in hepatocellular carcinoma (HCC) and tested whether PPARα activation can overcome FILM-associated resistance. FILM suppressed gasdermin E (GSDME)-dependent pyroptosis by driving NOS2+ inflammatory macrophage polarization and downstream SP1 S-nitrosylation, while PPARα activation restored GSDME-dependent pyroptosis and sensitized tumors to anti-PD-1 therapy. These findings support PPARα agonism as a mechanistically grounded strategy to overcome immunotherapy resistance in HCC patients with FILM-rich, immunosuppressive stroma.

Chen P, Xiong K, Huang K et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Evaluation of the UK Myeloma Research Alliance risk profile in transplant-ineligible multiple myeloma patients treated with novel agents.

This retrospective study evaluated the prognostic value of the UK Myeloma Research Alliance myeloma risk profile (MRP) in transplant-ineligible newly diagnosed multiple myeloma (TIE-NDMM) patients treated with novel agents using the J-CHARGE-MM database (n=799). Overall survival differed significantly across the three MRP risk groups, indicating that the easily available clinical-parameter-based MRP stratifies outcomes in this real-world transplant-ineligible population. Clinically, validating MRP in TIE-NDMM supports its use for risk-adapted counseling and treatment planning in patients receiving modern regimens.

Nakayama H, Nakazato T, Takahata A et al. · British journal of haematology · (2026) · View on PubMed ↗ · Free PDF ↗

Cannabigerol, a minor phytocannabinoid, prevents behavioral changes induced by psychotomimetic drugs.

This preclinical study tested whether cannabigerol (CBG), a minor phytocannabinoid from Cannabis sativa, prevents behavioral changes induced by psychotomimetic drugs in animal models relevant to schizophrenia-like phenotypes. CBG was reported to block psychotomimetic-drug–induced behavioral alterations, consistent with its lack of psychotomimetic effects and potential antipsychotic-like profile. These results support CBG as a candidate for further investigation as a schizophrenia-relevant therapeutic with potentially fewer side effects than conventional antipsychotics.

Pedrazzi JFC, Sales AJ, Hallak JEC et al. · Progress in neuro-psychopharmacology & biological psychiatry · (2026) · View on PubMed ↗

Biomimicry TRPV1 agonist 6SA attenuates corticosterone-induced depression via targeting Glul-Gm57375 signaling in microglia.

This study evaluated a biomimicry TRPV1 agonist analog of 6-shogaol, termed 6SA, in a mouse model of corticosterone-induced depression to determine whether it exerts antidepressant effects via microglial signaling. Using pharmacologic testing alongside single-cell RNA sequencing (scRNA-Seq), the authors investigated how 6SA modulates microglia-mediated neuroinflammation and identified involvement of Glul-Gm57375 signaling pathways. Scientifically, it links a TRPV1-targeting 6Sh analog to microglial inflammatory circuits in depression, supporting further development of 6SA/6Sh-derived therapeutics.

Sun Y, Liao W, Wing Sze SC et al. · Journal of advanced research · (2026) · View on PubMed ↗ · Free PDF ↗

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Solid tumor prognostic biomarkers & risk stratification

Distinct Prognostic Roles of Grade Group and Intraductal Carcinoma of the Prostate in Metastatic Hormone-Sensitive Prostate Cancer Treated With Androgen Receptor Signaling Inhibitors.

This retrospective analysis evaluated prognostic contributions of prostate grade group (GG 5) and intraductal carcinoma of the prostate (IDC-P) in 147 patients with metastatic hormone-sensitive prostate cancer (mHSPC) treated with androgen receptor signaling inhibitors (abiraterone, enzalutamide, or apalutamide) plus androgen deprivation therapy. The study assessed how GG and IDC-P status related to PSA progression-free survival (PSA-PFS), cancer-specific survival (CSS), and overall survival (OS) in this ARSI-treated population. Clarifying the independent prognostic roles of GG and IDC-P in ARSI-treated mHSPC could improve risk stratification and guide clinical decision-making.

Ikeda J, Taniguchi H, Inoue M et al. · International journal of urology : official journal of the Japanese Urological Association · (2026) · View on PubMed ↗

Spatial habitat radiomics predicts tertiary lymphoid structure status and identifies an IDO1+ migratory dendritic cell axis in breast cancer.

This study developed and validated a spatial heterogeneity-based radiomics signature (shTLS) from dynamic contrast-enhanced MRI to non-invasively predict tertiary lymphoid structure (TLS) status in breast cancer cohorts and to infer underlying immune cell programs. The spatial habitat radiomics signature predicted TLS status and highlighted an IDO1+ migratory dendritic cell axis associated with TLS, supported by integrated multi-omics analyses. This provides a clinically actionable imaging biomarker for TLS and links radiographic TLS patterns to a specific immunosuppressive/immune-regulatory dendritic cell pathway (IDO1+), potentially informing immunotherapy response prediction.

Yu Y, Wang Q, Lin Y et al. · Journal for immunotherapy of cancer · (2026) · View on PubMed ↗ · Free PDF ↗

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Cancer surgery, imaging, and procedural innovation

Long-term Oncological Outcomes of Retzius-sparing Versus Anterior Robot-assisted Radical Prostatectomy: Post Hoc Analysis of a Randomized Cohort.

This post hoc analysis of a randomized cohort compared long-term oncological outcomes of Retzius-sparing (RS) versus anterior robot-assisted radical prostatectomy (RARP) in 120 men aged 40–75 with low- to intermediate-risk prostate cancer. The trial originally randomized patients 1:1 to RS versus anterior surgical approaches to evaluate early continence, and this analysis extends follow-up to oncological endpoints. If oncological equivalence is demonstrated, RS RARP could be adopted more broadly as a technique that preserves early functional benefits without compromising cancer control.

Santangelo A, Jeong W, Silvani C et al. · European urology oncology · (2026) · View on PubMed ↗

Complete Pathologic Response to Neoadjuvant Pembrolizumab Captured on Intraoperative PET/CT: A Case Report and Exploratory Analysis.

This case report and exploratory analysis studied a 55-year-old man with cT3N2c supraglottic squamous cell carcinoma treated with two cycles of neoadjuvant pembrolizumab, using intraoperative micro-PET/CT to assess tumor and margins. The final laryngectomy pathology showed a pathologic complete response (pCR) after neoadjuvant pembrolizumab, captured by the intraoperative micro-PET/CT workflow. The result suggests intraoperative micro-PET/CT may help identify complete responders and guide margin assessment after neoadjuvant PD-1 blockade in head and neck cancer.

Austerlitz J, Radevic A, McAdoo A et al. · Head & neck · (2026) · View on PubMed ↗ · Free PDF ↗

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Genomics, epigenetics, and RNA biology

HUWE1 interactomes reveal sex-specific networks of nucleic acid-binding proteins.

This study mapped HUWE1 (an X-linked E3 ubiquitin ligase) protein interaction networks in brain tissue to identify sex-specific nucleic acid-binding protein networks. Using cross-linking-assisted immunoprecipitation coupled with mass spectrometry, the authors characterized HUWE1 interactomes in 26-month-old wild-type and Tg-SwDI mouse brains. Defining HUWE1 interactomes may clarify molecular mechanisms of brain aging and neurodegeneration with potential sex-dependent differences.

Escarcega RD, Vijay Kumar MJ, Abdul A et al. · Molecular and cellular neurosciences · (2026) · View on PubMed ↗

Monoallelic loss-of-function variants in ZNF536 are associated with a neurodevelopmental disorder with prominent behavioral features.

This genetic study analyzed an international cohort of 21 individuals with rare, heterozygous, protein-altering ZNF536 variants to define their contribution to a neurodevelopmental disorder with prominent behavioral features. Most identified alleles were predicted loss-of-function (15/18), supporting ZNF536 as a haploinsufficient transcriptional repressor whose monoallelic disruption causes disease. The results provide actionable evidence for ZNF536 variant interpretation in neurodevelopmental diagnostics and strengthen mechanistic links between transcriptional repression and behavioral phenotypes.

Hiatt SM, Zhao W, Wang Z et al. · American journal of human genetics · (2026) · View on PubMed ↗

Reconstitution of multistep recruitment of ULK1 to membranes in autophagy.

This study dissected the multistep mechanism by which the autophagy-initiating kinase ULK1 complex (ULK1, FIP200, and ATG13:ATG101) is recruited to membranes during autophagy. It showed that ATG13:ATG101 forms a complex with the PI3P-binding WIPI proteins (WIPI2 and WIPI3) via a PI3P-binding WD40 interaction, and that insertion of the ATG13:ATG101 WF finger into membranes—stabilized cooperatively by WIPIs—enables membrane association. Mechanistically, these findings clarify how PI3P-dependent recruitment is achieved without direct PI3P-binding domains in ULK1 complex subunits, informing models of autophagy initiation and potential intervention points.

Duan Y, Lu Y, Paul S et al. · Science advances · (2026) · View on PubMed ↗

Familial, neuropathological and cellular analysis identify ARPP21 as a major amyotrophic lateral sclerosis associated gene in French cohorts.

This genetic and neuropathological study analyzed a French ALS cohort of 1190 cases plus 50 relatives to characterize recurrent ARPP21 variants (including p.P529L and p.P713L) and determine their contribution to ALS risk. ARPP21 emerged as the most frequent rare ALS-associated gene in France after excluding the four major ALS genes, accounting for 2.7% of familial ALS and 0.1% of sporadic ALS cases. The findings establish ARPP21 as a clinically relevant ALS gene in French populations and justify incorporating ARPP21 into genetic testing and future functional studies of ALS pathogenesis.

de Bertier S, Amador MD, Guissart C et al. · Acta neuropathologica · (2026) · View on PubMed ↗

Beyond genes: EpiSwitch® and Orion platform-powered 3D genome architecture biomarkers reveal shared biology across ME/CFS, long COVID, PTSD, rheumatoid arthritis, and multiple sclerosis.

This study used the EpiSwitch® 3D genomics platform and the Orion knowledgebase to integrate chromosome conformation signatures with genome-wide association signals to identify shared regulatory biology across ME/CFS, long COVID, PTSD, rheumatoid arthritis, and multiple sclerosis. The key finding was that these clinically distinct disorders show convergent 3D genome architecture–linked biomarkers and shared biological pathways detectable by the platform. This supports a cross-disease epigenome/3D-genome biomarker framework that may help unify mechanisms and improve stratification across immune-neuroinflammatory conditions.

Hunter E, Alshaker H, Vugrinec D et al. · Journal of translational medicine · (2026) · View on PubMed ↗ · Free PDF ↗

High-throughput recovery of integron cassettes for gene discovery screens.

This study developed two high-throughput tools, cassette gatherer and cassette hunter, to recover integron cassettes for gene discovery screens using re-engineered class 1 integrons in genetically tractable strains and directly from DNA, including naturally competent Vibrio cholerae. The approach enabled sequence- and function-independent capture of single cassettes and recovered hundreds of single cassettes per assay from Vibrio strains and genomic libraries. This provides scalable methods to build gene libraries from integron cassettes for functional genomics and biotechnological gene discovery.

Trigo da Roza F, Carvalho A, Prieto A et al. · Nature microbiology · (2026) · View on PubMed ↗

Nuclear exosome targeting complexes modulate cohesin binding and enhancer-promoter interactions in 3D.

This study investigated whether nuclear RNA exosome targeting complexes regulate 3D genome architecture by modulating enhancer–promoter contacts in human cells. It found that nuclear exosome targeting complexes (including the nuclear RNA exosome and its targeting components) influence chromatin contact organization by controlling the decay of noncoding RNAs that contribute to enhancer–promoter connectivity. The significance is that it links RNA turnover machinery to spatial genome regulation, providing a mechanistic route by which noncoding RNA stability can reshape transcriptional programs.

Akkawi C, Heurteau A, Contreras X et al. · Nature communications · (2026) · View on PubMed ↗

DNTTIP2 coordinates RNA exosome activities to ensure fidelity of human ribosome assembly.

This study investigated how the RNA exosome adaptor DNTTIP2 coordinates RNA exosome activities to ensure fidelity of human ribosome assembly. It found that DNTTIP2, a component of the 90S pre-ribosome, docks an AIM-containing interface to the processive exosome core and coordinates with EXOSC10 to degrade RNA at distant sites on the 90S pre-ribosome, supported by structure-guided analyses. The significance is that it identifies a specific adaptor mechanism that safeguards ribosome biogenesis, with implications for diseases linked to defective ribosome assembly.

Pisano A, Bourdeaux J, Mazur J et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

New insights on Plasmodium gene expression from direct RNA sequencing.

This review studied how Oxford Nanopore Technology (ONT) direct RNA sequencing improves understanding of Plasmodium gene expression. It found that long-read, cDNA-free sequencing enables analysis of full-length transcripts including untranslated regions, isoforms, alternative splicing, non-coding RNAs, RNA modifications, and poly(A) tail dynamics. These advances are significant because they refine models of post-transcriptional regulation in Plasmodium beyond gametocyte/sporozoite translational repression.

Grünebast J, Serre D · Trends in parasitology · (2026) · View on PubMed ↗ · Free PDF ↗

Inositol hexakisphosphate is a Cofactor and Modulator of ADAR1 RNA Editing Activity.

This study examined how inositol hexakisphosphate (IP6) regulates adenosine-to-inosine (A-to-I) RNA editing by ADAR1 in IPPK-knockout cells and in response to a cell-permeable IP6 prodrug (Pro-IP6). IP6 depletion markedly reduced global ADAR1-mediated RNA editing, while Pro-IP6 supplementation restored and increased editing, and the authors identified a C6-phosphate requirement for ADAR1 modulation. These findings position IP6 as a biochemical cofactor/modulator of ADAR1 activity, with potential implications for Aicardi-Goutières syndrome (AGS) biology and therapeutic strategies targeting RNA editing.

Venegas Solis FA, Lu M, Cohen-Fultheim R et al. · RNA (New York, N.Y.) · (2026) · View on PubMed ↗

Clinical and molecular spectrum of VEXAS with multiple UBA1 variants: case study and literature review.

This case study and literature review characterized the clinical and molecular spectrum of VEXAS syndrome involving multiple somatic UBA1 variants, including a novel patient with three independent UBA1-mutated clones. Using droplet digital PCR and targeted next-generation sequencing on peripheral blood DNA, and evaluating bone marrow morphology, immunophenotype, and cytogenetics, the authors compared the patient’s features with the only three previously reported cases of multiple UBA1 mutations. The work expands the known VEXAS mutational landscape and supports ddPCR/NGS-based detection of multi-clonal UBA1 mosaicism for accurate diagnosis and risk understanding.

Das R, Prisneac I, Calvaresi E et al. · American journal of clinical pathology · (2026) · View on PubMed ↗

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Regenerative medicine & tissue repair

IGF2 acts downstream of Hippo signaling to regulate organ growth and restore liver regeneration in aging.

This work investigated how Hippo signaling regulates organ growth and liver regeneration in mice across development, chronic liver injury, and aging, focusing on Igf2 expression and function. Hippo signaling directly silenced Igf2 postnatally to enforce growth arrest and, during chronic injury, Hippo inactivation induced Igf2 that was required for regeneration but was defective in aged mice; ectopic Igf2 restored regenerative capacity. Clinically, restoring IGF2 signaling could be a strategy to improve liver regeneration in aging or in patients with impaired regenerative responses.

Zhong Z, Jin R, Zhong Y et al. · Cell stem cell · (2026) · View on PubMed ↗

Building and regenerating intestines by manipulating intestinal stem cells.

This article reviewed how intestinal stem cells (ISCs) can be manipulated to build and regenerate intestinal tissue, drawing on the 2009–2024 Intestinal Stem Cell Consortium (ISCC) efforts supported by the National Institute of Diabetes and Digestive and Kidney Diseases. The consortium’s work aimed to translate ISC biology toward in vivo mucosal repair and, ultimately, generation of functioning intestinal tissue ex vivo. The synthesis underscores a pathway for clinical translation of ISC-based regenerative strategies across developmental, infectious, inflammatory, and neoplastic intestinal disorders.

Kuo CJ, Blutt S, Donowitz M et al. · Nature reviews. Gastroenterology & hepatology · (2026) · View on PubMed ↗

MBNL depletion drives stem cell fusion and immature myonuclear states in myotonic dystrophy type 1.

This study examined myotonic dystrophy type 1 (DM1) muscle pathology in the context of MBNL loss, using patient muscle single-nucleus transcriptomics and functional analyses of muscle stem cells. It found that MBNL depletion drives activation of muscle stem cells and their fusion with existing muscle fibers, producing immature myonuclear transitional transcriptional states characterized by muscle stem cell-associated markers. The significance is that it clarifies a stem-cell–fusion mechanism underlying DM1 muscle remodeling, suggesting new targets to prevent maladaptive regeneration.

Todorow V, Lornage X, Hayashi S et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Regional diversity of cranial skeletal stem cells governs bone morphogenetic protein-2 mediated bone regeneration.

This study examined cranial skeletal stem cells (SSCs) and how their regional heterogeneity governs bone regeneration mediated by bone morphogenetic protein-2 (BMP2). It found that cranial SSCs show anatomically defined transcriptomic and functional heterogeneity, with region-specific lineage biases that alter osteogenic versus chondrogenic capacities, demonstrated using in vitro/in vivo functional assays and targeted qPCR gene expression analyses. The significance is that it provides a blueprint for improving BMP2-based regenerative strategies by accounting for SSC regional identity.

Takematsu E, Lachmansingh RN, Johnston K et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

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Cell death, inflammasomes, and innate immune mechanisms

Innate immune sensors of inflammasomes and PANoptosomes: structural-mechanistic insights and therapeutic implications.

This review synthesized structural and mechanistic evidence for innate immune sensors that form inflammasomes and PANoptosomes, focusing on how these multi-protein complexes drive caspase-1 activation and maturation of IL-1β/IL-18 and can integrate into PANoptosomes. It highlights that PANoptosome formation and function are supported by genetic, biochemical, and single-cell imaging evidence and culminate in lytic, inflammatory cell death pathways. The mechanistic framework is positioned to guide therapeutic targeting of inflammasome/PANoptosome signaling in inflammatory and infectious diseases.

Upadhyay S, Nagampalli R, Resende S et al. · Cell research · (2026) · View on PubMed ↗ · Free PDF ↗

Glycoprotein-induced phase separation drives unconventional secretion of galectin-3.

This study investigated an unconventional secretion pathway for galectin-3 in lysosome-damage models, using mechanistic assays of phase separation and particle release. It found that glycoprotein-induced galectin-3 phase separation drives rapid release of large, non-exosomal particles and is independent of pyroptosis and secretory autophagy, with the galectin-3 carbohydrate recognition domain and N-terminal tail dynamics enabling condensate formation and ALG-2 recruitment. The findings are clinically and scientifically significant because they reveal a new, non-classical route for galectin-3 export that could be targeted to modulate inflammation and lysosome stress responses.

Zhao Z, He Z, Gu H et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

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Infectious disease biology & immunity (including VZV/parasites)

Varicella zoster virus infection.

This Disease Primer studied varicella zoster virus (VZV) infection across human populations, covering primary infection, lifelong latency in ganglionic neurons, and reactivation leading to herpes zoster and complications. It found that immune dysfunction with age or immunosuppression triggers reactivation, which can cause not only post-herpetic neuralgia but also multisystem disease including vasculopathy, cranial neuropathies, and myelopathy. The significance lies in consolidating mechanisms and clinical patterns of VZV to improve risk recognition and management of severe neurologic and systemic complications.

Bubak AN, Warren-Gash C, Tommasi C et al. · Nature reviews. Disease primers · (2026) · View on PubMed ↗

What’s in a name? Discovering Leishmania.

This article studied the historical discovery and naming conventions of the protozoan parasite Leishmania. It found that the centenary of Sir William Boog Leishman’s death coincides with broader historical context showing he was not the first to describe the parasite, and it explains how etymological conventions preserved his name in scientific usage. While not a biomedical trial, the piece is significant for understanding scientific nomenclature and the history of parasitology research.

Barrett MP, Roy S, Vincent HM et al. · Trends in parasitology · (2026) · View on PubMed ↗

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Machine learning & AI in clinical decision-making

Artificial intelligence models for automated and semiautomated analysis and interpretation of clinical electroencephalography.

This review studied the evidence for artificial intelligence (AI), particularly neural networks, to automate or semi-automate interpretation of clinical electroencephalography (EEG) in epilepsy and related neurologic conditions. It found that AI-based EEG interpretation has progressed from research to increasingly clinically implementable systems that can augment expert reading and reduce workload. The review highlights AI EEG analysis as a scalable approach to address the shortage of EEG expertise and improve diagnostic throughput.

Beniczky S, Frauscher B, Nascimento FA et al. · The Lancet. Digital health · (2027) · View on PubMed ↗ · Free PDF ↗

Status, challenges, and future directions of machine learning in the management of epilepsy: a systematic review and meta-analysis.

This systematic review and meta-analysis studied how machine learning models perform in epilepsy management, focusing on predicting antiseizure medication outcomes, drug-resistant epilepsy, and epilepsy surgery outcomes. Across included human-only studies, the authors summarized the current state of evidence and identified challenges that limit clinical translation, such as heterogeneity in data and endpoints and the need for robust validation. The work is significant for guiding future development of ML decision-support tools that can reduce trial-and-error treatment selection in epilepsy.

Chang RS, Nguyen S, Mishra D et al. · The Lancet. Digital health · (2026) · View on PubMed ↗ · Free PDF ↗

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Cancer cell cycle & genomic stability

A temporal framework for error-free mitosis.

This article examined the spindle assembly checkpoint (SAC) and how its sequential, kinetochore-level molecular events ensure error-free mitosis. It reports that SAC silencing is a dynamic process and highlights how events unfold in a temporal order at individual kinetochores to prevent premature anaphase. Understanding this timing is clinically and scientifically important because SAC dysregulation can contribute to chromosomal instability and cancer.

Kletter T, Maiato H · Trends in cell biology · (2026) · View on PubMed ↗

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Generated automatically on September 06, 2026 from PubMed’s trending articles. Summaries are AI-generated; always consult the original publication for clinical or research decisions.