PubMed Trending Research Digest — September 27, 2026

Automated digest · 96 articles · 15 research areas · September 27, 2026

Overview

This week’s digest is dominated by mechanistic, multi-omic, and translational efforts that connect molecular states to clinical outcomes. Several studies use high-resolution “in situ” or spatial approaches—cryo-ET of human ribosome biogenesis in nucleoli, single-cell/spatial atlases of embryonic facial development, and spatial mapping of tumor recurrence or therapy-driven microenvironment remodeling—to build more faithful maps of dynamic biological processes. In parallel, cancer research repeatedly links specific molecular programs (e.g., mitochondrial dTMP synthesis as a PARPi resistance route, ceramide–Degs1–PP2A–YAP metastasis signaling, hypoxia-driven platelet hyperactivation, and OTUD1–SLC7A11 ferroptosis control) to therapeutic response or resistance, suggesting increasingly actionable biomarkers and targets.

Immunology and immune evasion also thread through multiple articles, spanning infectious and autoimmune mechanisms (EBV-driven immune dysregulation; autoimmune encephalitis diagnostic pathways; malaria epitope targeting) and cancer immune escape (FST/BMP axis in AR-independent prostate cancer; KAT5–HSPA1A lactylation promoting CD8+ T cell dysfunction in ESCC; resident macrophage selenium transfer driving ferroptosis resistance in PDAC; and multiple CAR-T/allogeneic CAR-T rejection/expansion mechanisms). Complementing these, microbiome-focused work continues to expand beyond gut symptoms into neurovascular and neurodegenerative contexts (FMT for IBS trial design; gut–brain axes in epilepsy and vascular cognitive impairment; and microbiota/tryptophan metabolite signaling affecting astrocyte pathways and glymphatic function).

Finally, the clinical translation layer is reinforced by consensus statements and pragmatic trial designs: frailty assessment in CKD, perioperative systemic-therapy trial standardization in HCC, and multiple randomized or prospective studies across oncology, cardiovascular risk interventions, and rehabilitation/exercise optimization. Together, the collection highlights a broader trend toward integrating mechanistic biology (often via spatial/single-cell or systems approaches) with biomarker-driven patient selection and standardized clinical pathways to improve both efficacy and equity in care.

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Precision oncology biomarkers & genomic predictors

Multi-target blood test for hepatocellular carcinoma early detection: a cross-sectional analysis of the prospective ALTUS study.

This prospective multicenter ALTUS study evaluated a multi-target blood test for hepatocellular carcinoma (mt-HBT) versus standard-of-care ultrasound in U.S. adults with cirrhosis or chronic hepatitis B eligible for routine HCC screening. The study reports whether mt-HBT is non-inferior to ultrasound for detecting early-stage HCC and compares specificity between the two approaches. If mt-HBT improves early detection with higher specificity than ultrasound, it could support more effective population screening strategies for HCC in high-risk HBV/cirrhosis patients.

John BV, Camardo M, Singal AG et al. · Journal of hepatology · (2026) · View on PubMed ↗

Independent and joint effects of lifestyle, human leukocyte antigen polymorphisms on cancer risk: findings from the UK Biobank.

Using UK Biobank participants of European ancestry (159,744 men and 175,037 women), this study assessed independent and joint effects of lifestyle profiles and imputed classical HLA alleles (50 alleles across 11 HLA genes) on overall and site-specific cancer risk. It identifies how specific HLA polymorphisms and lifestyle categories interact to modify cancer susceptibility beyond either factor alone. These findings could help refine personalized cancer risk stratification by combining immune-genetic background with modifiable lifestyle exposures.

Zheng J, Jiang S, Zhu H et al. · Frontiers in immunology · (2026) · View on PubMed ↗ · Free PDF ↗

The Expanding Multisystem Research Landscape of Hypermobile Ehlers-Danlos Syndrome: An Analysis of Orthopedic, Autonomic, Immunologic, and Neuropsychiatric Comorbidities.

This observational case series investigated whether adult-onset non-5q spinal muscular atrophy (SMA) is associated with CGG repeat expansions in the 5′ UTR of LRP12 and characterized clinical phenotypes. Across 8 genetically unresolved families meeting inclusion criteria, the study assessed LRP12 CGG expansions and their relationship to adult-onset proximal-predominant non-5q SMA presentations. Clinically, it aims to improve molecular diagnosis of adult-onset non-5q SMA by expanding the genetic testing targets beyond canonical SMA genes.

Tanuku S, Baer T, Viswanath O et al. · Orthopedic reviews · (2026) · View on PubMed ↗ · Free PDF ↗

LRP12 CGG Repeat Expansions in Patients With Adult-Onset Non-5q Spinal Muscular Atrophy.

This study assessed whether LRP12 CGG repeat expansions occur in patients with adult-onset non-5q spinal muscular atrophy and described associated clinical features. It enrolled 8 consecutive genetically unresolved families meeting prespecified criteria and evaluated the presence and phenotype correlates of LRP12 CGG expansions. The work is significant because it can reduce diagnostic uncertainty in adult-onset non-5q SMA by identifying a repeat-expansion mechanism amenable to targeted testing.

Naruse H, Mitsui J, Ishiura H et al. · Neurology. Genetics · (2026) · View on PubMed ↗ · Free PDF ↗

Unified long-read panel for Parkinson’s and repeat expansion disorders.

The study developed and evaluated a unified Nanopore long-read adaptive-sampling gene panel targeting 564 Parkinson’s disease (PD) and repeat expansion disorder genes in 18 individuals across known variant-positive, genetically negative, and repeat-expansion categories. It achieved high diagnostic yield by identifying 17/20 expected pathogenic variants (85%) with mean per-sample coverage of ~24X, including detection of repeat expansions in multiple loci. This demonstrates a scalable long-read panel approach for comprehensive genetic diagnosis of PD and repeat expansion disorders.

Fienemann A, Prietzsche JC, Laβ J et al. · NPJ Parkinson’s disease · (2026) · View on PubMed ↗ · Free PDF ↗

In-frame variants in TP53 gene identified in adult leukemia samples are predominantly deleterious: a study of the TP53 Network of Education and Research Initiative on CLL.

This study examined in-frame TP53 variants identified in adult leukemia samples from the TP53 Network of Education and Research initiative on CLL, focusing on variants that preserve the reading frame (in-frame deletions/insertions) and assessing their predicted deleteriousness. The authors found that these adult leukemia in-frame TP53 variants are predominantly deleterious, addressing a gap where such variants often rely on expert judgment rather than standardized functional evidence. Clinically, the results support more reliable interpretation and reporting of TP53 in-frame variants for prognosis and treatment decision-making in leukemia.

Pavlová Š, Gombíková J, Petrezsélyová S et al. · The Journal of pathology · (2026) · View on PubMed ↗ · Free PDF ↗

Pretreatment Tumor NECTIN4 RNA Expression Is Associated with First-line Enfortumab Vedotin Plus Pembrolizumab Efficacy in Metastatic Urothelial Cancer.

This retrospective real-world study evaluated whether pretreatment tumor NECTIN4 RNA expression and tumor mutational burden (TMB) predict outcomes in metastatic urothelial cancer patients receiving first-line enfortumab vedotin plus pembrolizumab (EV+P; N=322). NECTIN4-high tumors were associated with better overall survival (HR 0.67, 95% CI 0.46–0.98) and higher best overall response (OR 2.98, 95% CI 1.68–5.3) with improved objective response rate (truncated). Clinically, NECTIN4 RNA expression could serve as a practical predictive biomarker to refine patient selection for EV+P in metastatic urothelial cancer.

Cho BA, Perry CJ, Yoo SK et al. · European urology · (2026) · View on PubMed ↗

Association of ATM Alterations with Outcomes After 177Lu-PSMA-617 Treatment in Patients with Metastatic Castration-Resistant Prostate Cancer.

This retrospective genomic study analyzed next-generation sequencing data from 205 patients with metastatic castration-resistant prostate cancer treated at the University of Minnesota with 177Lu-PSMA-617 to test whether ATM alterations predict outcomes. The key finding was that ATM alterations were associated with differential clinical outcomes after 177Lu-PSMA-617, supporting ATM as a potential gene-level biomarker rather than relying on composite homologous recombination repair (HRR) categories. Clinically, this could enable more personalized selection of 177Lu-PSMA-617 based on DNA repair genotype.

Mahajan V, Yu L, Kollitz L et al. · Journal of nuclear medicine : official publication, Society of Nuclear Medicine · (2026) · View on PubMed ↗

Elexacaftor/tezacaftor/ivacaftor improves CFTR function to near-normal levels in children with cystic fibrosis.

This study quantified restoration of CFTR function in children with cystic fibrosis treated with the CFTR modulator elexacaftor/tezacaftor/ivacaftor (ETI), building on prior adult/adolescent data showing near-40% of median CFTR activity in non-CF controls. The key finding was the degree of CFTR function correction achieved in children (as measured in the study’s CFTR functional assay), addressing uncertainty about whether children achieve similar or different levels of CFTR activity restoration. Clinically, this informs expectations for ETI effectiveness in pediatric CF and supports dosing/monitoring decisions based on functional biomarker response.

Berger J, Yu Y, Berges J et al. · The European respiratory journal · (2026) · View on PubMed ↗ · Free PDF ↗

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Clinical trials, consensus, and guidelines (including CKD frailty, exercise/rehab, cardiovascular risk, dermatology, neuromodulation)

Comparative efficacy of neuromodulation techniques for Alzheimer’s disease: a systematic review and network meta-analysis of randomized controlled trials.

This systematic review and network meta-analysis compared the relative efficacy of different neuromodulation techniques (NMTs) for Alzheimer’s disease across randomized controlled trials, ranking effects on cognitive, activities of daily living, and neuropsychiatric outcomes. The analysis synthesizes which NMT modalities perform best for specific clinical endpoints in AD patients. Clinically, the ranked comparative evidence can guide selection of neuromodulation strategies for AD management and inform future trial design.

Liu Y, Liu S, Yan H et al. · Frontiers in neuroscience · (2026) · View on PubMed ↗ · Free PDF ↗

Recommendations for the management of frailty in chronic kidney disease: a consensus report.

This consensus report synthesized evidence to provide recommendations for assessing and managing frailty in patients with chronic kidney disease (CKD), addressing assessment tools, intervention targets, and how frailty should influence decisions between conservative care and kidney replacement therapy. It emphasizes frailty’s high prevalence and its associations with mortality, hospitalization, disability, and quality of life, while addressing gaps in reversibility and decision-making. Clinically, the 63 consensus statements aim to standardize frailty-informed care pathways in CKD.

Li PK, Chan GC, McAdams-DeMarco M et al. · Nature reviews. Nephrology · (2026) · View on PubMed ↗

Effects of Daily Rhythm-Aligned Training on Skeletal Muscle Adaptation in Older Adults: A Randomized Controlled Trial.

In a three-arm parallel-group randomized controlled trial, older adults were assigned to resistance training aligned to their daily peak versus trough time of day (daily rhythm-aligned training) to test effects on skeletal muscle adaptation. The study evaluates whether training at an individual’s peak time produces greater improvements in muscle outcomes than training at a trough time. If peak-time training is superior, it would support chronobiology-informed exercise prescriptions to better counter age-related sarcopenia risk.

Bruggisser F, Ritter S, Roth R et al. · Journal of cachexia, sarcopenia and muscle · (2026) · View on PubMed ↗ · Free PDF ↗

Efficacy and Safety of Risankizumab in Paediatric Patients With Psoriasis in the OptIMMize-1 Phase III Study.

The OptIMMize-1 phase III program evaluated the efficacy and safety of risankizumab, an interleukin-23 (IL-23) inhibitor, in pediatric patients with moderate-to-severe psoriasis over 52 weeks. It reports outcomes comparing risankizumab treatment strategies (including an initial randomized period versus ustekinumab) and subsequent longer-term follow-up/withdrawal components. Positive results would expand evidence for IL-23–targeted biologic therapy in children with psoriasis who need advanced treatment options.

Magnolo N, Lara WL, Reich A et al. · The British journal of dermatology · (2026) · View on PubMed ↗

10-year analysis of selective dissemination in glaucoma research from major conferences to journals.

This bibliometric analysis examined 10-year selective dissemination in glaucoma research by tracking full-text publication rates of abstracts presented at major conferences (AGS, EGS, ICGS, WGC) from 2010–2020 and relating publication to journal impact factors. It identifies determinants of whether abstracts reach full publication and how the resulting journals’ impact factors vary by study and presentation characteristics. The findings can inform researchers and stakeholders about publication bias and help improve transparency in glaucoma research dissemination.

Ghirardi A, Camisa L, De Cillà S et al. · The British journal of ophthalmology · (2026) · View on PubMed ↗

Global burden of liver disease: 2026 update.

This article updated the global burden of chronic liver disease (CLD) and quantified leading causes of cirrhosis and liver cancer across populations worldwide. It reports that CLD affects over 1.5 billion people, cirrhosis is the 12th leading cause of death globally, and alcohol-associated liver disease, metabolic dysfunction-associated steatotic liver disease (MASLD), and chronic viral hepatitis (HBV/HCV) are the dominant etiologies driving the burden. The update highlights major inequities and predicts rising CLD burden with demographic shifts, obesity, and increasing alcohol consumption, informing public health and prevention priorities.

Devarbhavi H, Asrani SK, Arab JP et al. · Gastroenterology · (2026) · View on PubMed ↗

Radiotherapy versus observation following surgical resection of WHO grade 2 atypical meningioma (ROAM/EORTC-1308): an international, multicentre, open-label, phase 3, randomised controlled trial.

This international phase 3 randomized controlled trial studied whether adjuvant radiotherapy versus observation reduces recurrence after complete surgical resection of newly diagnosed WHO grade 2 atypical meningioma in patients aged ≥16 years across 58 hospitals in 11 countries. The key finding is not included in the provided abstract text. Clinically, the trial directly addresses whether adding radiotherapy after surgery improves recurrence outcomes for grade 2 atypical meningioma, which would guide post-operative standard-of-care decisions.

Jenkinson MD, Rosala-Hallas A, Sahm F et al. · Lancet (London, England) · (2026) · 1 citations · View on PubMed ↗ · Free PDF ↗

Accelerating equitable cancer genomics and precision oncology in health care and research: a Lancet Oncology Commission.

This Lancet Oncology Commission analyzed the global landscape of implementing cancer genomics and precision oncology, focusing on scientific, structural, and health-system barriers to equitable delivery in health care and research. It found that access to guideline-indicated cancer genomics and precision oncology remains profoundly unequal across and within countries, leaving millions of patients without recommended interventions, and that genomic studies/clinical trials are concentrated in high-income settings and among underrepresented populations. The work is significant for policy and implementation planning, identifying where system-level changes are needed to improve equity and sustainability in precision oncology.

Casolino R, Mateo J, de Vries EGE et al. · The Lancet. Oncology · (2026) · 10 citations · View on PubMed ↗

Cluster-set rest vs. traditional during repeated sprint training: effects on creatine phosphokinase activity, sprint abilities and 100-m sprint performance.

This nonrandomized experimental study compared cluster-set rest versus traditional rest intervals during repeated sprint training in 20 well-trained male sprinters. After an 8-week, 24-session program, it measured creatine phosphokinase (CPK) activity, sprint abilities, and 100-m sprint performance to determine which rest configuration better modulates recovery and performance. The findings are relevant for optimizing training design to balance repeated-sprint performance gains with muscle damage markers.

Megahed M · PeerJ · (2026) · View on PubMed ↗ · Free PDF ↗

Effect of a community-based intervention for cardiovascular risk factor control on stroke mortality in rural Gadchiroli, India: a cluster-randomised controlled trial.

This cluster-randomised controlled trial studied a 3.5-year community-based cardiovascular risk factor intervention delivered by trained community health workers in 64 rural villages in Gadchiroli, India, targeting adults aged ≥50 years for screening of hypertension, diabetes, and stroke risk. The intervention was designed to improve cardiovascular risk factor control and thereby reduce stroke mortality in this underserved population. If effective, this scalable community-delivered screening-and-management approach could provide a practical public-health strategy to lower stroke deaths in rural India.

Kalkonde Y, Jadhao S, Bhusari V et al. · Wellcome open research · (2026) · View on PubMed ↗ · Free PDF ↗

Safety and Efficacy of Left Atrial Ablation After Percutaneous Left Atrial Appendage Occlusion in High-Bleeding-Risk Patients with Atrial Fibrillation: A Multicenter Analysis from the PROCEED-AF Ablation Registry.

This multicenter PROCEED-AF Ablation Registry analysis evaluated the safety and efficacy of catheter ablation for atrial fibrillation in high-bleeding-risk patients who already had left atrial appendage (LAA) occlusion devices, and characterized post-ablation anticoagulation patterns across 14 centers. The key finding was the registry-level assessment of complication rates and arrhythmia outcomes after ablation in this unique LAAO-pretreated population, addressing uncertainty about anticoagulation strategies. Clinically, the results inform how AF ablation can be integrated with LAAO in patients where long-term anticoagulation is challenging.

Kaplan RM, du Fay de Lavallaz J, Heeger CH et al. · Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · (2026) · View on PubMed ↗ · Free PDF ↗

Variations in Single-Point Insulin Sensitivity Estimator Index and the Risk of Cardiovascular Disease in Individuals With Cardiovascular-Kidney-Metabolic Syndrome Stages 0 to 3: A National Longitudinal Cohort Study.

This prospective national longitudinal cohort study used the CHARLS dataset to examine whether longitudinal changes in the single-point insulin sensitivity estimator (SPISE) index—calculated from body mass index, triglycerides, and HDL cholesterol—predict incident cardiovascular disease in individuals across cardiovascular-kidney-metabolic syndrome stages 0 to 3. The key finding was that dynamic SPISE trajectories (not just baseline SPISE) were associated with future cardiovascular disease risk in this preclinical population. This supports using longitudinal insulin-sensitivity metrics for earlier cardiovascular risk stratification in people with combined cardio-renal-metabolic risk.

Shi Y, Shen Y · Journal of the American Heart Association · (2026) · View on PubMed ↗ · Free PDF ↗

The effectiveness of resistance training for patients with degenerative arthritis after total joint arthroplasty: a pilot randomized controlled study.

This pilot randomized controlled study evaluated a volume-progressive staged bilateral resistance training program in patients with degenerative arthritis after total joint arthroplasty (total knee and hip), focusing on lower-limb muscular endurance, balance, pain intensity, and quality of life. The key finding was that the staged bilateral resistance training intervention improved targeted functional and symptom outcomes compared with the control approach used in post-arthroplasty rehabilitation. Clinically, it supports resistance training as a feasible, potentially more effective rehabilitation strategy when early progressive loading is limited by pain or surgical constraints.

Tian YR, Wu MC, Liao SJ · BMC musculoskeletal disorders · (2026) · View on PubMed ↗ · Free PDF ↗

Decentralized CAR-T production: clinical, economic, and regulatory perspectives. Worldwide Network for Blood & Marrow Transplantation (WBMT) special article.

This special review article assessed decentralized point-of-care (POC) CAR-T cell manufacturing from clinical, economic, and regulatory perspectives. It summarizes how decentralized production could address limitations of centralized manufacturing (cost, logistics, vein-to-vein time, and access) and outlines the current landscape of POC CAR-T implementation. The significance is guiding translation and policy decisions to expand CAR-T availability and enable faster manufacturing innovations.

Nasiri A, El Fakih R, Chabannon C et al. · Bone marrow transplantation · (2026) · View on PubMed ↗

Age-related molecular IgE sensitization to indoor and outdoor respiratory allergens: a two-step cross-sectional study in Algeria and Türkiye.

This two-step cross-sectional study assessed age-related molecular IgE sensitization to indoor and outdoor respiratory allergens in children and adults from Algeria and Türkiye using an experimental allergen microarray containing 105 allergen molecules. The key finding was that molecular IgE reactivity profiles differed by age, indicating age-related shifts in sensitization patterns across the two regions with similar climate/exposome (truncated). These data can inform age-stratified allergen-specific prevention and therapy design using molecular diagnostics.

Mahammed LL, Vrtala S, Akinfenwa O et al. · EBioMedicine · (2026) · View on PubMed ↗ · Free PDF ↗

DNA methylation: unifying framework for complex chronic conditions.

This article is a review proposing DNA methylation as a unifying epigenetic framework to study complex chronic conditions, specifically ME/CFS, long COVID, fibromyalgia, and hypermobile Ehlers-Danlos syndrome. It argues that shared symptom overlap may reflect shared or convergent pathophysiology that can be captured and compared longitudinally through DNA methylation patterns (truncated). Scientifically, it positions methylation profiling as a strategy to harmonize research across these conditions and potentially improve biomarker discovery and mechanistic understanding.

Sharma S, Rodger EJ, Chatterjee A et al. · Trends in genetics : TIG · (2026) · View on PubMed ↗ · Free PDF ↗

Expert consensus on clinical trials for use of systemic therapy in patients with hepatocellular carcinoma undergoing surgical and locoregional therapies.

This expert consensus from the HCC-Live Consortium evaluated how to design clinical trials testing systemic therapy in patients with hepatocellular carcinoma (HCC) undergoing surgical and/or locoregional therapies, focusing on perioperative and combination strategies and the heterogeneity of early/intermediate-stage disease. The panel agreed on >70% approval inclusion criteria, risk stratification approaches, treatment arms, and endpoint recommendations to improve trial comparability despite biological and clinical variability. These consensus recommendations are intended to standardize perioperative systemic-therapy trial design in HCC and thereby accelerate evidence generation for earlier-stage treatment settings.

Yarchoan M, Llovet JM, Kelley RK et al. · Gut · (2026) · View on PubMed ↗

Optimal exercise dose in adults with chronic low back pain disorders: systematic review with dose-response network meta-analysis.

This systematic review and non-linear dose-response network meta-analysis quantified exercise dose-response relationships to estimate an optimal exercise dose in adults (≥18 years) with chronic low back pain disorders (CLBDs). Across randomized controlled trials, it assessed clinically meaningful effects using a predefined ≥5-point change on a 0–100 scale and evaluated risk of bias with Cochrane RoB 2 and certainty with GRADE. The findings are intended to inform evidence-based exercise prescription (dose selection) for adults with CLBDs.

Arora NK, Saueressig T, Schleimer T et al. · British journal of sports medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Janus Kinase Inhibitor Use in Adults Aged 65 Years and Older: A Clinical Review Across Atopic Dermatitis, Alopecia Areata, and Psoriasis.

This clinical review synthesized evidence for Janus kinase (JAK) inhibitor use in adults aged ≥65 years with atopic dermatitis, alopecia areata, and psoriasis, focusing on efficacy, safety, and regulatory labeling. It found that in atopic dermatitis, upadacitinib 15 mg and abrocitinib 100 mg are effective in older adults, with higher doses generally avoided, reflecting age-related safety considerations. The significance is that it provides age-stratified guidance to support safer systemic treatment selection for older patients with inflammatory dermatoses.

Ezzat RZ, Paz M, Kreytak C et al. · Journal of the American Academy of Dermatology · (2026) · View on PubMed ↗ · Free PDF ↗

Diagnostic Accuracy of the Autism Diagnostic Interview-Revised and the Autism Diagnostic Observation Schedule, Second Edition, in a Naturalistic High-Risk Autism Spectrum Disorder Sample Aged 6-25 Years.

This retrospective diagnostic-accuracy study evaluated the Autism Diagnostic Interview-Revised (ADI-R) and the Autism Diagnostic Observation Schedule, Second Edition (ADOS-2) in 798 children and adolescents aged 6–25 years referred for autism spectrum disorder (ASD) assessment in a naturalistic, high-prevalence clinical setting without intellectual disability. ADI-R and ADOS-2 (individually and combined) showed diagnostic performance consistent with their use as gold-standard instruments in real-world specialized care. These findings support the clinical reliability of ADI-R/ADOS-2 for ASD diagnosis in routine practice and inform how to combine them when assessing high-risk patients aged 6–25 years.

Cartigny A, Gosling CJ, Chatzis G et al. · Journal of the American Academy of Child and Adolescent Psychiatry · (2026) · View on PubMed ↗

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Cell death regulation & senescence/fibrosis nanotherapies

Spatiotemporal Dynamics of Protein Recruitment During Cell Wound Repair.

This preprint investigated the spatiotemporal dynamics of protein recruitment during cell wound repair after cortical (plasma membrane and cytoskeleton) injury. It characterizes when and where key proteins are recruited to the wound site over time to coordinate repair. Understanding these recruitment dynamics can reveal mechanistic targets for improving tissue/cell repair in injury, infection, and cancer contexts.

Nakamura M, Hui J, Verboon JM et al. · bioRxiv : the preprint server for biology · (2026) · View on PubMed ↗ · Free PDF ↗

An endoplasmic reticulum-enriched nanogel couples ferroptotic tumor damage with macrophage reprogramming for triple-negative breast cancer immunotherapy.

This study developed an endoplasmic reticulum-enriched pH/redox-sensitive SPIONS@P-CpG-DOX nanogel to couple ferroptotic tumor damage with macrophage reprogramming for triple-negative breast cancer immunotherapy. In TNBC models, the nanogel induced ER stress that inhibited the GSH-GPX4 axis, accelerated lipid peroxidation to trigger ER-originated ferroptosis and immunogenic cell death, and simultaneously reprogrammed tumor-associated macrophages to support an innate-to-adaptive antitumor immune response. The approach is significant because it targets both tumor ferroptosis resistance and the immunosuppressive microenvironment to enhance therapeutic efficacy in TNBC.

Chen H, Ni Y, Tang J et al. · Bioactive materials · (2027) · View on PubMed ↗ · Free PDF ↗

Exosomal export of activated CASPASE-8 is linked to the prevention of TNF-induced cytotoxicity.

The study investigated how activated CASPASE-8 is exported via exosomes to prevent TNF-induced cytotoxicity by examining TNFR1 signaling outcomes and cell-death checkpoint regulation. It reports that exosomal export of activated CASPASE-8 functions as a protective mechanism that limits TNF cytotoxicity. The significance is defining a new cell-death control layer that could be leveraged to modulate inflammatory damage driven by excessive TNF signaling.

Huyghe J, Priem D, Haems A et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Breast cancer-associated fibroblast-derived exosomal miR-1290 promotes triple-negative breast cancer cell proliferation.

This study investigated whether exosomes derived from breast cancer-associated fibroblasts (CAFs) deliver microRNA cargo to promote triple-negative breast cancer (TNBC) proliferation, using CAF and MDA-MB-231 cell-derived exosomes and TNBC cell assays. CAF-derived exosomal microRNA (identified as miR-1290) promoted TNBC cell proliferation (truncated) by acting on downstream targets in recipient cancer cells. These findings highlight exosomal miR-1290 as a potential mechanistic driver and biomarker/therapeutic target in TNBC.

Lee J, Son T, Kim G et al. · Signal transduction and targeted therapy · (2026) · View on PubMed ↗ · Free PDF ↗

Senescence-directed nanotherapy ameliorates fibrosis and overcomes immune exclusion in cancer.

This study examined whether senescence-modulating nanoparticles can target senescent-like cells to treat fibrosis and improve antitumor immunity, using fibrotic tissues/tumors and cancer models. It found that P-selectin is expressed on a subset of senescent-like cells and that fucoidan-based P-selectin–binding senescence-modulating nanoparticles (SMNPs) selectively target these states, reducing fibrosis and overcoming immune exclusion while improving therapeutic response. The clinical significance is a potential nanotherapy approach to simultaneously remodel fibrotic barriers and enhance immunotherapy effectiveness.

Hinterleitner C, Barthet VJA, Goldberg HV et al. · Science (New York, N.Y.) · (2026) · View on PubMed ↗

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Autoimmunity & infectious immunology (EBV, autoimmune encephalitis, malaria epitopes)

Epstein-Barr Virus: More than Just an Infection.

This narrative review summarized how Epstein–Barr virus (EBV) drives immunopathological disease through switching between lytic replication and latency programs, with emphasis on the viral protein EBNA1. It highlights EBNA1-mediated molecular mimicry and downstream immune processes (including bystander activation and epitope spreading) that contribute to autoimmunity across disorders such as multiple sclerosis, rheumatoid arthritis, and systemic lupus erythematosus. The review underscores EBV as a mechanistic contributor to autoimmunity and supports EBV-targeted hypotheses for prevention or therapy.

Van de Perre E, Van Nieuwenhuyse B, Yombi JC · Viruses · (2026) · View on PubMed ↗ · Free PDF ↗

Diagnosing autoimmune encephalitis in psychiatry: clinical recommendations and unresolved challenges from the GENERATE network.

The paper reviewed and synthesized interdisciplinary clinical recommendations for diagnosing autoimmune encephalitis (AE) in psychiatric presentations, drawing on the German GENERATE network experience. It highlights that AE can initially present with predominant or isolated psychiatric symptoms and that diagnostic approaches vary across clinical settings, leaving unresolved challenges in classification and workup. The significance is improved, psychiatry–neurology–aligned diagnostic pathways to reduce missed or delayed AE diagnoses in patients presenting primarily with mental health symptoms.

Endres D, von Zedtwitz K, Tebartz van Elst L et al. · Molecular psychiatry · (2026) · View on PubMed ↗ · Free PDF ↗

Multi-omics characterization of Yao syndrome identifies three pathophysiological axes and disease-specific divergence from Blau syndrome.

The study performed integrated multi-omics profiling of peripheral blood mononuclear cells (PBMC RNA-seq), quantitative plasma proteomics (DIA-MS/DIA-NN; 7352 proteins), and untargeted metabolomics (1051 metabolites) in six Yao syndrome (YAOS) patients carrying NOD2 variants across functional domains and compared them with healthy controls. It identified three pathophysiological axes and reported disease-specific divergence from Blau syndrome, both linked to NOD2-driven autoinflammation. This patient-level systems characterization clarifies YAOS mechanisms and supports more precise biomarker and pathway targets for NOD2-associated disease.

Zhang J, Huang X, Liu G et al. · Inflammation research : official journal of the European Histamine Research Society … [et al.] · (2026) · View on PubMed ↗

Fatal Case of Severe Fever with Thrombocytopenia Syndrome Complicated by Profound Neutropenia and Invasive Trichosporonosis.

This case report described a 71-year-old woman with severe fever with thrombocytopenia syndrome (SFTS) who developed profound neutropenia followed by invasive trichosporonosis due to Cutaneotrichosporon dermatis. Despite prompt initiation of the antiviral favipiravir and treatment for hemophagocytic lymphohistiocytosis with corticosteroids and etoposide, the patient died. The report highlights invasive trichosporonosis as a rare but fatal secondary infection complication in SFTS patients with severe immunosuppression.

Koga K, Yamada A, Furuta R et al. · Journal of infection and chemotherapy : official journal of the Japan Society of Chemotherapy · (2026) · View on PubMed ↗

Targeting a site of vulnerability on circumsporozoite protein inhibits Plasmodium vivax malaria infection.

This study identified protective B cell epitopes on Plasmodium vivax circumsporozoite protein (PvCSP) and tested whether targeting them blocks infection. By screening inhibitory plasma from P. vivax–infected individuals, the authors mapped two PvCSP B cell epitopes (PvCSP-A and PvCSP-B/NAGG) outside the canonical central repeat region and isolated a monoclonal antibody (GRAM) against these epitopes, then showed that targeting a CSP vulnerability inhibited P. vivax malaria infection. The results advance PvCSP epitope-focused vaccine/antibody design by defining non-repeat protective targets for blocking sporozoite infection.

Visweswaran GRR, Mahdavi P, Vijayan K et al. · Immunity · (2026) · View on PubMed ↗ · Free PDF ↗

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Neurodegeneration biomarkers & Alzheimer’s disease pathology/monitoring

Advanced Eye Movement Features Measured by Quantitative Oculography as Candidate Biomarkers for Progressive Supranuclear Palsy.

This review evaluated quantitative oculography/video-oculography (VOG) measures of advanced eye movement tasks as candidate biomarkers for progressive supranuclear palsy (PSP), including prosaccades, antisaccades, memory-guided saccades, predictive saccades, overlap saccades, and gap saccades. It consolidates evidence that task-specific quantitative metrics can detect subtle abnormalities, help distinguish PSP subtypes, and potentially differentiate PSP from other neurodegenerative diseases. If validated, these digital eye-movement biomarkers could enable earlier and more accurate PSP diagnosis than conventional qualitative testing.

Ouyang H, Liu B, Peng Q et al. · Diagnostics (Basel, Switzerland) · (2026) · View on PubMed ↗ · Free PDF ↗

Spatiotemporal characterization of Alzheimer disease pathology in living human brain tissue.

This study used small brain biopsies obtained during ventriculoperitoneal shunt surgery from 18 individuals with suspected normal pressure hydrocephalus, with matched CSF and post-mortem control tissue, to map Alzheimer disease pathology and protein turnover in living human brain. Amyloid plaques were detected in 9/18 biopsies and matrix-assisted laser desorption/ionization (MALDI) mass spectrometry imaging was used to spatially map amyloid p (truncated) while mature tau tangles were rare. These findings support a minimally invasive, in vivo approach to characterize AD spatiotemporal pathology and protein dynamics, potentially enabling earlier and more direct biomarker studies than post-mortem-only methods.

Aslanyan A, Mukherjee S, Moncur EM et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Transcriptional risk score for chronic kidney disease: relation to Alzheimer’s disease.

This study developed a chronic kidney disease transcriptional risk score (CKD-TRS) from blood transcriptomes in the ADNI and AddNeuroMerge cohorts and related it to Alzheimer disease endophenotypes using brain transcriptomes from ROS/MAP (n=622). Higher blood-based CKD-TRS was associated with accelerated cognitive decline and with AD pathology measures including amyloidopathy and tauopathy, with mediation analyses supporting mechanistic links (truncated). The work suggests that CKD-related systemic transcriptional risk may help predict AD progression and identify shared biological pathways between CKD and Alzheimer disease.

Pyun JM, Park YH, Hwang J et al. · Alzheimer’s & dementia : the journal of the Alzheimer’s Association · (2026) · View on PubMed ↗ · Free PDF ↗

Circulating biochemical signatures of neurodegeneration in Alzheimer’s disease.

This International Review of Neurobiology article reviewed circulating biochemical signatures relevant to neurodegeneration in Alzheimer’s disease (AD) and emphasized that molecular changes occur before behavioral symptoms. It highlights that blood-based biomarkers could complement or extend neuroimaging approaches like MRI and PET, which are limited by cost and accessibility. The significance is that identifying circulating biochemical signatures may support earlier, more scalable diagnosis and monitoring of AD progression.

Eliazer GR, Kandasamy M · International review of neurobiology · (2026) · View on PubMed ↗

Dynamic changes in plasma biomarkers of Alzheimer’s disease in patients treated with lecanemab: a longitudinal cohort study.

This longitudinal cohort study analyzed changes in a panel of 130 plasma proteins in patients with early symptomatic Alzheimer’s disease who were treated with lecanemab and were amyloid PET positive at baseline. Plasma biomarker dynamics were characterized over time and related to conversion to amyloid PET negativity and cognitive changes during lecanemab infusions. These findings support the use of plasma protein panels as pharmacodynamic and disease-monitoring biomarkers for anti-amyloid therapy in early symptomatic AD.

Mu R, Hofmann A, Gong K et al. · The Lancet. Neurology · (2026) · View on PubMed ↗ · Free PDF ↗

Genome-wide cell-free DNA methylation profiling via TAPS for moyamoya disease diagnosis and postoperative collateral formation prediction.

This study applied low-input, bisulfite-free TET-assisted pyridine borane sequencing (TAPS) to genome-wide cell-free DNA (cfDNA) methylation profiling for moyamoya disease (MMD) diagnosis and prediction of postoperative collateral formation. Using plasma cfDNA from discovery (39 MMD, 37 atherosclerotic cerebrovascular disease [ACVD]) and external multicenter validation cohorts (40 MMD, 16 ACVD), the authors found that differentially methylated regions distinguished MMD from ACVD and that the same cfDNA libraries enabled additional analyses including fragmentation and tissue-of-origin signals. The work proposes a noninvasive cfDNA methylation assay as a diagnostic biomarker and potential tool to forecast postoperative collateral formation in MMD.

Chen T, Jia Z, Tang Y et al. · Cell reports. Medicine · (2026) · View on PubMed ↗ · Free PDF ↗

A pericyte-to-myofibroblast transition links APOE4 to cerebrovascular degeneration.

This study linked the Alzheimer’s disease genetic risk factor APOE4 to cerebrovascular degeneration by mapping human brain vasculature at single-cell resolution. In APOE4 carriers, pericyte abundance decreased and a myofibroblast-like population emerged, with immunostaining confirming non-vascular myofibroblasts in APOE4 human and mouse brains. The pericyte-to-myofibroblast transition provides a cellular mechanism for how APOE4 may promote vascular amyloid deposition and fibrosis.

Schuldt BR, Haworth-Staines D, Perez-Arevalo A et al. · Cell · (2026) · View on PubMed ↗ · Free PDF ↗

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Microbiome–immune–brain/gut–brain axis

Gut microbiota rescues vascular cognitive impairment by improving glymphatic function via the ILA-AHR-AQP4 pathway.

This study examined whether gut microbiota and the tryptophan metabolite indole-3-lactic acid (ILA) can prevent vascular cognitive impairment (VCI) caused by chronic cerebral hypoperfusion (CCH) in cognitively impaired CCH patients and in mice with bilateral carotid artery stenosis. In both cohorts, gut dysbiosis and reduced ILA preceded cognitive decline and were linked to astrocytic aryl hydrocarbon receptor (AHR) inactivation, aquaporin-4 (AQP4) depolarization, and glymphatic dysfunction, with microbiota/ILA acting as protective factors. These findings suggest a gut–brain therapeutic axis targeting the ILA–AHR–AQP4–glymphatic pathway to mitigate VCI progression.

Xie J, Ren Y, Lai M et al. · Pharmacological research · (2026) · View on PubMed ↗ · Free PDF ↗

Multi-modality profiling identifies Neisseria flavescens as a central geroprotective oral commensal in humans.

This human microbiome study used a generative multi-modality framework (AURORA) and multi-omics aging clocks to identify oral commensal taxa associated with decelerated aging, and then validated Neisseria flavescens (Nf) experimentally. The key finding was that Nf abundance correlated with favorable physiological signatures and that isolated Nf strains produced beneficial metabolites that supported geroprotective effects in functional assays. Scientifically, it nominates Nf as a candidate oral commensal for microbiome-based interventions to slow aspects of human aging.

Chen J, Ren Y, Zhou Y et al. · Nature aging · (2026) · View on PubMed ↗

The microbiota-gut-brain axis in epilepsy: Mechanistic insights and emerging probiotic-based therapeutics.

This International Review of Neurobiology review examined the microbiota–gut–brain axis in epilepsy and summarized mechanistic links between gut dysbiosis and seizure biology. It reports emerging evidence that epilepsy is associated with altered gut microbial composition (including reduced Lactobacillus, Bifidobacterium, and Faecalibacterium) and discusses how these changes may influence immune signaling, neurotransmitters, and gut–brain barrier integrity, alongside probiotic-based therapeutic concepts. The significance is that microbiome-targeted interventions could become adjunct strategies for pharmacoresistant epilepsy.

Matta T, Bishnoi M, Chopra K et al. · International review of neurobiology · (2026) · View on PubMed ↗

Faecal microbiota transplantation in irritable bowel syndrome (REFIT2): a randomised, double-blind, placebo-controlled, phase 3 trial.

This phase 3, randomized, double-blind, placebo-controlled trial (REFIT2) evaluated fecal microbiota transplantation (FMT) versus placebo in men and women aged 18–65 years with moderate-to-severe irritable bowel syndrome (IBS) diagnosed by Rome IV criteria and IBS-SSS ≥175. The study assessed whether FMT could improve IBS outcomes and was designed to determine efficacy and safety in a multicenter clinical setting in Norway. If effective, FMT would represent a microbiome-targeted therapeutic strategy for IBS; the trial’s results directly inform clinical adoption and regulatory decisions.

Johnsen PH, Juul FE, Hoff DAL et al. · Lancet (London, England) · (2026) · 1 citations · View on PubMed ↗

Fibroblasts restrain gut inflammation by IGF1-dependent regulation of innate lymphocytes.

This study investigated how fibroblast subsets regulate intestinal inflammation, focusing on insulin-like growth factor 1 (IGF1)–expressing fibroblasts and their effects on innate lymphocytes. It found that IGF1-expressing fibroblasts are reduced in inflammatory bowel disease (IBD) patients and that, in mouse models, IGF1 stimulation limits group 3 innate lymphoid cell (ILC3) CXCL10 production and reduces recruitment of plasmacytoid dendritic cells (pDCs), thereby restraining gut inflammation. The scientific significance is defining an IGF1–fibroblast–ILC3–pDC regulatory axis that may be conserved and therapeutically exploitable in IBD.

Lin Q, Liu RE, Wang Q et al. · Science (New York, N.Y.) · (2026) · View on PubMed ↗

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Immunotherapy & immune evasion (incl. TIGIT/PD-1, PD-L1/TGF-β, CAR-T, checkpoint combinations)

Iberdomide plus daratumumab and dexamethasone versus daratumumab, bortezomib, and dexamethasone in patients with relapsed or refractory multiple myeloma (EXCALIBER-RRMM): an open-label, randomised, controlled, phase 3 trial.

This phase 3 open-label randomized trial (EXCALIBER-RRMM) compared iberdomide plus daratumumab and dexamethasone versus daratumumab plus bortezomib and dexamethasone in patients with relapsed or refractory multiple myeloma, using minimal residual disease (MRD)-negative complete response and progression-free survival as dual primary endpoints. The abstract provided does not include the primary-analysis results for MRD-negative complete response. If iberdomide-based therapy improves MRD-negative complete response, it could change treatment sequencing for RRMM by leveraging cereblon E3 ligase modulation with anti-CD38 synergy.

Lonial S, Dimopoulos MA, Gavriatopoulou M et al. · The Lancet. Oncology · (2026) · View on PubMed ↗

Daratumumab Plus Bortezomib, Lenalidomide, and Dexamethasone in Newly Diagnosed Multiple Myeloma: Transplant-Ineligible Subgroup Analysis of CEPHEUS.

This analysis of the phase III CEPHEUS trial evaluated efficacy and safety of daratumumab plus bortezomib, lenalidomide, and dexamethasone (DVRd) versus bortezomib, lenalidomide, and dexamethasone (VRd) specifically in the transplant-ineligible (TIE) subgroup of newly diagnosed multiple myeloma patients. The abstract indicates that CEPHEUS overall improved MRD negativity and PFS with DVRd, but the provided text does not include the subgroup’s key numerical results. Clinically, clarifying benefit and tolerability of DVRd in TIE patients supports treatment selection for a common real-world population that cannot receive autologous stem cell transplant.

Usmani SZ, Facon T, Hungria V et al. · Journal of clinical oncology : official journal of the American Society of Clinical Oncology · (2026) · View on PubMed ↗ · Free PDF ↗

Venetoclax plus Inotuzumab Ozogamicin for Relapsed and Refractory Acute Lymphoblastic Leukemia.

This phase 1 trial evaluated venetoclax (BCL-2 inhibitor) plus standard-dose inotuzumab ozogamicin (CD22 antibody-drug conjugate) in 23 adults with relapsed/refractory CD22+ acute lymphoblastic leukemia or lymphoblastic lymphoma. The recommended dose was venetoclax 400 mg/day for 21 days per cycle, with no dose-limiting toxicities or early mortality reported. Clinically, the study supports the feasibility of combining BCL-2 inhibition with CD22 ADC therapy to improve outcomes in R/R B-cell ALL/LBL.

Luskin MR, Keating JH, Frost BF et al. · Blood · (2026) · View on PubMed ↗

Cellular and molecular mechanisms determining allogeneic CAR T cell rejection and expansion.

This study analyzed mechanisms of allogeneic CAR T cell rejection and expansion in 11 patients with large B-cell lymphoma treated with a single lot of the allogeneic anti-CD19 CAR T product cemacabtagene ansegedleucel (cema-cel). Integrated longitudinal TCRβ sequencing, single-cell molecular profiling, and mixed lymphocyte reaction assays showed that non-expanders had high frequencies of pre-existing recipient-derived alloreactive CD8+ T cells that rapidly rejected CAR T cells. These findings clarify why identical allogeneic CAR T infusions yield heterogeneous outcomes and suggest that recipient alloreactive T-cell profiling could guide patient selection and engineering strategies.

Jallouk AP, Ge Z, Kaimal V et al. · Cancer discovery · (2026) · View on PubMed ↗

Distinct intestinal eosinophil subsets in ulcerative colitis and their modulation by advanced inflammatory bowel disease therapies.

This study profiled intestinal eosinophil subsets in ulcerative colitis (UC) and tested how advanced inflammatory bowel disease therapies modulate these populations, using flow cytometry on colonic immune cells and matched stool measures (including fecal calprotectin and eosinophil-derived neurotoxin) in patients with UC. The key finding was that distinct eosinophil subsets exist in UC and that advanced therapies can shift eosinophil subset composition in relation to treatment response defined by Mayo endoscopic subscore 0–1. Clinically, eosinophil subset patterns may help refine histologic scoring and improve understanding of how modern UC therapies exert immunologic effects.

Jacobs I, Ceulemans M, Lenfant M et al. · Journal of Crohn’s & colitis · (2026) · View on PubMed ↗

Evorpacept plus trastuzumab, ramucirumab and paclitaxel in HER2-positive gastric cancer: a randomized phase 2 trial.

This randomized phase 2 trial (ASPEN-06) studied evorpacept, an anti-CD47 agent that blocks the CD47–SIRPα interaction to enhance antibody-dependent cellular phagocytosis, combined with trastuzumab, ramucirumab, and paclitaxel versus the same chemotherapy backbone without evorpacept in 127 patients with pretreated HER2-positive advanced gastric/gastroesophageal junction cancer. The key finding was the trial’s evaluation of investigator-assessed objective response rate (ORR) to determine whether evorpacept-containing therapy exceeded a historical 30% benchmark. Clinically, positive ORR would support evorpacept as an immunotherapy addition to standard HER2-directed regimens in this setting.

Shitara K, Wainberg Z, Tabernero J et al. · Nature medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Pseudomonas aeruginosa induces the generation of pathogenic IFNγ+Th17 cells that promote lung damage and chronic inflammation in cystic fibrosis.

The study examined how Pseudomonas aeruginosa infection in cystic fibrosis (CF) lungs drives pathogenic T helper responses by profiling IFNγ+ Th17 subsets in CF patients. It found two pathogenic Th17 subsets (Th1/17+ and pro-inflammatory pTh17) enriched in P. aeruginosa–colonized CF lungs that arise from conventional Th17 precursors and directly disrupt pulmonary epithelial integrity while amplifying inflammation. These findings implicate in situ T cell reprogramming and clonal selection as drivers of chronic CF lung damage, suggesting Th17-state targeting as a therapeutic strategy.

Dusetti I, Conte G, Chiara M et al. · Nature microbiology · (2026) · View on PubMed ↗ · Free PDF ↗

KAT5-mediated HSPA1A lactylation drives immunotherapy resistance by inhibiting STAT1 degradation in esophageal squamous cell carcinoma.

The study investigated whether KAT5-mediated lactylation of HSPA1A regulates immunotherapy resistance in esophageal squamous cell carcinoma (ESCC) by examining the STAT1/PD-L1 pathway. It showed that HSPA1A lactylation at lysine 108 (K108) by KAT5 promotes CD8+ T cell dysfunction and resistance to immunotherapy via stabilizing STAT1 by preventing TRIM25-mediated ubiquitination and proteasomal degradation. This identifies the KAT5–HSPA1A(K108)–STAT1 axis as a potential molecular target to overcome immune evasion in ESCC.

Wang Z, Li X, Luo P et al. · Oncogene · (2026) · View on PubMed ↗

AdvanTIG-105: a phase I/Ib dose-expansion study of ociperlimab plus tislelizumab with or without chemotherapy in metastatic non-small cell lung cancer and extensive-stage small cell lung cancer.

This phase I/Ib dose-expansion study (NCT04047862) evaluated ociperlimab (anti–TIGIT) plus tislelizumab (anti–PD-1) with or without chemotherapy in patients with unresectable locally advanced or metastatic non-small cell lung cancer (NSCLC) and extensive-stage small cell lung cancer (ES-SCLC). The key finding from the dose-expansion cohorts was the reported clinical outcomes and safety/tolerability profile of these combination regimens in this metastatic population. The study is significant because it tests an immunotherapy combination strategy aimed at improving outcomes in NSCLC and ES-SCLC beyond current checkpoint inhibitor approaches.

Lu S, Yu Y, Zhang J et al. · Journal for immunotherapy of cancer · (2026) · View on PubMed ↗ · Free PDF ↗

Teclistamab in relapsed, multi-refractory acquired hemophilia A after failure of anti-CD19 CAR-T cell therapy.

This report describes a patient with relapsed, multi-refractory acquired hemophilia A (AHA) after failure of autologous anti-CD19 CAR-T cell therapy and multiple immunosuppressive therapy lines. Treatment with teclistamab, a CD3×BCMA bispecific monoclonal antibody, was well tolerated aside from hypogammaglobulinemia and produced a prompt, durable remission lasting over one year. The case provides proof-of-concept that teclistamab may be a viable plasma-cell–targeted option for refractory AHA following anti-CD19 CAR-T failure.

Dobbelstein CE, Stoyanov K, Aleksandrova K et al. · Journal of thrombosis and haemostasis : JTH · (2026) · View on PubMed ↗ · Free PDF ↗

First-Line Retlirafusp Alfa Plus Chemotherapy for Human Epidermal Growth Factor Receptor 2-Negative Gastric or Gastroesophageal Junction Adenocarcinoma: A Randomized, Double-Blind, Phase III Study (RELIGHT).

This randomized, double-blind phase III trial studied retlirafusp alfa (an anti–PD-L1/TGF-β bispecific antibody) plus CAPOX chemotherapy (capecitabine and oxaliplatin) in 731 previously untreated patients with HER2-negative unresectable locally advanced or metastatic gastric or gastroesophageal junction adenocarcinoma. The key finding was that retlirafusp alfa improved outcomes versus placebo plus CAPOX as first-line therapy in this population. The clinical significance is that targeting the PD-L1/TGF-β axis with retlirafusp alfa could expand effective first-line treatment options for HER2-negative gastric/gastroesophageal junction cancer.

Peng Z, Wang J, Zhang Y et al. · Journal of clinical oncology : official journal of the American Society of Clinical Oncology · (2026) · View on PubMed ↗

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Neurobiology & brain circuits (including epilepsy, hydrocephalus/vasculature, hypothalamus)

A hypothalamic neuronal population coordinates metabolic adaptations to cold.

This Neuron study identified hypothalamic neuronal populations that coordinate metabolic adaptations to cold in mice, focusing on dorsal posterior periventricular hypothalamus neurons. It found that activation of GABAergic or cold-activated neurons increased food intake, body temperature, and brown adipose tissue thermogenesis, while inhibition blunted cold-induced hyperphagia and thermogenesis; single-nucleus RNA sequencing implicated Lef1 as a marker, with Lef1+ neuron activation reproducing cold responses and silencing attenuating them. These results define a specific Lef1+ cold-responsive hypothalamic circuit as a mechanistic target for modulating thermogenesis and energy balance.

Liu H, Liu Q, Bean JC et al. · Neuron · (2026) · View on PubMed ↗

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Ribosome biogenesis & RNA processing (in situ structural biology)

Single-cell visual proteomics of a minimal bacterium reveals structural coordination of gene expression machineries.

This Cell study used cryo-electron tomography to perform single-cell visual proteomics of native and antibiotic-perturbed Mycoplasma pneumoniae cells, resolving 140 structural maps of bacterial translation. It showed structural organization of translation initiation, elongation, and recycling, including multiple transcription–translation complexes that support a threading-based translation reinitiation mechanism and evidence for a proposed supercomplex coordinating translation-related processes. The work is significant because it provides direct structural insight into how gene expression machineries are coordinated and how antibiotics perturb translation in a minimal bacterium.

Dobbs JM, Jensen RK, Mahamid J · Cell · (2026) · View on PubMed ↗ · Free PDF ↗

Ligand-induced activation of RyR1 in native membranes.

This work determined high-resolution structures of the skeletal muscle ryanodine receptor RyR1 in native sarcoplasmic reticulum membranes using cryo-EM/ET, focusing on ligand-induced activation and the activation pathway including interfaces between adjacent RyR1 receptors. The authors captured conformational states along RyR1 activation and showed how receptor–receptor interactions at corner-to-corner interfaces contribute to coupled gating, enhancing calcium release compared with purified RyR1. Scientifically, the study clarifies the structural basis for how RyR1 arrays are activated in native membranes, informing mechanistic models of excitation–contraction coupling and related RyR1 dysfunctions.

Mikirtumov V, Golusik S, Huo R et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Escape of the BC200 gene to a human poxvirus reveals its persistent transposition in primates.

This study investigated the mobility of the human BC200 noncoding RNA gene after its escape into a human poxvirus, using molluscum contagiosum virus (MCV) as the viral system and comparative genomic analyses across primates. It found two BC200 insertions in MCV likely acquired via LINE-1 (L1)-mediated retrotransposition during modern human history and that BC200 retained its mobilization capacity, acting as a “master” source of L1-mediated germline retrotransposition events across anthropoid evolution. The scientific significance is that it reveals a mechanism for persistent transposable element activity across host–virus boundaries and long evolutionary timescales.

Gao P, Pritham EJ, Feschotte C et al. · Science (New York, N.Y.) · (2026) · View on PubMed ↗

In-cell structures visualize human pre-ribosome assembly in the nucleolus.

The study used cryogenic correlative light and electron tomography to visualize human pre-ribosome assembly within HeLa cell nucleoli, capturing structures including SSU processome and pre-60S intermediates. It found in-cell structural snapshots that recapitulate major previously known ex situ assembly states and additionally identify critical interaction partners such as the RNA exosome, rixosome, and the nuclear export receptor CRM1–RanGTP. These results provide a mechanistic, in situ map of human ribosome biogenesis that can refine models of nucleolar assembly and nuclear export control in eukaryotic cells.

Zhao X, Hayashi Y, Fung HKH et al. · Science (New York, N.Y.) · (2026) · View on PubMed ↗

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Cancer metabolism & metabolic resistance to therapy

mTORC1-TFEB/TFE3 signaling is associated with bile acid diversification during hepatic metabolic adaptation.

This Science Advances study investigated how mTORC1-TFEB/TFE3 signaling relates to bile acid diversification during hepatic metabolic adaptation, focusing on liver metabolic remodeling relevant to metabolic dysfunction-associated steatotic liver disease (MASLD). It found that altered hepatic mTORC1-TFEB/TFE3 signaling is associated with coordinated remodeling of bile acid metabolism, with cross-talk between mTORC1 and TFEB/TFE3 driving divergent regulation of bile acid synthesis and transformation, including changes in Cyp2c70 and Cyp8b1 expression and cholesterol trafficking. The findings are significant because they connect nutrient-sensing signaling (mTORC1) to bile acid pathway diversification, offering mechanistic targets for metabolic liver disease.

Zaufel A, Sun W, Pastore N et al. · Science advances · (2026) · View on PubMed ↗ · Free PDF ↗

Mitochondrial permeability transition in skeletal muscle phenocopies muscle alterations seen in cancer cachexia and other wasting conditions.

This study investigated whether mitochondrial permeability transition (mPT) in skeletal muscle can reproduce pathological features seen in cancer cachexia and other wasting conditions, using experimental models including tumor-conditioned media (TCM) and comparisons of differentially expressed genes. The key finding was that inducing or promoting mPT in skeletal muscle phenocopied muscle alterations characteristic of wasting, and that TCM could promote mPT-related pathology. Scientifically, this links a specific mitochondrial mechanism (mPT) to wasting biology and suggests potential therapeutic targets to mitigate muscle loss.

Semel M, Lukasiewicz C, Skinner S et al. · The Journal of physiology · (2026) · View on PubMed ↗

Inotodiol prevents age-related muscle wasting by restoring mitochondrial function through liver X receptor beta signaling.

This study tested whether the mycosterol inotodiol (Ino) can prevent age-related muscle wasting by restoring mitochondrial function via liver X receptor beta (LXRβ) signaling in aged mice and in a dexamethasone (DEX)-induced muscle atrophy model. Ino treatment significantly improved muscle mass and function in aged mice and prevented DEX-induced muscle (truncated) by restoring mitochondrial performance through LXRβ-dependent pathways. The results suggest a potential therapeutic strategy for sarcopenia that targets mitochondrial dysfunction through LXRβ signaling.

You CL, Bae JH, Jeong Y et al. · Signal transduction and targeted therapy · (2026) · View on PubMed ↗ · Free PDF ↗

Role of diallyl disulfide in cancer: Molecular mechanisms and therapeutic interventions.

This systematic review studied diallyl disulfide (DADS), a garlic-derived compound, focusing on its molecular mechanisms in cancer cells and potential therapeutic interventions. It found that DADS suppresses proliferation and invasion/metastasis, induces apoptosis and cell-cycle checkpoint arrest, and promotes differentiation through multiple regulatory effects on cancer-relevant pathways. The clinical significance is that DADS is a mechanistically supported candidate for anticancer strategies, though the evidence base and translational readiness depend on the included preclinical and clinical studies.

Liu MY, Wang B, Xu JX et al. · European journal of medicinal chemistry · (2026) · View on PubMed ↗

Ceramide synthesis mediates colorectal cancer metastasis through a YAP-driven regenerative program.

This study investigated how tumor-intrinsic ceramide metabolism drives colorectal cancer metastasis, using dietary fat exposure and mechanistic experiments in colorectal cancer models. It found that dietary fat increases de novo ceramide biosynthesis via the dihydroceramide desaturase Degs1, leading to ceramide accumulation that activates YAP through PP2A-mediated dephosphorylation and promotes a YAP-driven regenerative program (including Basp1) that enhances metastasis. The scientific significance is identifying a ceramide–Degs1–PP2A–YAP axis as a metabolic signaling mechanism that could be therapeutically targeted to prevent colorectal cancer spread.

Goswami S, Zhang Q, Yildiz AB et al. · Science (New York, N.Y.) · (2026) · View on PubMed ↗

Mitochondrial NADP(H)-dependent de novo dTMP biosynthesis counteracts the cytotoxicity of PARP inhibitors.

The study examined how mitochondrial NADP(H)-dependent de novo dTMP biosynthesis affects PARP inhibitor (PARPi) cytotoxicity by analyzing PARPi-responsive versus non-responsive human tumor cells and mitochondrial nucleotide metabolism. It found that in PARPi-non-responsive cells, PARP inhibition expands the mitochondrial NADP(H) pool, enabling de novo mitochondrial dTMP synthesis that preserves mitochondrial dTTP and prevents uracil misincorporation into mtDNA. This mechanistic link identifies a metabolic resistance pathway to PARPi therapy and suggests mitochondrial dTMP/mtDNA integrity as a potential biomarker or therapeutic target.

Li Q, Shu T, Liu C et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗ · Free PDF ↗

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Single-cell/spatial multi-omics atlases (development & tumors)

Distinct Arp2/3 isocomplexes drive axonal actin ring assembly and integrity.

This Science Advances study used superresolution imaging to determine how distinct Arp2/3 complex isocomplexes regulate axonal actin ring assembly and integrity in cells. It showed that Arp2/3 localizes to the membrane periodic skeleton (MPS) and that isoform-specific perturbations reveal functional specialization, with ARPC1A- and ARPC5-containing isocomplexes driving successive stages of MPS actin ring development. Mechanistically, the work advances understanding of how actin nucleation is partitioned by Arp2/3 subunit composition to maintain axonal cytoskeletal structure.

Costa AR, Lopes T, Rodrigues LP et al. · Science advances · (2026) · View on PubMed ↗ · Free PDF ↗

Multiplatform single-cell and spatial transcriptomics reveal sex-specific malignant states and architecture in male breast cancer.

This study generated a multiplatform single-cell and spatial transcriptomics atlas integrating scRNA-seq, SeekSpace, Visium HD, Xenium In Situ, and multiplex immunohistochemistry from male and female breast cancer cohorts (660,000+ cells) to define sex-specific malignant states. It identified male-specific tumor cells (MSTCs) enriched in male breast cancer, linked to worse disease-free survival, with neural transcriptional programs, higher transcriptome-inferred copy-number variation burden, and spatial coupling to fatty-acid metabolism signals. These findings suggest a male-specific tumor state that could refine prognostication and enable sex-tailored therapeutic strategies in breast cancer.

Shi H, Zhang X, Cai S et al. · Science advances · (2026) · View on PubMed ↗ · Free PDF ↗

Spatial Analysis Dissects the Microenvironmental Architecture of Local Recurrence after Breast-Conserving Surgery.

This study used single-cell spatial transcriptomics to map the microenvironmental architecture of ipsilateral breast tumor recurrence after breast-conserving surgery by profiling primary breast cancer and matched IBTR specimens from 22 patients (18 true recurrence, 4 new primary). Cellular neighborhood analysis identified a tumor cell–stroma region enriched in IBTR tumors, indicating spatially organized microenvironmental drivers of recurrence. The results provide a spatially resolved framework for understanding local recurrence progression and potentially stratifying patients based on recurrence-associated tissue architecture.

Qu FL, Zhu XH, Chen F et al. · Cancer research · (2026) · View on PubMed ↗

Longitudinal spatial multi-omics delineates tumor microenvironment remodeling across sequential EGFR-TKIs in EGFR-mutant NSCLC.

This longitudinal spatial multi-omics study analyzed tumor microenvironment (TME) remodeling within the same patients across sequential EGFR-TKI treatments in EGFR-mutant non-small-cell lung cancer (NSCLC), leveraging rare consecutive re-biopsy samples spanning baseline through resistance to first- and then third-generation EGFR-TKIs. The key finding was that spatially resolved multi-omics profiling revealed within-patient TME remodeling patterns associated with progression under successive EGFR-TKIs. Scientifically, the resulting atlas provides a hypothesis-generating resource for mechanisms of resistance and potential combination strategies.

Song X, Pan C, Li Z et al. · Journal of translational medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Atlas of cell types and regulatory elements underlying human facial diversity.

The study generated a multimodal single-cell atlas of human embryonic facial development (weeks 6–11) using single-cell transcriptomics, chromatin accessibility, and spatial transcriptomics to map mesenchymal cell states and their gene–enhancer cis-regulatory landscapes. It identified 56 cell states and showed that gene expression associations with facial traits are strongest in early mesenchymal progenitor cells and evolve over developmental time. This provides a mechanistic framework for how noncoding regulatory variation shapes craniofacial diversity and congenital facial anomalies.

Erickson AG, Gershtein Y, Galimullina R et al. · Nature genetics · (2026) · View on PubMed ↗ · Free PDF ↗

Fusion-driven oncogenic programs shape the immune landscape in translocation renal cell carcinoma.

This study analyzed single-cell transcriptomes and chromatin accessibility from translocation renal cell carcinoma (tRCC) to define oncogenic programs and the immune tumor microenvironment in relation to TFE3 gene fusions. Despite a proximal tubule-like origin, tRCC showed distinct oncogenic meta-programs and an immunosuppressive TME, including six conserved tumor meta-programs such as epithelial–mesenchymal transit (truncated). Clinically, these subtype-specific immune and transcriptional programs could improve biomarker development and guide more tailored immunotherapy strategies for aggressive TFE3-fusion RCC.

Konda P, Wakolbinger AJ, Cui Y et al. · Nature communications · (2026) · View on PubMed ↗

Metastatic pancreatic cancer: from human disease to preclinical modelling.

This Gut 2026 review synthesized clinical features of metastatic pancreatic ductal adenocarcinoma (PDAC) in patients and mapped how human disease biology is modeled in preclinical systems to address diagnosis challenges and therapeutic resistance. It highlights that metastatic PDAC is characterized by extensive molecular heterogeneity and frequent failure to detect disease clinically, and it emphasizes the need for models that capture tumor–organ/niche interactions. The review’s significance is to guide selection and development of more faithful preclinical models for biomarker discovery and therapy testing in metastatic PDAC.

Min J, Liaki V, Yu PY et al. · Gut · (2026) · View on PubMed ↗

Ancient introgression drives wild boar expansion and phenotypic diversification of domestic pigs.

This study used population genomics of 745 genomes across Eurasia to examine how ancient introgression shaped wild boar expansion and phenotypic diversification of domestic pigs. It found that wild boar expanded from South Asia during the Middle Pleistocene, preceded by a Pliocene introgression (~3–5 million years ago) from an archaic Suinae lineage that introduced a ~43 Mb X-chromosomal haplotype linked to increased body size and cold adaptation. The scientific significance is that it connects deep-time introgression to later demographic expansion and domestication-associated selection in pigs.

Chen JH, Du X, Zheng Z et al. · Science (New York, N.Y.) · (2026) · View on PubMed ↗

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Cancer signaling & microenvironment remodeling (incl. AR/BMP, hypoxia, ceramide, ferroptosis)

HIF-1α/ADPGK-driven glycolytic reprogramming provokes platelet hyperactivation by fueling RHOA lactylation.

This work investigated how hypoxia signaling drives platelet hyperactivation by studying HIF-1α-mediated glycolytic reprogramming and its downstream effects on RHOA lactylation, using chronic kidney disease and high-altitude cohorts. It found that HIF-1α upregulates ADP-dependent glucokinase (ADPGK) by shielding lysine 125 from ubiquitin-mediated degradation, enabling ADPGK-driven glycolysis that fuels RHOA activation and platelet hyperactivation under hypoxic conditions. The mechanism links hypoxia-driven metabolic remodeling to thrombosis biology, identifying the HIF-1α/ADPGK/RHOA lactylation axis as a potential therapeutic target.

Lan Q, Wang Y, Xie M et al. · Blood · (2026) · View on PubMed ↗

OTUD1-mediated deubiquitination stabilizes SLC7A11 to suppress ferroptosis in hepatocellular carcinoma.

This study examined whether the deubiquitinase OTUD1 regulates ferroptosis in hepatocellular carcinoma (HCC) and contributes to lenvatinib resistance by stabilizing SLC7A11. Using loss- and gain-of-function experiments, it showed that OTUD1-mediated deubiquitination stabilizes SLC7A11 and suppresses erastin-induced ferroptosis while affecting HCC sensitivity to lenvatinib. Scientifically, it positions OTUD1–SLC7A11 as a post-translational control node that may be exploited to overcome ferroptosis-related resistance in HCC.

Li R, Mo H, Zhang L et al. · Cellular oncology (Dordrecht, Netherlands) · (2026) · View on PubMed ↗ · Free PDF ↗

Divergent medulloblastoma chromatin states disclose KDM2B as a selective dependency.

This integrative genomics study analyzed medulloblastoma chromatin states across subgroups using multi-modal integration of histone modification data with mutation, DNA methylation, and transcriptomic profiles. The key finding was that KDM2B emerged as a selective dependency, with aberrant KDM2B binding at a bivalent/poised enhancer (EnhBiv) state enriched at neurodevelopmental gene promoters in Group 3/4 medulloblastoma. Scientifically, it identifies KDM2B as a subgroup-relevant vulnerability and links chromatin-state dysregulation to transcriptional programs driving medulloblastoma.

Tao R, Erkek-Ozhan S, Xu B et al. · Nature genetics · (2026) · View on PubMed ↗ · Free PDF ↗

Cardiovascular-kidney-metabolic syndrome as a mitochondrial systems disorder.

The review proposed that cardiovascular-kidney-metabolic (CKM) syndrome should be conceptualized as a mitochondrial systems disorder rather than comorbidity alone. It argues that chronic hemodynamic stress, substrate excess, hypoxia, and neurohormonal activation converge on mitochondrial programs controlling oxidative phosphorylation, redox balance, organelle dynamics, and quality control in energy-intensive tissues like myocardium and renal tubules. This reframing highlights mitochondrial pathways as unifying targets for CKM syndrome prevention and treatment.

Li S, Abel ED, Arany Z et al. · Nature reviews. Nephrology · (2026) · View on PubMed ↗

Selective dependency of CALR-mutant myeloproliferative neoplasms on TYK2 signaling.

The study tested whether TYK2 signaling is selectively required for CALR-mutant myeloproliferative neoplasms (MPNs) by comparing CALRdel52/ins5 and MPLW515K cells with JAK2V617F models and using receptor signaling and inhibitor approaches. It found constitutive TYK2 phosphorylation in CALR- and MPL-mutant cells but not in JAK2V617F-expressing cells, and it used micropatterning and modeling to support differential TYK2 engagement at the receptor, followed by evaluation of the TYK2 inhibitor deucravacitin. The significance is identifying a potential therapeutic vulnerability—TYK2 dependence—in CALR-mutant MPNs distinct from JAK2-driven disease.

Kalmer M, Wirths C, Lemanzyk R et al. · Leukemia · (2026) · View on PubMed ↗ · Free PDF ↗

A small molecule ACT004 targets four-and-a-half LIM domain protein 1 to disrupt TGF-β/Smad signaling and promote FHL1 degradation in renal fibrosis.

This preclinical study tested the synthetic small molecule ACT004 in mouse models of renal fibrosis (unilateral ureteral obstruction and unilateral ischemia-reperfusion injury) to define its molecular target and mechanism. ACT004 inhibited TGF-β/Smad signaling, promoted degradation of four-and-a-half LIM domain protein 1 (FHL1), and showed anti-fibrotic effects, with target engagement supported by RNA sequencing and HuProt human protein microarray approaches. By identifying ACT004 as an FHL1-directed disruptor of TGF-β/Smad signaling, the work provides a mechanistic rationale for developing ACT004-like therapies for chronic kidney disease–associated fibrosis.

He X, Peng F, Wang H et al. · Pharmacological research · (2026) · View on PubMed ↗ · Free PDF ↗

Resident tissue macrophages transfer selenium transporter protein to protect pancreatic cancer from ferroptosis.

This mechanistic cancer biology study investigated how resident tissue macrophages (RTMs) protect pancreatic ductal adenocarcinoma (PDAC) from ferroptosis by transferring selenium. Using single-cell profiling, spatial analysis, lineage tracing, RTM depletion, and selenium tracing, the authors showed RTMs localize at the tumor border and transfer the selenium transporter Selenop to tumor cells via LRP8-dependent uptake, increasing tumor-cell selenium and promoting EMT, growth, and metastasis. By identifying an RTM–Selenop–LRP8 axis that drives ferroptosis resistance, the study reveals a potential therapeutic vulnerability in PDAC.

Guo W, Li Z, Chen Q et al. · Cell · (2026) · View on PubMed ↗

The promise of biased ligands in therapeutics.

This review studied the concept of biased agonism in G protein-coupled receptors (GPCRs) and how different ligands can preferentially activate distinct downstream signaling pathways in drug discovery. It found that biased agonists stabilize different agonist–GPCR complex ensembles, producing signaling “bias” that can yield pharmacological effects distinct from endogenous agonists or antagonists. This supports the scientific significance of designing therapeutics that selectively tune GPCR signaling to improve efficacy and potentially reduce adverse effects.

Eiger DS, Smith JS, Rajagopal S · Pharmacological reviews · (2026) · View on PubMed ↗

Mammals produce cyclo-octasulfur to suppress lipid peroxidation and ferroptosis.

This study investigated sulfur metabolism in mammals, identifying cyclo-octasulfur (S8) as a biological sulfur allotrope and testing its effects on ferroptosis and lipid peroxidation in mouse and human cells. It found that S8 accumulates in mitochondrial membranes and lipid droplets, is produced via lipid droplet-associated nitric oxide synthase, and suppresses lipid peroxidation and ferroptosis; in vivo, intra-articular S8 reduced lipid peroxidation in a mouse osteoarthritis model. The clinical significance is that S8 biology may represent a new therapeutic angle for diseases where ferroptosis and lipid peroxidation contribute to pathology.

Barayeu U, Ogata S, Takata T et al. · Science (New York, N.Y.) · (2026) · View on PubMed ↗

Targeting an atypical G protein-coupled receptor signaling pathway for cardiac fibrosis therapy.

This study aimed to develop cardiac fibrosis therapy by targeting an atypical GPCR signaling pathway, using a human induced pluripotent stem cell (iPSC)-based multidimensional drug discovery pipeline. It found that high-throughput screening identified CGS15943 (CGS) as a lead antifibrotic compound with activity in human cardiac fibroblasts, engineered heart tissues, and heart failure animal models, and mechanistically revealed an atypical adenosine receptor (AR)-dependent pathway converging on Gβγ signaling. The clinical significance is a potential new pharmacologic strategy to directly modulate fibrotic remodeling in heart failure, addressing a lack of FDA-approved targeted therapies.

Zhang H, Shivnaraine RV, Ren L et al. · Science (New York, N.Y.) · (2026) · View on PubMed ↗

Follistatin drives AR-independent prostate cancer through BMP signaling inactivation and microenvironmental remodeling.

The study investigated how follistatin (FST) drives androgen receptor (AR)-independent prostate cancer by suppressing BMP signaling and remodeling the tumor microenvironment, focusing on resistance to AR-targeted therapy such as enzalutamide. It found that during anti-AR treatment, loss of an AR–BMP positive feedback loop leads to FST upregulation, which antagonizes BMP11-dependent AR maintenance, induces SOX9-mediated lineage plasticity, and promotes stem-like, metastatic phenotypes. These findings position FST/BMP pathway disruption as a driver of treatment resistance and a potential target to counteract AR-independent progression in prostate cancer.

Shi X, Fan Z, Qu M et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗ · Free PDF ↗

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Surgical imaging & cancer staging (ICG/theranostics)

Glypican-3 as a Theranostic Target in Hepatocellular Carcinoma.

This Journal of Nuclear Medicine review described glypican-3 (GPC3) as a theranostic target in hepatocellular carcinoma (HCC), focusing on how GPC3 expression enables both imaging and therapy. It reports that GPC3 can be visualized with PET using radiolabeled antibodies (with noted pharmacokinetic limitations of full-size antibodies) and that newer approaches include GPC3-directed antibodies, antibody-drug conjugates, cellular immunotherapies, and therapeutic radiopharmaceuticals. The significance is that GPC3-targeted theranostics may improve patient stratification and treatment selection in HCC where tumor-specific targeting is needed.

Weber WA, Eiber M, Lapa C et al. · Journal of nuclear medicine : official publication, Society of Nuclear Medicine · (2026) · View on PubMed ↗

Impact of indocyanine green on nodal dissection and staging for gastric cancer surgery: iGreenGO prospective multicentre study.

This prospective multicentre iGreenGO study evaluated whether intraoperative indocyanine green (ICG) fluorescence imaging changes surgical conduct and stage migration during D2 lymphadenectomy for minimally invasive distal or total gastrectomy in Western patients with cT2-4a N0-3 M0 gastric adenocarcinoma. It tested the association between ICG fluorescence and lymph node dissection/staging outcomes across 15 Italian referral centers. If confirmed, the results would support or limit the clinical adoption of ICG-guided nodal dissection to improve staging accuracy and prognostication in gastric cancer surgery.

Lombardi PM, Mazzola M, Baiocchi GL et al. · The British journal of surgery · (2026) · View on PubMed ↗

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RNA modifications & developmental genetics

Role of the m6A methyltransferase Mettl16 in Drosophila development.

The study investigated the role of the m6A RNA methyltransferase Mettl16 in Drosophila development by analyzing Mettl16 mutant phenotypes and Mettl16-GFP localization in flies. It found that, unlike mammals, Drosophila Mettl16 mutants are viable but show developmental and behavioral defects, with both sexes sterile due to severe gametogenesis defects, including impaired spermatid elongation and individualization. This establishes Mettl16 as a conserved but context-dependent regulator of RNA methylation required for male fertility and specific germline differentiation steps in vivo.

Song P, Ma L, Yan D · PLoS genetics · (2026) · View on PubMed ↗ · Free PDF ↗

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Drug safety pharmacovigilance & reproductive risk

Androgenetic alopecia drugs and male infertility: Evidence from pharmacovigilance and testicular transcriptomics.

The study combined pharmacovigilance disproportionality analyses using FAERS (2004–2025) and EudraVigilance (2002–2025) with testicular transcriptomic analyses (including single-cell RNA-seq and intercellular communication modeling) to assess whether androgenetic alopecia drugs—finasteride, dutasteride, and minoxidil—are linked to male infertility-related adverse events. It identified disproportionality signals for infertility-related outcomes and used testicular transcriptomic datasets to characterize infertility-associated biological features consistent with drug-related effects. These findings suggest candidate mechanisms and safety signals for AGA therapies that warrant further clinical validation regarding male reproductive risk.

Gong Z, He J, Feng Q et al. · PloS one · (2026) · View on PubMed ↗ · Free PDF ↗

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Generated automatically on September 27, 2026 from PubMed’s trending articles. Summaries are AI-generated; always consult the original publication for clinical or research decisions.