PubMed Trending Research Digest — August 27, 2026

Automated digest · 99 articles · 15 research areas · August 27, 2026

Overview

This week’s digest is dominated by two converging trends: (1) increasingly scalable, mechanism-informed biomedical tools (from AI models to spatial multi-omics and next-generation delivery platforms), and (2) a shift toward precision stratification—using biomarkers, imaging, genomics/epigenomics, and immune or metabolic “endotypes” to better match patients to therapies and predict outcomes.

On the clinical/translation side, multiple studies emphasize improved risk prediction and treatment personalization across diverse diseases. Examples include an externally validated EEG foundation model (MORGOTH) for broader automated interpretation, radiomics/ML approaches for pancreatic cancer staging, and immune endotyping in type 2 diabetes. In oncology, several papers connect intratumoral heterogeneity, tumor–immune states (e.g., interferon-rich B-cell trajectories in melanoma), and pathway-specific vulnerabilities (e.g., AR-pathway intensification in biochemical recurrent prostate cancer; NANS–USP7–LATS2 in HR+/HER2− breast cancer) to more rational therapy timing and selection. In parallel, radiation and cardiovascular studies highlight practical “planning” and “prevention” levers—such as thymic dose constraints during NSCLC radiotherapy and refined ASCVD risk prediction using coronary artery calcium.

Mechanistically, the biological thread running through many articles is how cellular regulation and microenvironmental signaling propagate disease. Work spans mitochondrial control of cancer and immunity, cGAS–STING activation shaped by mitophagy, persistent inflammaging via transposable element derepression or splicing memory in macrophages, and neuroimmune/neurodegenerative pathways involving synaptic scaffolds, oligodendrocyte NRF2 signaling, and convergent neuroinflammation/oxidative/protein-homeostasis disturbances across neurodegenerative disorders. Together, these studies reinforce a broader message: durable clinical gains will likely come from combining high-resolution measurement (spatial genomics, single-cell profiling, biomarker panels) with targeted interventions that interrupt the specific upstream regulatory nodes driving downstream pathology.

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AI/Computational Models for Clinical Diagnostics

Predicting Synchronous Liver Metastasis in Pancreatic Cancer Using CT Radiomics and Clinical Features: A Machine Learning Approach.

This retrospective machine-learning study used CT radiomics features combined with clinical variables to predict synchronous liver metastasis in pancreatic ductal adenocarcinoma, comparing linear (LDA) and nonlinear (multilayer perceptron, MLP) models. In 340 patients (190 with liver metastasis, 150 without), the model selected radiomics features using mRMR and LASSO and evaluated performance and interpretability between architectures. If validated, this CT-radiomics approach could improve preoperative staging and treatment planning for pancreatic cancer patients at risk of synchronous liver metastasis.

Han Y, Xiang S, Jing H et al. · Academic radiology · (2026) · View on PubMed ↗

Toward unified and comprehensive automated electroencephalogram interpretation: a multicentre development and validation of an electroencephalogram foundation model.

This multicentre study developed and externally validated the EEG foundation model MORGOTH (MORGOTH) using EEG data from 18,677 patients across Massachusetts General Hospital and Brigham and Women’s Hospital. MORGOTH achieved expert-level performance across diverse EEG tasks and clinical settings by learning a broadly applicable “omnibus” representation for EEG interpretation. This supports more scalable, globally deployable automated EEG reading that can generalise beyond narrow, single-task AI systems.

Sun C, Karakis I, Herlopian A et al. · The Lancet. Digital health · (2026) · View on PubMed ↗ · Free PDF ↗

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Microbiome and Immune-Mediated Disease Risk

A geroprotective probiotic and its functional metabolite counteract inflammaging to extend healthspan.

This study examined whether a geroprotective probiotic, Bifidobacterium pseudocatenulatum, and its functional metabolite can counter inflammaging and extend healthspan in naturally aged mice, alongside human microbiome analyses across multiple Chinese cohorts. B. pseudocatenulatum was consistently depleted during aging, and oral monotherapy rescued intestinal homeostasis, reduced multiorgan inflammaging, improved cognitive-motor performance, and extended healthspan. These findings support a microbiome-based therapeutic concept targeting inflammaging with a specific candidate species and metabolite mechanism for promoting healthier aging.

Lu X, Ping J, Han Z et al. · Nature aging · (2026) · View on PubMed ↗

Childhood exposure to a sibling with Crohn’s disease alters gut microbiome and Crohn’s disease susceptibility.

This prospective study in the GEM Project cohort and a nationwide South Korean database assessed whether childhood exposure to a sibling with Crohn’s disease (CD) alters gut microbiome composition and increases CD susceptibility, with mechanistic testing in a T-cell transfer colitis model in germ-free mice. Childhood (vs adult) exposure was associated with gut microbial perturbations and higher CD onset risk, and stool-derived effects contributed to colitis susceptibility in the mouse model. These findings implicate early-life sibling exposure as a modifiable environmental factor acting through the gut microbiome to influence CD risk.

Chen R, Kim HJ, Bushra M et al. · Gut · (2026) · View on PubMed ↗

Unraveling the toxicological mechanisms of PFAS in metabolic diseases by network toxicology and molecular docking.

This study used network toxicology and molecular docking to investigate how perfluoroalkyl and polyfluoroalkyl substances (PFAS) may drive metabolic diseases including type 2 diabetes mellitus, obesity, non-alcoholic fatty liver disease, osteoporosis, and hyperuricemia. The authors integrated disease–gene associations from the Comparative Toxicogenomics Database (CTD) and performed docking to identify key molecular pathways and candidate targets implicated in PFAS-related metabolic toxicity. These findings provide mechanistic hypotheses and prioritized targets that can guide future experimental validation of PFAS effects on metabolic health.

Qiao Z, Liu T, Hu X et al. · Environmental pollution (Barking, Essex : 1987) · (2026) · View on PubMed ↗

Immunometabolic endotypes define distinct clinical trajectories in type 2 diabetes.

This study analyzed routine blood immune cell counts from >1,500 newly diagnosed type 2 diabetes patients across three European cohorts to derive immune-based clinical endotypes. Unsupervised clustering produced four stable immune endotypes—severe inflammatory diabetes (SIND), mild inflammatory diabetes (MIND), lymphocyte-rich diabetes (LYRD), and lymphocyte-deficient diabetes (LYDD)—that were reproducible and independent of age, sex, BMI, and HbA1c. The identified endotypes define distinct clinical trajectories (with SIND and LYDD associated with worse cardiovascular outcomes, truncated), supporting immune endotyping for precision risk stratification and tailored care in type 2 diabetes.

Vuong BT, Delépine CM, Ratter-Rieck JM et al. · Cell metabolism · (2026) · View on PubMed ↗

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Mechanistic Cell Biology & Gene Regulation

Aberrant alternative splicing memorized in adipose tissue macrophages impedes efferocytosis during postobesity weight loss.

This mechanistic study examined how obesity-induced epigenetic memory persists in adipose tissue macrophages (ATMs) during postobesity weight loss by focusing on aberrant alternative splicing. It showed that dysfunction of CWC22/exon junction complex impairs macrophage efferocytosis, and multiomics plus gene-targeting approaches demonstrated that a large fraction of obesity-associated differentially spliced genes remained altered after weight loss. Scientifically, it links persistent splicing changes to impaired efferocytosis and provides a targetable pathway (CWC22/EJC) for improving metabolic recovery after obesity.

Miyazaki T, Shiraishi A, Sugiura Y et al. · Science translational medicine · (2026) · View on PubMed ↗

cGAS-deficient mice display premature aging associated with derepression of LINE1 elements and inflammation.

This work characterized aging in cGAS knockout (KO) mice to determine how loss of cyclic GMP-AMP synthase affects inflammaging and genome instability. cGAS KO mice showed accelerated aging with shorter median lifespan and increased frailty, accompanied by increased LINE1 retrotransposon transcription, reduced LINE1 DNA methylation, and elevated cytoplasmic LINE1 that promotes inflammatory signaling. The study is significant because it reveals that cGAS can be protective against age-related transposable element derepression, reframing cGAS’s role in inflammaging and aging biology.

Martinez JC, Morandini F, Rechsteiner C et al. · Nature aging · (2026) · View on PubMed ↗

Mitophagy mitigates mitochondrial DNA-induced activation of cGAS-STING in autoimmune thyroiditis.

This study examined how mitophagy regulates mitochondrial DNA-driven activation of the cGAS-STING pathway in autoimmune thyroiditis using mouse models. It identified a mitochondrial DNA–cGAS–STING inflammatory axis as a driver of disease, while ubiquitin-dependent mitophagy mediated by PINK1 and Parkin protected mice from autoimmune thyroiditis; mechanistically, mitochondrial dysfunction increased mitochondrial ROS, activated ATM–CHK2, and led to TAX1BP1 phosphorylation (Ser722) that promoted autophagy. These findings are significant because they connect a defined mitophagy–TAX1BP1 signaling cascade to suppression of cGAS-STING inflammation, suggesting potential therapeutic targets for autoimmune thyroiditis.

Xie XC, Guo Y, Guo R et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

TDP-43 promotes allergen-induced inflammation and influenza A virus replication in airway epithelium.

This study investigated the role of the RNA-binding protein TDP-43 in airway epithelial cells during allergen-induced inflammation and influenza A virus replication. TDP-43 was induced by allergen exposure and promoted asthmatic airway responses by dampening nonsense-mediated decay (NMD) through modulation of UPF1, leading to accumulation of pathogenic transcripts including CHRM1 that drives vagally derived neurotransmission signaling. The findings are clinically significant because they implicate TDP-43–NMD regulation as a potential target to reduce asthma recurrence and to influence viral replication in airway epithelium.

Yuan Y, Tang W, Feng X et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

DICER1-related tumour predisposition mutations increase 3p-miRNA function and HERVH activity.

This study examined how DICER1-related tumor predisposition hotspot mutations affect small RNA processing and endogenous retroelement activity by generating cell lines with catalytic RNase IIIa (S1344L) or RNase IIIb (D1709N) substitutions in endogenous DICER1. Both mutations caused widespread loss of 5p miRNAs and increased 3p passenger strand loading into AGO2, and they were associated with increased HERVH activity. The scientific significance is that it links specific DICER1 catalytic mutations to altered miRNA strand usage and activation of human endogenous retrovirus elements, providing mechanistic insight into how these variants promote cancer predisposition.

Gordon K, Bellora N, Witteveldt J et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Structural insights into ligand recognition and activation of the human oxoglutarate receptor OXGR1.

This work used cryo-electron microscopy to determine structures of the human oxoglutarate receptor OXGR1 (GPR99) bound to the Gq protein in complex with the immunometabolites α-ketoglutarate (α-KG) and itaconate (ITN). The structures revealed key ligand-binding interactions and the conformational changes underlying OXGR1 activation. These mechanistic insights can guide rational design of modulators targeting OXGR1 for metabolic and airway innate-immune signaling.

Ma T, Chen Z, Liang E et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

MEIOSIN retains a STRA8-independent activity that contributes to meiotic gene activation across vertebrates.

Using comparative genomics plus genetic and single-cell analyses in zebrafish and mice, this study investigated whether MEIOSIN has meiotic gene activation activity independent of the MEIOSIN–STRA8 axis. MEIOSIN retained an intrinsic STRA8-independent function, supported by orthologs in vertebrate lineages lacking Stra8 (e.g., zebrafish and hagfish) that preserve the HMG domain but lack the bHLH domain needed for canonical MEIOSIN–STRA8 interaction. This revises the ancestral regulatory logic of vertebrate meiosis and clarifies how meiotic transcription can be initiated without STRA8.

Shimada R, Imai Y, Araki K et al. · Genes & development · (2026) · View on PubMed ↗ · Free PDF ↗

Integrative spatial profiling of 3D genome organization and gene expression in tissue.

The researchers developed Spatial Hi-C-RNA, a multimodal platform that simultaneously measures genome-wide chromatin contacts and transcriptomes from the same tissue section at near-single-cell resolution, and applied it to mouse brain, developing embryos, and human melanoma. Spatial Hi-C-RNA produced multimodal maps aligned with tissue anatomy and revealed complementary spatial patterns in chromatin organization (A/B compartments, topologically associating domains, and chromatin loops) and gene expression. This technique enables in situ mapping of how 3D genome architecture coordinates transcription across intact tissues, advancing mechanistic studies of spatial gene regulation in development and cancer.

Guo P, Cui Y, He J et al. · Cell · (2026) · View on PubMed ↗

Multidomain interaction governs the filamentous assembly of the dominant-negative DNMT3A R882H mutant.

This work used single-particle cryo-EM to determine the filamentous assembly mechanisms of DNMT3A homo-oligomers, comparing wild-type DNMT3A (DNMT3A^WT) with the acute myeloid leukemia/developmental disorder mutant DNMT3A R882H (DNMT3A^R882H). The key finding is that multidomain interactions govern higher-order polymer/filament formation, with distinct structural features explaining how the dominant-negative DNMT3A^R882H mutant assembles differently from DNMT3A^WT. Understanding this structural basis for DNMT3A^R882H polymerization provides a mechanistic framework for how this hotspot mutation disrupts de novo DNA methylation and genomic stability.

Chen J, Lu J, Long Z et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗ · Free PDF ↗

SET7-mediated methylation of IRF3 at lysine 98 attenuates antiviral innate immunity.

This study identified SET7 (SETD7), a lysine methyltransferase, as a regulator of the antiviral transcription factor IRF3 and tested how IRF3 methylation affects innate immune signaling. SET7 monomethylates IRF3 at lysine 98, which attenuates type I interferon responses by decreasing IRF3 phosphorylation, dimerization, and nuclear translocation. These results define a specific posttranslational modification that dampens antiviral innate immunity, suggesting SET7–IRF3 methylation as a potential lever for tuning interferon-driven inflammation.

Deng H, Sun X, Zha H et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗ · Free PDF ↗

RNA aptamers for sodium and lithium are abundant in mammals.

This comparative bioinformatics and biochemical study searched mammalian genomes for RNA motifs resembling bacterial riboswitch aptamers for sodium and lithium. It identified numerous candidate structured RNA aptamers in humans and other mammals, enriched in mRNA transcripts for ~70 genes related to ion conductance, neuronal development/function, and neurological disease, supporting selective Na^+ and Li^+ binding. If validated experimentally, these abundant mammalian RNA aptamers would expand the regulatory repertoire beyond proteins to include ion-responsive RNA control of gene expression.

White N, Belem de Andrade G, Narunsky A et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗ · Free PDF ↗

Mutant p53 gains RNA-binding activity to reprogram translation and mitochondrial function.

This study used an intein-based μMap photoproximity labeling approach and CLIP to map interactomes and RNA binding for five hotspot mutant p53 proteins, focusing on how mutant p53 gains new functions. The key finding is that mutant p53 acquires RNA-binding activity, shifts toward the cytoplasm, and shows increased proximity to structured RNA and RNA-binding proteins, with CLIP supporting an RNA-binding motif for mutant p53. This provides a mechanistic basis for how gain-of-function p53 mutants can reprogram translation and mitochondrial function, potentially revealing new therapeutic vulnerabilities in p53-mutant cancers.

Zhou W, Long A, Douglas CJ et al. · Cell reports · (2026) · View on PubMed ↗ · Free PDF ↗

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Cancer Immunotherapy & Tumor Microenvironment

LTBP4 deficiency induces MRC1+/CD44+ macrophages to drive cancer progression in preclinical colorectal cancer models.

This preclinical colorectal cancer study investigated how latent transforming growth factor-β binding protein 4 (LTBP4) deficiency alters tumor-associated macrophages to promote cancer progression. In immunocompetent mouse models, Ltbp4 knockout increased MRC1+/CD44+ macrophages that coordinated immune evasion and extracellular matrix (ECM) remodeling, enhancing tumor growth and metastasis, with effects attenuated by macrophage-targeted intervention. The findings identify an LTBP4–macrophage axis as a potential therapeutic target to limit CRC progression.

Ji S, Du S, Miao G et al. · Science translational medicine · (2026) · View on PubMed ↗

Comparative Efficacy and Safety of Treatments for Parkinson’s Disease With Depression: A Systematic Review and Bayesian Model-Based Network Meta-Analysis.

This mechanistic study investigated how phosphorylation of the CD28 cytoplasmic tyrosine 218 (Y218) regulates IL-2 secretion and antitumor efficacy in second-generation CAR-T cells. Using a CD28 Y218F (218F) mutant, the authors found that loss of Y218 phosphorylation impaired IL-2 production and abrogated antitumor activity, with transcriptomic profiling revealing altered CAR-T functional programs. The scientific significance is that CD28 Y218 phosphorylation is a tunable molecular determinant of CAR-T potency, informing future CAR design and optimization.

Zhao Y, Mo Q, Liu Y et al. · Brain and behavior · (2026) · View on PubMed ↗ · Free PDF ↗

Tumor-infiltrating B cells evolve towards interferon-rich trajectories aligned with immunotherapy in melanoma.

This study profiled tumor-infiltrating B cells in melanoma patients undergoing immunotherapy using bulk, single-cell, and spatial transcriptomics, long-read antibody sequencing, and CyTOF to map differentiation states and evolutionary trajectories. It found that tumor-resident B cells evolve toward interferon-rich trajectories that align with immunotherapy-associated antitumor immune programs. These findings suggest that interferon-associated B-cell states could serve as biomarkers or therapeutic targets to improve immunotherapy responses in melanoma.

Stoker K, Laddach R, Booth L et al. · Journal of experimental & clinical cancer research : CR · (2026) · View on PubMed ↗ · Free PDF ↗

Galanin impairs tumor immunity in glioblastoma by promoting infiltration and ferroptosis resistance of myeloid-derived suppressor cells.

This study investigated how the neuropeptide galanin (GAL) shapes glioblastoma immune evasion by examining its effects on myeloid-derived suppressor cells (mMDSCs) and immunotherapy resistance. GAL acting via GALR3 on monocytic mMDSCs activated a USP51-mediated deubiquitination of estrogen receptor-α and downstream signaling that increased mMDSC infiltration and conferred ferroptosis resistance in the tumor microenvironment. Targeting GALR3 and/or ferroptosis pathways is proposed as a way to overcome GBM immunotherapy resistance driven by GAL–mMDSC interactions.

Pang L, Liu Y, Zhou F et al. · Nature cancer · (2026) · View on PubMed ↗ · Free PDF ↗

All-trans retinoic acid suppresses CD8+ T-cell terminal exhaustion and potentiates anti-PD-1 therapy in glioblastoma.

This study investigated whether all-trans retinoic acid (ATRA) modulates CD8+ T-cell terminal exhaustion and thereby improves immune checkpoint blockade in glioblastoma. ATRA suppressed CD8+ T-cell terminal exhaustion by inducing a specific exhaustion-regulating gene program during CD8+ T-cell activation in vitro, preserving effector cytokine production and potentiating anti-PD-1 therapy. Clinically, this suggests ATRA as a potential adjunct to PD-1 blockade to overcome intrinsic resistance driven by exhausted T cells in glioblastoma.

Kang I, Kim Y, Kang BH et al. · Signal transduction and targeted therapy · (2026) · View on PubMed ↗ · Free PDF ↗

Targeting Regnase-1 in B7-H3-CAR T cells reprograms the tumor microenvironment and enhances antitumor efficacy for osteosarcoma.

The study evaluated whether deleting the CAR T cell intrinsic negative regulator Regnase-1 (Reg-1/Regnase-1) in B7-H3-CAR T cells can reshape the tumor microenvironment to improve osteosarcoma therapy in human and murine models. Reg-1 knockout enhanced antitumor activity in vivo and, in immune-competent settings, promoted a proinflammatory microenvironment characterized by increased IFN-γ–associated immune infiltration (truncated). These results support targeting Regnase-1 in B7-H3-CAR T cells as a strategy to overcome solid-tumor immunosuppression and improve therapeutic efficacy.

Adeshakin AO, Shi H, Perry SS et al. · Cell reports. Medicine · (2026) · View on PubMed ↗ · Free PDF ↗

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Cancer Genomics, Subtyping & Biomarkers

Intratumoral heterogeneity as a potential biomarker for immunotherapy response and postoperative recurrence in NSCLC.

This study analyzed intratumoral heterogeneity (ITH) as a biomarker for immunotherapy response and postoperative recurrence in advanced non-small cell lung cancer (NSCLC) using somatic variant data from public cohorts (POPLAR, OAK, Hellmann2018; n=504) and an in-house surgical cohort (n=121) with 733-panel NGS. Using Shannon entropy to quantify ITH, the authors found that ITH relates to immunogenic markers and has prognostic value for immunotherapy outcomes and postoperative recurrence. The clinical significance is that quantifying ITH from sequencing data could help stratify NSCLC patients for immunotherapy benefit and recurrence risk.

Wang Y, Dong X, Yin Y et al. · Frontiers in immunology · (2026) · View on PubMed ↗ · Free PDF ↗

Patient-partnered multiomics reveals the molecular architecture of angiosarcoma.

This study analyzed 254 angiosarcoma patients in the patient-partnered Angiosarcoma Project by integrating transcriptomic, somatic, and germline variant data to define molecular subtypes. Subcutaneous angiosarcomas showed upregulation of TGF-β and receptor tyrosine kinase signaling with driver alterations in KDR, PLCG1, and POT1, while cutaneous angiosarcomas were enriched for MYC-driven programs, UV mutational signatures, immune checkpoint expression, and mutations in TP53, FLT4, and BRAF. The resulting subtype-specific genomic and pathway architecture supports more precise biomarker-driven stratification and therapeutic targeting in this rare, heterogeneous cancer.

Chu H, Hollyer M, Borden BA et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Actionable biomarker co-expression in advanced ovarian cancer: folate receptor alpha expression and related markers.

This single-institution cohort study of 110 patients with platinum-resistant ovarian cancer treated with mirvetuximab soravtansine (2019–2025) assessed co-expression patterns among folate receptor-α and other actionable biomarkers. It used immunohistochemistry, fluorescence in situ hybridization, and next-generation sequencing to characterize how folate receptor-α expression relates to additional therapeutic targets and their potential implications for treatment selection. The findings aim to refine biomarker co-expression strategies to better identify patients most likely to benefit from mirvetuximab soravtansine.

Shachar EK, Silverstein J, Gornbein J et al. · International journal of gynecological cancer : official journal of the International Gynecological Cancer Society · (2026) · View on PubMed ↗ · Free PDF ↗

Fibroblast-derived Spondin-2 promotes dysplastic transition in metaplastic gastric epithelial cells.

This study used single-cell RNA sequencing of patient-derived fibroblast populations and coculture/gastroid models to determine how fibroblast-derived Spondin-2 (SPON2) drives the transition from metaplasia to dysplasia in gastric epithelial cells. Fibroblast-derived SPON2 promoted dysplastic transition in metaplastic gastric epithelial cells, identifying SPON2 as a key mediator of early gastric carcinogenesis progression. This mechanistic insight highlights SPON2 as a potential therapeutic target or biomarker for preventing progression from metaplasia to dysplasia.

Rhodes JD, Hur S, Zhang C et al. · Gastroenterology · (2026) · View on PubMed ↗

Splenic extramedullary hematopoiesis in myelofibrosis is shaped by transcriptomic and epigenetic dysregulation.

This Cell Stem Cell study investigated the cellular basis of splenic extramedullary hematopoiesis (EMH) in myelofibrosis by performing single-cell transcriptional and chromatin profiling on cells from surgically removed MF spleens. The key finding was that EMH involved expansion of hematopoietic stem and progenitor cells with aberrant erythroid and megakaryocytic differentiation, accompanied by enrichment of inflammatory pathways with enhanced NF-κB signaling and interferon (IFN) responses. These results identify transcriptomic/epigenetic dysregulation programs that could be targeted to modulate pathological EMH in myelofibrosis.

Austin R, Kowalski MH, Wang X et al. · Cell stem cell · (2026) · View on PubMed ↗

Spatial profiling of the spleen in mouse and human myelofibrosis reveals complement-driven immune-stromal interactions as a therapeutic target.

The study used spatial and single-nucleus transcriptomics of human spleens and spatial/single-cell transcriptomics plus imaging of mouse spleens to map extramedullary hematopoiesis niches in myelofibrosis. It found that activated red pulp reticular cells shift from hematopoiesis-supportive to inflammatory and pro-fibrotic states, driven by complement-driven immune–stromal interactions, with early marginal zone disruption and lymphoid depletion preceding stromal remodeling. These findings identify complement-mediated stromal reprogramming in the spleen as a tractable therapeutic target to slow progression of myelofibrosis.

Dugué B, Wanner P, Ruiz Tejada Segura ML et al. · Cell stem cell · (2026) · View on PubMed ↗ · Free PDF ↗

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Cancer Therapeutics (Drugs, Trials, and Delivery Platforms)

A binding-to-release strategy for targeted anticancer drug delivery.

The study developed a binding-to-release (BTR) targeted drug delivery strategy for anticancer drug conjugates, focusing on decoupling payload release from receptor-mediated endocytosis in poorly internalizing targets. Using phosphorus(V)-phenol exchange (PhoPEx) chemistry to place an electrophile for direct cleavage by a proximal nucleophilic residue in the binding pocket, the authors reported improved release behavior relative to endocytosis-dependent designs. This provides a mechanistic platform to expand the therapeutic applicability of antibody-drug conjugates (ADCs) and small molecule-drug conjugates (SMDCs) to targets that internalize inefficiently.

Wen Z, Xu M, Yan Z et al. · Nature · (2026) · View on PubMed ↗

Structure-Guided Optimization of a Molecular Glue Targeting the KBTBD4-HDAC1/2 Complex.

This work used cryo-EM structure-guided medicinal chemistry to optimize UM171-derived molecular glues that target the KBTBD4–HDAC1/2 complex, aiming to enhance ternary complex formation and neosubstrate degradation. The optimized compounds showed a ~20-fold increase in glue activity with improved stability of the KBTBD4–HDAC2 ternary complex and robust degradation of LSD1 and CoREST1, with variable toxicity in HepG2 cells. The results demonstrate that structural design can potentiate KBTBD4-based molecular glue efficacy while highlighting the need to manage complex, context-dependent cellular toxicity.

Balo T, Chen Z, Palluaud L et al. · ChemMedChem · (2026) · View on PubMed ↗ · Free PDF ↗

Targeting tumour-neuron synapses with intracavitary RNA delivery prevents glioblastoma recurrence.

This study used analyses of intact human glioblastoma specimens with spatial and transcriptomic profiling to identify malignant tumor–neuron synapse features and highlighted TrkB as a candidate target at the tumor-brain interface. It then engineered an intracavitary, multiresponsive hydrogel for local RNA delivery that targeted tumor-neuron synapses and prevented glioblastoma recurrence. Scientifically, it provides a strategy to modulate synaptic signaling locally to avoid systemic neurotoxicity while improving recurrence outcomes in GBM models.

Li Z, Hao ZZ, Zhang Y et al. · Nature biomedical engineering · (2026) · View on PubMed ↗ · Free PDF ↗

Enzymatic activity-independent NANS stabilizes LATS2 to drive growth and therapeutic resistance in HR+/HER2- breast cancer.

This study examined the role of N-acetylneuraminate synthase (NANS) in HR+/HER2- breast cancer and its contribution to growth and resistance to endocrine therapy and CDK4/6 inhibitors. NANS promoted tumor growth and conferred resistance to tamoxifen and CDK4/6 inhibitors independently of its enzymatic activity by recruiting USP7 to deubiquitinate and stabilize LATS2. Scientifically, it identifies an enzymatic-activity-independent NANS–USP7–LATS2 axis as a therapeutic vulnerability in HR+/HER2- disease.

Cai JY, Huang MY, Yang SY et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Suzetrigine (Journavx) for Acute Dental Pain: First Clinical Case Series of a Selective Naᵥ1.8 Inhibitor in Endodontics.

This first clinical case series evaluated suzetrigine (Journavx), a selective Naᵥ1.8 inhibitor, for acute dental pain in endodontic settings where inflammatory Naᵥ1.8 upregulation contributes to persistent nociception and local anesthetic failure. The reported cases describe clinical use outcomes of suzetrigine for acute dental pain, targeting the peripheral sodium channel mechanism underlying pain and anesthetic failure. These early real-world data support further controlled trials of Naᵥ1.8 inhibition as a mechanism-based analgesic strategy in dental emergencies.

James Z, Al-Barrak Moqbel M, Shirodkar G et al. · Journal of endodontics · (2026) · View on PubMed ↗

Embarking on a new era in high-risk biochemical recurrent prostate cancer: redefining early systemic intervention.

This article reviews the clinical rationale and evidence for early systemic intervention in high-risk biochemical recurrent prostate cancer, focusing on patients with short PSA doubling time after definitive local therapy. It highlights that persistent androgen receptor (AR) signaling sustains occult micrometastatic disease and that the phase III EMBARK trial showed improved metastasis outcomes with enzalutamide intensification of AR pathway inhibition given with androgen deprivation therapy or as monotherapy. The work supports redefining treatment timing for selected high-risk patients to reduce metastatic progression and prostate cancer mortality.

Izzi M, Lapucci A, Catalano M et al. · Pharmacology & therapeutics · (2026) · View on PubMed ↗ · Free PDF ↗

Crizotinib versus observation or placebo for surgically resected early-stage ALK-positive non-small-cell lung cancer (Eastern Cooperative Oncology Group-American College of Radiology Imaging Network E4512): a phase 3 trial.

This phase 3 randomized trial (E4512) studied adjuvant crizotinib versus observation in patients with surgically resected early-stage ALK-positive NSCLC. The key finding was that adjuvant crizotinib improved disease-free survival compared with observation (with the trial designed to assess DFS as the primary endpoint). This supports using the ALK inhibitor crizotinib as a post-resection systemic therapy strategy to reduce recurrence risk in early-stage ALK-positive NSCLC.

Gerber DE, Wang Y, Langer CJ et al. · The Lancet. Respiratory medicine · (2026) · View on PubMed ↗

On-demand transarterial chemoembolisation combined with atezolizumab and bevacizumab in patients with untreated hepatocellular carcinoma (TALENTACE): a multicentre, randomised, open-label, phase 3 trial.

This multicentre, randomized, open-label phase 3 trial (TALENTACE) studied whether adding atezolizumab and bevacizumab to on-demand transarterial chemoembolisation (TACE) improves outcomes versus on-demand TACE alone in systemically untreated unresectable intermediate-to-high tumor burden hepatocellular carcinoma. The key finding was that the combination strategy with atezolizumab (anti–PD-L1) plus bevacizumab (anti-VEGF) improved clinical outcomes compared with TACE alone. Clinically, it provides evidence for an immunotherapy–antiangiogenic regimen integrated with TACE to extend survival in this patient population.

Kudo M, Ogasawara S, Liu R et al. · The lancet. Gastroenterology & hepatology · (2026) · View on PubMed ↗

Engineered human iPSC-derived dendritic cells dressed with tumor MHC complexes as a cancer vaccine.

This study engineered universal MHC-deficient human iPSC-derived CCR7+ migratory dendritic cells and “dressed” them with tumor-derived full repertoires of MHC–antigen complexes to create a personalized cancer vaccine product. The key finding was that these TumorDressed dendritic cells effectively activated tumor antigen–specific T cells, overcoming limitations of antigen diversity and DC yield/quality in autologous approaches. Scientifically, it demonstrates a scalable iPSC-based platform for personalized cancer vaccination using tumor membrane–derived MHC complexes.

Xu H, Kamei C, Gökbuget D et al. · Cell stem cell · (2026) · View on PubMed ↗ · Free PDF ↗

Becotatug Vedotin Combined With Pucotenlimab in Platinum- and Immunotherapy-Resistant Recurrent or Metastatic Nasopharyngeal Carcinoma.

This phase I/II open-label study (Magic-C001; NCT05688605) evaluated the EGFR-directed antibody-drug conjugate becotatug vedotin (BV) combined with the PD-1 inhibitor pucotenlimab in patients with EGFR-positive, platinum- and anti–PD-1/PD-L1–resistant recurrent or metastatic nasopharyngeal carcinoma (R/M NPC). The abstract indicates the trial was designed to determine efficacy and safety using BV dose escalation (1.8–2.3 mg/kg in phase I; 2.0 mg/kg in phase II) with pucotenlimab 3.0 mg/kg, but the provided text is truncated before reporting the key efficacy/safety results. If effective, this combination would provide a targeted ADC plus checkpoint blockade strategy for a population with limited options after failure of platinum and PD-1/PD-L1 therapy.

Ruan DY, Wang FH, Zhou Y et al. · Journal of clinical oncology : official journal of the American Society of Clinical Oncology · (2026) · View on PubMed ↗

Phase 1 Trial with Soquelitinib, a Selective ITK Inhibitor for Treatment of Relapsed/Refractory T Cell Lymphomas.

This phase 1 clinical trial evaluated soquelitinib, a covalent selective ITK inhibitor, in patients with relapsed/refractory peripheral T cell lymphomas. The study assessed safety and ITK target occupancy while leveraging soquelitinib’s ability to block Th2 differentiation with Th1 sparing (Th1 skewing). If effective, ITK inhibition with soquelitinib could provide a targeted immunomodulatory therapy for R/R mature T cell lymphomas driven by tonic TCR signaling and an immunosuppressive microenvironment.

Miller RA, Ding N, Reneau JC et al. · Blood · (2026) · View on PubMed ↗

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Neurodegeneration, Brain Aging & Cognitive Outcomes

Exome analysis of 22,319 individuals links extremely rare copy-number variants and 22q11.21 dosage to Alzheimer risk.

This exome-based genetic study analyzed rare copy-number variants (CNVs) in 22,319 individuals (4,150 early-onset AD, 8,519 late-onset AD, and 9,650 controls) to identify CNV dosage effects on Alzheimer disease risk. It found that extremely rare CNVs and increased dosage at 22q11.21 were linked to Alzheimer risk, with early-onset AD showing higher burdens of rare coding-gene CNVs, particularly deletions in AD-related genes. These results strengthen the role of non-monogenic CNV dosage—especially 22q11.21—in Alzheimer susceptibility and support gene-set burden approaches for risk discovery.

Quenez O, Schramm C, Cassinari K et al. · American journal of human genetics · (2026) · View on PubMed ↗

Nicotinamide Mononucleotide Adenylyltransferase 1 and NAD+ Homeostasis in Neuroprotection and Aging.

This review synthesized evidence on nicotinamide mononucleotide adenylyltransferase 1 (NMNAT-1), the final enzyme in NAD+ biosynthesis, and how NAD+ homeostasis contributes to neuroprotection and aging, including human genetic data. The key finding is that NMNAT-1 is a causal gene for inherited retinal degeneration and that NMNAT-1–dependent NAD+ maintenance is positioned as a limiting, compartment-specific node relevant to neuronal survival and age-related decline. Scientifically, it supports NMNAT-1/NAD+ pathway targeting as a mechanistic strategy for neuroprotection and for understanding tissue-specific aging biology.

Sun Y, Li B, Qian Z · Metabolites · (2026) · View on PubMed ↗

Hormone replacement therapy and dementia risk among postmenopausal women: Identifying responsive subgroups in the UK Biobank.

Using UK Biobank data from 183,450 postmenopausal women followed for a mean of 13.3 years, this study evaluated whether hormone replacement therapy (HRT) for ≥1 year is associated with all-cause dementia and dementia subtypes and whether effects differ by menopause type, lifetime estrogen exposure, APOE ε4 genotype, and age at HRT initiation. HRT use was associated with a modestly lower risk of all-cause dementia (HR 0.90, 95% CI 0.84–0.96), and the analysis aimed to identify responsive subgroups based on these modifiers. Clinically, the results suggest that HRT’s dementia risk profile may vary across biologically defined groups, supporting more personalized risk–benefit discussions.

Squires S, Saleh RN, Pilling LC et al. · Alzheimer’s & dementia : the journal of the Alzheimer’s Association · (2026) · View on PubMed ↗ · Free PDF ↗

Unraveling Neurodegeneration: Common Molecular Mechanisms and Novel Therapeutic Concepts in Major Neurodegenerative Disorders.

This review integrated evidence across major neurodegenerative disorders—Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, multiple sclerosis, and Huntington’s disease—to identify shared molecular disturbances in neuroinflammation, oxidative imbalance, mitochondrial impairment, and disrupted protein homeostasis. It concludes that despite distinct clinical phenotypes, these diseases converge on common pathogenic pathways that can be leveraged for multi-target, disease-modifying therapeutic strategies. The synthesis supports a shift from single-pathway interventions toward combination approaches aimed at convergent mechanisms across neurodegeneration.

Aldaghi FS, Siahpoosh Z, Salehi Z et al. · Brain and behavior · (2026) · View on PubMed ↗ · Free PDF ↗

Oligodendrocyte dysfunction in human age-related cognitive decline.

This study linked human neuropathology and transcriptomic changes in white matter to individual rates of cognitive decline in aging, focusing on oligodendrocyte biology and NRF2 signaling. Worse cognitive trajectories were associated with smaller myelinated axon size, thicker myelin, more oligodendrocytes, and downregulation of NRF2, and oligodendrocyte-specific NRF2 knockout mice showed attenuated cognitive improvement. The findings implicate oligodendrocyte NRF2 dysregulation as a mechanistic contributor to age-related cognitive decline and a potential therapeutic axis.

Craig GA, Merour E, Seeker LA et al. · Nature medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Sex-specific aging clocks from a large-scale human phenome reveal distinct aging transitions and circulating signatures.

This study developed sex-specific human aging clocks using large-scale phenome data from the X-Age Project and the Multicentric Chinese Aging Study (mCAS), profiling 172 clinical measures in >100,000 participants aged 18–98 years across three centers. The resulting clocks revealed divergent midlife aging transitions between women and men that later converged, and phenome-wide analyses highlighted age-related accumulation of metabolic factors such as LDL, triglycerides, glucose, and uric acid. These findings are clinically important because they enable sex-tailored biomarkers of aging progression and circulating signatures that may improve risk stratification for age-associated diseases.

Li J, Gao DD, Li J et al. · Nature aging · (2026) · View on PubMed ↗

Mitochondria as central regulators of cancer progression and antitumor immunity.

This review summarizes how mitochondria regulate cancer progression and antitumor immunity through metabolic and signaling outputs, including redox control, metabolite production, and mitochondrial genome dynamics. It highlights emerging mechanisms such as mitochondrial DNA variation, intercellular mitochondrial transfer, and mitochondrial dysfunction that can reshape tumor–immune interactions. The synthesis supports mitochondria as actionable targets for therapies designed to both suppress tumor growth and enhance antitumor immunity.

Gomez-Duran A, Martínez-Reyes I · Trends in endocrinology and metabolism: TEM · (2026) · View on PubMed ↗ · Free PDF ↗

Prevalence of chronic traumatic encephalopathy at death in National Football League players: retrospective population based cohort study, 2008-21.

This retrospective, population-based cohort study examined chronic traumatic encephalopathy (CTE) at death in 1,712 deceased National Football League players (2008–2021), including 338 brain donors evaluated neuropathologically at UNITE and UCSF ADRC brain banks. The study estimated a range of CTE prevalence at death and assessed how CTE severity related to dementia risk. These results strengthen epidemiologic evidence linking repetitive head impacts in NFL players to neurodegenerative outcomes and inform risk estimates for CTE and dementia.

Daneshvar DH, Nowinski CJ, Abdolmohammadi B et al. · BMJ (Clinical research ed.) · (2026) · View on PubMed ↗ · Free PDF ↗

Cardiovascular-Kidney-Metabolic Syndrome in neurological and psychiatric disorders: a large multi-national cohort study.

This large multinational cohort study examined long-term cerebral outcomes of cardiovascular-kidney-metabolic (CKM) syndrome stages in relation to neuropsychiatric disorders using data from Health and Retirement Study, UK Biobank, China Health and Retirement Longitudinal Study, and NHANES. The study found that increasing CKM stage was associated with higher risk of dementia, Parkinson’s disease, depression, anxiety, and sleep disorders after adjustment for demographic, lifestyle, and medical history factors. These results extend CKM syndrome from a multisystem homeostasis framework to clinically meaningful brain and mental health outcomes.

Huang Y, Li K, Yangybrbi Y et al. · Brain, behavior, and immunity · (2026) · View on PubMed ↗

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Neurology: Pain, Synapses & Neuropsychiatric Mechanisms

Divergent recovery trajectories after mild traumatic brain injury are characterized by distinct acute profiles of neurofilament light, 4R-tau, and white matter diffusivity.

This prospective study examined 36 adults with acute mild traumatic brain injury (mTBI) (≤9 days post-injury) and 35 healthy controls using blood biomarkers (including neurofilament light-chain and 4R-tau) alongside diffusion MRI to define recovery subtypes. It identified divergent recovery trajectories characterized by distinct acute profiles of neurofilament light, 4R-tau, and white-matter diffusivity, and related these to recovery patterns while evaluating moderating effects of resilience and coping style. The work supports using combined blood-based and diffusion MRI biomarkers to stratify mTBI patients by likely recovery course.

Papini MG, Thorne J, Gozt AK et al. · Journal of neurology · (2026) · View on PubMed ↗ · Free PDF ↗

G3BP1 depletion, observed in Parkinson’s Disease, drives Golgi-lysosome-autophagy defects.

This study investigated how depletion of the RNA-binding protein G3BP1, observed in Parkinson’s disease, affects intracellular trafficking and autophagy in cellular models. G3BP1 stabilized the COPI vesicle protein beta-COP by promoting its interaction with the deubiquitinase USP10; G3BP1 loss disrupted this interaction, increased beta-COP ubiquitination and proteasomal degradation, leading to Golgi-lysosome dysfunction and impaired autophagic flux, including reduced clearance of α-synuclein. The work is significant because it links a Parkinson’s-associated factor (G3BP1) to a mechanistic pathway controlling autophagy and α-synuclein homeostasis.

Ramakrishna S, Ryan L, Son SM et al. · Cell death and differentiation · (2026) · View on PubMed ↗ · Free PDF ↗

BRAF recruitment to spinal sensory synapses promotes neuropathic pain by potentiating transsynaptic NMDA receptor activity.

This work investigated how the kinase BRAF regulates neuropathic pain by promoting transsynaptic NMDA receptor activity in rat models of spinal nerve injury and in mouse/human spinal cord and synapse samples. Spinal injury induced BRAF translocation from dorsal root ganglion neurons to spinal cord synaptosomes, increased MEK/ERK phosphorylation, and enhanced NMDAR–BRAF/MEK/ERK interactions, while pharmacologic inhibition or genetic ablation of BRAF in DRG neurons reversed injury-induced NMDAR phosphorylation. The results identify BRAF as a critical upstream regulator of spinal NMDAR hyperactivity, suggesting BRAF/MEK/ERK pathway targeting as a potential therapeutic approach for chronic neuropathic pain.

Jin D, Chen H, Huang Y et al. · Science signaling · (2026) · View on PubMed ↗

WNK-dependent phosphorylation of gephyrin tunes GABAA receptors at inhibitory synapses and modulates anxiety behavior.

This study investigated how WNK1/SPAK signaling regulates inhibitory synapses by controlling the phosphorylation-dependent behavior of the gephyrin scaffold and GABA_A receptors (GABA_A R) in neurons and in vivo. WNK-dependent phosphorylation of two residues in gephyrin tunes GABA_A R synaptic diffusion/clustering and membrane stability, where WNK activation stabilizes receptors at inhibitory synapses and WNK inhibition increases receptor internalization, altering GABAergic current kinetics and anxiety-related behavior. These results link a chloride-sensitive kinase pathway to inhibitory synapse organization and behavior, highlighting WNK–gephyrin–GABA_A R signaling as a potential target for neuropsychiatric modulation.

Merlaud Z, Delhaye C, Nabais 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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Cardiovascular, Metabolic & Kidney Outcomes

Glucagon-Like Peptide 1 Receptor Agonists, Mortality, and Cardiovascular Outcomes in Serious Mental Illness.

This retrospective target-trial emulation study used TriNetX data to compare outcomes after initiating glucagon-like peptide-1 receptor agonists (GLP-1 RAs) versus sodium-glucose cotransporter-2 (SGLT2) inhibitors in adults with and without serious mental illness (SMI). It assessed associations with all-cause mortality and major adverse cardiovascular events (MACEs) following treatment initiation. The clinical significance is that it evaluates whether GLP-1 RA initiation could reduce cardiovascular risk in high-mortality psychiatric populations compared with an alternative cardiometabolic class.

McIntyre RS, Zhang-James Y, Kwan ATH · JAMA psychiatry · (2026) · View on PubMed ↗

Predictive Utility of Coronary Artery Calcium Score Added to the PREVENT Atherosclerotic Cardiovascular Disease Equations.

This longitudinal observational cohort study tested whether adding coronary artery calcium (CAC) scores improves ASCVD risk prediction beyond the PREVENT (Predicting Risk of Cardiovascular Disease EVENTS) equations. The analysis evaluated changes in predictive utility when CAC was incorporated for adults whose 10-year risk fell in the guideline-recommended “selective CAC use” range (3% to <10%). The results are significant for refining risk stratification and guiding more personalized prevention decisions in cardiovascular prevention practice.

Huang X, Petito LC, Allen NB et al. · JAMA · (2026) · View on PubMed ↗

Hepatic ChREBP Drives Cardiac Remodeling via ApoM Nontranscriptional Repression.

This mouse study investigated how hepatic carbohydrate response element binding protein (ChREBP) regulates cardiac remodeling through apolipoprotein M (ApoM) using hepatocyte-specific ChREBP knockout/overexpression, global ApoM knockout, and adeno-associated virus–mediated hepatic ApoM knockdown or overexpression, alongside cardiomyocyte-specific ChREBP overexpression and S1PR1 knockdown. The key finding is that hepatic ChREBP drives cardiac remodeling by nontranscriptionally repressing ApoM, linking liver–heart signaling to pathological remodeling in models induced by isoproterenol and transverse aortic constriction. These mechanistic results highlight the ChREBP–ApoM axis as a potential therapeutic target for preventing or treating heart failure–associated remodeling.

Zhang S, Zhang Z, Ma Z et al. · Circulation research · (2026) · View on PubMed ↗ · Free PDF ↗

Case Report: A rare case of multi-vessel coronary artery-coronary sinus fistula combined with multiple coronary aneurysms initially presenting with frequent premature ventricular complexes.

This case report describes a 63-year-old woman with a rare Sakakibara type B multi-vessel coronary artery–coronary sinus fistula combined with multiple coronary aneurysms, initially presenting with frequent premature ventricular complexes (PVCs). Holter monitoring showed very high PVC burden (up to 40,804 complexes) and imaging (including transthoracic echocardiography) demonstrated cardiac chamber dilation consistent with the underlying vascular anomaly. The report is clinically significant because it highlights an uncommon anatomical cause of high-burden PVCs and supports considering coronary fistula/aneurysm in atypical arrhythmia presentations.

Yi H, Li J, Bao Y · Frontiers in cardiovascular medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Prescription of SGLT-2 inhibitors alone or in combination with RAS-inhibitors in patients with diabetes mellitus and comorbid cardiovascular disease, chronic kidney disease or cardiorenal disease: a real-world evidence study from the REPOSI registry.

This real-world study analyzed prescription patterns of SGLT-2 inhibitors alone versus combined with renin-angiotensin system (RAS) inhibitors in older (≥65 years) hospitalized patients with diabetes mellitus and comorbid cardiovascular disease, chronic kidney disease, or cardiorenal disease using the Italian REPOSI registry. Among 1372 multicenter patients (2008–2024), the authors assessed how clinicians used these drug combinations across relevant comorbidity groups and time periods. The results are clinically significant because they inform real-world uptake of guideline-concordant SGLT-2–based strategies intended to reduce cardiovascular and renal risk in high-risk diabetic populations.

Lido P, Ratti S, Ronchetti C et al. · Internal and emergency medicine · (2026) · View on PubMed ↗

Cardiorenal Mortality and Safety Outcomes of GLP-1 Receptor Agonists in Type 2 Diabetes With BMI Below 27 kg/m2: A Target Trial Emulation.

This target trial emulation used the TriNetX US Collaborative Network to compare cardiorenal outcomes in adults with type 2 diabetes and BMI <27 kg/m2 initiating non-tirzepatide GLP-1 receptor agonists versus DPP-4 inhibitors, SGLT2 inhibitors, or usual care. The study assessed all-cause mortality and safety outcomes over up to 24 months using 1:1 propensity score matching. The results address an evidence gap for GLP-1 RA effectiveness and safety in leaner T2D populations, informing risk-benefit decisions beyond overweight/obesity trial cohorts.

Chen SC, Huang YN, Li PY et al. · Diabetes, obesity & metabolism · (2026) · View on PubMed ↗ · Free PDF ↗

New Cardiovascular Diagnoses, Symptoms and Functional Status Following SARS-CoV-2 Infection in a National Cohort of 1,734 Patients in Italy.

This multicentre Italian cohort study followed 1,734 patients after SARS-CoV-2 infection to characterize new cardiovascular diagnoses, symptoms, and functional status. It collected acute COVID-19 severity and timing, comorbidities, and 30 post-acute symptoms, then classified new diagnoses as cardiovascular versus non-cardiovascular and tested associations with clinical covariates. The results provide population-level evidence for the burden and correlates of post-COVID cardiovascular sequelae, informing follow-up and risk stratification.

Floridia M, Parati G, Soranna D et al. · Heart, lung & circulation · (2026) · View on PubMed ↗

Detection of Potential MetALD and ALD Using Phosphatidylethanol in a Large Multicenter MASH Trial Screening Cohort.

In a large multicenter MASH trial screening cohort of patients considered for MASLD pharmacologic therapies, this study assessed detection of potential MetALD and ALD using phosphatidylethanol (PEth) blood testing. Elevated PEth was used to estimate the prevalence of alcohol-associated phenotypes and to evaluate how well PEth separates dominant MASLD from MetALD/ALD in the clinical trial context. This improves phenotype classification in liver disease trials where self-reported alcohol use may be underreported.

Noureddin M, Schattenberg JM, Patil R et al. · Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association · (2026) · View on PubMed ↗

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Radiation Oncology & Treatment Planning

Thymic Radiation is Associated with Worse Outcomes in Patients with NSCLC.

This multicohort analysis studied whether incidental thymus radiation during radiotherapy is associated with outcomes in 1,107 patients with non-small cell lung cancer (NSCLC), including participants from the phase III RTOG-0617 trial and two real-world chemoradiotherapy cohorts. The key finding was that higher thymic radiation dose correlated with worse clinical outcomes, indicating that thymic exposure during RT is clinically relevant. Clinically, it suggests that radiotherapy planning should consider thymic dose constraints to potentially improve survival and reduce treatment-related harm.

Prudente V, Bernatz S, Pai S et al. · Annals of oncology : official journal of the European Society for Medical Oncology · (2026) · View on PubMed ↗ · Free PDF ↗

Salvage Hypofractionated Accelerated Versus Standard Radiotherapy for Biochemical Recurrence After Radical Prostatectomy: A Phase III Randomized Clinical Trial.

This phase III randomized clinical trial compared hypofractionated salvage radiotherapy (65 Gy in 26 fractions) versus conventional salvage radiotherapy (66 Gy in 33 fractions) for biochemical recurrence after radical prostatectomy in 316 intermediate- to high-risk prostate cancer patients. The primary endpoint was biochemical progression-free survival (bPFS), with intensity-modulated RT and daily image guidance used and pelvic nodal irradiation at clinician discretion (results truncated). If hypofractionated RT is non-inferior or superior on bPFS and toxicity, it could change standard salvage RT fractionation to improve convenience without compromising disease control.

Song Y, Park W, Pyo H et al. · Journal of clinical oncology : official journal of the American Society of Clinical Oncology · (2026) · View on PubMed ↗

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Infectious Disease, Vaccines & Host-Pathogen Mechanisms

Finding the perfect promoter for Cas9 in homing gene drives using single cell transcriptome data.

This study evaluated 35 CRISPR-Cas9 homing gene drive constructs with different promoters in Drosophila melanogaster and linked promoter choice to single-cell RNA expression patterns in reproductive and germline cells. Higher drive conversion was associated with elevated expression of promoter-associated genes in reproductive cells, whereas embryo resistance allele formation correlated with excessive female germline expression. These findings provide promoter-selection rules to improve homing drive performance while reducing resistance in gene-drive engineering.

Wu Y, Xia Y, Yao Z et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Bundibugyo virus glycoprotein seroreactivity following recombinant vesicular stomatitis virus-Zaire Ebola virus glycoprotein vaccination in outbreak-affected populations of the Democratic Republic of the Congo: a longitudinal cohort study.

This longitudinal cohort study measured Bundibugyo virus (BDBV) glycoprotein seroreactivity after vaccination with recombinant vesicular stomatitis virus–Zaire Ebola virus glycoprotein (rVSVΔG-ZEBOV-GP) in outbreak-affected populations in the Democratic Republic of the Congo. The key finding was that vaccination induced cross-reactive BDBV glycoprotein antibodies, with durability and longitudinal kinetics characterized over follow-up. This is significant for understanding breadth of vaccine-induced immunity and for informing preparedness against BDBV where no licensed vaccine exists.

Halbrook M, Merritt S, Hoff NA et al. · Lancet (London, England) · (2026) · View on PubMed ↗ · Free PDF ↗

Host eicosanoid signals define a granuloma fibroblast population that coordinates mycobacterial containment.

The authors studied zebrafish mycobacterial infection models using single-cell profiling to define how leukotriene A4 hydrolase (lta4h/LTA4H)-dependent host signals recruit and program granuloma fibroblasts. They identified a peripheral granuloma fibroblast population with mesenchymal/stem-like features (including aldh1a3) whose ablation impairs bacterial containment, and they report that apolipoprotein disruption similarly affects containment (details truncated). This work links LTA4H-driven eicosanoid signaling to granuloma-edge fibroblast function, suggesting host-pathway modulation as a strategy to enhance tuberculosis control.

Hughes EJ, Pyle CJ, Chambers M et al. · Cell host & microbe · (2026) · View on PubMed ↗ · Free PDF ↗

The long and winding road: On the endoplasmic reticulum of Plasmodium and implications for pathogenesis.

This PLoS Pathogens “Pearl” review summarized how the Plasmodium endoplasmic reticulum (ER) supports parasite survival and contributes to malaria pathogenesis across life-cycle stages. It highlights ER roles in conserved processes such as cell signaling, protein synthesis/secretion, lipid production, and stress responses, and links ER functions to motility, egress/invasion, host-cell remodeling, and transmission. The synthesis frames the Plasmodium ER as a multi-stage vulnerability and a source of potential therapeutic targets.

Blank A, Ngwira S, Fierro MA · PLoS pathogens · (2026) · View on PubMed ↗ · Free PDF ↗

A gut symbiotic filamentous fungus reprograms host metabolism and the microbiota to confer radioprotection.

This study identified the gut symbiotic filamentous fungus Mucor racemosus and tested how it confers radioprotection in host intestinal tissues and microbiota. M. racemosus produces L-glutamate, L-aspartate, and DL-lysine that are transferred to radiation-exposed intestinal epithelial cells to enhance DNA damage repair, with additional radioprotection amplified through microbiota-mediated metabolic coupling. These findings suggest a mechanistic, metabolite-transfer route by which a filamentous mycobiome member can protect against radiation injury, informing microbiota- or metabolite-based radioprotective strategies.

Xiao H, Liu J, Zhao J et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗

Plasmodium thiamine pyrophosphokinase is essential for sporozoite formation and activation of an antiplasmodial thiamine analogue.

This study examined the role of Plasmodium falciparum thiamine pyrophosphokinase (TPK) in oxythiamine (a thiamine analogue) antiplasmodial activity and generated genetic models to test TPK function across parasite development. Whole-genome sequencing of oxythiamine-resistant P. falciparum lines identified a single-point mutation in the TPK gene that reduces TPK activity, likely limiting conversion of oxythiamine into its active toxic form, and TPK knockout in Plasmodium berghei impaired sporozoite formation and activation. The findings establish TPK as an essential enzyme for parasite life-cycle progression and as a mechanistic determinant of oxythiamine susceptibility, supporting TPK as a drug target.

Fathoni I, Kina ÜY, Chan AHY 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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Hematologic Malignancies: Trials, Guidelines & Risk Stratification

Superior 12-month progression-free survival with frontline DVd versus VRd in patients with newly diagnosed multiple myeloma: a multicenter propensity score-matched analysis.

This multicenter propensity score-matched analysis compared frontline daratumumab plus lenalidomide-bortezomib-dexamethasone (DVd) versus lenalidomide-bortezomib-dexamethasone (VRd) in patients with newly diagnosed multiple myeloma. DVd produced superior 12-month progression-free survival compared with VRd. Clinically, the findings strengthen evidence for incorporating daratumumab into induction regimens to improve early disease control in NDMM.

Jiang H, Li Q, Wang L et al. · Journal of translational medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Ivosidenib monotherapy in IDH1 mutated myelodysplastic neoplasm/syndrome.

This multicenter phase 2 trial evaluated ivosidenib (IVO) monotherapy, an inhibitor of mutant IDH1 (IDH1m), in patients with IDH1-mutated myelodysplastic neoplasm/syndrome (MDS) across three cohorts (post–azacitidine HR-relapsed/refractory, treatment-naïve HR, and low-risk refractory to erythropoiesis-stimulating agents). The study reported an overall response rate of 63% after 3 cycles and characterized safety and efficacy across these groups. The results support IVO monotherapy as a potential treatment option for IDH1m MDS, extending IDH1-targeted therapy beyond AML.

Sébert M, Clappier E, Chevret S et al. · Leukemia · (2026) · View on PubMed ↗

Real-world effectiveness and safety of Zanubrutinib in Spanish patients with relapsed/refractory marginal zone lymphoma.

This retrospective real-world study evaluated the effectiveness and safety of zanubrutinib in 118 Spanish patients with relapsed/refractory marginal zone lymphoma (R/R MZL) after at least one prior anti-CD20 regimen. It reports patient and disease characteristics (median age 75; 56% female; multiple MZL subtypes including splenic, MALT, and nodal; median 1.5 prior lines; with refractory and POD24 proportions, truncated) to contextualize outcomes of zanubrutinib use outside the MAGNOLIA trial setting. The findings are clinically relevant for informing treatment expectations and safety monitoring for zanubrutinib in routine care for R/R MZL.

Martin-Moro F, Muntanola Prat A, Gutierrez Lopez De Ocariz X et al. · Blood advances · (2026) · View on PubMed ↗ · Free PDF ↗

Inhibition of nucleoporin 214 depletes leukemia stem cells by promoting heme catabolism and lipid peroxidation.

This study investigated the role of nucleoporins in acute myeloid leukemia (AML) and identified nucleoporin 214 (NUP214) as a driver of leukemia stem cell (LSC) fitness. Through a NUP-family screen, NUP214 was found to be frequently overexpressed and required for LSC survival by restricting heme catabolism, limiting Fe2+ accumulation, and suppressing lipid peroxidation; NUP214 deficiency increased HMOX1 and ALOX15, leading to heme exhaustion and excessive lipid peroxidation. These mechanistic findings suggest that targeting NUP214 could selectively impair AML LSCs by forcing lethal oxidative/heme stress.

Chen Z, Wu F, Zhang W et al. · Blood · (2026) · View on PubMed ↗

International Consensus Criteria for the Diagnosis, Treatment Initiation, and Response Assessment for T-LGL Leukemia.

This article presents International Consensus Criteria for diagnosing, initiating treatment, and assessing response in T-cell large granular lymphocytic (T-LGL) leukemia. It addresses the clinical problem that heterogeneous diagnostic and response criteria have limited comparability across studies and reflects recent advances and emerging therapies in T-LGL/LGLL. Standardized criteria are scientifically and clinically significant because they enable consistent trial enrollment, endpoints, and response assessment in this under-diagnosed, often autoimmune-associated leukemia.

Brammer JE, Pflug N, Zambello R et al. · Blood · (2026) · View on PubMed ↗

Epigenetic markers expand genetic risk estimation in acute myeloid leukemia.

This study evaluated whether DNA methylation patterns can expand genetic risk estimation in acute myeloid leukemia (AML) beyond mutations and cytogenetics. In 1,262 patients with de novo AML, unsupervised DNA methylation clustering defined 13 methylation subtypes (“epitypes”), which were largely driven by predominant genetic alterations but also included “genetic alteration-like” patients lacking cardinal genetic changes. The work indicates that epigenetic markers can refine risk stratification for AML patients even when key genetic alterations are absent, improving prognostic modeling.

Abdelbaky SB, Giacopelli B, Kohlschmidt J et al. · Blood · (2026) · View on PubMed ↗ · Free PDF ↗

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Ophthalmology & Vision Science

Early anatomical rescue after switching to aflibercept 8 mg in faricimab-refractory neovascular AMD.

This retrospective study evaluated early anatomical outcomes after switching from faricimab to aflibercept 8 mg in 32 eyes from 31 patients with faricimab-refractory neovascular age-related macular degeneration (nAMD). After the switch, central subfield thickness decreased and a proportion of eyes achieved a fluid-free macula by weeks 8 and 16, with subgroup analyses by polypoidal choroidal vasculopathy (PCV) versus non-PCV and prior treatment history. The results suggest that aflibercept 8 mg can provide early anatomical benefit in faricimab-refractory nAMD.

Chang W · International ophthalmology · (2026) · View on PubMed ↗

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Reproductive/Developmental Biology & Tissue Patterning

Development of mitochondrial mutator pigs exhibiting increased mitochondrial DNA mutations and premature aging via prime editing.

This experimental study created a mitochondrial mutator pig model by introducing proofreading-deficient POLG (DNA polymerase gamma catalytic subunit) using prime editing combined with somatic cell nuclear transfer. The resulting pigs accumulated increased somatic mitochondrial DNA (mtDNA) mutations and developed premature aging phenotypes, including weight loss and a rough hair coat. The model provides a large-animal system to study how POLG proofreading loss drives mtDNA mutagenesis and aging biology and to test mitochondrial-targeted interventions.

Chen F, Liang Y, Zheng W et al. · Science advances · (2026) · View on PubMed ↗

Atypical E2F transcription factors couple Polycomb Repressive Complex 2 to endosperm cell division and differentiation.

This study investigated how the ancestral maize gene ZmFIE2 and the atypical E2F transcription factor ZmE2F12 regulate PRC2-mediated H3K27me3 control of endosperm cell division and differentiation in flowering plants. ZmFIE2 mutations (not ZmFIE1) abrogated global H3K27me3, caused aberrant early endosperm proliferation with impaired differentiation, and seed lethality, and ZmFIE2 physically interacted with ZmE2F12 to couple PRC2 to endosperm developmental programs. These findings identify a ZmFIE2–ZmE2F12 mechanism that links atypical E2F factors to PRC2 repression, providing a molecular explanation for how epigenetic silencing prevents precocious overproliferation in plant reproductive development.

Wang Y, Shi D, Wei Y et al. · Nature plants · (2026) · View on PubMed ↗

Disruption of the insulin/IGF-1 signaling pathway in Caenorhabditis elegans dramatically increases male longevity and enhances reproductive health late in life.

This study used the Caenorhabditis elegans male model to test whether disrupting insulin/IGF-1 signaling by degrading the DAF-2/IGF-1 receptor with an auxin-inducible degron system increases lifespan and improves late-life reproductive health. Ubiquitous DAF-2 degradation in males increased median lifespan by more than 440% and enhanced reproductive health late in life. These findings support a strong, sex-specific pro-longevity role for insulin/IGF-1 pathway suppression and highlight DAF-2 as a mechanistic target for extending healthy lifespan.

Al-Saadi RS, Lewack HB, Phillips PC · Aging · (2026) · View on PubMed ↗ · Free PDF ↗

Recognition of pathogenic bacteria by intestinal stem cells promotes adult Drosophila midgut regeneration.

This study examined whether adult Drosophila intestinal stem cells (ISCs) directly sense invading pathogens to drive regeneration after infection. Adult midgut ISCs recognized pathogenic bacteria via peptidoglycan recognition proteins PGRP-LC and PGRP-LE and translated this into ISC proliferation through Imd–Mkk3–p38 signaling, with PGRP-LC/LE–Imd–Mkk3–p38 regulating p38 activation across the midgut epithelium after infection. The findings establish a direct stem-cell innate immune sensing mechanism that couples bacterial recognition to regenerative proliferation.

Uttekar B, Srotyr M, Ravale SS et al. · PLoS biology · (2026) · View on PubMed ↗ · Free PDF ↗

Brachyury expression levels predict lineage potential and axis-forming ability of in vitro-derived neuromesodermal progenitors.

This study assessed whether Brachyury (TBXT) expression levels in in vitro-derived neuromesodermal progenitors (NMPs) predict their lineage potential and ability to form the body axis. Using a dual Sox2/Tbxt reporter mouse embryonic stem cell line to generate SOX2/TBXT-positive NMP-like cells, the authors found that TBXT levels correlate with functional differences in lineage potential and axis-forming capacity (details truncated in the provided abstract). If validated, TBXT expression quantification could become a practical biomarker for selecting higher-potency NMPs for developmental modeling and regenerative applications.

Binagui-Casas A, Granés A, Ceccarelli AS et al. · PLoS biology · (2026) · 3 citations · View on PubMed ↗ · Free PDF ↗

Auxin-induced ARF transcription factor degradation defines tissue boundaries.

This study investigated how plant tissues establish boundaries in the gynoecium apex by analyzing auxin and the ARF transcription factor ETTIN (ETT). It found that auxin induces ETT protein destabilization through the ubiquitin–proteasome pathway, requiring a short motif in an intrinsically disordered region for auxin-triggered degradation, and that disrupting this motif causes ectopic ETT accumulation and boundary defects. The work links hormone signaling to targeted protein degradation as a mechanism for defining tissue domains during organ patterning.

Ahn J, Yuan Q, Ding YN et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗

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Clinical Trials, Guidelines & Evidence Synthesis (Non-oncology and Cross-cutting)

Comparative Evaluation of Tooth Type and Pulp Chamber Depth on the Accuracy of Endocrown Scans Acquired Using Various Intraoral Scanners.

This dental imaging study evaluated how pulp chamber depth (2 vs 5 mm), tooth type (molar vs premolar), and intraoral scanner (Dexis, iTero, 3Shape) affect the accuracy of endocrown digital impressions. Across standardized endocrown preparations, all three factors significantly influenced scanning accuracy, with cavity base and axial regions showing differential performance depending on scanner and preparation geometry. Clinically, the findings guide selection of intraoral scanners and preparation parameters to improve endocrown fit and reduce restoration errors.

Erkul S, Ozkurt-Kayahan Z, Özden YE et al. · Journal of esthetic and restorative dentistry : official publication of the American Academy of Esthetic Dentistry … [et al.] · (2026) · View on PubMed ↗

De-Escalating and Discontinuing Immunotherapies in Patients With NMOSD and MOGAD.

This review examined evidence on de-escalating or discontinuing immunotherapies in patients with antibody-mediated CNS diseases, specifically aquaporin-4 antibody neuromyelitis optica spectrum disorder (AQP4-Ab NMOSD) and myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD). It concluded that while targeted therapies and sensitive antibody assays have reduced relapse rates, the risk of relapse—often severe in AQP4-Ab NMOSD—makes treatment duration and discontinuation decisions highly individualized and still uncertain. The work is significant for informing safer long-term management strategies that balance relapse prevention against treatment burden.

Hacohen Y, Androdias G, Arrambide G et al. · Neurology · (2026) · View on PubMed ↗

Blood Biochemical Acute Daily Responses During an Intensive Training Microcycle: A Case Report of an Olympic Kayaker.

This case report monitored acute blood biochemical, hematological, and hormonal responses in a 35-year-old Olympic flat-water kayaker across two consecutive 7-day microcycles (pre-intensified vs intensified). During the intensified microcycle, fasting venous blood samples collected over five mornings showed marked physiological changes consistent with training load stress. While limited to one athlete, the report supports using biochemical monitoring to better understand and manage acute responses to intensified training in elite endurance sports.

Dos Santos JAR, Zacca R, Fernandes DG et al. · Sports (Basel, Switzerland) · (2026) · View on PubMed ↗

Surgical Management of Early-Onset Breast Cancer Among Young BRCA1 and BRCA2 Carriers.

This international retrospective cohort study (BRCA BCY Collaboration) examined surgical decision-making in women aged ≤40 with germline pathogenic BRCA1 or BRCA2 and early-onset breast cancer across 109 centers on 5 continents. Uptake of bilateral mastectomy varied by patient and clinical factors, with the study identifying determinants associated with choosing bilateral mastectomy versus breast-conserving surgery (BCS) and/or contralateral risk-reducing mastectomy. These findings can inform counseling and shared decision-making for young BRCA1/2 carriers considering the tradeoffs between BCS and bilateral mastectomy.

Wong SM, Blondeaux E, Delucchi V et al. · JAMA network open · (2026) · View on PubMed ↗

Cutaneous lymphomas reported following the use of dupilumab, nemolizumab, tralokinumab, or lebrikizumab: A case investigation based on JADER database and disproportionality analysis.

This Japanese pharmacovigilance study used the JADER adverse drug event database (April 2004–August 2025) and disproportionality analyses to assess cutaneous lymphomas reported after dupilumab, nemolizumab, tralokinumab, or lebrikizumab. The key finding is that cutaneous lymphoma signals were evaluated across these anti–IL-4/IL-13 and related biologics, extending beyond dupilumab to other atopic dermatitis treatments. Scientifically and clinically, it provides safety signal characterization that can guide clinicians and regulators in monitoring rare lymphoproliferative adverse events.

Tanaka H, Ishii T · Intractable & rare diseases research · (2026) · View on PubMed ↗ · Free PDF ↗

C-terminus CD28 phosphorylation, Y218, modulates IL-2 secretion and therapeutic effect of CAR-T cells.

This systematic review and Bayesian network meta-analysis compared randomized controlled trials for depression treatments in patients with Parkinson’s disease (PD) and depression, using standardized mean differences for efficacy and odds ratios for safety and ranking interventions with SUCRA. The key finding is the relative comparative efficacy and safety ordering of available interventions, synthesized across the RCT evidence base up to September 30, 2025. Clinically, it provides an evidence-ranked framework to guide selection of depression treatments in PD patients, where comorbidity-specific effectiveness and tolerability are critical.

Martinez-Planes E, Ramello MC, Fontela MG et al. · Molecular therapy : the journal of the American Society of Gene Therapy · (2026) · View on PubMed ↗

APOE-guided lecanemab dosing dissociates ARIA-E from ARIA-H: The K-ROAD study.

In the K-ROAD study, 508 patients with early Alzheimer’s disease received APOE genotype-guided lecanemab escalation with MRI-based ARIA surveillance across eight Korean centers. The key finding is that APOE-guided dosing dissociated ARIA-E from ARIA-H, with ARIA-E incidence differing by APOE ε4 carrier status while ARIA-H behaved differently, supporting mechanistic distinctness between these ARIA phenotypes. Clinically, this supports genotype-informed dosing strategies to mitigate edema risk while clarifying that ARIA-E and ARIA-H may require different risk management considerations.

Kang H, Jang H, Ahn J et al. · Alzheimer’s & dementia : the journal of the Alzheimer’s Association · (2026) · View on PubMed ↗ · Free PDF ↗

Genetic testing in pituitary adenomas: a Pituitary Society International Consensus Statement.

This consensus statement reviewed evidence for genetic testing strategies in pituitary adenomas, covering both germline and somatic testing approaches. It specifies actionable germline predisposition genes (e.g., AIP, MEN1, CDKN1B, PRKAR1A, SDHx, MAX), recurrent copy-number events (GPR101-containing Xq26.3 microduplications), and postzygotic gain-of-function GNAS variants, while also outlining somatic testing to identify aggressive pituitary adenoma types and rare pituitary carcinomas. The clinical significance is that it provides evidence-based guidance for implementing precision medicine via genotype-based risk assessment and management in patients with pituitary tumors.

De Sousa SMC, Andoniadou CL, Daly AF et al. · Nature reviews. Endocrinology · (2026) · View on PubMed ↗ · Free PDF ↗

Efficacy and safety of mirogabalin in patients with fibromyalgia: protocol for a multicentre, Prospective, Randomised, Open-label, Blinded Endpoint (PROBE) study.

This BMJ Open protocol describes a multicentre, prospective, randomised, open-label trial with blinded endpoints (PROBE) to test mirogabalin in patients with fibromyalgia compared with standard care (including reference to pregabalin as the comparator context). The key aim is to determine mirogabalin’s efficacy and safety in fibromyalgia, addressing the evidence gap that preclinical and other neuropathic pain data have not yet been fully translated to FM. If successful, the trial could establish mirogabalin as an alternative α2δ ligand option for chronic pain with a potentially improved tolerability profile.

Liu M, Li Y, Yao X et al. · BMJ open · (2026) · View on PubMed ↗ · Free PDF ↗

Electronic cigarettes for smoking cessation.

This living Cochrane systematic review evaluated electronic cigarettes (EC) for smoking cessation by comparing safety, tolerability, and effectiveness for long-term smoking abstinence against non-nicotine EC, other cessation treatments, and no treatment. Across included trials, the review synthesises evidence on whether EC increase cessation rates and what adverse effects occur. The updated evidence base supports clinical and regulatory decisions about EC use as a cessation strategy.

Lindson N, Livingstone-Banks J, Butler AR et al. · The Cochrane database of systematic reviews · (2026) · 1 citations · View on PubMed ↗

Evidence and Consensus Based Guidelines in Behçet Disease Uveitis. Multimodal imaging in Uveitis (MUV) Taskforce Report 18.

This international MUV Taskforce Report 18 used a nominal group technique (NGT) consensus process informed by systematic literature review and representative multimodal imaging datasets to develop imaging and clinical guidelines for Behçet disease (BD) uveitis. The key output was consensus recommendations on multimodal imaging approaches for diagnosis, monitoring, and detection of complications in BD uveitis. These guidelines standardise imaging practice across expert centres and can improve detection of sight-threatening complications in BD uveitis.

Bansal R, Tugal-Tutkun I, Androudi S et al. · Ophthalmology. Retina · (2026) · View on PubMed ↗ · Free PDF ↗

Executive Summary of the American Radium Society Appropriate Use Criteria for a Multidisciplinary Treatment Approach to the Management of Resectable Esophageal and Gastroesophageal Junction Adenocarcinoma.

This American Radium Society (ARS) guideline executive summary evaluated evidence for multidisciplinary management of resectable esophageal and gastroesophageal junction adenocarcinoma using a systematic review framework (PICO) to produce appropriate use criteria. The key finding is the consensus set of recommended treatment approaches across specialties (radiation oncology, medical oncology, gastroenterology, and thoracic surgery) for resectable disease. Scientifically and clinically, it standardizes care pathways and supports consistent decision-making for thoracic and gastrointestinal cancer treatment planning.

Anker CJ, Juloori A, Chamil Codipilly D et al. · International journal of radiation oncology, biology, physics · (2026) · View on PubMed ↗

Biological rhythms, sleep disturbances, and the skin - a narrative review.

This narrative review synthesized evidence on how sleep, circadian rhythms, light exposure, and environmental factors regulate skin physiology and contribute to dermatoses. It concludes that skin peripheral clocks govern rhythmic barrier function, immune activity, pigmentation, temperature, blood flow, and repair, and that sleep loss/circadian disruption can impair immune function and barrier integrity, promoting inflammatory skin outcomes (details truncated). The review highlights circadian and sleep interventions as potential adjuncts for preventing or managing inflammatory skin disease.

Biegański K, Takamine S, Sato M et al. · Sleep medicine reviews · (2026) · View on PubMed ↗ · Free PDF ↗

Endothelial HSPA1A preserves microvascular integrity in HFpEF via HIF-1α-dependent glycolysis and NNT K1079 lactylation.

The authors investigated HFpEF pathophysiology in a mouse model induced by high-fat diet plus l-NAME, focusing on endothelial HSPA1A and metabolic mechanisms. They found endothelial HSPA1A was reduced in HFpEF, and endothelial-targeted HSPA1A knockdown worsened diastolic dysfunction and microvascular rarefaction, while HSPA1A overexpression preserved microvascular integrity via HIF-1α-dependent glycolysis and NNT K1079 lactylation (with lactylome profiling and AAV9-based endothelial manipulation, truncated). This mechanistic link between HSPA1A, HIF-1α glycolysis, and NNT lactylation identifies potential metabolic targets to protect microvascular function in HFpEF.

Zhou C, Li F, Xia Z et al. · Redox biology · (2026) · View on PubMed ↗ · Free PDF ↗

NMOSD and MOGAD in Latin America: A consensus-informed regional perspective.

This consensus-informed regional perspective addressed the clinical challenges of diagnosing and treating neuromyelitis optica spectrum disorder (NMOSD) and myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) across Latin America. It emphasizes that diagnosis increasingly depends on sensitive antibody assays and timely access to targeted therapies, but that substantial system-level barriers continue to compromise patient care in LATAM (methods truncated). The article’s significance is to guide region-specific improvements in diagnostic pathways and treatment access for these antibody-mediated CNS autoimmune diseases.

Boldrini V, Samadzadeh S, Carnero Contentti E et al. · Multiple sclerosis and related disorders · (2026) · View on PubMed ↗ · Free PDF ↗

Frequency and prognostic outcomes of emergency diagnosis in 13 non-neoplastic conditions in England: A population-based cohort study using linked electronic health records of 1.7 million patients.

This population-based cohort study used linked electronic health records from 1.7 million patients in England to quantify the frequency and prognostic impact of emergency diagnosis across 13 non-neoplastic conditions. Emergency diagnosis frequency and outcomes were characterized across conditions, and the study aimed to determine whether emergency presentation is associated with worse clinical outcomes beyond cancer-specific mechanisms (the provided abstract is truncated before reporting the main effect estimates). Clinically, the work supports using emergency-diagnosis status as a general risk marker for adverse outcomes and informs health-system planning for non-cancer conditions.

Whitfield E, White B, Barclay ME et al. · PLoS medicine · (2026) · View on PubMed ↗ · Free PDF ↗

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