PubMed Trending Research Digest — June 21, 2026
A curated digest of 97 trending PubMed articles, automatically categorised and summarised across 15 research areas.
Jump to category
PubMed Trending Research Digest — June 21, 2026
Automated digest · 97 articles · 15 research areas · June 21, 2026
Overview
Across this week’s set of studies, a dominant theme is immune modulation—both for cancer and for inflammatory/autoimmune disease. Multiple papers describe strategies to reprogram immune responses (e.g., poxvirus-driven extracellular vesicles, mRNA “cytokine + antigen” cocktails for PDAC, neuron–immune crosstalk disruption in melanoma, and nanoparticle adjuvants for HSV-2), while others dissect immune-pathway mechanisms that could be therapeutically targeted (TLR7 in SLE, CD95L/sCD95L-driven neutrophil ROS in AAV, IL-6 signaling linking atopic dermatitis to depressive-like behavior, and neutrophil subsets driving steroid-resistant GI GVHD). Together, these works emphasize moving from descriptive immunology toward pathway-specific interventions and better target selection.
A second major theme is mechanistic biology connecting metabolism, stress, and disease risk. Several studies link cellular stress/nutrient sensing to outcomes—cysteine availability via LRRC58–CDO1 regulation, lysosomal metabolite compartmentalization (dimethylarginine) and systemic morbidity, and ER stress alternative splicing programs under PERK control. In parallel, clinical and translational research highlights cardiometabolic consequences of circadian disruption (night shift → mitochondrial dysfunction → hypertension risk), and the ongoing need to clarify long-term benefits and safety of weight-loss and lipid-lowering strategies (including lean body mass preservation and uncertainty of mortality/morbidity endpoints in hypertension). Liver-focused papers further reinforce that MASLD/MASH biology and progression (including neurobiology of hepatic nerves and zonation-driven early steatosis control) remain active targets for prevention.
Finally, the digest shows a strong push toward precision stratification and better clinical implementation. Studies and reviews address improved endpoints and risk models (unclassified pulmonary hypertension phenotyping, KDIGO kidney protection adherence in ICU, Lp(a) variability in youth-onset diabetes, and AI/ML readiness in glioblastoma perioperative care). In oncology, advances span biomarker discovery (ATR inhibitor sensitivity via origin firing capacity), understanding metastatic convergence (recurrent prostate cancer populations), and overcoming resistance mechanisms (lysosome/autophagy resistance via HSPA8–CMA, ferroptosis suppression linked to ICB non-response). Collectively, the field is converging on more reproducible biomarkers, phenotype-aware trial design, and interventions that are mechanistically grounded.
Cancer immunotherapy & tumor immune microenvironment
A Self-Immunoregulatory Nanosensitizer for Sonodynamic Cancer Therapy.
This study developed a porphyrin–biguanide-loaded albumin nanoparticle sonosensitizer (POR-BG@Alb) to improve sonodynamic cancer therapy by addressing ROS-driven immune resistance. The authors report that immune resistance is a shared mechanism across major classes of clinically used SDT sensitizers and that POR-BG@Alb induces mitochondrial dysfunction to activate AMPK and suppress c-MYC, leading to downregulation of PD-L1 and CD (as described) and improved antitumor immune responses. This is significant because it proposes a self-immunoregulatory SDT platform designed to enhance durable immunity rather than only inducing tumor cell killing.
Liu J, Zhou Z, Li C et al. · Advanced materials (Deerfield Beach, Fla.) · (2026) · View on PubMed ↗
Neuron-tumor crosstalk in cancer: molecular mechanisms and translational advances.
This review article examined molecular mechanisms of neuron–tumor crosstalk and summarized translational advances targeting this interaction in cancer. It highlights how tumor cells hijack neural and neuro-immune signaling to drive growth, invasion, metastasis, immune escape, treatment resistance, and cancer-associated pain. The synthesis supports emerging therapeutic strategies that disrupt tumor–nervous system communication to improve cancer outcomes.
Jia B, Zhao L, Tang M et al. · Molecular cancer · (2026) · View on PubMed ↗ · Free PDF ↗
Neuron-targeting piezoelectric microneedles disrupt pro-tumorigenic neuron-immune crosstalk and restore anti-tumor immunity in melanoma.
This study investigated whether neuron-targeting piezoelectric microneedle patches can disrupt pro-tumor neuron–immune crosstalk and enhance anti-tumor immunity in melanoma in female mice. Using manganese-doped titanium-based MOF piezoelectric microneedles coated with dorsal root ganglia neuron-derived membranes, the authors found that a single administration deposits the material at the melanoma site and accelerates anti-tumor immune responses by interfering with neuron–immune signaling. This is significant because it combines targeted neuroimmune modulation with a minimally invasive delivery platform, suggesting a new therapeutic direction for melanoma immunotherapy.
Song A, Zhang Y, Ji Y et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗
Multiplexed cytokine and antigen mRNA administration generates durable anti-tumor immunity against pancreatic cancer.
This study tested whether multiplexed administration of cytokine and antigen mRNAs can generate durable anti-tumor immunity against pancreatic ductal adenocarcinoma (PDAC) in mouse models. The key finding is that intratumoral injection of mRNAs encoding IL-12, IL-18, CCL5, CXCL10, and IFNβ produces robust (though transient) cytokine expression that activates NK cells and CD8+ T cells, reduces tumor growth and fibrosis, and that adding tumor antigen mRNAs improves dendritic cell antigen presentation and CD8+ T-cell priming. Scientifically and clinically, it provides a strategy to overcome PDAC’s cytokine-poor immune microenvironment by programming local immune activation with mRNA cocktails.
Parikh CN, DeMarco KD, Bhalerao N et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗
The search for safe and effective CAR-T targets in AML.
The article reviewed the challenges of identifying safe and effective CAR-T targets in acute myeloid leukemia (AML), focusing on leukemic stem cell persistence and the risk of on-target/off-tumor toxicity. It highlights that AML-specific antigen scarcity and shared antigen expression on normal hematopoietic stem cells (HSCs) or mature blood cells have limited CAR-T success. The review underscores the need for target discovery and engineering strategies that selectively eliminate AML leukemic stem cells while sparing normal hematopoiesis.
Van Oers F, Flumens D, Haentjens S et al. · Blood cancer journal · (2026) · View on PubMed ↗ · Free PDF ↗
First-in-human study of lomvastomig, a PD-1-TIM-3 bispecific antibody, in patients with advanced and/or metastatic solid tumors.
The first-in-human phase 1 study investigated lomvastomig, an IgG1-based Fc-silenced PD-1–TIM-3 bispecific antibody, in patients with advanced and/or metastatic solid tumors. The trial used dose escalation and expansion cohorts including checkpoint inhibitor (CPI)-experienced melanoma and non-small-cell lung cancer (NSCLC) patients to assess safety, tolerability, and preliminary antitumor activity. This establishes early clinical characterization of a dual PD-1/TIM-3 checkpoint strategy that may overcome resistance to single-checkpoint blockade.
Rohrberg KS, Melero I, F Sanmamed M et al. · Journal for immunotherapy of cancer · (2026) · View on PubMed ↗ · Free PDF ↗
Expansion and CAR engineering of granulocyte-monocyte progenitors for cellular immunotherapy.
This Cell study developed defined culture conditions to expand and genetically engineer mouse and human granulocyte-monocyte progenitors (GMPs) for cellular immunotherapy. The key finding was that myeloperoxidase regulates GMP proliferation, enabling long-term expansion while preserving progenitor identity and myeloid potential, and engineered GMPs reconstituted myelopoiesis and restored antibacterial defense in chronic granulomatous disease mouse models. This establishes GMPs as a renewable, tractable platform for engineered myeloid immunotherapies with improved ex vivo expansion and post-transfer function.
Yue S, Guo Z, Pan C et al. · Cell · (2026) · View on PubMed ↗ · Free PDF ↗
Beyond the GH-IGF-1 Axis: A Network Perspective Integrating Clinical Observations and Mechanistic Insights.
This case-based network perspective integrated clinical observations with mechanistic insights on obesity beyond the GH–IGF-1 axis using three representative patient cases. It found distinct obesity–GH/IGF-1 interactions in acromegaly improved by the PPAR-α agonist pemafibrate, Prader-Willi syndrome treated with dulaglutide, and a third case illustrating alternative pathway relationships. The significance is that it supports a more individualized, pathway-based view of obesity phenotypes rather than relying solely on the GH–IGF-1 axis.
Yoshimichi G · Endocrine connections · (2026) · View on PubMed ↗ · Free PDF ↗
Therapeutic Poxviruses Induce the Secretion of Immunostimulating and Anti-Tumoral Extracellular Vesicles.
This study examined how therapeutic poxviruses, including Modified Vaccinia Ankara (MVA), affect extracellular vesicle (EV) secretion by peripheral blood mononuclear cells (PBMCs). Poxvirus infection stimulated release of small EVs containing viral proteins and immune-related signatures. These findings suggest poxvirus-based cancer immunotherapy may enhance antitumor efficacy by reprogramming immune-cell EV biogenesis and function.
Walther L, Mittelheisser V, Claudepierre MC et al. · Journal of extracellular vesicles · (2026) · View on PubMed ↗ · Free PDF ↗
Epidermal radionuclide therapy with rhenium-188 in non-melanoma skin cancer: a short narrative review.
This narrative review summarized epidermal radionuclide therapy using rhenium-188 (Re-188) epidermal radionuclide therapy (ERT) for non-melanoma skin cancer (NMSC), focusing on indications, efficacy, safety, and radiobiological rationale. The key finding is that Re-188 ERT provides a non-surgical, superficial high-dose treatment option with clinically reported efficacy and an acceptable safety profile in appropriate patients. Scientifically and clinically, it supports Re-188 ERT as an emerging alternative for patients who are poor candidates for surgery.
Castellucci P, Vetrone L, Baraldi C et al. · Frontiers in medicine · (2026) · View on PubMed ↗ · Free PDF ↗
Oncology therapeutics, biomarkers & targeted drug discovery
Ibrutinib in early stage CLL: Genetic risk factors and treatment outcome in the GCLLSG CLL12 trial.
This analysis of the GCLLSG CLL12 trial evaluated genetic risk factors for treatment outcome in early-stage chronic lymphocytic leukemia (CLL) by stratifying 515 participants randomized to ibrutinib versus placebo. In the placebo arm, shorter event-free survival was associated with del(17p), del(11q), +12, unmutated IGHV (U-IGHV), and mutations in NOTCH1, ATM, NRAS/KRAS/BRAF, and NFKBIE, and the study assessed whether ibrutinib benefit differed across these genetic subgroups. The findings are significant for precision risk stratification and for identifying which early-stage CLL patients may derive the greatest benefit from ibrutinib.
Riecke A, Robrecht S, Yosifov DY et al. · Blood · (2026) · View on PubMed ↗
Machine learning-driven QSAR modeling combined with single cell transcriptomics identifies novel drug targets for lung cancer.
This study used machine learning-driven quantitative structure–activity relationship (QSAR) modeling combined with single-cell RNA sequencing (scRNA-seq) to identify novel conserved and metastasis-relevant drug targets in non-small cell lung cancer (NSCLC). By analyzing scRNA-seq profiles from primary tumors and matched brain and bone metastases, it prioritized candidate targets using pathway-based interpretation (e.g., Ingenuity Pathway Analysis). The clinical significance is that it proposes druggable targets conserved across primary and metastatic sites, potentially supporting precision oncology strategies against NSCLC brain/bone metastasis.
Nagarajan N, Shakyawar SK, Raheem K et al. · Journal of translational medicine · (2026) · View on PubMed ↗ · Free PDF ↗
Lysosome-derived methylated arginine is a signalling metabolite controlling the lipidome.
This study developed an unbiased platform integrating human plasma metabolomics with single-lysosome metabolomics to identify lysosome-derived signaling metabolites controlling the lipidome. It showed that dimethylarginine is produced in lysosomes, predicts patient morbidity, and that genetic depletion of the lysosomal exporter cystinosin (CTNS) causes lysosomal dimethylarginine accumulation with compartmentalization plasticity that maintains cellular and tissue homeostasis. These findings link lysosomal metabolite compartmentalization to systemic metabolic regulation and highlight dimethylarginine as a clinically relevant signaling metabolite.
Nguyen ST, Watson RL, Gao F et al. · Nature cell biology · (2026) · View on PubMed ↗
FKBP8 connects the Hsp70-Hsp90 chaperone machinery to the folding of membrane proteins.
This study investigated how the ER-anchored chaperone FKBP8 connects the Hsp70–Hsp90 machinery to folding of membrane protein cytoplasmic domains. Using a genome-wide CRISPR-Cas9 screen, the authors identified FKBP8 as essential for membrane protein folding and showed with ABC transporter model substrates that FKBP8 cooperates with Hsp70–Hsp90 to remodel nascent or misfolded cytosolic domains into native conformations, supported by cryo-EM structural insights into a conserved hydrophobic client-binding cavity. These findings are significant because they define a specific molecular link in the ER chaperone network that could be targeted to modulate membrane protein biogenesis and proteostasis.
Ge MX, Wu MZ, Ji J et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗
Conformational cycling of the Wntless transporter drives trafficking and secretion of Wnt morphogens.
This study examined how conformational cycling of the Wntless (WLS) transporter controls trafficking and secretion of Wnt morphogens. By solving cryo-EM structures of Wnt-bound and unliganded WLS and performing structure-guided functional experiments, the authors found that Wnts engage WLS via three conserved hairpins required for cell-surface trafficking and carrier-mediated secretion, and that Wnt release is driven by large conformational changes in WLS. Scientifically, this provides a mechanistic, structural explanation for how WLS regulates Wnt morphogen export, informing models of development and Wnt-driven diseases.
Ge Y, de Almeida Magalhaes T, Wu H et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗
Replication origin firing capacity indicates ATR inhibitor sensitivity.
The study investigated whether DNA replication origin firing capacity predicts sensitivity to ATR inhibitors (ATRi) in cancer cell lines, using parallel proteomics, transcriptomics, and functional assays. ATRi-sensitive lines showed higher expression of DNA replication initiation factors, higher origin firing, increased pan-nuclear γH2AX, and greater cell death, and origin firing rates causally modulated ATRi sensitivity. These findings suggest origin firing capacity could serve as a mechanistic biomarker to stratify patients for ATRi therapy.
Lumeau A, Pfuderer PL, Scarth JA et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗
Structure of the NAT10 acetyltransferase and mechanism of tRNA acetylation.
The study determined the structure and mechanism of the NAT10 acetyltransferase, the sole eukaryotic enzyme that catalyzes N4-acetylcytidine (ac4C) RNA modification, and how it coordinates catalysis and RNA binding. Using single-particle cryo-electron microscopy, it resolved NAT10 as a heart-shaped symmetrical dimer in complex with a designer cytidine-CoA ligand with and without ADP, revealing an atypically opened GNAT active site. This structural mechanism of NAT10-mediated tRNA/RNA acetylation advances understanding of how NAT10 dysregulation contributes to cancer and premature aging syndromes.
Zhou M, Thalalla Gamage S, Tran KA et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗
LRRC58 defines an E3 ubiquitin ligase complex sensitive to cysteine abundance.
This molecular cell study investigated how human cells sense cysteine availability by characterizing the LRRC58-defined Cullin-RING E3 ubiquitin ligase complex that regulates conditional degradation of CDO1. The authors found that LRRC58 activity is restrained by ubiquitination and proteasomal degradation when cysteine is replete, but LRRC58 stabilizes during cysteine deprivation to enable CDO1 degradation. This provides a specific nutrient-sensing ubiquitin–proteasome mechanism that could be leveraged to understand or manipulate cysteine metabolism in disease.
Ramage DE, Wieske LHE, Crowe C et al. · Molecular cell · (2026) · 2 citations · View on PubMed ↗ · Free PDF ↗
Cell-based screen identifies translation state modulators that extend lifespan in D. melanogaster and C. elegans.
This study used a cell-based phenotypic screen to identify translation state modulators that extend lifespan in Drosophila melanogaster and Caenorhabditis elegans. The authors report that compounds mimicking dietary restriction/cold-induced longevity shift translation in a way linked to the 4E-BP/eIF4E pathway and mRNA 5′-UTR–dependent regulation. These results suggest drug-like translation modulators could reproduce conserved pro-longevity translational programs across species.
Wu B, Wang LJ, Godbole AA et al. · The journals of gerontology. Series A, Biological sciences and medical sciences · (2026) · View on PubMed ↗
SIRT2 antagonizes MOF function during mitotic entry.
This study examined mitotic entry regulation in the G2–M transition by characterizing functional antagonism between the deacetylase SIRT2 and the acetyltransferase MOF in cell models. SIRT2 deacetylated MOF and antagonized MOF function to regulate key histone marks, including H4K16ac deacetylation and H4K20me1 dynamics, thereby controlling mitotic progression. The findings connect SIRT2–MOF enzymatic interplay to chromatin-state control during mitotic entry, offering a mechanistic handle on how epigenetic regulators coordinate cell-cycle transitions.
Espinosa-Alcantud M, Sima N, Fernández-Duran I et al. · Science advances · (2026) · View on PubMed ↗ · Free PDF ↗
Targeting the HSPA8-CMA-ATP6V1A Axis Triggers Lysosomal Hyperacidification and Catastrophic Vacuolation in Prostate Cancer.
This study examined the role of Heat Shock Protein Family A Member 8 (HSPA8) in prostate cancer lysosome/autophagy resistance to therapy, focusing on the Aloperine (ALO) mechanism. ALO inhibited HSPA8 function, impairing chaperone-mediated autophagy (CMA) by blocking ATP6V1A degradation, which triggered lysosomal hyperacidification and catastrophic vacuolation. The results support the HSPA8–CMA–ATP6V1A axis as a therapeutic vulnerability to overcome lysosome-driven drug resistance in prostate cancer.
An B, Gao Z, Chen S et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗ · Free PDF ↗
Single-Cell Reveal GALNT7-Dependent Ferroptosis Suppression as a Mechanism of Immunotherapy Resistance in Non-Small Cell Lung Cancer.
This study used integrative multi-omics (single-cell RNA-seq, bulk RNA-seq, and spatial transcriptomics) to identify mechanisms of immune checkpoint blockade (ICB) resistance in non-small cell lung cancer (NSCLC). GALNT7, a glycosyltransferase, was selectively upregulated in non-responders and enriched in malignant epithelial cells, and its expression was linked to suppression of ferroptosis-related signaling compared with responders. Mechanistically, GALNT7-dependent ferroptosis suppression provides a potential biomarker and target to improve ICB response rates in NSCLC.
Gan J, Zheng Q, Liu D et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗ · Free PDF ↗
Harnessing MDM2-Mediated Targeted Degradation of Transcriptional and Epigenetic Machinery to Disrupt Oncogenic Addictions in Pediatric Sarcoma.
This study explored how MDM2 overexpression drives oncogenic dependencies in pediatric sarcoma and developed MDM2-recruiting proteolysis-targeting chimeras (PROTAC-like degraders). It showed that MDM2 rewires transcriptional programs via p53-independent chromatin occupancy and p53-dependent proteasome-mediated degradation, and the resulting MDM2-targeted chimeras selectively degraded the CDK9/Cyclin T complex to disrupt oncogenic transcription. The work supports targeted degradation of transcriptional machinery as a precision therapeutic strategy for pediatric sarcomas with MDM2 overexpression.
Zhou J, Guan X, Li N et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗ · Free PDF ↗
Cancer genomics, heterogeneity & evolution
Clinical Characteristics and Prognostic Risk Factors in Breast Cancer With Liver Metastasis.
This retrospective study assessed prognostic risk factors for breast cancer liver metastasis (BCLM) using SEER data (n=560,908) and an external Jiangsu Province Hospital cohort (n=294). Liver metastasis occurred in 1.3% of SEER patients, and the authors used multivariate logistic regression plus Kaplan–Meier and Cox models to identify determinants associated with development and overall survival in BCLM. The results are clinically relevant for risk stratification and prognosis in patients with breast cancer metastatic to the liver.
Yu D, Zhu C, Yang S et al. · The breast journal · (2026) · View on PubMed ↗ · Free PDF ↗
Recurrent intra-tumour heterogeneity is a hallmark of metastatic prostate cancer.
The study examined metastatic castration-resistant prostate cancer in 9 patients by profiling 34 metastatic lesions using single-cell multi-omics and whole-genome sequencing to characterize intra-tumour heterogeneity. It found recurrent tumour populations that repeatedly emerge across lesions, indicating evolutionary convergence of heterogeneity and that these populations act as functional components of the metastatic tumour ecosystem. This supports a model where targeting convergent, recurrent subclones may be more effective than targeting lesion-specific diversity in late-stage prostate cancer.
Weng S, Cain L, Comben J et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗
Cardiovascular risk, hypertension & vascular biology
Longitudinal variability of lipoprotein(a) in youth-onset type 1 diabetes: implications for cardiovascular risk stratification.
This retrospective single-centre study characterized intra- and inter-individual longitudinal trajectories of lipoprotein(a) [Lp(a)] in a paediatric cohort with youth-onset type 1 diabetes. Lp(a) showed meaningful longitudinal variability across childhood/adolescence, challenging the assumption of lifelong stability and affecting how individuals are classified for cardiovascular risk. These findings support more nuanced, potentially repeated Lp(a) measurements for lifetime coronary artery disease risk stratification in type 1 diabetes youth.
Iafrate-Luterbacher F, Jimenez-Sanchez C, Anastasiadou ML et al. · Cardiovascular diabetology · (2026) · View on PubMed ↗ · Free PDF ↗
Diagnostic and therapeutic inertia for LDL cholesterol management of consecutively verified patients with acute myocardial infarction.
The study audited real-world acute myocardial infarction (AMI) care to quantify diagnostic and therapeutic inertia in LDL cholesterol (LDL-C) management after discharge among consecutively verified patients. Diagnostic inertia was defined as no post-discharge LDL-C measurement, and therapeutic inertia reflected failure to intensify or manage LDL-C appropriately over follow-up. By quantifying these quality gaps, the study identifies actionable system-level barriers to guideline-concordant LDL-C management after AMI.
Gragnano F, Artana C, Carrara G et al. · European journal of internal medicine · (2026) · View on PubMed ↗ · Free PDF ↗
Mitochondrial Dysfunction Unravels the Potential Molecular Link Between Night Shift Work-Related Circadian Disruption and Elevated Blood Pressure in Human and Mouse Models.
This study investigated whether night shift work–related circadian disruption increases blood pressure and identified mitochondrial dysfunction as the mechanistic link in both human night-shift workers and mouse models. Simulated night shift elevated blood pressure, dysregulated circadian genes (e.g., PER1 and BMAL1), and triggered mitochondrial dysfunction and oxidative stress. The results support mitochondrial dysfunction as a targetable pathway connecting circadian disruption to hypertension risk.
Jiang Z, Dou Y, Lei Y et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗ · Free PDF ↗
Glycine Receptor α2 Mediates Vasodilation via Endothelial eNOS Signaling.
This study tested the role of the glycine receptor α2 subunit (GLRA2) in regulating endothelial nitric oxide synthase (eNOS) signaling and vasodilation using endothelial-specific Glra2-deficient mice and adeno-associated virus (AAV)-transfected mice. GLRA2 mediated vasodilation through endothelial eNOS signaling, assessed via endothelium-dependent relaxation and whole-cell patch clamp recordings. The findings identify GLRA2–eNOS signaling as a mechanistic contributor to blood pressure regulation and a potential hypertension therapeutic target.
Bai X, Wang Y, Zhou W et al. · Circulation research · (2026) · View on PubMed ↗
Metabolic disease, obesity & cardiometabolic outcomes
Solasodine, a Natural Steroidal Alkaloid, Attenuates RANKL-Induced Osteoclastogenesis and Bone Resorption: A Study Based on Network Pharmacology and Experimental Validation.
This experimental study investigated whether solasodine (SOL), a natural steroidal alkaloid, attenuates RANKL-induced osteoclastogenesis and bone resorption and explored mechanisms involving MAPK, NF-κB, and JAK-STAT signaling. Using network pharmacology with molecular docking and in vitro assays in bone marrow-derived macrophages stimulated with M-CSF and RANKL (including TRAcP staining), the authors found SOL downregulated key targets such as NFκB1, JAK1/2, and STAT3 and reduced osteoclast differentiation and resorptive activity. These findings suggest SOL as a potential therapeutic candidate for osteoporosis by targeting RANKL-driven osteoclast activation pathways.
Jiang Y, Jin Z, Ji X et al. · Journal of cellular and molecular medicine · (2026) · View on PubMed ↗ · Free PDF ↗
Myostatin Signaling in Skeletal Muscle: Implications for Athletic Performance.
This comprehensive physiology review summarizes myostatin biology in skeletal muscle, focusing on the MSTN gene’s role as a negative regulator of muscle growth and homeostasis. It explains how myostatin signals through Smad-dependent and non-Smad pathways to influence satellite cell function and protein synthesis, and how reduced myostatin activity can enhance muscle regeneration largely via modulation of IGF-1/Akt/mTOR signaling. The review is significant for understanding therapeutic opportunities to improve muscle mass, recovery, metabolic function, and athletic performance through targeted myostatin pathway modulation.
Chandel S, Uvarajan D, Iyer M et al. · Comprehensive Physiology · (2026) · View on PubMed ↗
Comparative Cardiovascular, Lipid, and Safety Effects of Lipid-Modifying Therapies in Diabetes: An Agent-, Class-, and Dose-Level Network Meta-Analysis.
This network meta-analysis studied the comparative efficacy and safety of lipid-modifying therapies in patients with diabetes across agent-, class-, and dose-levels using randomized controlled trials. The key finding is that the analysis provides a fine-grained ranking of major adverse cardiovascular events (MACE), stroke, and myocardial infarction outcomes (and safety endpoints) across different lipid-lowering strategies and dosing intensities in diabetes. Clinically, it supports more evidence-based selection of lipid therapies for cardiovascular risk reduction in diabetes by integrating comparative effectiveness beyond head-to-head trials.
Zhao X, Zheng S, Tang C et al. · Cardiovascular drugs and therapy · (2026) · View on PubMed ↗
The Effects of Glucagon-Like Peptide-1 Receptor Agonists and Sodium-Glucose Co-Transporter-2 Inhibitors on Lean Body Mass in Humans: A Systematic Review and Meta-Analysis of Randomised Controlled Trials.
This systematic review and meta-analysis of randomized controlled trials evaluated how GLP-1 receptor agonists and SGLT2 inhibitors affect lean body mass in humans. Across 36 RCTs in populations with obesity and type 1 or type 2 diabetes, the authors assessed body composition outcomes focused on lean body mass changes (full quantitative results were not visible in the truncated abstract). The findings clarify whether these widely used weight-loss–associated drugs preserve or reduce metabolically important lean tissue, informing safer long-term prescribing.
Jobanputra R, Sargeant JA, Plekhanova T et al. · Diabetes/metabolism research and reviews · (2026) · View on PubMed ↗ · Free PDF ↗
Statins promote muscle metabolic danger and NLRP3-mediated myopathy via lower protein-prenylation and YAP.
This study investigated statin-induced low-level myopathy in muscle cells and in mice, testing whether NLRP3 inflammasome activation and protein prenylation/YAP signaling mediate statin muscle toxicity. Statin priming of NLRP3 (enhanced by lipopolysaccharide) lowered the statin dose that caused myopathy, and statin-induced muscle cell death and increased Atrogin-1 were prevented by NLRP3 blockade or restoring isoprenoids but not by cholesterol restoration, with statins reducing glycolysis in a manner requiring lower protein prenylation and involving YAP. The work links statin intolerance to an NLRP3–prenylation–YAP mechanism, suggesting that targeting inflammasome activation or prenylation pathways could improve statin tolerability without relying on cholesterol effects.
Robin N, Barra NG, Foley KP et al. · Science advances · (2026) · View on PubMed ↗ · Free PDF ↗
Long-term effects of weight-reducing drugs in people with hypertension.
This Cochrane systematic review evaluated long-term weight-reducing drugs in adults with essential hypertension to determine effects on all-cause mortality, cardiovascular morbidity, and adverse events. The key finding is that the evidence base for patient-relevant long-term outcomes in people with hypertension remains unclear and requires better data beyond weight loss and short-term effects. This is significant because it informs clinicians and guideline developers about the current uncertainty in cardiovascular benefit and safety when using anti-obesity medications in hypertensive populations.
Spary-Kainz U, Posch N, Radl-Karimi C et al. · The Cochrane database of systematic reviews · (2026) · View on PubMed ↗
GLP-1 Agonists in Adolescent Obesity: A Narrative Review of Single, Dual, and Triple Agonists.
This narrative review evaluated clinical efficacy and safety of glucagon-like peptide-1 (GLP-1) receptor agonists, including single-, dual-, and triple-incretin regimens, for adolescent obesity. The key finding is that incretin-based therapies show beneficial effects on weight and metabolic outcomes in adolescents, with safety considerations varying by regimen and trial design. Clinically, the review supports expanding pharmacologic options for adolescent obesity while emphasizing the need to balance efficacy with tolerability.
Abid M, Sheikh KS, Ahmad MS et al. · Diabetes, metabolic syndrome and obesity : targets and therapy · (2026) · View on PubMed ↗ · Free PDF ↗
Liver disease (MASLD/MASH) & related cancer
Burden and Regional Disparities of MASH-Related Liver Cancer in the Asia-Pacific Region From 1990 to 2023.
This study quantified the burden and temporal trends of metabolic dysfunction-associated steatohepatitis (MASH)-related liver cancer across Asia-Pacific countries and subregions from 1990–2023 using the Global Burden of Disease (GBD) 2023 dataset. It found substantial regional variation in age-standardized prevalence, deaths, and disability-adjusted life years (DALYs) for MASH-related liver cancer and assessed how these trends related to Socio-demographic Index (SDI). These findings help identify where MASH-driven liver cancer prevention and surveillance may be most urgently needed across the Asia-Pacific region.
Zhou XD, Chen QF, Huang DQ et al. · Liver international : official journal of the International Association for the Study of the Liver · (2026) · View on PubMed ↗
Hepatic neurons and metabolically induced liver dysfunction.
This review studied the role of hepatic nerves in metabolic dysfunction-associated steatotic liver disease (MASLD) progression, including how sympathetic and parasympathetic signaling changes with disease stage. The key finding is that as MASLD advances, hepatic sympathetic activity increases while hepatic sympathetic innervation diminishes, and emerging evidence implicates both parasympathetic and sympathetic pathways in driving progression toward steatohepatitis and hepatocellular carcinoma. Scientifically, it highlights hepatic neurobiology as a potential therapeutic target and motivates mechanistic studies linking neural remodeling to metabolic liver dysfunction.
Pauss SN, Chhabra KH, Stec DE et al. · Nature reviews. Endocrinology · (2026) · View on PubMed ↗
Efficacy of Initiation of Semaglutide versus SGLT2 inhibitors in Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD): A Multicenter Propensity-Matched Real-World Study.
This multicenter retrospective propensity-matched real-world study used TriNetX U.S. data to compare new initiators of semaglutide versus SGLT2 inhibitors in adults with metabolic dysfunction-associated steatotic liver disease (MASLD) and at least one metabolic comorbidity. The study found comparative effectiveness favoring semaglutide over SGLT2 inhibitors on downstream outcomes after balancing >50 covariates (exact effect sizes were not visible in the truncated abstract). These findings support GLP-1 receptor agonist–based initiation as a potentially more effective strategy than SGLT2 inhibition for MASLD patients with cardiometabolic risk in routine clinical practice.
Khalil I, Sarker P, Hossain MI et al. · Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists · (2026) · View on PubMed ↗
Liver endothelial zonation orchestrates hepatic steatosis onset through retinoic acid-regulated FGF1.
This study examined how liver sinusoidal endothelial cell (LSEC) zonation regulates the onset of metabolic dysfunction-associated steatotic liver disease (MASLD) in a liver zonation model, focusing on c-Kit/RXRG-driven FGF1 signaling in mice and corroborating with human clinical correlations. Pericentral LSEC c-Kit transcriptionally activated FGF1 via the nuclear receptor RXRG, and FGF1 suppressed hepatocellular lipid accumulation through FGFR4 signaling; retinoic acid phenocopied FGF1’s antisteatotic effects. These findings identify a retinoic-acid–RXRG–FGF1 axis in pericentral LSECs as a mechanistic control point for early MASLD and a potential therapeutic target to prevent steatosis progression.
Fang Z, Che B, Ling Y et al. · Science advances · (2026) · View on PubMed ↗ · Free PDF ↗
Neuroimmunology & neuroinflammation
Environmental enrichment mitigates sevoflurane-induced neurodevelopmental injury via cGAS-STING-dependent microglial modulation.
This study tested whether environmental enrichment (EE) can mitigate neonatal sevoflurane-induced neurodevelopmental injury by modulating cGAS-STING-dependent microglial activation and aberrant synaptic pruning in mice. It found that EE after neonatal sevoflurane exposure improved cognitive outcomes and altered microglial activity and synaptic/mitochondrial-related pathology through the cGAS-STING pathway. The significance is that it links a modifiable post-exposure environment to a defined innate-immune signaling mechanism that may be actionable for reducing anesthesia-associated neurodevelopmental risk.
Li F, Gong B, Wu H et al. · Cell & bioscience · (2026) · View on PubMed ↗ · Free PDF ↗
Gastrointestinal symptoms correlate with core clinical features and systemic inflammation in myalgic encephalomyelitis/chronic fatigue syndrome.
This study assessed gastrointestinal (GI) symptom burden in 116 patients with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and tested associations with core clinical features and systemic inflammation. It found that GI symptoms correlated with key clinical domains and specific immune/inflammatory markers, supporting a link between gut-related symptom expression and systemic disease biology. The significance is that GI symptom profiling may help stratify ME/CFS patients and guide investigations into inflammatory mechanisms relevant to disease severity.
Brown M, Vernon SD, Indart AC et al. · Journal of translational medicine · (2026) · View on PubMed ↗ · Free PDF ↗
Blood IL-6 is a critical trigger of depressive symptoms in a mouse model for human atopic dermatitis.
The study tested whether peripheral blood IL-6 and soluble IL-6Rα (sIL-6Rα) trigger depressive symptoms in NC/Tnd mice with spontaneous atopic dermatitis (AD), focusing on blood-brain barrier disruption and hippocampal circuit effects. Increased IL-6 and sIL-6Rα specifically disrupted the blood-brain barrier and induced depressive-like symptoms in these AD mice. This provides a mechanistic link between AD-associated cytokine signaling and depression, supporting IL-6 pathway modulation as a potential therapeutic strategy.
Matsuda K, Muko R, Moon C et al. · Translational psychiatry · (2026) · View on PubMed ↗ · Free PDF ↗
Epstein-Barr virus and multiple sclerosis: from associations to mechanisms to potential therapies.
This narrative review examined how Epstein-Barr virus (EBV) contributes to multiple sclerosis (MS) from epidemiologic associations to mechanistic pathways and potential therapies. It highlights evidence that EBV can interact with MS susceptibility loci to alter B-cell transcriptional programs and differentiation, including expansion of neuroinvasive atypical B cells enriched in inflamed CNS compartments. Mechanistic EBV–B-cell insights support the scientific rationale for EBV-targeted interventions as potential MS therapies.
Luünemann JD, Münz C · The Lancet. Neurology · (2026) · View on PubMed ↗ · Free PDF ↗
CXCL16-mediated recruitment of γδ T cells to the brain reduces sociability in mice.
This study investigated immune contributions to autism spectrum disorder using 15q11-13 duplication (15q dup) mice, focusing on CXCL16-driven recruitment of γδ T cells to the brain. Elevated brain CXCL16 promoted infiltration of Vγ6+ γδ T cells producing IL-17A, and developmental deletion or neutralization of Vγ6+ γδ T cells reduced the sociability phenotype. These results implicate a CXCL16–Vγ6+ γδ T cell–IL-17A axis in genetic ASD-like behavior and suggest that modulating this pathway could be a strategy to alter neuroimmune risk.
Takayama N, Shiraishi K, Matsui A et al. · Science immunology · (2026) · View on PubMed ↗
Neurodegenerative disease & dementia
Evaluating emerging amyloid-β centric drugs for the treatment of Alzheimer’s disease.
This review evaluated emerging amyloid-β (Aβ)-directed therapies for Alzheimer’s disease, emphasizing mechanisms, clinical efficacy, safety, and regulatory status across the current pipeline. It highlights that recent approvals of the anti-Aβ monoclonal antibodies lecanemab and donanemab provide the first convincing evidence that Aβ reduction can modestly slow cognitive decline in early Alzheimer’s disease, while next-generation agents (e.g., trontinemab) aim to improve brain penetration and include strategies for presymptomatic disease. The synthesis is significant for guiding therapeutic selection and trial design as the field moves from first-generation Aβ antibodies toward more targeted and earlier interventions.
Lozupone M, Dibello V, Sardone R et al. · Expert opinion on emerging drugs · (2026) · View on PubMed ↗
Unveiling a unique microglial phenotype promoting oxidation in the iBRB: insights from single-cell transcriptomics in the NPDR rat model.
This study used single-cell transcriptomics to characterize microglial heterogeneity in the inner blood-retinal barrier (iBRB) microenvironment in a non-proliferative diabetic retinopathy (NPDR) rat model (Zucker Diabetic Fatty rats). It identified a unique microglial phenotype that promotes oxidation and used cell-cell gene interaction, differentiation potential, and trajectory analyses to link microglial states to early iBRB lesions. The results suggest a mechanistic cellular target for early intervention in NPDR-related iBRB impairment.
Geng Y, Zhang Y, Xu X et al. · Cell & bioscience · (2026) · View on PubMed ↗ · Free PDF ↗
Dementia risk by metabolic health and obesity in two prospective cohorts.
This study evaluated how obesity (BMI ≥ 30 kg/m²) and metabolic health phenotypes (hyperglycemia, hypertension, dyslipidemia) jointly associate with dementia risk in two prospective cohorts, examining differences by midlife (≤65 years) versus late-life (>65 years) and by sex. It analyzed combined risk patterns to determine whether metabolic health modifies the dementia risk associated with obesity across the life course. The significance is that it clarifies which metabolic/obesity profiles may be most important for dementia prevention at different ages.
Nakash M, Ojalehto Lindfors E, Zhan Y et al. · BMC medicine · (2026) · View on PubMed ↗ · Free PDF ↗
Neuronal YTHDF2 suppresses innate immune activation in Aβ pathology by promoting m6A-dependent decay of cytosolic mitochondrial mRNAs.
This Science Advances study investigated how neuronal YTHDF2 regulates innate immune activation in Alzheimer’s disease (Aβ) pathology via m6A-dependent decay of cytosolic mitochondrial mRNAs. The authors found that cytosolic m6A-modified mt-Nd4 is normally recognized and degraded by YTHDF2 to prevent aberrant RIG-I–MAVS pathway activation, but YTHDF2 is downregulated in Aβ conditions leading to mt-Nd4 accumulation and innate immune activation. This identifies a specific m6A–YTHDF2–mitochondrial RNA axis that could be targeted to dampen neuroinflammation in AD.
Pan W, Yang L, Zhang Y et al. · Science advances · (2026) · View on PubMed ↗ · Free PDF ↗
Sleep, circadian biology & neuromodulation
Tryptamine from wake-active monoaminergic neurons regulates sleep homeostasis.
This study investigated whether tryptamine (TrpA) in cerebrospinal fluid is produced by wake-active monoaminergic neurons and whether it tracks sleep homeostatic pressure in nocturnal mice and diurnal pigs. Using a ratiometric fluorescent TrpA sensor, the authors found that TrpA levels correlate with homeostatic sleep pressure independent of light–dark cycles and that TrpA is secreted in an activity-dependent manner from wake-active monoaminergic nuclei in the diencephalon and brainstem. These findings identify TrpA as a candidate sleep-homeostasis signal and provide a mechanistic framework for how wake circuits generate a measurable biochemical drive toward sleep.
Cao H, Wang K, Zhao J et al. · Nature neuroscience · (2026) · View on PubMed ↗
Transcranial Alternating Current Stimulation at 40 Hz Improves Social Functioning in Children With Autism Spectrum Disorder: A Randomized Clinical Trial.
The randomized, double-blind, sham-controlled trial studied whether 40 Hz high-definition transcranial alternating current stimulation (tACS) targeting the right temporoparietal junction (rTPJ) improves social functioning in 47 children with autism spectrum disorder (ASD). Compared with sham stimulation, active 40 Hz rTPJ tACS improved social functioning at post-intervention timepoints. These results support gamma-band–linked neuromodulation as a potentially rapid, noninvasive intervention for core social difficulties in ASD.
Gao B, Lin L, Smith RC et al. · Biological psychiatry · (2026) · View on PubMed ↗
Wearable-Derived Diurnal Alignment Between Physical Activity and Device Temperature Predicts Future Disease and Mortality Risk.
This study tested whether wearable-derived diurnal alignment between physical activity and device temperature predicts future disease and mortality in free-living humans. In ~90,000 UK Biobank participants (median age 63) with week-long wrist-worn acceleration and device temperature recordings, the authors decomposed circular cross-correlation into alignment features (including 24 h coupling strength and phase deviation) and related these to long-term outcomes. If validated, this provides a scalable digital biomarker of circadian disruption that could improve risk prediction for disease and mortality.
Chen H, Wei J, Cedernaes J et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗ · Free PDF ↗
Infectious diseases, vaccines & antimicrobial strategies
HPV vaccination in people living with HIV: A network meta-analysis highlighting safety, immunogenicity, and evidence gaps.
This network meta-analysis evaluated HPV vaccination in people living with HIV (PLWH) by synthesizing evidence from systematic reviews of randomized controlled trials, focusing on safety and immunogenicity and identifying evidence gaps. Across included studies, the analysis aimed to compare HPV vaccine performance in PLWH and summarize adverse events and immune responses relative to other regimens or comparators. The work is significant because it supports clinical decision-making for HPV vaccination in PLWH while clarifying where stronger efficacy or long-term safety data are still needed.
Neto AAS, Souza ATB, Sarmento ACA et al. · International journal of gynaecology and obstetrics: the official organ of the International Federation of Gynaecology and Obstetrics · (2026) · View on PubMed ↗
Deep learning reveals antimicrobial peptides within prions.
Using deep learning, this study screened 19.3 million fragments from 2,897 curated prion-related proteins to identify antimicrobial peptides termed “prionins.” Among 75 synthesized prionins, 59 inhibited bacterial pathogens, 53 disrupted membranes, and 2 reduced Acinetobacter baumannii infection burden in mice. The work expands the functional repertoire of prion-like sequences and provides a computational pipeline for discovering antimicrobial peptides.
Torres MDT, Wan F, de la Fuente-Nunez C · Nature microbiology · (2026) · View on PubMed ↗ · Free PDF ↗
Effects of ethanol and acetaldehyde on multi-organ genomic mutation landscapes.
This study examined how chronic in vivo exposure to ethanol or its metabolite acetaldehyde reshapes genome-wide mutational landscapes in rats, focusing on head-and-neck tumors and tumors of the forestomach and liver. The key finding is that alcohol-related mutational signatures (including SBS16, DBS4, and ID11) are present in these tissues but are not confined to alcohol-associated cancers, indicating broader, multi-organ mutagenic effects. Scientifically, this clarifies how ethanol/acetaldehyde contribute to cancer risk through tissue-specific mutation patterns that may inform biomarker interpretation and mechanistic models of alcohol carcinogenesis.
Chavanel B, Tibaldi E, Virard F et al. · Cell biology and toxicology · (2026) · View on PubMed ↗ · Free PDF ↗
Coxsackievirus B escapes antiviral CD8+ T cells but triggers robust CD4+ memory responses.
This study analyzed how Coxsackievirus B3 (CVB3) modulates antigen presentation at the intestinal entry site and downstream T cell immunity in vitro and in CVB-seropositive individuals. CVB3-infected enterocytes evaded immune recognition by down-regulating HLA class I and viral peptide presentation, impairing CD8+ T cell responses, while CVB infection also triggered robust CD4+ memory responses. These results clarify a viral immune evasion strategy that may contribute to persistent CVB infection and islet autoimmunity relevant to type 1 diabetes risk.
Burgos-Morales O, Vecchio F, Samassa F et al. · Science advances · (2026) · View on PubMed ↗ · Free PDF ↗
Bioactive enhanced adjuvant chemokine oligonucleotide nanoparticles (BEACONs) for mucosal vaccination against genital herpes.
This study developed and tested bioactive enhanced adjuvant chemokine oligonucleotide nanoparticles (BEACONs) for mucosal vaccination against genital herpes (HSV-2), using CpG oligodeoxynucleotides (CpG ODNs) electrostatically complexed with the chemokine CXCL9. BEACONs enhanced antigen-presenting cell engagement and innate immune signaling, promoted CD8 T cell recruitment, and reduced local neutrophilic inflammation compared with CpG ODNs alone. The approach supports a nanoparticle adjuvant strategy to improve local cellular immunity for HSV-2 vaccination.
Bhagchandani SH, Ehrenzeller S, Pires IS et al. · Science immunology · (2026) · 1 citations · View on PubMed ↗ · Free PDF ↗
Bacterial infection reshapes monocyte and macrophage ontogeny at the CNS borders.
This study examined how bacterial infection reshapes monocyte and macrophage ontogeny at CNS borders using an intravenous mouse model of streptococcal meningoencephalitis. Although bacteria localized mainly to the leptomeninges and dura, monocyte infiltration into leptomeninges and parenchyma correlated with disease severity; in the dura, infection activated and depleted resident macrophages followed by rapid engraftment of inflammatory monocytes that transiently replenished the macrophage niche. The work clarifies site-specific immune cell replacement dynamics at CNS borders, informing how meningitis severity is linked to monocyte-derived macrophage remodeling.
Gres V, Lohrmann F, Fuchs V et al. · Science immunology · (2026) · View on PubMed ↗
Efficacy of doxycycline in treatment of Staphylococcus spp. prosthetic joint infections: a CRIOGO multicentre case-control study.
This multicentre retrospective matched case-control study (CYCLIOS) assessed doxycycline as part of curative antibiotic regimens for adult patients with staphylococcal hip or knee prosthetic joint infections (PJI). The key finding was the observed efficacy of doxycycline-containing regimens compared with matched controls receiving alternative standard regimens, addressing the need for oral options when rifampicin and fluoroquinolones are limited by resistance or intolerance. The significance is that doxycycline may expand feasible treatment strategies for staphylococcal PJI, particularly when first-line agents cannot be used.
Fiorenza V, Millot R, Lecomte R et al. · The Journal of antimicrobial chemotherapy · (2026) · View on PubMed ↗
SERS Facemask for Rapid and Portable Sensing Mycobacterium Tuberculosis Antigens for TB Screening.
This study evaluated a portable surface-enhanced Raman spectroscopy (SERS) facemask biosensor for detecting Mycobacterium tuberculosis antigens ESAT-6/CFP-10 in droplet or sputum samples from clinical settings. Using an Ag@Au nanoflower (NF) array-based sensing facemask combined with a catalytic/plasmonic urchin-shaped Au–Ag embedded covalent organic framework (U@COF) sensor, the assay classified TB-negative (n=12) and TB-positive (n=17) patients with reported sensitivity of 76.5%. The approach offers a non-invasive, rapid, and field-deployable screening tool that could complement conventional TB diagnostics.
Chen L, Yu J, Xu J et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗ · Free PDF ↗
Targeting Lipopolysaccharide Transport Induces Membrane Lipid Remodeling and Sensitizes Acinetobacter baumannii to Colistin Treatment.
This study investigated how disrupting the lipopolysaccharide (LPS) transport (Lpt) system in Acinetobacter baumannii affects membrane lipid remodeling and antibiotic susceptibility. A structure-based virtual screen identified a somatostatin octapeptide analogue (C4) that had modest direct antibacterial activity but produced strong synergy with colistin, supported by integrated lipidomic and transcriptomic analyses. Scientifically, it highlights Lpt-targeted membrane perturbation as a strategy to resensitize multidrug-resistant A. baumannii to colistin.
Luo J, Zhang H, Cai J et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗ · Free PDF ↗
Andes virus outbreak linked to expedition cruise ship travel, multi-country investigation and response, April to June 2026.
This multi-country outbreak investigation and response report described an Andes orthohantavirus outbreak linked to travel on the Dutch-flagged expedition cruise ship MV Hondius from April to June 2026. Thirteen cases (12 confirmed, 1 probable) with 23% case-fatality were identified among passengers and crew from 23 nationalities, prompting coordinated contact tracing, isolation/quarantine, and ongoing source/risk-factor investigations. Public-health significance lies in demonstrating how cruise-ship travel can seed hantavirus outbreaks and the need for rapid international surveillance and control measures.
van den Berg OE, Severi E, Mutoka-Banza F et al. · Euro surveillance : bulletin Europeen sur les maladies transmissibles = European communicable disease bulletin · (2026) · View on PubMed ↗ · Free PDF ↗
Microbiome & host–microbe metabolite signaling
Bacteria-derived glutarate mitigates Alzheimer’s disease model pathology through autophagy-lysosomal pathway.
This study tested whether bacteria-derived glutarate from Escherichia coli strain HB101 mitigates Alzheimer’s disease (AD) model pathology in Caenorhabditis elegans. It showed that HB101 improved learning deficits and neurodegeneration/paralysis phenotypes by reducing amyloid-β (Aβ) aggregation through enhanced autophagy-lysosomal activity and mitochondrial/endoplasmic reticulum unfolded protein responses (UPRmt/UPRer), with UPRmt driven by atfs-1 and sphk-1 and UPRer by pek-1; metabolomics implicated glutarate as the bioactive mediator. The significance is that it identifies a gut-bacteria metabolite–autophagy/UPR mechanism that could inform future AD disease-modifying strategies.
Deng C, Qu M, Yao W et al. · Cell communication and signaling : CCS · (2026) · View on PubMed ↗ · Free PDF ↗
Commensal yeast Malassezia produces tryptophan metabolites to promote tissue homeostasis via the aryl hydrocarbon receptor in mice.
This mouse study investigated how the skin commensal yeast Malassezia furfur promotes tissue homeostasis through tryptophan-derived metabolites acting on the aryl hydrocarbon receptor (AhR). Malassezia-derived tryptophan derivatives activated AhR in human epidermal equivalents and upregulated epidermal barrier/structure proteins in mouse epidermis, while in atopic dermatitis models colonization plus tryptophan supplementation reduced inflammation and restored barrier function. These results support a mechanistic, AhR-dependent role for Malassezia metabolites in skin homeostasis and suggest potential microbiome–metabolite therapeutic avenues for inflammatory skin disease.
Gushiken-Ibañez E, Stokmaier M, Barone G et al. · Nature microbiology · (2026) · View on PubMed ↗ · Free PDF ↗
Inflammation, autoimmunity & immune signaling pathways
Retinoic acid-driven expansion of CD16hiCD177+ neutrophils mediates steroid-resistant GI-GVHD.
This study used single-cell RNA sequencing of patient blood to define neutrophil heterogeneity in steroid-resistant gastrointestinal graft-versus-host disease (SR-GI-GVHD) after allogeneic hematopoietic stem cell transplantation. The authors identified an expanded CD16hiCD177+ neutrophil subset that uses CD177 to bind endothelial CD31 for intestinal transmigration, then triggers epithelial damage via MyD88-mediated sensing of translocated gut bacteria and neutrophil extracellular trap (NET) release. These mechanistic insights are clinically important because they nominate CD177–CD31 interactions, MyD88 signaling, and NET formation as potential therapeutic targets for SR-GI-GVHD.
Liang W, Xu D, Zhang L et al. · Blood · (2026) · View on PubMed ↗ · Free PDF ↗
Narcolepsy is (not) an autoimmune disease.
This Nature Reviews Neurology article reviewed evidence on whether narcolepsy type 1 (NT1) is autoimmune, focusing on its relationship to hypocretin (HCRT) neuron loss and the strong genetic association with HLA-DQB1*06:02. It argues that the autoimmune hypothesis remains unresolved—autoreactive immune responses could be a cause or a consequence of disease—while emphasizing the centrality of HCRT deficiency. The review frames future research directions for clarifying NT1 pathogenesis and for developing immune-targeted therapies if autoimmunity is causal.
Vassalli A, Tafti M, Liblau RS · Nature reviews. Neurology · (2026) · View on PubMed ↗
TLR7 in systemic lupus erythematosus: genetics and emerging therapies.
This review summarized genetic evidence and emerging therapies implicating Toll-like receptor 7 (TLR7) in systemic lupus erythematosus (SLE). It describes how gain-of-function variants in TLR7 and its chaperone UNC93B1 can cause monogenic childhood-onset SLE, while other rare variants alter ligand availability or downstream signaling, with both self RNA–protein complexes and viruses implicated in TLR7 activation. The article positions TLR7 as a key pathogenic pathway and supports ongoing development of targeted therapies to modulate endosomal nucleic-acid sensing in SLE.
Vinuesa CG, Shrotri M, Rahman A · Nature reviews. Rheumatology · (2026) · View on PubMed ↗
Soluble CD95L triggers Caspase-10-driven reactive oxygen species production in neutrophils and aggravates anti-neutrophil cytoplasmic antibody-vasculitis.
This study investigated whether soluble CD95L (sCD95L) triggers caspase-10-driven reactive oxygen species (ROS) production in neutrophils and worsens ANCA-associated vasculitis (AAV). The key finding is that inflamed tissues from AAV patients express CD95L on blood vessels, which is cleaved by metalloproteases to release sCD95L, and that sCD95L stimulates neutrophils to produce ROS via caspase-10, aggravating disease pathology. Clinically, it identifies a mechanistic pathway (CD95L→sCD95L→caspase-10→neutrophil ROS) that could be targeted for more precise therapies in AAV.
Boizard-Moracchini A, Msalbi D, Huot-Marchand S et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗
PERK orchestrates an endoplasmic reticulum stress alternative splicing program via CLK1/SRSF1.
The study investigated how PERK (EIF2AK3) orchestrates an endoplasmic reticulum stress alternative splicing program through CLK1/SRSF1, using O-propargyl-puromycin (OPP) labeling of de novo peptides followed by LC-MS/MS to map stress-induced translation. It identified PERK-dependent splicing regulation mediated by the CLK1/SRSF1 axis that reshapes the stress-response translatome early during unfolded protein response. These results clarify a pathway connecting ER stress signaling to alternative splicing and translation rewiring, informing how cells adapt under stress.
Philippe C, Burke S, Carrasco-Leon A et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗
Teclistamab for treatment-refractory autoimmune diseases: a multicentre case series.
This multicentre retrospective case series evaluated teclistamab, a T cell-redirecting bispecific antibody targeting B-cell maturation antigen (BCMA), in 18 patients with treatment-refractory autoimmune diseases across 5 European centers. The report focused on safety and efficacy outcomes in patients with systemic sclerosis, idiopathic inflammatory myopathies, systemic lupus erythematosus, undifferentiated connective tissue disease, and IgG4-related disease after a median of 5 prior therapies. The findings support further clinical investigation of BCMA-directed T cell redirection as a potential option for refractory autoimmune disease.
Albach FN, Phithak E, Biesen R et al. · Annals of the rheumatic diseases · (2026) · View on PubMed ↗ · Free PDF ↗
Kidney disease & critical care implementation
Implementation of the kidney protection strategy in critically ill patients with acute kidney injury - a multi-center prospective cohort study.
This multicenter prospective cohort study evaluated real-world implementation of the Kidney Disease: Improving Global Outcomes (KDIGO) kidney protection strategy (KPS) in critically ill adults with moderate-to-severe acute kidney injury (KDIGO stage 2–3) requiring vasopressors and/or mechanical ventilation across five European centers. It measured timely and sustained adherence to KPS and tested associations between adherence and clinical outcomes. The study’s significance is that it benchmarks how guideline-based kidney protection is applied in intensive care and informs whether improving adherence could reduce AKI-related harm.
Sadjadi M, Marcello M, Köhler A et al. · Critical care (London, England) · (2026) · View on PubMed ↗ · Free PDF ↗
SMN deficiency contributes to osteoporosis in spinal muscular atrophy by impairing Snap23 meditated muscle-derived extracellular vesicle secretion.
This study investigated how survival motor neuron 1 (SMN) deficiency contributes to osteoporosis in spinal muscular atrophy (SMA) by impairing Snap23-mediated muscle-derived extracellular vesicle (EV) secretion, combining human imaging with SMA mouse models. It showed that SMA-associated SMN loss leads to bone pathology and muscle atrophy phenotypes and mechanistically links defective Snap23-dependent EV secretion to impaired EV-mediated signaling relevant to bone loss. These findings identify the SMN–Snap23–EV axis as a potential therapeutic target to mitigate osteoporosis in SMA.
Lin W, Sui W, Deng Y et al. · Journal of translational medicine · (2026) · View on PubMed ↗ · Free PDF ↗
Association between prognostic nutritional index and mortality in critically ill patients with atrial fibrillation: a retrospective cohort study.
This retrospective cohort study evaluated whether the prognostic nutritional index (PNI), derived from serum albumin and total lymphocyte count, predicts mortality in critically ill patients with atrial fibrillation using MIMIC-IV v3.1. Lower PNI was associated with higher 30-day all-cause mortality and was also assessed for associations with in-hospital and 90-day mortality outcomes. The findings suggest PNI could be a practical prognostic biomarker to identify high-risk critically ill AF patients.
Kong X, Hu Z, Huang X et al. · BMC cardiovascular disorders · (2026) · View on PubMed ↗ · Free PDF ↗
Geriatrics, comorbidity & risk prediction
Establishment of the China Elderly Comorbidity Medical Database (CECMed) and its application in machine learning-based prediction.
This multicenter study established the China Elderly Comorbidity Medical Database (CECMed) and applied machine learning to predict in-hospital adverse events using geriatric comorbidity data from elderly patients across northern, central, and southern China. The dataset showed high comorbidity burden (over 90% with at least one geriatric syndrome) and machine learning models were used for early warning of adverse events during hospitalization. This resource and modeling approach can support earlier risk stratification and preventive care for hospitalized older adults in China.
Shi J, Wan D, Tang W et al. · BMC geriatrics · (2026) · View on PubMed ↗ · Free PDF ↗
Global burden of fall-related injuries attributable to low bone mineral density in women aged 50-69 years: inequalities, projections to 2050, and Mendelian randomisation.
This study quantified the global burden of fall-related injuries attributable to low bone mineral density (LBMD) in women aged 50–69 years using Global Burden of Disease (GBD) 2021 estimates (1990–2021) and applied Mendelian randomisation to assess causality. LBMD-attributable fall-related disability-adjusted life years (DALYs) and years lived with disability (YLDs) showed substantial inequality and a projected trajectory to 2050, consistent with LBMD increasing fracture susceptibility and post-fall disability rather than directly causing falls. These findings support targeting LBMD to reduce downstream disability from falls and help prioritize prevention strategies by age and geography.
Zhang B, Chen Q, Chen Y et al. · Journal of global health · (2026) · View on PubMed ↗ · Free PDF ↗
Clinical practice, trials, diagnostics & health systems
RNU4ATAC-opathy: Clinical, molecular and transcriptomic insights from a large cohort.
This study characterized the genotype–phenotype spectrum of RNU4ATAC-opathy in 60 individuals with molecularly confirmed biallelic variants in the noncoding minor spliceosome gene RNU4ATAC, using RNA sequencing in a subset of seven affected patients. The authors identified 33 distinct RNU4ATAC variants (including 13 novel) and demonstrated that RNA sequencing can help classify variants and clarify detection challenges for noncoding RNU4ATAC changes. These findings expand diagnostic variant interpretation and improve clinical counseling for RNU4ATAC-opathy by strengthening evidence for pathogenicity beyond DNA-only approaches.
Matalon DR, Duker AL, Arriaga TM et al. · Genetics in medicine : official journal of the American College of Medical Genetics · (2026) · View on PubMed ↗
Expanding the clinical spectrum of RNU4ATAC-opathies: more frequent and diverse than assumed.
This study refined the clinical spectrum of biallelic RNU4ATAC-opathies by collecting clinical and molecular data from 69 individuals across French and European networks, focusing on phenotypes previously described as Taybi-Linder/MOPD1, Roifman, and Lowry-Wood syndromes. The authors report that RNU4ATAC-opathies are more frequent and more diverse than previously assumed, with a large proportion presenting with the most severe Taybi-Linder syndrome. Clinically, this supports broader recognition and more accurate diagnosis of RNU4ATAC-related disorders and informs expectations for microcephaly, skeletal dysplasia, neurodevelopmental impairment, and immunodeficiency.
Cuinat S, Cormier-Daire V, Rosain J et al. · Genetics in medicine : official journal of the American College of Medical Genetics · (2026) · View on PubMed ↗ · Free PDF ↗
Retinoic acid as a stage-specific modulator of hematopoietic lineage fate from human pluripotent stem cells.
This study examined how retinoic acid (RA) directs hematopoietic lineage fate from human pluripotent stem cells (hPSCs) using a stepwise differentiation system. It found RA has a stage-specific role, with minimal or inhibitory effects during early mesoderm/hemogenic endothelial stages but significant lineage-modulating effects when applied during days 13–15 of differentiation. This provides a practical and mechanistic framework for optimizing RA timing to steer hematopoietic outcomes in hPSC-based differentiation.
An SH, Kim JY, Mao YY et al. · Cell communication and signaling : CCS · (2026) · View on PubMed ↗ · Free PDF ↗
Patient journeys mapping in health management for older patients with chronic obstructive pulmonary disease: a qualitative descriptive study.
This qualitative descriptive study mapped the patient journey across the COPD care continuum in older adults, covering screening, diagnosis, inpatient care, and home-based rehabilitation. It identified multidimensional needs, challenges, and critical touchpoints where care is fragmented and fails to meet patients’ longitudinal requirements. The results provide actionable targets for redesigning COPD services to improve continuity and effectiveness for older patients.
Tan Y, Xu J, Liu J et al. · BMC public health · (2026) · View on PubMed ↗ · Free PDF ↗
Cancer burden and control in China: landscape, trends and challenges.
This article studied the cancer burden in China by synthesizing landscape, temporal trends, and control challenges across the population. The key finding is that China contributes about 25% of the global cancer burden despite ~17% of the world’s population, with rapidly increasing new diagnoses driven by population ageing and expanded diagnostic capacity, particularly for cancers common in high-income countries (e.g., lung, colorectal, prostate, thyroid, female breast, and cervical). Clinically and policy-wise, it frames why shifting incidence patterns and system-level constraints must be addressed to improve prevention, early detection, and treatment outcomes.
Xia C, Li H, Wu C et al. · Nature reviews. Clinical oncology · (2026) · View on PubMed ↗
Should triple inhaled therapy be initiated earlier in the disease course of COPD to modify long-term outcomes, including mortality, exacerbations, and cardiovascular risk?
This article is a clinical question framing study evaluating whether earlier initiation of single-inhaler triple therapy (ICS/LABA/LAMA) in COPD could improve long-term outcomes such as mortality, exacerbations, lung-function decline, and cardiovascular risk. The authors synthesize emerging evidence suggesting that starting triple therapy earlier than current guideline triggers may reduce exacerbation burden and related downstream harms. If confirmed, earlier triple inhaled therapy could shift COPD treatment timing to better modify disease trajectory and cardiovascular outcomes.
Quaranta VN, Dragonieri S, Cosentino G et al. · Respiratory medicine · (2026) · View on PubMed ↗
Balancing benefit and burden: rethinking post-polypectomy colonoscopy surveillance strategies.
This Viewpoint reviewed post-polypectomy colorectal cancer surveillance strategies, focusing on whether current risk stratification leads to overuse in patients with high-risk labels but low absolute risk. The key argument is that surveillance intervals may be misaligned with true benefit while imposing meaningful procedural risks, costs, and endoscopy capacity burdens. Rebalancing surveillance based on absolute risk could improve patient safety and resource allocation without sacrificing colorectal cancer prevention.
IJspeert JEG, Bretthauer M, Jover R et al. · The lancet. Gastroenterology & hepatology · (2026) · View on PubMed ↗
Extracorporeal life support in adult critically ill patients: mechanisms of benefit in respiratory and cardiac failure.
This review article analyzed the mechanisms by which extracorporeal life support (ECLS) benefits adult critically ill patients with severe, potentially reversible respiratory and/or cardiac failure. It summarizes mechanistic pathways including restoration of gas exchange, optimization of circulatory dynamics, and mitigation of secondary organ injury to create conditions for tissue repair and adjunctive therapies. Understanding these mechanisms can guide better patient selection and optimization of ECLS strategies in critical care.
Zochios V, Brewer JM, Velia Antonini M et al. · American journal of respiratory and critical care medicine · (2026) · View on PubMed ↗
AI for prognosis and treatment stratification in glioblastoma neurosurgery: a systematic review.
This study systematically reviewed AI, machine learning, and deep learning approaches for glioblastoma neurosurgery tasks using MRI-derived and/or multimodal perioperative data, focusing on prognosis and treatment stratification. The review found heterogeneous, difficult-to-translate evidence across studies for clinically relevant endpoints such as prognosis, risk stratification, and treatment-response assessment. By mapping the current evidence landscape, it highlights gaps in standardization and clinical readiness for AI tools in GBM perioperative decision-making.
Reyes JS, Snyder MH, Roguski M et al. · Journal of neuro-oncology · (2026) · View on PubMed ↗
Quantitative ultrasound evaluation of the thoracolumbar fascia after manual and acupuncture therapies: an exploratory mechanistic randomized controlled trial with a sequential within-subject phase.
This exploratory mechanistic randomized controlled trial evaluated thoracolumbar fascia (TLF) biomechanics and microstructure after acupuncture, chiropractic care, or massage in adults with nonspecific low back pain (NSLBP). Participants were randomized to acupuncture, chiropractic, or a 3-week waitlist control, and after the waitlist control received massage to enable sequential within-subject comparisons; outcomes included TLF shear strain (ShS) and other pre/post imaging-based measures. The study aims to link manual and acupuncture therapies to measurable TLF biomechanical changes that could explain NSLBP symptom mechanisms.
Tomita N, Croteau D, Roy-Cardinal MH et al. · European radiology experimental · (2026) · View on PubMed ↗ · Free PDF ↗
Characterizing the post-market safety profile of cemiplimab: a pharmacovigilance study of the FDA adverse events reporting system database.
This pharmacovigilance study characterized the post-market safety profile of cemiplimab by analyzing FDA Adverse Events Reporting System (FAERS) reports where cemiplimab was the primary suspect drug. Using proportional reporting ratios (PRR), reporting odds ratios (ROR), and chi-squared signal detection with predefined thresholds, it identified 1,460 cemiplimab reports and detected 22 adverse event signals meeting criteria. These findings provide an evidence-based update on potential risks associated with the PD-1 inhibitor cemiplimab to support ongoing immune checkpoint inhibitor safety monitoring.
Frey C · Investigational new drugs · (2026) · View on PubMed ↗
Left ventricular non-compaction in heart failure: contemporary perspective on diagnostic challenges and treatment opportunities.
This review examined left ventricular non-compaction (LVNC) versus left ventricular hypertrabeculation (LVHT) in patients with heart failure, focusing on diagnostic imaging criteria and the genetic/pathophysiologic background of these cardiomyopathy phenotypes. It highlights that physiologic or adaptive hypertrabeculation in healthy individuals can mimic LVNC, making misclassification clinically consequential for both unnecessary interventions and failure to identify high-risk patients. The article emphasizes the need for improved, phenotype-specific diagnostic approaches that integrate imaging features with genetic risk to better guide treatment decisions in HF.
Geavlete O, Tschöpe C, Angermann CE et al. · Heart failure reviews · (2026) · View on PubMed ↗
Development of a robotic training curriculum for visceral and gastrointestinal surgical trainees: an international Delphi study.
This international Delphi study surveyed 83 experts and trainees to develop a platform-agnostic robotic training curriculum for visceral and gastrointestinal (GI) surgical trainees. The key finding was consensus on a structured, 106-item (Delphi) curriculum intended to standardize training, assessment, and certification across different robotic systems. This supports more consistent competency development in GI robotic surgery and may improve training quality and patient safety as robotic adoption expands globally.
Fadel MG, Walshaw J, Yiasemidou M et al. · Surgical endoscopy · (2026) · View on PubMed ↗ · Free PDF ↗
Disease modification in advanced Parkinson’s disease: a review and roadmap for paving the way for next-generation interventions.
This review assessed the current state of disease-modifying strategies and the evidence base for endpoints in advanced Parkinson’s disease (aPD), addressing biomarker and clinical-measure limitations across heterogeneous patient trajectories. It finds that existing milestone-based definitions and biomarkers (e.g., aggregated α-synuclein, MRI, PET) correlate only modestly with clinical progression, underscoring the need for robust, reproducible, phenotype-aware endpoints. The roadmap is significant because it guides next-generation trials toward measurable outcomes that can more reliably test disease modification across genetic background, age of onset, and motor/autonomic/cognitive domains.
Groppa S, Fasano A, Urso D et al. · Journal of neural transmission (Vienna, Austria : 1996) · (2026) · View on PubMed ↗ · Free PDF ↗
Incidence, Mechanistic Insights, and Ablation of Atrial Tachycardia Occurring After Pulsed Field Ablation for Atrial Fibrillation: Results From a Large International Registry.
This registry study analyzed 4,144 patients who underwent repeat ablation for atrial tachycardia (AT) occurring after first-time atrial fibrillation ablation using a pentaspline pulsed field ablation (PFA) catheter. Using high-density electroanatomical mapping and topology-based circuit analysis, it identified mechanistic substrates and assessed lesion durability to explain post-PFA ATs and inform targeted re-ablation strategies. Clinically, these findings support more precise mapping and ablation planning for AT after PFA, potentially improving repeat-procedure success and reducing recurrence.
Nakasone K, Duytschaever M, Almorad A et al. · JACC. Clinical electrophysiology · (2026) · View on PubMed ↗
High- and Low-Load Resistance Training Produce Distinct Skeletal Muscle Growth but Similar Changes in Tendon Morphology.
This randomized controlled trial studied 201 non-resistance-trained adults comparing high-load versus low-load isotonic resistance training to task failure on skeletal muscle growth and distal biceps brachii tendon thickness, with a time-matched non-exercise control group. The key finding was that high- and low-load training produced distinct skeletal muscle growth responses while tendon morphology changes were similar between loading conditions. This is significant for exercise prescription because it suggests tendon adaptations may be less load-dependent than muscle hypertrophy when training is taken to failure.
Hammert WB, Yamada Y, Sallberg RW et al. · Medicine and science in sports and exercise · (2026) · View on PubMed ↗ · Free PDF ↗
From Policy to Practice: Brazil’s Pathway to Eliminating Vertical Transmission of HIV as a Public Health Milestone.
This policy-to-practice article reviewed Brazil’s national pathway toward eliminating vertical transmission of HIV as a public health milestone within the Unified Health System (SUS). It reports that sustained universal health policies and rights-based governance across federal, state, and municipal levels enabled prevention, diagnosis, treatment, and monitoring services needed to reduce mother-to-child HIV transmission. The significance is that Brazil’s SUS-centered model provides a transferable framework for other countries aiming to meet PAHO/WHO elimination goals.
Gaspar PC, Miranda AE, Lannoy LH et al. · Journal of the International AIDS Society · (2026) · View on PubMed ↗ · Free PDF ↗
Magnetic resonance imaging-targeted biopsy with index lesion ipsilateral or bilateral systematic biopsy in prostate cancer: A multicenter, paired, noninferiority, observational trial.
This multicenter, paired, noninferiority observational trial evaluated MRI-targeted prostate biopsy with index lesion ipsilateral systematic biopsy (iSB) versus MRI-targeted biopsy plus systematic biopsy (TB+SB) in biopsy-naïve men with PI-RADS ≥4 lesions or PI-RADS 3 with PSA density ≥0.15 ng/mL/cm³. The key finding (from core-level reclassification simulation) was the comparative performance of TB+iSB as a potential core-reduction alternative to TB+SB. Clinically, if noninferiority holds, this approach could reduce biopsy cores while maintaining cancer detection accuracy in men undergoing MRI-targeted biopsy.
Cheng Y, Huang H, Wang M et al. · Cancer · (2026) · View on PubMed ↗
KMT2A and KMT2B episignatures address diagnostic challenges associated with rare neurodevelopmental disorders.
This work developed and validated DNA methylation (DNAm) episignatures for rare neurodevelopmental disorders caused by pathogenic variants in KMT2A (Wiedemann–Steiner syndrome, WDSTS) and KMT2B (Dystonia 28, DYT28). The KMT2A-WDSTS signature (264 CpG sites) and KMT2B-DYT28 signature (752 mostly hypermethylated CpG sites) achieved high sensitivity/specificity with >80% and >85% pathogenicity scores, respectively, and showed limited overlap between the two. Clinically, these episignatures improve molecular diagnosis when variant interpretation is challenging, enabling more accurate classification of KMT2A- vs KMT2B-associated disorders.
Awamleh Z, Chen A, Choufani S et al. · Genetics in medicine : official journal of the American College of Medical Genetics · (2026) · View on PubMed ↗
Is achieving higher standards in real-world migraine care feasible with anti-CGRP monoclonal antibodies preventive therapies?: Insights from the EUREkA cohort.
This prospective, real-world European multicenter EUREkA cohort study assessed how many adults with migraine achieved International Headache Society prevention targets after 6 months of treatment with anti-CGRP monoclonal antibodies. The key finding was the proportion of patients meeting migraine freedom (no monthly migraine days), optimal control (<4 MMD), modest control (4–6 MMD), or insufficient control (>6 MMD) categories under real-world anti-CGRP therapy. This informs whether higher guideline-based prevention standards are feasible outside trials and can guide expectations and treatment optimization in routine care.
Caronna E, Mas-de-Les-Valls R, Egeo G et al. · Cephalalgia : an international journal of headache · (2026) · View on PubMed ↗
Phenotypic Characterization of Unclassified Pulmonary Hypertension.
This study characterized “unclassified” pulmonary hypertension in PVDOMICS participants using dynamic right heart catheterization and transpulmonary metabolomics, with additional validation using exercise right heart catheterization. The key finding was that unclassified PH represents a distinct clinical/metabolic phenotype despite normal pulmonary vascular resistance and pulmonary artery wedge pressure. This improves scientific understanding of unclassified PH and may guide more precise diagnostic stratification beyond conventional hemodynamic categories.
Reddy YNV, Frantz RP, Egbe AC et al. · Circulation. Heart failure · (2026) · View on PubMed ↗
Safety and Efficacy of a Sandwich Total Neoadjuvant Therapy Strategy for Low-Risk Distal Locally Advanced Rectal Cancer: Results From the TESS Phase II Trial.
This prospective phase II multicenter trial assessed a sandwich total neoadjuvant therapy (TNT) strategy for low-risk distal locally advanced rectal cancer using capecitabine plus oxaliplatin (CapeOx) around radiotherapy, followed by surgery or watch-and-wait and additional adjuvant capecitabine. The key finding was a clinical complete response (cCR) rate of 46.9% with high radiotherapy completion (98/98) and most patients receiving six cycles of neoadjuvant chemotherapy (88.8%). These results suggest the sandwich TNT approach may be an effective neoadjuvant option for selected low-risk LARC patients.
Liu S, Lv G, Xu G et al. · MedComm · (2026) · View on PubMed ↗ · Free PDF ↗
Generated automatically on June 21, 2026 from PubMed’s trending articles. Summaries are AI-generated; always consult the original publication for clinical or research decisions.