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PubMed Trending Research Digest — October 18, 2026

A curated digest of 96 trending PubMed articles, automatically categorised and summarised across 15 research areas.

PubMed Trending Research Digest — October 18, 2026

Automated digest · 96 articles · 15 research areas · October 18, 2026

Overview

This week’s papers cluster around a unifying theme: biological systems are increasingly understood as dynamic networks rather than static categories. In neuroscience, circuit-level mechanisms for sleep homeostasis (Drosophila dFBN slow-wave activity) and mechanistic dissociations of therapeutic-like versus hallucinogenic plasticity (5-HT2A in cortical layer 5) highlight how specific neural dynamics map onto behavior. In immunology and inflammation, multiple studies emphasize context dependence—whether STAT3’s role in adaptive NK responses shifts with the inflammatory milieu, or how interferon programs coordinate maternal-fetal immune balance across space and time—reinforcing that “the same pathway” can produce different outcomes depending on cellular state and environment.

A second dominant thread is precision medicine built from high-resolution biology plus better risk accounting. Cancer-focused work spans large-scale genomic driver mapping (RAS in AML; whole-genome prostate cancer drivers), tumor microenvironment heterogeneity (TAM plasticity; spatial immune programs), and next-generation therapeutics (bispecific non-relapse mortality pharmacovigilance; EGFR-targeted antibody-toxin conjugates; radiotherapy-combined PD-1 strategies). Complementing these, several studies and reviews push toward actionable biomarkers and endpoints—such as integrating clonal hematopoiesis with cardiovascular risk (LE8+CH), using MRI enhancement to refine glioma prognosis, and linking patient-reported outcomes to imaging burden in Crohn’s fistulising disease.

Finally, the digest repeatedly returns to the gut–immune–metabolic interface as a lever for disease modification. Diet and microbiome studies connect omega-3/omega-6 fatty acids, Akkermansia, and microbial metabolites (e.g., kynurenic acid) to immune signaling and therapeutic responsiveness, while cardiometabolic and liver papers explore insulin resistance surrogates, GLP-1 digital-first implementation, and targeted MASH pharmacology. Together, these findings suggest that future interventions—whether drugs, diet, or engineered immune cells—will increasingly be optimized by measuring the right biological state at the right time.


Neural circuits, sleep homeostasis & circadian/behavioral states

Symptom Profiles Compatible With Disorders of Gut-Brain Interaction in Individuals With Coeliac Disease on a Long-Term Gluten-Free Diet.

This cross-sectional survey study of adult members of the Dutch Coeliac Society evaluated the prevalence and correlates of disorders of gut-brain interaction (DGBI)-compatible symptom profiles in individuals with coeliac disease (CD) on a long-term gluten-free diet (GFD). Using Rome IV criteria plus validated measures of psychological distress, non-GI somatic symptom severity, and health-related quality of life, the authors identified factors associated with DGBI-compatible symptom patterns despite adherence to GFD. The results support DGBI as a plausible contributor to persistent symptoms in treated CD and may guide more targeted symptom management beyond gluten avoidance.

van Gils T, Törnblom H, van Overveld F et al. · United European gastroenterology journal · (2026) · View on PubMed ↗ · Free PDF ↗

Beyond Excitotoxicity: Glutamate-Independent Mechanisms Underlie Noise-Induced Synaptopathy and Compromise Gene Therapy for Hereditary Deafness.

This animal study investigated noise-induced synaptopathy and its implications for hereditary deafness gene therapy by testing whether glutamate release is required, using Vglut3 knockout (Vglut3-KO) mice lacking glutamatergic transmission from inner hair cells. After 116 dB SPL noise exposure, Vglut3-KO mice still showed significant ribbon synapse loss despite the absence of glutamate release, indicating glutamate-independent mechanisms underlying noise-induced synaptopathy and limiting assumptions about excitotoxicity-only protection. These findings are important for designing and interpreting gene therapy strategies for NIHL and hereditary deafness by broadening the mechanistic targets beyond glutamate excitotoxicity.

Yu C, Xu H, Tong L et al. · Molecular therapy : the journal of the American Society of Gene Therapy · (2026) · View on PubMed ↗

Autoimmune diseases and autoimmune polyglandular syndromes in adult patients with biopsy-confirmed celiac disease: A prospective study.

This prospective observational study followed 102 adults with biopsy-confirmed celiac disease to determine the prevalence and spectrum of additional autoimmune diseases (ADs) and autoimmune polyglandular syndromes (APS), along with micronutrient deficiencies and gluten-free diet adherence. It assessed demographic/clinical features, laboratory parameters, APS subtypes, and micronutrient status using the celiac dietary adherence test (CDAT). The study is clinically significant because it quantifies comorbidity risk in adult CD and supports systematic screening for ADs/APS and nutritional deficiencies during routine follow-up.

Kuşaksizoğlu Kara S, Basat S, Kara Ç · Medicine · (2026) · View on PubMed ↗ · Free PDF ↗

The β-cells in type 1 diabetes mellitus: findings from human pancreas studies.

This narrative review summarized findings from human pancreas studies of pancreatic β-cells in type 1 diabetes mellitus (T1DM), emphasizing how immune–β-cell interactions evolve over time. It highlights that advances such as high-resolution imaging, single-cell and spatial multi-omics, and AI-assisted histopathology have shown that β-cell loss and/or dysfunction may begin early, reshaping models of disease initiation and progression. The review is clinically and scientifically important because it supports earlier detection and more precise targeting of β-cell dysfunction in T1DM based on human tissue evidence.

Eizirik DL, Martin-Vazquez E, Roca-Rivada A et al. · Nature reviews. Endocrinology · (2026) · View on PubMed ↗

Autistic burnout: Early insights from a systematic review on characteristics, precipitating factors, and protective mechanisms.

This systematic review examined autistic burnout by synthesizing research on its characteristics, precipitating factors, and protective/recovery mechanisms, and compared it with depression. Using PRISMA-guided searches across databases including PubMed and PsychINFO, it consolidated early evidence on how autistic burnout presents and what factors may trigger or buffer it. The review is significant because it clarifies a distinct construct within autism research and can inform more accurate assessment and targeted supports for autistic individuals.

Bory P, Fiorentino M, Bérenguier L et al. · L’Encephale · (2026) · View on PubMed ↗ · Free PDF ↗

Processed meat, unprocessed red meat, poultry, seafood, and egg intake and stomach cancer risk: a pooled analysis of 20 cohorts.

This pooled cohort analysis studied associations between intakes of processed meat, unprocessed red meat, poultry, seafood, and eggs and stomach cancer risk in 1,100,370 females and 891,919 males from 20 cohorts. Using harmonized baseline diet data and Cox regression, it estimated multivariable-adjusted, study- and sex-specific hazard ratios for each food group. The findings help clarify whether specific dietary animal-food categories—particularly processed versus unprocessed red meat—contribute to stomach carcinogenesis and can inform cancer-prevention dietary guidance.

Peng Y, Wang M, Abe SK et al. · International journal of epidemiology · (2026) · View on PubMed ↗

RiboTRAP-seq identifies spatially distinct functions for the anterior and posterior intestine in immune and metabolic regulation in Caenorhabditis elegans.

This study used RiboTRAP-seq with cell-type-specific translatome profiling in Caenorhabditis elegans to compare anterior intestinal cells (INT1) versus posterior intestinal cells (INT2–9) during fasting and refeeding. The key finding was that INT1 forms a translationally distinct intestinal subcompartment enriched for immune and stress response gene programs, supported by functional assays using newly identified INT1-specific genes. Scientifically, it demonstrates spatial specialization of intestinal translation programs that coordinate immune and metabolic regulation across intestinal regions.

Liu CC, Seban N, Srinivasan S · eLife · (2026) · View on PubMed ↗ · Free PDF ↗

GLP-1 Receptor Agonists, Gut Microbiota, and Chronic Pain: Nutritional Signaling at the Gut-Brain Axis.

This narrative review studied how GLP-1 receptor agonists (GLP-1RAs) interact with the gut microbiota and influence chronic pain through gut–brain axis mechanisms. The key finding is that GLP-1RAs can reshape gut microbial communities and modulate pain across phenotypes, aligning with dysbiosis patterns involving reduced SCFA-producing taxa such as Faecalibacterium prausnitzii, Lachnospiraceae, and Roseburia. This is significant because it supports a mechanistic rationale for exploring GLP-1RA-based microbiome modulation as a potential adjunct strategy for chronic pain.

Odonkor CA, Dodurgali MR, Cox FR et al. · Nutrients · (2026) · View on PubMed ↗ · Free PDF ↗

Multi-Omic Integration of the miRNome and Transcriptome in Dermal Fibroblasts from Hypermobile Ehlers-Danlos Syndrome and Hypermobility Spectrum Disorders Identifies Convergent Candidate miRNA-mRNA Regulatory Networks Linking Extracellular Matrix Remodeling and Inflammation.

This study investigated miRNA-mediated post-transcriptional regulation by integrating miRNome sequencing with transcriptome data in dermal fibroblasts from individuals with hypermobile Ehlers-Danlos syndrome (hEDS; n=12), hypermobility spectrum disorders (HSD; n=12), and controls (n=24). It found 25 differentially expressed miRNAs in pooled discovery material and identified 88 differentially expressed miRNAs in pooled hEDS/HSD analysis, leading to candidate miRNA–mRNA regulatory networks linked to extracellular matrix remodeling and inflammation. The scientific significance is that these convergent regulatory networks provide candidate molecular biomarkers and pathways for hEDS/HSD, which currently lack validated biomarkers.

Pelisenco IA, Cinquina V, Chiarelli N et al. · International journal of molecular sciences · (2026) · View on PubMed ↗ · Free PDF ↗

Eating Behavior in Menopausal Women: From Molecular to Clinical Aspects-What Changes?

This narrative review studied how menopausal transition alters eating behavior through molecular mechanisms involving hypothalamic neuropeptide systems, neurotransmitter pathways, and peripheral hormonal signals in menopausal women. The key finding is that estrogen deficiency disrupts hypothalamic appetite regulation via estrogen receptors ERα and ERβ, contributing to dysregulated appetite-related signaling that manifests as changes in eating behavior. This is clinically significant because it frames menopause-related eating changes in receptor-level biology that could inform targeted interventions.

La Vignera S, Calogero AE, Cannarella R et al. · International journal of molecular sciences · (2026) · View on PubMed ↗ · Free PDF ↗

Changes in Medical Interns’ Psychological Well-Being and Work Investment Perceptions During the Internship Year: An Interim Prospective Repeated-Measures Study at a Single Tertiary Medical Center.

This interim prospective repeated-measures study assessed changes in psychological well-being and work investment perceptions across the internship year among 42 medical interns (126 questionnaires) at a single tertiary medical center. General life satisfaction (measured by the Satisfaction With Life Scale, SWLS) and related outcomes such as stress and fatigue changed over Q1–Q3, indicating time-dependent shifts in intern well-being and perceived work investment. These findings are important for designing interventions to support interns’ mental health and retention during the transition to supervised clinical responsibility.

Sabih M, Vishnevsky G, Hamoud Y et al. · Healthcare (Basel, Switzerland) · (2026) · View on PubMed ↗ · Free PDF ↗

Novel antibody-based regimens for large B-cell lymphoma: latest updates from the 2026 ASCO Annual Meeting.

This article reviewed 2026 ASCO Annual Meeting updates on novel antibody-based regimens for large B-cell lymphoma (LBCL), emphasizing agents beyond conventional anti-CD20 monoclonal antibodies. It highlights phase 3 evidence for tafasitamab plus lenalidomide with R-CHOP in newly diagnosed high-risk disease (frontMIND) and ongoing exploration of CD20×CD3 bispecific strategies (including OLYMPIA-3). The update is significant for clinicians because it consolidates emerging targeted antibody combinations that may improve outcomes in high-risk and relapsed/refractory LBCL.

Luo G, Jiang H, Chen Z et al. · Journal of hematology & oncology · (2026) · View on PubMed ↗ · Free PDF ↗

A half-center oscillator regulates sleep pressure.

This study investigated how sleep-control neurons in Drosophila—dorsal fan-shaped body (dFBN) neurons—regulate sleep pressure and sleep-stage transitions. The authors found that a dFBN half-center circuit generates slow-wave activity (SWA) via bistable UP/DOWN membrane-voltage oscillations, and that restricting glutamate release from dFBNs disrupts SWA as well as baseline and rebound sleep. These results establish a causal neural-oscillator mechanism for sleep homeostasis in vivo, linking specific circuit dynamics to SWA-driven sleep regulation.

Hasenhuetl PS, Sarnataro R, Vrontou E et al. · Nature neuroscience · (2026) · View on PubMed ↗ · Free PDF ↗

MAP2-mediated integrin dysregulation reprograms cancer cell plasticity in hepatocellular carcinoma.

This study investigated whether repurposing estramustine phosphate (EMP) can target hepatocellular carcinoma (HCC) cell plasticity by inhibiting MAP2, a gene enriched in CD133+ HCC stemness cells. Using lineage-tracing and lineage-ablation approaches, the authors found that MAP2-mediated integrin dysregulation drives reprogramming of cancer cell plasticity, and that EMP suppresses this MAP2-dependent program to preferentially affect the CD133+ stem-like subset. Clinically, this suggests a drug-repurposing strategy to eliminate therapy-resistant, dedifferentiated HCC populations defined by CD133 and MAP2.

Lou UK, Wong TL, Huang IB et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Next-generation natural killer cell therapy: bench to bedside and beyond.

This review studied next-generation natural killer (NK) cell therapies, focusing on how NK subset heterogeneity, epigenetic regulation, metabolism, and intracellular immune checkpoints shape therapeutic performance. It summarizes the clinical progression from unmodified adoptive NK transfer to cytokine-induced memory-like NK cells and, most notably, to CAR-NK cell platforms, including strategies to address intratumoral NK heterogeneity. The significance is that it consolidates mechanistic and translational insights to guide rational engineering of more effective, durable NK-based cancer immunotherapies.

Zhao A, Xu J, Deng W et al. · Signal transduction and targeted therapy · (2026) · View on PubMed ↗ · Free PDF ↗

LENG8 granule regulates alternative polyadenylation in mammals.

This study investigated how the membraneless organelle LENG8 granule regulates alternative polyadenylation (APA) in mammals. The authors found that deleting LENG8 causes widespread 3’UTR lengthening in cultured cells and male germ cells, and that phase separation-driven LENG8 granule formation promotes LENG8–CPSF4 interactions to control APA site usage. These findings identify LENG8 granules as a nuclear hub for APA regulation, linking a specific gene and nuclear condensate mechanism to transcript isoform control in mammalian cells.

Wu Z, Du C, Li Y et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗


Neurodevelopmental genetics & synaptic mechanisms (ASD/NLGN3)

NLGN3 autism variants have distinct functional impact on synapses and sleep behavior in Drosophila.

This study examined how different autism-associated Neuroligin-3 (NLGN3) variants (including de novo p.R175W) affect synaptic function and sleep behavior in transgenic Drosophila models. The p.R175W variant produced distinct in vivo synaptic and behavioral phenotypes compared with other NLGN3 variants, indicating variant-specific functional impact on neural circuits governing sleep. These findings support NLGN3 variant–specific mechanisms for ASD risk and provide Drosophila models to test targeted synapse- and circuit-level interventions.

Townsley RE, Andrews JC, Srivastav S et al. · PLoS genetics · (2026) · View on PubMed ↗ · Free PDF ↗


Pain & sensory transduction (thermomechanosensation, nociception)

The mechanosensitive channel TMEM63B contributes to noxious heat sensation in the dorsal root ganglia.

This study investigated the mechanosensitive cation channel TMEM63B in dorsal root ganglion (DRG) neurons to determine its role in noxious heat sensation. Global TMEM63B knockout and DRG-specific conditional knockout both markedly reduced heat sensitivity, and TMEM63B deletion attenuated heat-evoked calcium responses and currents in DRG neurons. The results identify TMEM63B as a contributor to thermonociception, expanding the set of ion channels that may be targeted for pain therapeutics.

Ye C, Zang YY, Duan GF et al. · PLoS biology · (2026) · View on PubMed ↗ · Free PDF ↗

Membrane contact activation of Piezo2 drives lysosome-mitochondrion Ca2+ transfer and signaling in Trypanosoma cruzi.

This study characterized how the mechano/osmosensitive channel TcPiezo2 regulates lysosome-to-mitochondrion Ca2+ transfer in the protozoan Trypanosoma cruzi. Using ultrastructural methods, biochemical assays, and live-cell superresolution imaging, the authors defined lysosome–mitochondrion contact sites (LMCs) where TcPiezo2 triggers Ca2+ release that drives mitochondrial Ca2+ uptake and downstream signaling. These mechanistic insights link Piezo2-mediated mechanotransduction to organelle communication in a Chagas disease pathogen, suggesting potential intervention points in parasite survival pathways.

Huang G, Docampo R · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗ · Free PDF ↗

Rapid-Onset Opioid-Induced Neurotoxicity During Morphine Therapy.

This report described a clinical case of rapid-onset opioid-induced neurotoxicity (OIN) occurring during morphine therapy in a hospice/palliative care context. The key finding was that the patient developed visual and auditory hallucinations shortly after morphine exposure, with prompt reversibility after opioid rotation and recurrence upon morphine rechallenge. Scientifically and clinically, it strengthens the causal link between morphine and OIN and underscores the importance of early recognition and opioid switching when delirium or hallucinations emerge.

Weilein E, Amoateng MD, Bruera E · The American journal of hospice & palliative care · (2026) · View on PubMed ↗ · Free PDF ↗


Neurodegeneration, brain clearance & neuromodulation (glymphatic/AD/MDD)

Associations of Antibodies Against Several Infections With Alzheimer Disease Neuropathology: A Prospective Cohort Study Analysis.

This prospective cohort study analyzed whether circulating antibodies to 14 pathogens measured at ages 60–64 in the 1946 British birth cohort are associated with Alzheimer disease (AD) neuropathology. The key finding is that specific serologic infection measures (including serostatus, pathogen burden indices, and seroreactivity tertiles) show associations with AD neuropathologic outcomes consistent with an infection–Aβ aggregation defense hypothesis. This is clinically significant because it links lifetime infectious exposure to AD brain pathology and supports further work on infection-related risk mechanisms.

Felici C, Green RE, Warren-Gash C et al. · Neurology · (2026) · 1 citations · View on PubMed ↗ · Free PDF ↗

MFN2-associated astrocyte dysfunction contributes to neuronal hyperexcitability and depressive-like behaviors.

This study examined whether mitofusin-2 (MFN2)-associated astrocyte dysfunction contributes to neuronal hyperexcitability and depressive-like behaviors in a mouse model of major depressive disorder (MDD). The key finding is that chronic social defeat stress (CSDS) induces MFN2 up-regulation in hippocampal astrocytes (using SMART-seq profiling) and that MFN2-associated astrocyte mitochondrial dysfunction contributes to altered neuron-glia glutamate handling and depressive-like phenotypes. This is significant because it identifies MFN2-linked astrocytic mitochondrial pathways as a mechanistic driver of depression-relevant circuit dysfunction and a potential target.

Ma FX, Wang M, Fang SY et al. · Science advances · (2026) · View on PubMed ↗ · Free PDF ↗

Noninvasive ultrashort wave neuromodulation enhances glymphatic clearance to alleviate traumatic brain edema and Alzheimer’s pathology.

This study tested whether noninvasive ultrashort wave (USW) neuromodulation can enhance glymphatic clearance to treat traumatic brain edema and Alzheimer-like pathology in vivo. The key finding is that 40.68 MHz USW rapidly increases glymphatic bulk flow (influx and efflux) within minutes in healthy mice, with effects requiring neuronal activity (chemogenetic silencing) and astrocytic AQP4 (pharmacological blockade), and is accompanied by increased Delta-wave neuronal synchronization. This is clinically significant because it provides a noninvasive, mechanism-linked strategy to boost glymphatic clearance for brain edema and AD pathology.

Liu J, Xu C, Ruan H et al. · Science advances · (2026) · View on PubMed ↗ · Free PDF ↗

PINK1-mediated mitophagy supports lung cancer initiation and limits the efficacy of KRAS-targeted therapy.

This study investigated the role of PINK1-mediated mitophagy in lung cancer initiation and in limiting the efficacy of KRAS-targeted therapy, using human lung adenocarcinoma analyses and mito-QC reporter mice to monitor mitophagy in vivo. The key finding is that PINK1 activity and mitophagy increase from the earliest stages of tumorigenesis, and genetic inhibition of PINK1 impairs oncogenic transformation but has limited impact once tumor cells are established. This is significant because it positions PINK1-dependent mitophagy as an early vulnerability in lung cancer and suggests timing-dependent constraints on KRAS-targeted therapeutic benefit.

Gonçalves D, Guilbaud E, Di Mascio L et al. · Science advances · (2026) · View on PubMed ↗ · Free PDF ↗

Multiomics Profiling Supports Cathepsin B as a Protective Factor in White Matter Hyperintensities and Cognition.

This 4-stage proteogenomic study used a WMH polygenic risk score and plasma proteomics in UK Biobank participants (n=52,560; neuroimaging subset n=5,443) to identify circulating proteins linked to white matter hyperintensities (WMH) and cognition. The key finding was that cathepsin B emerged as a protective factor, with multiomics evidence supporting an upstream relationship between cathepsin B levels, reduced WMH burden, and better cognitive outcomes. Clinically, it nominates cathepsin B as a potential biomarker and mechanistic target for cerebral small vessel disease and cognitive decline.

Rivier CA, Diaz-Perez S, Bories G et al. · Stroke · (2026) · View on PubMed ↗

Neuron-Derived Vesicular circMagi1 Restrains Vascular Repair After Ischemic Stroke by Promoting TRIM65-Mediated ANXA2 Degradation.

This study investigated how neuron-derived extracellular vesicles containing the circular RNA circMagi1 affect vascular repair after ischemic stroke, focusing on endothelial mechanisms. The key finding was that circMagi1 is enriched in EVs from injured neurons and accumulates in endothelial cells, where it binds ANXA2 and promotes TRIM65-mediated ANXA2 ubiquitination and proteasomal degradation, thereby restraining vascular repair. These results identify a circMagi1–ANXA2–TRIM65 axis as a mechanistic regulator of post-stroke vascular dysfunction and a potential therapeutic target.

Bi Y, Liu Q, Zou B et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗ · Free PDF ↗

An aging-sensitive secreted phospholipase confers neuroprotection and cognitive resilience.

This preclinical and translational study identified an aging-sensitive secreted phospholipase, Pla2g2f, in hippocampal dentate granule cells (DGCs) and tested its role in cognitive resilience during aging. Pla2g2f deletion in DGCs worsened aging-associated synapse loss, neuroinflammation (microglial activation), reactive astrogliosis, impaired neurogenesis, lipid dysregulation, and memory decline, while boosting Pla2g2f promoted neuroprotection and resilience. The work is significant because it points to Pla2g2f as a potential therapeutic target to preserve synaptic function and cognition during aging.

Vicidomini C, Goode TD, Yu R et al. · Nature neuroscience · (2026) · View on PubMed ↗ · Free PDF ↗

5-HT2A receptors in layer 5 pyramidal neurons mediate the neuroplastic but not the hallucinogenic effects of psilocybin.

This neuroscience study tested how serotonin 2A receptors (5-HT2ARs) in cortical layer 5 pyramidal neurons contribute to psilocybin-induced neuroplasticity versus hallucination-like behavior in rodents. It found that 5-HT2AR signaling in layer 5 pyramidal neurons is necessary and sufficient for psilocybin-driven synapse formation/maturation and synaptic remodeling, but is dispensable for the head-twitch response (a rodent proxy for hallucination). The results are clinically relevant because they dissociate the neural mechanisms of therapeutic-like plasticity from those associated with hallucinogenic effects, informing safer drug design.

Baker JJ, Kogan E, Ma S et al. · Nature neuroscience · (2026) · View on PubMed ↗


Cancer immunotherapy & immune cell engineering (NK/T/NK, CAR, checkpoints)

NKG2D overexpression potentiates CAR-T cells through costimulation by tumor NKG2D ligands.

This study investigated how NKG2D overexpression alters CAR-T cell behavior by engineering CAR-T cells to overexpress full-length NKG2D (CAR-NG) and assessing effects on tumor ligand interactions. NKG2D overexpression reduced surface accessibility of endogenous NKG2D ligands while tumor-expressed NKG2D ligands provided additional costimulatory signals, thereby potentiating CAR-T function and persistence-related efficacy. The work supports a gene-engineering strategy to enhance CAR-T performance by leveraging NKG2D–ligand biology.

Li J, Han L, Zhu Q et al. · Cell reports. Medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Targeting MMGT1 enhances immunotherapy efficacy in triple-negative breast cancer.

This study examined the senescence-associated gene membrane magnesium transporter 1 (MMGT1) as a target to enhance immunotherapy in triple-negative breast cancer (TNBC). MMGT1 was upregulated in TNBC and promoted lipid metabolism via SCAP–SREBP1 complex translocation to the Golgi, suppressing cellular senescence; MMGT1 knockout in mammary tissue impaired tumor growth and senescent TNBC cells increased CD8+ T cell proliferation and cytotoxicity. Targeting MMGT1 may therefore improve TNBC immunotherapy by reshaping tumor senescence and the CD8+ T cell–mediated immune response.

Liu S, Liu H, Zhang M et al. · Cell reports. Medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Embracing macrophage complexity for research and translation.

This article reviewed how macrophage identity and function emerge from integrated developmental origin, tissue niche, epigenetic history, local environmental cues, and disease-associated signals rather than fixed subsets or single markers. It highlights advances in single-cell genomics, spatial profiling, epigenomics, in vivo perturbation, and computational modeling showing macrophage states are organized by modular gene programs. The synthesis is significant for improving translational macrophage research by guiding more accurate experimental design and therapeutic targeting strategies.

Ginhoux F, Mulder K, Arcila-Barrera S et al. · Immunity · (2026) · View on PubMed ↗

STAT3 operates as an inflammation-dependent transcriptional switch in antiviral NK cells.

This study examined how STAT3 functions as an inflammation-dependent transcriptional switch in antiviral natural killer (NK) cells during mouse cytomegalovirus (MCMV) infection. The key finding is that STAT3 recruitment and activity can either promote or impair adaptive NK-cell responses depending on the inflammatory milieu present during infection. This is scientifically significant because it explains context-specific STAT3 control of NK immunity and suggests that modulating STAT3 may require tailoring to the inflammatory state.

Grassmann S, Kim H, Rückert T et al. · Science immunology · (2026) · View on PubMed ↗

Antiviral and inflammatory immune signatures in anti-CD20-treated multiple sclerosis: a cross-sectional study.

This cross-sectional study examined how anti-CD20 therapy reshapes antiviral T-cell immunity and innate inflammatory signatures in adults with relapsing multiple sclerosis, comparing 45 untreated, 25 ocrelizumab-treated patients, and additional healthy donors. Using high-parameter flow cytometry across 40+ immune populations and blood markers of neuroaxonal injury, the authors found distinct antiviral and inflammatory immune signatures associated with anti-CD20 treatment. These results are clinically relevant because they may explain how ocrelizumab alters immune defense (e.g., against EBV/CMV/SARS-CoV) while modulating neuroinflammatory activity.

D’Orso S, Picozza M, Guerrera G et al. · Journal of neurology · (2026) · View on PubMed ↗ · Free PDF ↗

IRF7 signalling in tanycytes controls brain-body-immune response across the ovarian cycle.

This study investigated how IRF7 signaling in tanycytes regulates brain–body–immune communication across the ovarian cycle in mice and humans. Using single-cell transcriptomics and cross-species cellular mapping, the authors identified a cyclic interferon response in tanycytes that is sex- and oestrous-cycle dependent and linked to IRF7-dependent control of immune-related programs. The work is significant because it connects a specific immune transcriptional pathway (IRF7) in a defined hypothalamic cell type (tanycytes) to physiological immune variation across the reproductive cycle.

Nampoothiri S, Fernandois D, Journiac N et al. · Nature metabolism · (2026) · View on PubMed ↗


Cancer genomics, molecular drivers & risk stratification

The molecular heterogeneity and clinical impact of genomic driver alterations in prostate cancer.

This study analyzed genomic driver alterations in prostate cancer using the Pan Prostate Cancer Group whole genome sequencing dataset from 1,001 men, integrating point mutations, structural variants, and copy number alterations across 961 primary tumors. It found that at least one recurrent somatic or germline alteration was present in 97% of tumors and identified putative driver genes and mechanisms of dysregulation, addressing the previously noted scarcity of clinically relevant drivers. The results are significant for improving molecular stratification and understanding the heterogeneity of prostate cancer by mapping recurrent driver events across diverse genomic alteration types.

Pellegrina D, Kiriy D, C L Cheng K et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Genomic and clinical landscape of RAS mutations in acute myeloid leukemia.

This study mapped the genomic and clinical landscape of RAS mutations in acute myeloid leukemia (AML) using centralized molecular profiling from 8,553 newly diagnosed patients. RAS mutations were present in 1,775 patients (21%), with NRAS (1,103; 13%) and KRAS (445; 5%) predominating, clustering in P-loop hotspots (G12/G13; 70%) and showing subtype-specific patterns such as higher NRAS Q61 prevalence. The findings highlight convergent evolution of RAS signaling mutations as a key feature of RAS-mut AML, informing risk stratification and therapeutic targeting of the RTK/RAS pathway.

Rodríguez-Arbolí E, Soria-Saldise E, Barragan E et al. · Blood · (2026) · View on PubMed ↗

Ataxin-2 downregulation rewires neuronal and astrocytic metabolism to protect against TDP-43 toxicity.

This study examined whether downregulating ataxin-2 (ATXN2; yeast pbp1 ortholog) protects against TDP-43 toxicity by rewiring metabolism in yeast and mouse TDP-43 models. Global proteomic profiling showed that pbp1/ATXN2 reduction activates orthogonal stress-adaptive pathways in neurons and glia, including neuronally driven glycolysis and reductive glutamine carboxylation via IDH1 to restore ATP independently of impaired mitochondria. These results position ATXN2 as a mechanistically grounded therapeutic target in ALS by linking ATXN2 suppression to metabolic resilience against TDP-43 toxicity.

Gastaldo D, Vito S, Black HH et al. · Cell reports · (2026) · View on PubMed ↗ · Free PDF ↗

Distinct Clinical Features of Multiple Myeloma With t(11;14): A Post Hoc Analysis of JSH-MM-15 Study.

This post hoc analysis of the prospective JSH-MM-15 study evaluated newly diagnosed multiple myeloma patients with t(11;14) cytogenetics (131/482; 27%) to identify t(11;14)-specific prognostic features and treatment factors affecting outcomes. The study found that overall survival differed for t(11;14)-positive disease compared with other cytogenetic risk categories, supporting distinct clinical behavior within MM. These findings are clinically significant because they refine risk stratification and may guide more tailored therapeutic decision-making for the ~15–25% of MM patients with t(11;14).

Tsukamoto T, Shimura Y, Mizutani S et al. · Cancer science · (2026) · View on PubMed ↗ · Free PDF ↗

Prognostic Significance of p53 Immunohistochemical Expression and Molecular Characterization of TP53 Variants in Triple-Negative Breast Cancer After Neoadjuvant Chemotherapy.

This retrospective study evaluated 43 patients with triple-negative breast cancer (TNBC) treated with neoadjuvant chemotherapy (NAC) to determine whether p53 immunohistochemical expression and TP53 sequence variants (including longitudinal changes in variant detection and allele frequency) predict clinical outcomes. The key finding is that p53 IHC status and specific TP53 variant profiles/allele-frequency dynamics after NAC are associated with prognosis in TNBC. This is significant because it supports integrating p53 IHC with TP53 genotyping to improve risk prediction and potentially guide post-NAC management in TNBC.

Berenguer-Marí JR, Álvarez L, Sierra-Roca J et al. · Diagnostics (Basel, Switzerland) · (2026) · View on PubMed ↗ · Free PDF ↗


Tumor microenvironment, inflammation & diet–immunity interactions

The Hidden Conductor: HDL-Gut Microbiome Interplay in the Pathophysiology of Inflammatory-Based Diseases.

This article reviewed and synthesized evidence on how high-density lipoprotein (HDL) functionality interacts with the gut microbiome to influence inflammatory-based diseases. It highlights mechanisms whereby HDL’s anti-inflammatory and immunomodulatory effects—through altered lipid raft composition and membrane protein signaling—intersect with gut microbial metabolites and community dynamics, potentially shaping disease pathophysiology. The review frames HDL–gut microbiome interplay as a mechanistic target for future translational studies and therapeutic strategies in inflammatory disorders.

Hafiane A, Kiss RS, Favari E et al. · BioFactors (Oxford, England) · (2026) · View on PubMed ↗

Omega-3 fatty acids reprogram tumor-associated macrophage cytokine signaling and suppress pancreatic cancer growth.

This study tested how dietary omega-3 versus omega-6 polyunsaturated fatty acids (PUFAs) reprogram cytokine signaling in the pancreatic tumor microenvironment using orthotopic pancreatic ductal adenocarcinoma (PDAC) models. An n-3-enriched diet suppressed PDAC growth in a T cell–independent manner by reducing pro-inflammatory cytokines, whereas an n-6-enriched diet accelerated tumor growth. The work supports a diet–immune-microenvironment mechanism in PDAC and suggests omega-3 PUFA strategies to modulate tumor-associated macrophage inflammatory signaling.

Sakuma S, Zhao S, Hildreth A et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗ · Free PDF ↗

Skeletal Muscle Index, Tumor and Systemic Immunity, and Survival in Advanced Pancreatic Ductal Adenocarcinoma.

This retrospective study assessed whether skeletal muscle index (SMI) relates to tumor immune microenvironment (TIME), peripheral immune phenotypes, serum biomarkers, and survival in 119 patients with advanced pancreatic ductal adenocarcinoma (PDAC). The key finding was that SMI—derived from sex-specific sarcopenia cut-offs using baseline L3-level CT—was associated with features of systemic immunity and the tumor immune microenvironment measured by multiplex immunofluorescence (mIF) and flow cytometry, with prognostic implications for survival. Clinically, SMI may serve as an accessible imaging biomarker reflecting immune status and risk stratification in advanced PDAC.

Ma Y, Jia R, Fan M et al. · Cancer medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Research progress of SPP1 in cancer regulation: Tumorigenesis, metastasis, tumor microenvironment, immunity and therapeutic targets (Review).

This review summarized how secreted phosphoprotein 1 (SPP1/osteopontin) regulates cancer across tumorigenesis, metastasis, tumor microenvironment (TME), immunity, and therapeutic targeting. The key finding was that SPP1 acts as a central signaling hub by binding integrins (e.g., αvβ3, αvβ5, α5β1) and CD44 variants to activate oncogenic pathways such as PI3K/AKT, NF-κB, MAPK/ERK, and Wnt/β-catenin while promoting immune evasion. Scientifically and therapeutically, the review supports SPP1 as a multi-pathway driver and a candidate target for interventions aimed at both tumor growth and immunosuppression.

Xia Y, Han D, Tang S et al. · International journal of oncology · (2026) · View on PubMed ↗ · Free PDF ↗

Spatiotemporal multi-omics reveals lineage, spatial and functional heterogeneity of tumor-associated macrophages and therapeutic vulnerabilities in the tumor microenvironment.

This review studied how emerging single-cell and spatial multi-omics approaches redefine tumor-associated macrophage (TAM) lineage, spatial organization, and functional heterogeneity across solid tumors. It reports that fate-mapping, single-cell transcriptomics, and spatial profiling reveal TAM plasticity beyond the classical M1/M2 framework and identify therapeutic vulnerabilities linked to specific TAM states and locations. Scientifically, it provides a roadmap for using multi-omics to stratify TAM subpopulations and improve immunotherapy and combination targeting strategies.

Wang T, Yang D, Wu J et al. · NPJ precision oncology · (2026) · 1 citations · View on PubMed ↗ · Free PDF ↗


Cancer therapeutics (targeted drugs, antibodies, radiotherapy, clinical trials)

This systematic review and meta-analysis studied palliative radiotherapy for gastric cancer-related bleeding across published clinical studies (patients with advanced gastric cancer) to quantify bleeding response rates and dose–fractionation/dose-response relationships. It found that radiotherapy can achieve clinically meaningful bleeding control and that outcomes are associated with dose and fractionation patterns (with the review aiming to identify the most effective regimens). Clinically, the work is intended to guide selection of optimal dose-fractionation schedules for palliation of bleeding in advanced gastric cancer.

Iguchi R, Imano N, Saito T et al. · Japanese journal of radiology · (2026) · View on PubMed ↗ · Free PDF ↗

EGFR-targeted antibody-toxin conjugate in recurrent glioma: a phase 1 trial.

This phase 1, single-arm, open-label trial studied the EGFR-targeted antibody-toxin conjugate D2C7-ATC in 81 patients with biopsy-confirmed recurrent malignant glioma, including targeting wild-type EGFR and EGFR variant III (EGFRvIII). Using a single infusion delivered by convection-enhanced delivery into enhancing disease, the trial assessed toxicity and determined the recommended phase 2 dose (RP2D), while also evaluating overall survival and the relationship between EGFR expression and outcomes. The study is significant for advancing a next-generation EGFR-directed targeted cytotoxic approach for recurrent glioma and for defining dosing and biomarker-relevant signals for future trials.

Chandramohan V, Herndon JE, Barnwal A et al. · Nature medicine · (2026) · View on PubMed ↗

Targeting FEN1 disrupts EIF4A3-mediated MUC1-C autoregulation: a novel strategy to suppress lung adenocarcinoma progression.

This study investigated whether targeting flap endonuclease 1 (FEN1) can suppress lung adenocarcinoma (LUAD) progression by disrupting EIF4A3-mediated MUC1-C autoregulation. In LUAD models, FEN1 was upregulated and its genetic depletion reduced proliferation via G0/G1 cell-cycle arrest and senescence while impairing migration and invasion, with mechanistic work using integrated proteomics and molecular analyses linking FEN1 knockdown to disruption of the EIF4A3–MUC1-C regulatory axis. The findings support a novel therapeutic strategy in LUAD that targets FEN1 to interfere with oncogenic MUC1-C signaling controlled by EIF4A3.

Wu M, Wu B, Yan X et al. · Cell death & disease · (2026) · View on PubMed ↗ · Free PDF ↗

IFM 2026 Recommendations for First-line Treatment of Newly Diagnosed Multiple Myeloma.

This IFM 2026 guideline review studied evidence for first-line treatment strategies in newly diagnosed multiple myeloma (NDMM), focusing on transplant-eligible and transplant-ineligible patients. It recommends anti-CD38-based quadruplets—daratumumab-VRd for transplant-eligible patients and isatuximab-VRd informed by PERSEUS and GMMG-HD7 trials—as standard induction options, with subsequent autologous stem-cell transplantation for eligible patients. The recommendations are clinically significant because they unify current trial evidence into practical, evidence-based treatment pathways for NDMM.

Perrot A, Manier S, Hulin C et al. · Clinical lymphoma, myeloma & leukemia · (2026) · View on PubMed ↗ · Free PDF ↗

Efficacy and safety of camrelizumab plus docetaxel and carboplatin as neoadjuvant therapy for stage II-III triple-negative breast cancer: the HELEN-Trio 011 randomized clinical trial.

This phase 3 randomized clinical trial studied camrelizumab combined with an anthracycline-free neoadjuvant regimen of docetaxel plus carboplatin in women aged 18–70 with previously untreated stage II–III triple-negative breast cancer (TNBC). Compared with standard neoadjuvant therapy, the trial evaluated efficacy and safety outcomes for the camrelizumab–chemo strategy across 14 Chinese hospitals. If effective and tolerable, this regimen could expand neoadjuvant immunotherapy options for TNBC while avoiding anthracycline-associated toxicity.

Jiao D, Sun X, Qiao J et al. · Annals of oncology : official journal of the European Society for Medical Oncology · (2026) · View on PubMed ↗

Firmonertinib in advanced non-small cell lung cancer with epidermal growth factor receptor P-loop and αC-helix compressing mutations.

This study evaluated firmonertinib, a brain-penetrant mutant-selective EGFR tyrosine kinase inhibitor, in advanced non-small cell lung cancer (NSCLC) harboring P-loop and αC-helix compressing (PACC) mutations. In preclinical models and the phase 1b FURTHER study (NCT05364073), firmonertinib showed high anti-proliferative activity and, in a randomized first-line comparison of 160 mg versus 240 mg, reported confirmed objective response rates of 43% and 68%, respectively. These results support firmonertinib as a promising targeted option for a structurally distinct EGFR-mutant subgroup with limited therapies.

Le X, Wang J, Yu Y et al. · Cancer cell · (2026) · View on PubMed ↗ · Free PDF ↗

Akkermansia muciniphila attenuates macrophage efferocytosis to enhance anti-PD-1 efficacy in microsatellite-stable colorectal cancer.

This study tested whether oral Akkermansia muciniphila (Akk) can overcome intrinsic resistance to anti–PD-1 therapy in microsatellite-stable (MSS) colorectal cancer by modulating macrophage efferocytosis. In MSS CRC mouse models, Akk attenuated macrophage efferocytosis via the TLR2/NF-κB pathway, increasing apoptotic cancer cell accumulation that activated cGAS–STING signaling, boosted type I interferon production, enhanced effector CD8+ T cells, and improved anti–PD-1 efficacy. The findings suggest a microbiome–immunotherapy combination strategy to sensitize MSS colorectal tumors to checkpoint blockade.

Jiang YT, Li GQ, Zhou YW et al. · Cell host & microbe · (2026) · View on PubMed ↗ · Free PDF ↗

Pan-Asian adapted ESMO Clinical Practice Guidelines for the diagnosis, treatment and follow-up of patients with early and locally advanced non-small-cell lung cancer.

This article describes Pan-Asian adapted ESMO Clinical Practice Guidelines for the diagnosis, treatment, and follow-up of early and locally advanced non-small-cell lung cancer (NSCLC) in Asian patients, produced by an expert panel representing oncological societies across Asian countries. The key finding is that the 2025 ESMO NSCLC guideline recommendations were systematically adapted (consensus methodology) to reflect clinical practice considerations relevant to Asian populations. This provides a regionally tailored, evidence-based framework to standardize NSCLC care and follow-up across early and locally advanced disease stages in Asia.

Hayashi H, Zer A, Kenmotsu H et al. · ESMO open · (2027) · View on PubMed ↗

Prognostic Significance of Contrast Enhancement in Newly Diagnosed Grade 2 IDH-mutant Glioma.

This study evaluated the prognostic significance of preoperative contrast enhancement on MRI in newly diagnosed grade 2 IDH-mutant glioma patients. In a retrospective cohort of consecutive patients treated at two institutions (2010–2021) with enhancement assessed by independent readers, the authors analyzed overall survival (OS) and progression-free survival (PFS) in relation to intratumoral enhancement status. The clinical implication is that contrast enhancement may refine risk prediction in grade 2 IDH-mutant glioma, which is particularly relevant for interpreting and optimizing use of the mutant IDH inhibitor vorasidenib.

Nakhate V, Lasica AB, Aker L et al. · Neuro-oncology · (2026) · View on PubMed ↗

Non-Relapse Mortality With Bispecific Antibodies in Hematologic Malignancies: A Dual Systematic Review and Pharmacovigilance Analysis.

This dual systematic review and pharmacovigilance analysis evaluated non-relapse mortality (NRM) associated with bispecific antibodies (BsAbs) in patients with relapsed/refractory hematologic malignancies. The key finding was that BsAb therapy—driven by indefinite treatment exposure and immune toxicities such as neutropenia, B-cell aplasia, and hypogammaglobulinemia—substantially contributes to NRM, with pharmacovigilance signals consistent with clinically meaningful infection-related and treatment-related deaths. Clinically, the study highlights the need to monitor and mitigate immune toxicity and to incorporate NRM as a patient-centered endpoint when assessing BsAb benefit-risk.

Irfan S, Khosla H, Nasir S et al. · Hematological oncology · (2026) · View on PubMed ↗ · Free PDF ↗

Radiotherapy combined with serplulimab, and chemotherapy as first-line treatment for metastatic pancreatic adenocarcinoma: a multicenter, single-arm, phase II trial.

In a multicenter, single-arm phase II trial (ChiCTR2300073237), investigators studied first-line metastatic pancreatic adenocarcinoma patients treated with a combined regimen of serplulimab plus gemcitabine/nab-paclitaxel and stereotactic body radiotherapy (ICSBR). The key finding was that adding serplulimab to chemotherapy with radiotherapy was feasible and produced clinically meaningful antitumor activity alongside biomarker analyses to characterize responders. This supports further development of radiotherapy-combined PD-1 pathway blockade strategies for mPDAC and provides a framework for biomarker-guided optimization.

Cheng K, Zhang C, Liu J et al. · Clinical cancer research : an official journal of the American Association for Cancer Research · (2026) · View on PubMed ↗

Complement Activation Within Minutes Following Systemic Administration of AAV in the Presence of AAV Immunity.

This preclinical translational study evaluated complement activation after systemic administration of AAVrh.10 in the presence of preexisting AAV immunity, focusing on timing after dosing. The key finding was that complement activation can occur within minutes of AAV exposure when anti-AAV antibodies are present, rather than only days later as previously observed in some settings. This is significant for gene therapy safety planning, suggesting that rapid monitoring and mitigation strategies may be needed immediately after systemic AAV dosing in antibody-positive patients.

Caragiulo A, Rosenberg JB, De BP et al. · Human gene therapy · (2026) · View on PubMed ↗

This review evaluated targeted therapy options for renal cell carcinoma (RCC) in the precision medicine era, emphasizing molecular pathway drivers and immune checkpoint inhibitor (ICI) integration. The key finding was that RCC can be stratified by dysregulated pathways (including von Hippel–Lindau–hypoxia-inducible factor signaling, chromatin remodeling alterations, and immune regulatory pathways), which underpins current targeted regimens and pivotal phase III trial evidence. Clinically, the synthesis helps guide selection and sequencing of VEGF-targeted therapies and ICIs based on molecular and pathway context.

Cui H, Song J, Yang P et al. · Molecular medicine reports · (2026) · View on PubMed ↗ · Free PDF ↗


Gene regulation & RNA biology (APA, miRNA, condensates, RNA helicases)

The advances and challenges of mRNA-LNP application in fields of hematology and oncology therapeutics.

This review examined how mRNA delivered by lipid nanoparticles (mRNA-LNPs) is being applied in hematology and oncology therapeutics, building on the clinical feasibility established by COVID-19 mRNA-LNP vaccines. It reports expanding use cases including cancer immunotherapy, personalized neoantigen vaccination, in vivo immune-cell engineering, protein replacement, mRNA-encoded biologics, and genome editing, while noting that hematologic/oncologic efficacy is limited by biological barriers. The synthesis supports continued development of mRNA-LNP platforms tailored to tumor and blood-system constraints to improve therapeutic success in cancer and related disorders.

Wang Y, Ge Y, Chen Y et al. · Journal of hematology & oncology · (2026) · View on PubMed ↗ · Free PDF ↗

Toward a Platform PBPK Model to Characterize the Plasma and Tissue Disposition of Unconjugated Antisense Oligonucleotides and GalNAc-Conjugated Small Interfering RNAs in Preclinical Species and Human.

This study developed a cross-species physiologically based pharmacokinetic (PBPK) platform to characterize plasma and tissue disposition of unconjugated antisense oligonucleotides (ASOs) and GalNAc-conjugated small interfering RNAs (siRNAs) in preclinical species and humans. The key finding was the creation of a mechanistic modeling framework intended to capture rapid plasma clearance, heterogeneous tissue uptake, and prolonged intracellular retention across chemistries and species. Scientifically, this platform aims to improve translation of oligonucleotide dosing and exposure predictions, supporting more efficient development of ASO and GalNAc-siRNA therapeutics.

Desai DA, Cristofoletti R · Clinical pharmacology and therapeutics · (2026) · View on PubMed ↗


DNA repair & chromatin/histone interactions

TONSL/TONSOKU binding to histone H3.1 is required for DNA repair.

This study investigated the molecular requirement for TONSL/TONSOKU binding to histone H3.1 in DNA repair, focusing on the TONSL (TONSOKU-like) histone-binding interface and disease-linked mutations. The key finding is that, beyond a shallow pocket in the TPR domain, additional binding pockets are required for histone H3.1 binding and TONSL-dependent DNA repair, and sponastrime dysplasia-linked TONSL TPR mutations disrupt H3.1 binding and fail to rescue repair. This is significant because it links specific TONSL–H3.1 interaction determinants to genome stability and provides mechanistic insight into a histone-binding DNA repair defect.

Davarinejad H, Laflamme C, Dupont B et al. · Science advances · (2026) · View on PubMed ↗ · Free PDF ↗


Cell biology, mechanobiology & developmental tissue mechanics

A cellular view of seed development and germination.

This article is a review that synthesizes single-cell and spatial transcriptomics studies to provide a cellular-resolution view of seed development and germination. It focuses on how cell-type-specific regulatory programs emerge across the developmental continuum from fertilization to seedling establishment, drawing examples from Arabidopsis thaliana and major crops including rice, maize, barley, and soybean. The review highlights how modern transcriptomic techniques can overcome “bulk” masking of heterogeneity, guiding future mechanistic studies in plant reproduction and crop improvement.

He C, Auroux L, Lewsey M et al. · The Plant cell · (2026) · View on PubMed ↗ · Free PDF ↗

Cell and nuclear scaling constrains tissue fluidity in a doubly-dense remodeling epithelium.

This developmental biology study investigated how cell and nuclear scaling constrains tissue fluidity in doubly dense remodeling epithelia using mh mutant embryos and mechanical/shape analyses. The key finding was that nuclear volume scaled non-linearly with cell volume, producing rounder, more compact nuclei that behaved like a jammed state and reduced tissue fluidity, impairing extension movements. These findings clarify how subcellular geometry and mechanical constraints regulate epithelial remodeling dynamics.

Russell LJ, Budhathoki R, Weber HD et al. · Development (Cambridge, England) · (2026) · View on PubMed ↗

MTR4: A Conserved Youth Factor for Vascular Endothelium.

This mechanistic study examined the role of the RNA helicase MTR4 in vascular endothelial cell (VEC) senescence in senescent human umbilical vein endothelial cells (HUVECs) and aged mouse aortas. The key finding was that senescence-associated upregulation of the E3 ubiquitin ligase SYVN1 promotes K638-linked ubiquitination and proteasomal degradation of MTR4, and that MTR4 depletion drives premature endothelial senescence while MTR4 overexpression preserves youthfulness. These findings identify MTR4 as a conserved “youth factor” and suggest a potential molecular target pathway (SYVN1–MTR4) for age-related vascular dysfunction.

Guo Z, Chen Z, Sun J et al. · Aging cell · (2026) · View on PubMed ↗ · Free PDF ↗


Cardiometabolic health, diabetes & obesity (including GLP-1, insulin resistance)

Association between triglyceride-glucose index and stages of T2DM: potential indirect effects of inflammatory indicators.

This retrospective cross-sectional study of 1,117 participants examined whether the triglyceride-glucose (TyG) index is nonlinearly associated with glycemic status categories spanning normal glucose to type 2 diabetes mellitus (T2DM), and whether inflammatory indicators mediate this relationship. Using generalized additive models (GAM) with mediation/indirect-effect analyses, higher TyG index levels were associated with more advanced glycemic stages, with inflammatory markers providing potential indirect contributions to the TyG–T2DM association. These findings support TyG as an insulin-resistance surrogate linked to T2DM progression and suggest inflammation as a mechanistic pathway that could inform risk stratification and targeted prevention strategies.

Tian J, Li H, Li M et al. · Frontiers in endocrinology · (2026) · View on PubMed ↗

Real-world, digital-first delivery of GLP-1 receptor agonist therapy in women.

This observational real-world study evaluated digital-first implementation of GLP-1 receptor agonist therapy in 8,127 women in the UK, with 99.8% initiating tirzepatide. The program used mandatory biochemical monitoring, weekly video-supported follow-up, and clinician-guided dose titration, producing mean weight loss of 16.1 kg (15.5% of baseline) with most participants achieving ≥10% weight reduction. The findings support that structured digital care can deliver substantial weight and cardiometabolic benefits outside randomized trials, informing scalable implementation of GLP-1RA therapy in women.

Deanfield J, Wong JLC, Katsoulis M et al. · Nature medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Vitamin D Supplementation in Community-Dwelling Adults.

This article reviewed evidence on vitamin D supplementation and the role of vitamin D testing in community-dwelling adults. It concludes that evidence does not support routine vitamin D screening or supplementation in the general population regardless of baseline serum 25-hydroxyvitamin D levels, while noting that recommended daily intakes (e.g., 600 IU for ≤70 years and 800 IU for >70 years) can prevent levels from dropping below 12 ng/mL in most people. The clinical significance is guidance toward targeted supplementation rather than universal testing, aligning practice with evidence and National Academy of Medicine recommendations.

Nohria R, Bagatelas P, Martin S · American family physician · (2026) · View on PubMed ↗

Association of Life’s Essential 8 With Clonal Hematopoiesis and Coronary Artery Disease.

This UK Biobank study (n=427,295) examined whether the American Heart Association Life’s Essential 8 (LE8) cardiovascular health score is associated with clonal hematopoiesis (CH) and how LE8 and CH jointly relate to incident coronary artery disease (CAD). The key finding was that LE8 cardiovascular health and CH prevalence independently contributed to future CAD risk, with combined risk effects indicating that poorer LE8 scores and presence of CH identify higher-risk individuals. These results support integrating CH status with LE8-based cardiovascular risk stratification to improve prediction of CAD in population-based settings.

Liu Y, Li L, Liang S et al. · JACC. CardioOncology · (2026) · View on PubMed ↗ · Free PDF ↗

Dietary anthocyanins as multifunctional bioactives targeting obesity across experimental and clinical models.

This review evaluated the anti-obesogenic effects of dietary anthocyanins across in vitro, preclinical, and clinical studies relevant to obesity. The key finding was that anthocyanins improve lipid and glycemic profiles and show multifunctional mechanisms (e.g., antioxidant and anti-obesity actions) across experimental and human evidence. Clinically, the work positions anthocyanins from dark-pigmented fruits as promising natural bioactives for obesity management, while highlighting the need for clearer translational evidence.

Amjad L, Gamage D, Rupasinghe HPV · Food & function · (2026) · View on PubMed ↗ · Free PDF ↗

Pancreatic steatosis is not associated with impaired insulin secretion among individuals with diabetes.

This cross-sectional study examined whether pancreatic steatosis (PS) and hepatic steatosis (HS) are associated with residual insulin secretion and insulin resistance in 170 individuals with diabetes. Using MRI-derived pancreatic/liver fat fractions (PFF/LFF) and insulin secretion/resistance measures (HOMA2-B, ΔC-peptide after i.v. glucagon, PI:C, HOMA2-IR, Adipo-IR, and i.v. insulin tolerance testing), the key finding was that PFF did not correlate with insulin secretion metrics but did correlate with fasting indices of insulin resistance. These results suggest that, in diabetes, pancreatic fat may be more closely linked to insulin resistance than to impaired insulin secretory capacity.

Laitinen A, Johansson K, Käräjämäki AJ et al. · The Journal of clinical endocrinology and metabolism · (2026) · View on PubMed ↗ · Free PDF ↗

Is There a Relationship Between the Gut Microbiome and the Functional Capabilities of Skeletal Muscle? A Narrative Review.

This narrative review examined whether the gut microbiome’s composition and metabolic functional capabilities relate to skeletal muscle physiology and performance in humans and experimental models. The key finding is that a “gut–muscle axis” is supported by evidence linking diet-driven microbial metabolites (including fiber- and protein-associated outputs) to muscle metabolism, strength, function, and physical performance. Scientifically, this supports microbiome-targeted nutritional strategies as potential modulators of muscle health and sarcopenia risk.

Ondrak KS, Seicshnaydre EA, Duffy SJ et al. · Nutrients · (2026) · View on PubMed ↗ · Free PDF ↗

Ketogenic Dietary Therapies and β-Hydroxybutyrate as Modulators of Mitochondrial Function: From Molecular Mechanisms to Clinical Translation.

This review studied ketogenic dietary therapies (KDTs) and the ketone body β-hydroxybutyrate (BHB) as modulators of mitochondrial function, integrating molecular mechanisms with evidence for clinical translation in drug-resistant epilepsy and related contexts. It found that BHB can alter mitochondrial redox balance and oxidative phosphorylation and also act via epigenetic and signaling pathways, including inhibition of class I histone deacetylases, promotion of lysine β-hydroxybutyrylation, activation of hydroxycarboxylic acid receptor 2 (HCA2/FFAR3), and suppression of the NLRP3 inflammasome. These mechanistic insights are significant because they provide testable targets for improving and extending ketogenic approaches beyond seizure control.

Na JH, Lee YM · Nutrients · (2026) · View on PubMed ↗ · Free PDF ↗

This narrative review evaluated GLP-1-based pharmacotherapies in relation to skeletal muscle health in obesity, focusing on body composition, muscle quantity/composition/function, and sarcopenia-related outcomes across preclinical and clinical studies. The key finding is that while GLP-1 receptor agonists and related agents promote weight loss, their effects on lean/fat-free mass and muscle function depend on the balance between reduced adiposity/inflammation and potential loss of muscle mass. Clinically, this matters for optimizing obesity treatment regimens that preserve muscle and reduce sarcopenic obesity risk.

Knapik J, Fic W, Polak-Szczybyło E · Nutrients · (2026) · View on PubMed ↗ · Free PDF ↗

Nutritional Accuracy and Clinical Applicability of Large Language Model-Generated Therapeutic Diet Plans for Phenylketonuria: A Comparative Simulation Study.

This comparative simulation study evaluated the nutritional accuracy and clinical applicability of large language model (LLM)-generated therapeutic diet plans for classical phenylketonuria (PKU) using standardized simulated patient cases (infancy, adolescence, adulthood, and maternal PKU). The key finding is that diet plans generated by ChatGPT-5.2, Claude 4.5, and Gemini 3 under different prompting conditions showed variable nutrient composition performance against the precise requirements needed for therapeutic PKU diets. Scientifically and clinically, the results highlight limitations of current consumer-facing LLM outputs for high-precision medical nutrition and support the need for validation before use.

Kulu B, Süzen B, Mintaş NE et al. · Nutrients · (2026) · View on PubMed ↗ · Free PDF ↗


Liver disease & metabolic dysfunction-associated steatotic liver disease (MASLD/MASH)

Efficacy and safety of imeglimin hydrochloride for metabolic dysfunction-associated steatotic liver disease with type 2 diabetes: Single-center, single-arm phase 2 (IMELD study).

This single-center, single-arm phase 2 trial evaluated imeglimin hydrochloride, an oral glimin antidiabetic agent, in patients with metabolic dysfunction-associated steatotic liver disease (MASLD) and type 2 diabetes (T2D). Over 24 weeks of imeglimin 1000 mg twice daily, the primary endpoint was change in alanine aminotransferase (ALT) from baseline, with secondary endpoints including HbA1c and insulin resistance/β-cell function measures. If effective and safe, imeglimin could offer a dual metabolic–hepatic therapeutic option for MASLD patients with T2D.

Yamada H, Ida Y, Kaji S et al. · Medicine · (2026) · View on PubMed ↗ · Free PDF ↗

NNMT enhances hyperandrogenism in polyendocrine metabolic ovarian syndrome through epigenetic remodelling.

This study investigated the role of nicotinamide N-methyltransferase (NNMT) in polyendocrine metabolic ovarian syndrome (PMOS) using mouse granulosa-cell models and mechanistic epigenetic assays. NNMT overexpression reduced histone H3 lysine 27 trimethylation (H3K27me3), increased retinoic acid receptor beta (RARB) expression, and promoted ovarian androgen synthesis, creating a feedforward loop that sustains hyperandrogenism. Scientifically, it identifies an NNMT–H3K27me3–RARB axis as a driver of PMOS progression and a potential therapeutic target for hyperandrogenic ovarian disease.

Huang W, Yu C, Wang Y et al. · Nature metabolism · (2026) · View on PubMed ↗

Low-dose Juglone Attenuates Pressure Overload-Induced Cardiac Hypertrophy through Lys207-dependent FoxO1 activation and Mitochondrial protection.

This preclinical study tested whether low-dose juglone mitigates pressure overload-induced cardiac hypertrophy in mice subjected to transverse aortic constriction (TAC) and in Ang II–stimulated cardiomyocytes, focusing on lysine 207–dependent FoxO1 activation and mitochondrial protection. Low-dose juglone (1 mg/kg/day) was well tolerated and attenuated TAC-induced hypertrophy while preserving mitochondrial membrane potential, respiration, ATP production, and redox homeostasis, whereas high-dose juglone caused toxicity. Mechanistically, the protective effects depended on Lys207-dependent FoxO1 activation, supporting juglone as a potential redox-targeted therapeutic candidate for hypertrophy.

Chen H, Yang Z, Zhang C et al. · Pharmacological research · (2026) · View on PubMed ↗ · Free PDF ↗

Thyroid hormone receptor-β agonist simedeutirom (HSK31679) for Chinese patients with metabolic dysfunction-associated steatohepatitis: a 52-week, multicentre, randomised, double-blind, placebo-controlled, phase 2b trial.

This multicentre, randomized, double-blind, placebo-controlled phase 2b trial evaluated the thyroid hormone receptor-β agonist simedeutirom (HSK31679) in Chinese adults with biopsy-confirmed metabolic dysfunction-associated steatohepatitis (MASH) and F2–F3 fibrosis. Over 52 weeks, it tested whether simedeutirom improves liver fat and histologic/clinical endpoints versus placebo in an Asian-descent population. The results are significant for developing targeted, mechanism-based pharmacotherapy for MASH with clinically meaningful fibrosis.

Xue F, Liu J, Chen J et al. · The lancet. Gastroenterology & hepatology · (2026) · 1 citations · View on PubMed ↗

Curcumin alleviates metabolic dysfunction-associated steatotic liver disease via gut microbiota-dependent epigenetic alterations.

This study investigated whether curcumin alleviates metabolic dysfunction-associated steatotic liver disease (MASLD) through gut microbiota-dependent epigenetic changes. In high-fat diet rat models, curcumin reduced hepatic lipid accumulation and metabolic dysfunction, but these benefits were weakened in antibiotic-induced pseudo–germ-free rats, indicating microbiota dependence. The findings support a gut microbiota–epigenetic mechanism for curcumin’s metabolic effects, providing a rationale for microbiome-informed MASLD therapies.

Zhu Y, Ma J, Wang D et al. · Molecular biomedicine · (2026) · View on PubMed ↗ · Free PDF ↗


Autoimmunity & inflammatory disease (including interferons, RA, MG, pericarditis, COPD consensus)

Targeted intestinal ROS scavenging alleviated rheumatoid arthritis by microbial metabolite kynurenic acid mediated Treg/Th17 balance through AhR pathway activation.

This preclinical study used black phosphorus nanosheets (BPNSs) as intestinal reactive oxygen species (ROS) scavengers in collagen-induced arthritis (CIA) mice to test whether microbial metabolite kynurenic acid (KYNA) mediates Treg/Th17 balance via the aryl hydrocarbon receptor (AhR) pathway. Oral BPNS treatment significantly ameliorated arthritis severity and modulated gut microbial KYNA metabolism, shifting immune balance toward Tregs over Th17 cells through AhR pathway activation. The results identify an ROS–microbiome–KYNA–AhR immunoregulatory axis as a potential therapeutic mechanism for rheumatoid arthritis.

Ling Z, Xiang T, Yang C et al. · Gut microbes · (2026) · View on PubMed ↗ · Free PDF ↗

Objective validation of the Crohn’s Anal Fistula Quality of Life questionnaire using quantitative MRI fistula volume in perianal fistulising Crohn’s disease.

This prospective validation study enrolled adults with perianal fistulising Crohn’s disease (pfCD) to test construct validity of the Crohn’s Anal Fistula Quality of Life (CAF-QoL) questionnaire against objective disease burden measured by quantitative pelvic MRI fistula volume. CAF-QoL scores showed a relationship with MRI-derived fistula volume quantified independently by two radiologists using ITK-SNAP, supporting that the PROM reflects clinically meaningful fistula burden. This strengthens the clinical utility of CAF-QoL for monitoring pfCD by linking patient-reported outcomes to objective imaging endpoints.

Anand E, Pelly T, Patel U et al. · Colorectal disease : the official journal of the Association of Coloproctology of Great Britain and Ireland · (2026) · View on PubMed ↗ · Free PDF ↗

Transition From Child to Adult Care in Paediatric Neurological Disorders in Europe-A Joint EAN-EPNS Survey of Current Practices for Healthcare Providers.

This cross-sectional web-based survey assessed current healthcare provider practices for transition from paediatric to adult care in neurological disorders across Europe using a 22-item questionnaire distributed to European Paediatric Neurology Society/European Academy of Neurology Task Force members. The study characterized variability in transition structures, identified key barriers to effective transition, and gathered perceived priorities for improvement. These findings are significant for informing standardized, evidence-aligned transition pathways for young people with paediatric-onset neurological conditions.

Craiu D, Cazacu C, Papadopoulou MT et al. · European journal of neurology · (2026) · View on PubMed ↗ · Free PDF ↗

Hepatic Progenitor Cells and the Ductular Reaction: Pathophysiological Role in the Progression of Liver Disease.

This mechanistic review summarized how hepatic progenitor cells (HPCs) and the ductular reaction (DR) interact during liver injury progression, emphasizing spatiotemporal HPC activation and niche crosstalk. It proposes that early, transient HPC activation supports parenchymal restoration, whereas persistent dysregulated HPC expansion drives progressive fibrogenesis, integrating developmental signaling pathways such as Hippo-YAP, Hedgehog, and Notch. The synthesis is significant because it frames HPC/DR dynamics as a potential therapeutic leverage point for halting progression of diverse liver diseases.

Wang P, Li M, Zhou Z et al. · Liver international : official journal of the International Association for the Study of the Liver · (2026) · View on PubMed ↗

Comparative efficacy and safety of antihistamines, increased antihistamine dosing, and antihistamine adjuncts for chronic urticaria: a systematic review, dose-response, and network meta-analysis of randomized trials.

This systematic review, dose-response, and network meta-analysis evaluated comparative efficacy and safety of H1 antihistamines, increased H1 antihistamine dosing, and adjuncts (H2 blockers or montelukast) for chronic urticaria using randomized trial evidence. It synthesized outcomes across treatment strategies to determine relative benefits and harms and to characterize dose-escalation effects. Clinically, the results aim to guide stepwise management of chronic urticaria by identifying the most effective and safest antihistamine-based regimens.

Chu AWL, Zhao IX, Rayner DG et al. · The Journal of allergy and clinical immunology · (2026) · View on PubMed ↗ · Free PDF ↗

Decoding interferon-mediated spatiotemporal regulation at the maternal-fetal interface.

This review studied how interferons (IFNs) regulate the maternal-fetal immune microenvironment at the maternal-fetal interface across pregnancy, focusing on IFN sources including endometrial cells, decidual stromal cells, trophoblasts, and decidual immune cells. The key finding is that locally produced IFN signaling forms a coordinated spatiotemporal network that governs endometrial receptivity, decidualization, trophoblast differentiation and invasion, spiral artery remodeling, and immune homeostasis. This mechanistic synthesis is significant because it clarifies how IFN activity balances maternal immune tolerance with antimicrobial defense, informing reproductive immunology and potential therapeutic targeting.

Ye Y, Yin T, Li Y · Journal of reproductive immunology · (2026) · View on PubMed ↗

Glycome remodeling programs pathogenic γδ T17 cell responses in autoimmunity.

This study investigated how glycosylation controls activation and function of type 3/γδ T17 (IL-17A-committed) γδ T cells in autoimmunity, using single-cell RNA sequencing and genetic/functional perturbations of glycosylation pathways. The key finding is that MGAT1–MGAT5-mediated branched N-glycosylation is required for γδ T17 cell programs, and loss of branched N-glycans drives a peripheral signal that promotes an IL-17A pro-inflammatory phenotype. This is significant because it identifies the MGAT1–MGAT5 branched N-glycan axis as a mechanistic regulator of pathogenic γδ T17 responses and a potential therapeutic target in autoimmune disease.

Santos-Pereira B, Nogueira R, Tafesse Y et al. · Science immunology · (2026) · View on PubMed ↗

SIK2 antagonizes postinfarction cardiac repair by driving macrophage proinflammatory and impairing efferocytosis.

This study examined how salt-inducible kinase 2 (SIK2) affects post–myocardial infarction (MI) cardiac repair by modulating macrophage inflammation and efferocytosis. The key finding is that macrophage-specific SIK2 deletion reduces infarct size and improves healing, while SIK2 knockout macrophages decrease proinflammatory factor expression and enhance efferocytosis, increasing repair-associated factors. This is significant because it identifies SIK2 as a macrophage-intrinsic regulator of maladaptive inflammation after MI and a potential therapeutic target to improve cardiac repair.

Rong WW, Xu ZQ, Shao S et al. · Science advances · (2026) · View on PubMed ↗ · Free PDF ↗

Early Introduction and Prolonged Full-Dose Anakinra Reduce Recurrence Risk After Discontinuation in Recurrent Pericarditis: An International Multicenter Cohort.

This international multicenter cohort retrospectively analyzed 185 adults with corticosteroid-dependent and colchicine-resistant recurrent pericarditis who achieved clinical remission and then permanently discontinued anakinra. The key finding was that early introduction of anakinra and prolonged full-dose treatment were associated with a lower risk of pericarditis recurrence after discontinuation. Clinically, the results provide evidence-based guidance on treatment duration and timing to improve the likelihood of sustained remission after stopping anakinra.

Malandrino D, Bettiol A, Andreis A et al. · Journal of the American Heart Association · (2026) · View on PubMed ↗ · Free PDF ↗

A Proposed Consensus Definition of Severe COPD: a modified Delphi Study.

This modified Delphi consensus study surveyed 55 international COPD experts to develop a consensus definition of severe COPD and a minimal diagnostic work-up set. The key finding was the establishment of an expert-based, standardized framework for identifying severe COPD and specifying which clinical and diagnostic characteristics should be assessed. Scientifically and clinically, it aims to reduce heterogeneity in “severe COPD” labeling and improve consistency of patient selection for advanced interventions.

Melles MC, van Dijk M, Duiverman ML et al. · Annals of the American Thoracic Society · (2026) · View on PubMed ↗ · Free PDF ↗

Additional Effects of Manual Therapy to Exercise on Pain and Function in Individuals With Knee Osteoarthritis: A Systematic Review and Meta-Analysis.

This systematic review and meta-analysis studied whether adding manual therapy (MT) to exercise (EX) improves pain, function, and pain pressure threshold (PPT) in people with knee osteoarthritis (KOA) using randomized clinical trials. Across 29 included trials, MT combined with exercise showed additional benefits over exercise alone for patient-relevant outcomes (pain/function/PPT), with effects synthesized using standardized mean differences (SMD) and random-effects models. These findings support MT as a potentially useful adjunct to exercise-based care in KOA, informing evidence-based rehabilitation strategies.

da Silva VR, Ramalho RB, de Noronha M et al. · European journal of pain (London, England) · (2026) · View on PubMed ↗ · Free PDF ↗

Nutritional Management of Polyendocrine Metabolic Ovarian Syndrome: Current Evidence on Dietary Strategies, Supplementation, and Lifestyle Support.

This narrative review studied nutritional management strategies for polyendocrine metabolic ovarian syndrome (PMOS; formerly PCOS), synthesizing evidence on diet, supplementation, gut microbiota, and lifestyle support. The key finding is that lifestyle intervention remains foundational, while the optimal dietary pattern and adjunct supplementation approach for PMOS is still debated and likely individualized based on metabolic and inflammatory features. This is significant because it informs evidence-based nutritional counseling aimed at improving insulin resistance, hyperandrogenism, and long-term cardiometabolic risk.

Murawski M, Góral A, Miszczak MM et al. · Nutrients · (2026) · View on PubMed ↗ · Free PDF ↗

IgM- and IgA-Enriched Polyclonal Intravenous Immunoglobulin Therapy in Sepsis: A Single-Center Retrospective Cohort Study.

This single-center retrospective cohort study evaluated adjunctive IgM- and IgA-enriched polyclonal intravenous immunoglobulin (IgGAM) versus standard sepsis management in 50 adults with sepsis or septic shock (Sepsis-3) treated between 2006 and 2010. Patients receiving IgGAM had improved 28-day intensive care outcomes, with post hoc analyses suggesting benefit may depend on the appropriateness of initial empiric antibiotic therapy (IEAT). These findings support further prospective trials of IgGAM as an adjunct to standard care in adult sepsis, potentially stratified by IEAT appropriateness.

Yılmaz H, Tulunay M, Yılmaz AA · Journal of clinical medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Heterogeneity in Self-Reported Management of Blunt Chest Trauma: An International Cross-Sectional Survey.

This international cross-sectional web survey studied self-reported diagnostic and management practices for blunt chest trauma among healthcare professionals, comparing Italian respondents with respondents from other participating countries (509 total responses). The survey found substantial heterogeneity in how clinicians report managing blunt chest trauma across settings and countries. The results highlight the need for harmonized, evidence-based guidelines and targeted education to reduce variability in blunt chest trauma care.

Cimino M, Notaro S, Esquinas AM et al. · Journal of clinical medicine · (2026) · View on PubMed ↗ · Free PDF ↗

From Rescue Therapy to Mechanism-Based Sequencing in Refractory Myasthenia Gravis: A Narrative Review with an Illustrative Clinical Case.

This narrative review synthesized evidence on mechanism-based sequencing for refractory acetylcholine receptor antibody-positive generalized myasthenia gravis (AChR-Ab-positive gMG), focusing on how to choose next targeted therapies after incomplete response to a prior targeted class. It summarizes data across conventional immunosuppression, rescue strategies, B-cell/B-lineage depletion, terminal complement inhibition, and neonatal Fc receptor (FcRn) inhibition, and provides an illustrative clinical case to demonstrate sequencing logic. The review is clinically significant because it offers a structured framework for selecting subsequent mechanisms in refractory AChR-Ab-positive gMG, where trial evidence is limited.

Ilves A, Nikitin V · Journal of clinical medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Clinical phenotype and treatment response in AQP4-IgG-positive NMOSD and MOGAD: insights from the Italian I-MS&RD registry.

Using the Italian I-MS&RD registry, this study characterized clinical phenotype and treatment response in 664 patients with AQP4-IgG-positive neuromyelitis optica spectrum disorder (NMOSD; n=406) and MOGAD (n=258). It assessed predictors of rituximab response and compared relapse outcomes across treatment classes, aiming to identify factors associated with time to first relapse. The findings are important for personalized management of NMOSD and MOGAD by clarifying which patient features may predict rituximab effectiveness and relapse risk.

Tortorella C, Cruciani A, Patti F et al. · Journal of neurology · (2026) · View on PubMed ↗


Infectious disease, vaccines & epidemiology (including viruses, norovirus, dengue)

Symmetry-breaking antibody binding reveals extensive capsid malleability in pandemic human norovirus.

This study investigated how symmetry-breaking antibody binding reveals capsid plasticity in pandemic human norovirus, focusing on GII.4 variants and VP1-based virus-like particles (VLPs). The key finding was that human norovirus capsids exhibit extensive malleability that reshapes antigenic landscapes, consistent with a metastable balance between stability and flexibility required for entry, infectivity, and immune escape. Scientifically, the results refine understanding of norovirus immune recognition and support rational design of VP1/VLP vaccines targeting evolving antigenic sites.

Apostol CV, Anish R, Pham S et al. · Research square · (2026) · View on PubMed ↗ · Free PDF ↗

Dengue virus infection.

This article reviewed dengue virus infection caused by Aedes-borne DENV-1 to DENV-4 and summarized epidemiology, clinical progression, and diagnostic approaches in humans. It highlights that dengue can range from acute febrile illness to life-threatening inflammation-driven circulatory failure and that diagnosis relies on viral RNA/antigen detection or serology. The review’s clinical significance is to guide recognition and testing strategies as dengue expands beyond urban centers due to travel and climate change.

Ooi YS, Cattrall J, Brady O et al. · Nature reviews. Disease primers · (2026) · View on PubMed ↗ · Free PDF ↗



Generated automatically on October 18, 2026 from PubMed’s trending articles. Summaries are AI-generated; always consult the original publication for clinical or research decisions.