PubMed Trending Research Digest — July 31, 2026

Automated digest · 96 articles · 29 research areas · July 31, 2026

Overview

Across this week’s set of studies, a dominant theme is mechanism-first biology that connects microenvironmental cues to cell-state control—spanning plants, brain immune cells, and cancer. Plant root epidermal cells use spatial mechanical tension versus root-cap shielding to trigger distinct growth programs, while Drosophila intestinal stem cells maintain tissue homeostasis by an intrinsic “division-counting” fate switch. In the brain, iPSC-derived microglia work identifies state-specific regulators that could enable selective modulation of neuroimmune activation, and multiple studies link innate immune signaling (e.g., cGAS–STING in drug-refractory epilepsy; NLRC3–STING in cancer) to disease progression and therapeutic opportunity.

A second major cluster centers on immunotherapy and immune evasion—both as biomarkers and as modifiable biology. Several papers dissect why responses succeed or fail: TIL infusion composition and tumor spatial immune programs in melanoma, aged-tumor CD8+ persistence regulators, and CAR NK/T-cell dysfunction mechanisms (including trogocytosis-driven antigen sinks and phenotype-dependent CAR-T efficacy at limited doses). Complementing these, tumor microenvironment engineering emerges via bile-acid and microbiome effects on antigen presentation and immunotherapy resistance, tumor-derived autophagosomes that reprogram CAFs to create immune-excluded niches, and nanoparticle/antibody-PROTAC strategies aimed at improving delivery and durable anti-tumor memory.

Finally, translational and systems-level efforts show up repeatedly: evidence synthesis and trial design (network meta-analyses, consensus, and platform trials) inform clinical decision-making; tuberculosis reviews highlight diagnostic and treatment advances with WHO policy translation; and metabolic/aging studies connect mitochondrial, lysosomal, and epigenetic control to pathology (e.g., mitophagy failure in Alzheimer’s, mitochondrial–epigenetic coupling to SASP, CMA regulation of cardiac fibrosis, and metabolic checkpoints linking glycolysis to autophagy). Together, these articles underscore a trend toward integrating high-resolution mechanistic data (single-cell/spatial, structural biology, multi-omics) with targeted interventions and better stratification to improve outcomes across diverse diseases.

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Plant mechanobiology and developmental patterning

The Arabidopsis SPFH protein HIR2 modulates receptor signaling and plasma membrane organization.

This study investigated the Arabidopsis SPFH-family protein HIR2 and how it modulates receptor signaling and plasma membrane organization, focusing on interactions with receptor kinases including BAK1-interacting receptors BIR2 and BIR3 and BAK1. It reports that HIR2 interacts with these membrane proteins and that hir2 mutants show impaired growth and immunity phenotypes consistent with disrupted BAK1-mediated signaling. The scientific significance is defining HIR2 as a regulator linking SPFH-domain membrane organization to receptor-kinase signaling control in plants.

Weber H, Ehinger A, Kolb D et al. · The EMBO journal · (2026) · View on PubMed ↗ · Free PDF ↗

Fgfr3-Wnt signaling crosstalk is involved in maintaining cranial suture integrity.

The study examined the role of Fibroblast Growth Factor Receptor 3 (Fgfr3) in cranial suture formation and maintenance using an fgfr3 loss-of-function (LoF) zebrafish model with abnormal suture morphology. It showed that Fgfr3 has pleiotropic functions in both suture formation and homeostasis, with transmission electron microscopy and second harmonic generation imaging indicating essential organization of suture-associated structures (details truncated). This clarifies Fgfr3–Wnt pathway crosstalk in cranial suture integrity and strengthens mechanistic understanding of craniosynostosis linked to FGFR3 disruption.

Pereur R, Marc Y, Lim Y et al. · Bone research · (2026) · View on PubMed ↗ · Free PDF ↗

Plant cells at the organ surface use mechanical cues to activate a specific growth-control program.

The study examined how plant epidermal cells at the root organ surface versus root-cap–covered epidermal cells use mechanical cues to activate distinct growth-control programs during organ morphogenesis. It found that surface epidermal cells experience high mechanical tension that triggers a specific growth-control program, whereas root-cap coverage mechanically shields covered epidermal cells and prevents that activation. This mechanobiology insight clarifies how spatial mechanical environments pattern tissue growth in roots and could inform strategies to manipulate plant organ development.

Nemec-Venza Z, Kiss A, German N et al. · Current biology : CB · (2026) · View on PubMed ↗

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Insect chemosensation and vector control

Gustatory function of Aedes aegypti opsins and TRPA1 in avoiding a natural insect repellent.

The study investigated gustatory roles of the Aedes aegypti opsins Op1 and Op2 and the ion channel TRPA1 in detecting natural insect-repellent chemicals that suppress blood feeding. It found that Op1 and Op2 function as chemical sensors activated by flavonoids such as catechin, and that catechin suppresses blood feeding in an artificial skin-mimicking membrane system (VectaDerm), with the effect disrupted in op1,op2 double mutants. These findings identify catechin/Op1/Op2 as a mechanistic pathway for repellent action, supporting rational development of next-generation mosquito repellents.

Chandel A, Dhavan P, Ganguly A et al. · Current biology : CB · (2026) · View on PubMed ↗ · Free PDF ↗

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Global mental health epidemiology

Burden of 10 mental disorders in low- and middle-income countries, 1990-2023, with forecasts to 2050: a Global Burden of Disease Study.

The study used the Global Burden of Disease Study 2023 to quantify 1990–2023 prevalence and disability-adjusted life years (DALYs) for 10 mental disorder subcategories across 76 low- and middle-income countries/low-income countries and projected trends to 2050. It found that age-standardized prevalence increased substantially from 1990 to 2023 in LMICs and LICs, with modeled forecasts extending the burden into 2050. This provides long-term, cross-country evidence to prioritize mental health resources and planning in LMIC/LIC settings.

Med (New York, N.Y.) · (2026) · View on PubMed ↗

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Cancer immunotherapy biomarkers and cellular products (TIL/immune cell engineering)

Quantifying target antigen-dependent CAR T-cell performance against AML.

This study quantified CAR T-cell performance against acute myeloid leukemia (AML) by integrating mathematical modeling with in vitro assay data and Bayesian inference to evaluate target antigen-dependent dynamics. It specifically addresses how different CAR target constructs (e.g., CD33, CD123, CD371) perform against AML variants, including those with resistance mechanisms such as TP53 loss mutations. The resulting quantitative framework aims to enable more systematic, predictive comparison of CAR designs for improving efficacy in antigen- and genotype-defined AML.

Shah S, Mueller J, Vogel E et al. · Cancer cell international · (2026) · View on PubMed ↗ · Free PDF ↗

A distinct CAR-T cell phenotype mediates therapeutic response at limited doses.

The study analyzed anti-CD19 CAR-T cell products from a phase I/II dose-escalation trial to determine how a distinct CAR-T phenotype mediates therapeutic response at limited CAR-T doses. Through deep phenotyping of CAR-T cells and matched leukapheresis starting materials, it identified a CAR-T phenotype associated with clinical response when administered at lower doses (clinical outcomes described but truncated). This provides mechanistic insight into efficacy under manufacturing-limited dosing and could guide biomarker-driven optimization of CAR-T dosing strategies.

Yousefian S, Schubert ML, Minafra AR et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

B cell CD19 is transferred between immune cells in mice and humans.

The study tested whether the B cell marker CD19 is strictly B-lineage–restricted or can be transferred between immune cells, using mouse and human B–T cell co-cultures. It found that CD19 is transferred via trogocytosis when B cells activate T cells, and in a B cell-driven experimental autoimmune encephalomyelitis model, CD19+ T cells expanded and showed enhanced activation, differentiation, and encephalitogenic potential ex vivo. This challenges the assumption that CD19 is exclusive to B cells and has implications for interpreting immune phenotyping and for therapeutic monoclonal antibody targeting.

Ochs J, Schweineberg P, Thode J et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Depletion of an immature cord blood NK subset reverses trogocytosis-driven CAR NK dysfunction.

This mechanistic cancer immunology study examined cord blood-derived allogeneic CAR NK cell dysfunction, identifying an immature CD16-CD161 double-negative (DN) NK subset associated with poor outcomes and trogocytosis-driven hypofunction. After CAR engineering, DN-derived CAR NK cells remained hypofunctional but showed exaggerated trogocytosis, forming an intra-product trogocytic-antigen sink (TAS) that diverted CAR engagement from tumor targets and promoted on-target off-tumor interactions. The findings are significant because depleting this immature DN subset can reverse CAR NK dysfunction and improve the consistency of off-the-shelf CAR NK potency.

Li Y, Fan H, Wang G et al. · Cancer cell · (2026) · View on PubMed ↗ · Free PDF ↗

Immunologic determinants of infusion products and the tumor microenvironment govern response to TIL therapy in advanced melanoma.

The study analyzed immunologic determinants within tumor-infiltrating lymphocyte (TIL) infusion products and matched tumor microenvironments that govern response to TIL therapy in advanced/metastatic melanoma patients. Using integrated immunophenotyping and spatial transcriptomics of TIL products and tumor samples from early-phase clinical trials, it found that responders had infusion products enriched for CD8+ T cells with stem-like features and that tumor microenvironment immunologic context aligned with durable objective responses. This supports biomarker-driven selection and engineering of TIL products by linking specific immune composition and spatial tumor programs to clinical benefit.

Karapetyan L, Xu J, Ward K et al. · Med (New York, N.Y.) · (2026) · View on PubMed ↗

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Microglia states and neuroimmune regulation

Persistent cytolytic CD8+ T cells recognize SARS-CoV-2 and herpesvirus epitopes in long COVID.

This study profiled viral-specific CD8+ T cells in long COVID by using combinatorial tetramers to measure SARS-CoV-2 and herpesvirus (CMV and EBV) epitopes in post-acute samples from long COVID individuals versus recovered controls. It found that long COVID–associated CMV-specific CD8+ T cells were biased toward T central memory (Tcm) rather than terminally differentiated Temra phenotypes, contrasting with severe COVID patterns (abstract truncated before full quantitative details). The work is significant because it characterises persistent cytolytic CD8+ T cell specificity and memory-state remodeling in long COVID, informing immune monitoring and potential interventions.

Ma T, Ryu H, Yin K et al. · Cell reports. Medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Transcriptional regulation of disease-relevant microglial activation programs.

The study sought transcriptional regulators of disease-relevant microglial activation states by performing CRISPR interference screens in induced pluripotent stem cell (iPSC)-derived microglia. It identified 31 regulators and characterized state-specific protein markers using single-cell transcriptomics and cell-surface proteomics across two iPSC-derived microglia models, then functionally validated several regulators of microglial activation programs. This advances mechanistic targets for selectively driving or inhibiting microglial states relevant to brain disorders.

McQuade A, Mishra R, Hagan V et al. · Neuron · (2026) · View on PubMed ↗

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Metabolic disease therapeutics and mitochondrial function (MASLD/MASH/steatosis)

Efficacy and Safety of Dual and Triple Glucagon-Like Peptide-1-Based Polyagonists in Metabolic Dysfunction-Associated Steatotic Liver Disease and Steatohepatitis: A Systematic Review and Meta-Analysis.

This systematic review and meta-analysis evaluated randomized controlled trials in adults with metabolic dysfunction-associated steatotic liver disease (MASLD) and metabolic dysfunction-associated steatohepatitis (MASH) to compare dual or triple GLP-1-based polyagonists versus placebo. The analysis synthesized efficacy and safety outcomes across trials to determine whether polyagonist regimens improve steatotic and inflammatory liver disease endpoints. Clinically, the results aim to clarify which GLP-1 polyagonist strategies may offer the best benefit–risk profile for MASLD/MASH patients.

Santos Solis R, Baeza-Zapata AA, Negrete-Najar JP · Cureus · (2026) · View on PubMed ↗ · Free PDF ↗

Clinical Trial: Phase 3 Trial of Resmetirom Versus Placebo in Metabolic Dysfunction-Associated Steatohepatitis-Reanalysis of Fibrosis Stage 2-3 Subset.

This post hoc reanalysis of a phase 3 clinical trial evaluated resmetirom versus placebo in adults with metabolic dysfunction-associated steatohepatitis (MASH) restricted to fibrosis stages F2–F3, using endpoints consistent with the approved label population. It reports treatment effects of resmetirom on co-primary outcomes including MASH resolution and fibrosis improvement measures in the F2–F3 subset. The significance is that it refines the evidence base for resmetirom’s efficacy specifically in the clinically targeted F2–F3 fibrosis group.

Mironova M, Padmanabhan K, Schneider D et al. · Alimentary pharmacology & therapeutics · (2026) · View on PubMed ↗

p21-activated kinase 4 drives hepatic stellate cell activation and liver fibrosis through the phosphorylation of YAP at T428.

The study investigated how p21-activated kinase 4 (PAK4) regulates hepatic stellate cell (HSC) activation and liver fibrosis by phosphorylating YAP at threonine 428 (T428). It reported that PAK4 is upregulated in activated HSCs from patients and mouse models of liver fibrosis, and that PAK4 silencing suppressed HSC activation features by reducing YAP T428 phosphorylation (details truncated). This identifies a PAK4→YAP(T428) signaling axis as a mechanistic driver and potential antifibrotic therapeutic target.

Kim GH, Rho H, Lee CH et al. · Signal transduction and targeted therapy · (2026) · View on PubMed ↗ · Free PDF ↗

Proteomic resolution of the MASLD cardiometabolic spectrum identifies sex-driven endotypes and predicts systemic mortality.

This study investigated molecular heterogeneity across the metabolic dysfunction-associated steatotic liver disease (MASLD) cardiometabolic spectrum by integrating MRI-based phenotyping with large-scale proteomics in UK Biobank participants. Using latent class analysis (LCA) in 48,806 participants followed for >15 years, the authors identified sex-driven endotypes and used proteomic profiling to define molecular subtypes that predicted systemic mortality. Scientifically and clinically, the work supports more precise MASLD risk stratification beyond traditional cardiometabolic labels by linking sex-specific molecular endotypes to long-term outcomes.

Diambra L, Sookoian S, Pirola CJ · Gut · (2026) · View on PubMed ↗

PYY3-36 potentiates Semaglutide‑mediated mitochondrial modulation in MASLD.

The study tested whether PYY3-36 potentiates semaglutide-mediated mitochondrial effects in metabolic dysfunction-associated steatotic liver disease (MASLD) using obese rats. In male Wistar rats fed a high-fat/fructose diet with L-NAME, it assessed how the GLP-1 receptor agonist semaglutide and the NPY2 receptor agonist PYY3-36 (alone and in combination) modulate hepatic mitochondrial oxygen consumption and ROS emission. The results support a combined incretin–NPY signaling mechanism for improving mitochondrial function in MASLD, informing therapeutic strategy refinement.

Geiger N, Nickel AG, Kohlhaas M et al. · American journal of physiology. Endocrinology and metabolism · (2026) · View on PubMed ↗ · Free PDF ↗

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Allergy/dermatology therapeutics (atopic dermatitis/eczema)

Antihistamines for atopic dermatitis (eczema): systematic review and network meta-analysis of randomised trials.

This systematic review and network meta-analysis evaluated add-on oral antihistamines (H1 antihistamines, H2 blockers, and mast cell stabilisers such as nedocromil sodium and sodium cromoglycate, alone or in combination) for atopic dermatitis/eczema in randomized trials. The study synthesized comparative benefits and harms across these drug classes to determine which oral antihistamine strategies most effectively improve eczema outcomes. These findings are clinically significant for guiding evidence-based selection of adjunct oral therapies in atopic dermatitis where antihistamines are commonly used despite uncertain comparative effectiveness.

Chu AWL, Wen A, Guyatt GH et al. · BMJ (Clinical research ed.) · (2026) · View on PubMed ↗

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Migraine therapeutics and cardiovascular comorbidity (PFO-associated)

Antithrombotic treatment for migraine in patients with patent foramen ovale: multicentre, randomised, active controlled, open label trial.

This multicentre, randomized, active-controlled, open-label trial with blinded outcome assessment studied antithrombotic treatment for migraine prevention in 1000 Chinese adults (18–64 years) with patent foramen ovale (PFO) confirmed by echocardiography. The key finding reported in the abstract would determine whether the antithrombotic regimen improves migraine outcomes and safety versus the active comparator in this PFO-associated migraine population. If effective, the results would be scientifically and clinically important for establishing whether targeting PFO-related mechanisms with antithrombotics can reduce migraine burden in adults.

Li Z, Wang C, Tang Y et al. · BMJ (Clinical research ed.) · (2026) · 1 citations · View on PubMed ↗ · Free PDF ↗

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Targeted protein/RNA degradation therapeutics (RiboTAC/PROTAC)

A first-in-class RNA degrader reduces c-MYC expression and myeloma cell survival in preclinical models.

This preclinical study tested a first-in-class RNA degrader, a MYC-RiboTAC ribonuclease-targeting chimera, designed to degrade MYC mRNA in multiple myeloma using RNase L-dependent mechanisms across primary patient samples and myeloma cell lines. The key finding was that MYC-RiboTAC reduced MYC mRNA and MYC protein levels and decreased myeloma cell survival in an RNase L-dependent manner. This is significant because it provides a tractable strategy to pharmacologically suppress the intrinsically disordered MYC protein by degrading its mRNA, supporting further development of RiboTAC therapeutics for MYC-driven cancers.

Maisano D, Wang T, Kulp SB et al. · Blood · (2026) · View on PubMed ↗

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GPCR drug discovery and screening methods

A high throughput screening platform for label-free identification and characterization of GPCR ligands using impedance-based real-time cellular analysis.

This methods-focused study developed a high-throughput screening platform using impedance-based real-time cellular analysis (RTCA) to label-free identify and characterize GPCR ligands. The key finding is that RTCA can kinetically monitor integrated cellular responses to pharmacological modulation of GPCRs, enabling characterization beyond downstream signaling readouts. This is clinically and scientifically important because it supports more efficient GPCR drug discovery by providing a scalable, label-free assay for early ligand profiling.

Bangnowski F, Ries R, Karnath M et al. · SLAS discovery : advancing life sciences R & D · (2026) · View on PubMed ↗ · Free PDF ↗

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Neurodegeneration mechanisms and targeted gene regulation (AD/ALS/HD/epigenetics)

Transaldolase 1 contributes to pentose phosphate pathway disruption and synaptic dysfunction in Alzheimer’s disease.

This study investigated how transaldolase 1 (TALDO1) and pentose phosphate pathway (PPP) disruption relate to synaptic dysfunction in Alzheimer’s disease using proteomic analyses of temporal cortex synaptosomes from AD patients and controls. It reports that TALDO1 contributes to reduced PPP flux and associated synaptic impairment in AD. The findings are significant because they implicate a specific metabolic enzyme–pathway axis (TALDO1/PPP) as a mechanistic driver of synaptic dysfunction, suggesting potential metabolic targets for AD intervention.

Hu X, Yu Y, Luo H et al. · Translational neurodegeneration · (2026) · View on PubMed ↗ · Free PDF ↗

In vivo CRISPR base editing for treatment of Huntington’s disease.

The study developed in vivo CRISPR base editors for Huntington’s disease by disrupting the splice acceptor of HTT exon 13 to generate proteolysis-resistant huntingtin isoforms. The key finding is that base editing targets exon 13 splice regulation to prevent formation of aggregation-prone N-terminal mutant HTT fragments implicated in toxicity. This supports a gene-regulatory therapeutic strategy for HD that aims to reduce pathogenic proteolysis rather than directly replacing the gene.

Shirguppe S, Gapinske M, Swami D et al. · Nature biomedical engineering · (2026) · View on PubMed ↗

Mitochondrial accumulation and lysosomal dysfunction result in mitochondrial plaques in Alzheimer’s disease.

The study examined Alzheimer’s disease mechanisms in AD model mice expressing a mitophagy reporter (APP/PSEN1/mt-Keima) to test whether dysfunctional mitophagy produces in vivo pathological structures. The key finding is that mice develop mitochondrial plaques composed of accumulated acidic and neutral mitochondria in neuronal processes, driven by abnormal mitochondrial buildup and delayed lysosomal recruitment, with incomplete degradation due to impaired lysosomal function. This provides direct in vivo evidence linking mitophagy failure and lysosomal dysfunction to a distinct AD pathology.

Dan X, Croteau DL, Liu W et al. · Nature neuroscience · (2026) · View on PubMed ↗

Ferroptosis modulation enhances astrocyte-to-neuron conversion induced by a novel chemical cocktail in the hemorrhagic brain.

The study aimed to develop and validate a small-molecule cocktail to induce astrocyte-to-neuron (AtN) conversion in vivo after intracerebral hemorrhage (ICH), and to test ferroptosis modulation as part of the reprogramming strategy. It identified a seven-compound cocktail (DFGKLRV) that converted astrocytes into neurons under both physiological and ICH conditions, using immunostaining, RT–qPCR, electrophysiology, RNA sequencing, neural circuit tracing, and additional assays (details truncated). This work supports a chemically defined, ferroptosis-influencing approach to promote brain regeneration after ICH, with translational relevance for limiting neuronal loss and improving functional recovery.

Wang J, Chen S, Li J et al. · Signal transduction and targeted therapy · (2026) · View on PubMed ↗ · Free PDF ↗

Endothelial Cell-Pericyte Interactions in Ischemic Stroke: From Microvascular Pathology to Repair.

This review synthesized evidence on endothelial cell–pericyte interactions in ischemic stroke, focusing on microvascular pathology and repair mechanisms after ischemic injury. The key finding is that post-stroke endothelial cells and pericytes can communicate via processes including mitochondrial transfer and exosome release through multiple pathways, forming a signaling interaction network. This is scientifically significant because it highlights mechanistic targets within the blood–brain barrier unit that could be leveraged to promote vascular repair and improve outcomes after ischemic stroke.

Feng S, Zhang C, Zhao Y et al. · Pharmacological research · (2026) · View on PubMed ↗ · Free PDF ↗

Targeting TDP-43 in ALS: Regulatory hurdles, trial design deficiencies, and the causal evidence gap for CTx1000.

This review evaluated the therapeutic rationale and translational challenges for targeting TDP-43 in amyotrophic lateral sclerosis (ALS), with emphasis on the PROTAC CTx1000 approach that aims to selectively degrade mislocalized TDP-43. The key finding is that despite the causal evidence gap and historical trial design/regulatory shortcomings, PROTAC-based target degradation may address limitations of prior TDP-43-directed strategies. This is significant because it frames what evidence, trial design elements, and regulatory considerations are needed to close the target-engagement and efficacy gaps for CTx1000 in ALS.

Guth MAS · Drug discovery today · (2026) · View on PubMed ↗

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Tuberculosis diagnostics and biomarkers (policy/implementation)

Aerobiology and Transmission of Mycobacterium tuberculosis.

This article reviewed the aerobiological mechanisms of Mycobacterium tuberculosis (Mtb) transmission, tracing how bacilli are expelled in respiratory aerosols, survive in the environment, and deposit to infect new hosts. It highlights that host, mycobacterial, and environmental factors jointly determine transmission efficiency and that recent direct aerosol sampling studies have challenged older assumptions about aerosol generation and infectious dose. Scientifically, the synthesis refines how airborne exposure pathways should be measured and modeled to better inform TB transmission risk and control strategies.

Patterson B, Warner D, Wood R · Cold Spring Harbor perspectives in medicine · (2026) · View on PubMed ↗

Advances in tuberculosis treatment: novel regimens, new drug pipelines, host-directed therapies, and updated management guidelines.

This Lancet Microbe review summarized advances in tuberculosis diagnostics and biomarkers from 2020–2025 and how they translated into WHO policy guidance. The key finding is that digital chest radiography with computer-aided detection and expanded decentralized molecular diagnosis using WHO-recommended rapid test classes have improved integrated screening, diagnosis, and drug-resistance detection across specimen types and populations. This is significant because it identifies evidence-backed diagnostic pathways and remaining gaps to prioritize for future development and implementation.

Marais BJ, Goletti D, McHugh TD et al. · The Lancet. Microbe · (2027) · 1 citations · View on PubMed ↗ · Free PDF ↗

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Tuberculosis treatment optimization and regimen trials (WHO impact)

Advances in tuberculosis diagnostics and biomarkers, 2020-26: scientific evidence, recommendations, gaps, and developmental priorities.

This Lancet Microbe review described major advances in tuberculosis treatment from 2020 onward, including results from pivotal randomized trials (e.g., TB-PRACTECAL, ZeNix, Nix-TB, endTB, BEAT-TB, SHINE, and Study 31/A5349) and their impact on WHO guidelines. The key finding is that these trials enabled shorter, fully oral regimens with improved efficacy and safety for both drug-susceptible and drug-resistant TB across adult and pediatric populations, including people with HIV. This is clinically significant because it supports updated global treatment strategies that can reduce TB mortality while improving tolerability and feasibility.

Walzl G, McHugh TD, Chakaya J et al. · The Lancet. Microbe · (2027) · View on PubMed ↗ · Free PDF ↗

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Autoimmune disease genetics and precision medicine (thyroiditis/Hashimoto; programs)

Multi-ancestry genome-wide association analyses provide insights into the genetic basis of Hashimoto’s thyroiditis.

The study performed multi-ancestry genome-wide association meta-analyses for Hashimoto’s thyroiditis using 48,694 cases and 1,044,134 controls with precise case definitions. The key finding was identification of 155 significant independent associations (P<5×10^-8), including 45 variants and 19 loci not previously linked to hypothyroidism, with functional enrichment implicating immune cells and the spleen and highlighting T-cell importance. This improves genetic resolution across ancestries and refines biological pathways for autoimmune hypothyroidism risk prediction and mechanism discovery.

Bujnis MN, Sterenborg RBTM, Li Y et al. · Nature genetics · (2026) · View on PubMed ↗ · Free PDF ↗

Translating genomic data into healthcare practice with the Singapore National Precision Medicine program.

The study described the Singapore National Precision Medicine (NPM) program’s phase II (2020–2025), including translation of genomic research into healthcare using large-scale datasets such as PRECISE-SG100K. The key finding is that NPM enabled scalable precision-health solutions tailored to Singapore’s multi-ancestry Asian population and successfully translated findings into mainstream care using familial hypercholesterolemia as a use case. This demonstrates a practical framework for converting genomic data into clinical workflows and policy-ready precision medicine.

Seow SW, Mina T, Hebrard M et al. · Nature genetics · (2026) · View on PubMed ↗

Retinal microvascular alterations detected by optical coherence tomography angiography in patients with inflammatory bowel disease.

This study evaluated retinal microvascular changes in inflammatory bowel disease (IBD) patients using optical coherence tomography angiography (OCTA) compared with healthy controls. Among 114 participants (65 IBD, 49 controls), it assessed superficial and deep capillary plexus vessel density, foveal avascular zone metrics, and FD300, reporting that IBD is associated with measurable microvascular alterations on OCTA. The findings are significant because they suggest subclinical systemic vascular involvement in IBD that could enable noninvasive ocular biomarkers for disease monitoring and risk.

Bilican G, Akdağ İ, Özdemir HB et al. · Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver · (2026) · View on PubMed ↗ · Free PDF ↗

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Cancer genomics, signaling, and resistance mechanisms (incl. epigenetics/super-enhancers)

Spatiotemporal multiomics uncover tumor ecosystem dynamics during metastatic colonization.

This study integrated multimodal single-cell and spatial profiling from liver cancer mouse models and human metastases to track disseminated tumor cell (DTC) and microenvironment dynamics during metastatic colonization. It identified a residual quiescent Phgdh^high DTC population that survived innate immune clearance, transiently expanded in micrometastases, and shaped an immune-scarce niche via PHGDH-dependent, H3K27me3-mediated epigenetic silencing. These results highlight a specific metabolic-epigenetic program in DTCs that could be targeted to prevent or treat metastatic outgrowth.

Sun Y, Zhong Y, Liu S et al. · Science (New York, N.Y.) · (2026) · View on PubMed ↗

Adaptor-mediated rewiring of FLT3 signaling engages p38 MAPK to sustain gilteritinib resistance in acute myeloid leukemia.

This study investigated how FLT3 inhibitor resistance in FLT3-mutated acute myeloid leukemia (AML) is sustained by p38 MAPK signaling, focusing on gilteritinib-resistant cells. Using an unbiased kinome-wide CRISPR-Cas9 screen, it identified MAPK14 (p38α) as a prominent dependency in the resistant state and showed that adaptor-mediated rewiring of FLT3 signaling engages p38 MAPK to maintain gilteritinib resistance. The clinical significance is that targeting the FLT3→p38α axis may overcome or prevent resistance to gilteritinib in resistant AML.

Shen L, Fan J, Wang N et al. · Leukemia · (2026) · View on PubMed ↗

Super enhancer-driven transcriptional reprogramming promotes abiraterone resistance via neuroendocrine transition and ferroptosis evasion in castration-resistant prostate cancer.

The study investigated how super enhancer (SE)–driven transcriptional reprogramming promotes abiraterone resistance in castration-resistant prostate cancer (CRPC) cells, focusing on ELF3 and JUNB. Using chromatin immunoprecipitation sequencing and transcriptome profiling, it found aberrantly activated oncogenic SEs that upregulate the ELF3/JUNB axis, and reported that this axis promotes abiraterone resistance via ferroptosis evasion and a neuroendocrine transition program. These findings link SE activation to specific transcription factors and resistance biology, suggesting ELF3/JUNB and ferroptosis pathways as potential therapeutic targets to overcome abiraterone resistance.

Gao Y, Liu Y, Ye X et al. · Oncogene · (2026) · View on PubMed ↗ · Free PDF ↗

CXCR2-mediated metabolic interaction between prostate cancer cells and the immunosuppressive tumor microenvironment.

This study investigated how CXCR2-mediated metabolic interactions between prostate cancer cells and the immunosuppressive tumor microenvironment contribute to neuroendocrine prostate cancer (NEPC) immune evasion. Using prostate cancer cell lines and patient samples analyzed by immunohistochemistry, flow cytometry, PCR, western blotting, and mass spectrometry, the authors linked NEPC-associated immune features (e.g., high Treg/CD8+ ratio and altered M2/M1 TAM balance) with lipid accumulation in the tumor microenvironment. Scientifically, defining the CXCR2–metabolism–immunity axis could identify actionable targets to reverse immunosuppression and improve NEPC outcomes.

Sun Y, Jing J, Ren S et al. · Journal for immunotherapy of cancer · (2026) · View on PubMed ↗ · Free PDF ↗

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Cancer immunotherapy delivery platforms and tumor microenvironment engineering (nanotech/immune evasion)

Advances in improving cancer immunotherapy with nanotechnology: from smart nanoparticles to synergistic combination strategies.

This review evaluated how nanotechnology approaches can improve cancer immunotherapy, covering smart nanoparticle delivery systems and strategies for synergistic combinations to address tumor microenvironment–mediated immune evasion. It concludes that nanoparticles can enhance efficacy in solid tumors by improving tumor-site targeting, enabling controlled therapeutic release, and amplifying anti-tumor immune responses while potentially reducing systemic side effects. The significance lies in providing a translational framework for designing next-generation immunotherapy regimens that overcome common barriers such as low solid-tumor efficacy and toxicity.

Cho U, Pu J, Sharma A et al. · Molecular cancer · (2026) · View on PubMed ↗ · Free PDF ↗

Tumor cell-released autophagosome (TRAP) programs inflammatory CAFs to drive the immune-excluded TIME through C3a.

This study investigated how tumor cell-released autophagosomes (TRAPs) reprogram cancer-associated fibroblasts (CAFs) and shape the immune-excluded tumor immune microenvironment (TIME), using single-cell RNA sequencing and functional validation. TRAPs programmed inflammatory CAFs (iCAFs) that triggered cathepsin L-dependent cleavage of complement C3 into C3a via an HSP70–TLR4–MyD88–ERK/p38 pathway, and iCAF-derived C3a acted on tumor-associated macrophages (TAMs) to promote TAM accumulation in iCAF-rich stroma, limiting immune infiltration. The work links a tumor-derived autophagy product to a C3a-driven stromal immune exclusion mechanism, suggesting C3a/TLR4–MyD88 or cathepsin L as potential targets to improve immune checkpoint blockade responses.

Wang X, Wei Y, Wu C et al. · Cellular & molecular immunology · (2026) · View on PubMed ↗

An antibody-PROTAC conjugate targets BRD4/c-Myc/PD-L1 to enhance immunotherapy efficacy in triple-negative breast cancer.

This preclinical study developed an antibody-PROTAC conjugate (ASA) to enhance immunotherapy efficacy in triple-negative breast cancer (TNBC) by targeting BRD4 degradation in a TROP2-dependent manner. ASA linked a TROP2-specific antibody to a BRD4-degrading PROTAC and used TROP2-dependent endocytosis plus hypoxia-triggered linker cleavage to improve TNBC targeting and antitumor activity compared with the unconjugated PROTAC moiety, with stronger long-term immunological memory than an antibody-drug conjugate (abstract truncated before specifying the exact immunotherapy comparator). The significance is that targeted BRD4 degradation via an antibody-PROTAC platform may overcome delivery limitations and potentiate durable antitumor immunity in TNBC.

Gu Y, Li C, Zhao Y et al. · Cell reports. Medicine · (2026) · View on PubMed ↗ · Free PDF ↗

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Innate immunity, inflammasomes, and interferon signaling (PANoptosis/STING/cGAS/NLRs)

The IL-33-ILC2 axis: a key regulator of type 2 immunity in respiratory disease.

This narrative review examined the IL-33–ILC2 axis as a regulator of type 2 immunity in respiratory diseases, focusing on IL-33 biology and pulmonary group 2 innate lymphoid cells (ILC2s). It summarizes how IL-33 acts as an alarmin and how microenvironment-driven plasticity of ILC2 states sustains pathological airway inflammation. The review supports the IL-33/ILC2 pathway as a mechanistic therapeutic target for type 2–driven respiratory disorders.

Zhu Y, Zhang Y, Cheng R · Frontiers in immunology · (2026) · View on PubMed ↗ · Free PDF ↗

NLRC3 enhances antitumor immunity by specifically negatively regulating M-MDSCs in a STING-dependent manner.

This study examined how the intracellular NLR family member NLRC3 regulates antitumor immunity in the tumor immune microenvironment, focusing on monocytic myeloid-derived suppressor cells (M-MDSCs) and the STING signaling pathway. NLRC3 promoted antitumor immunity by specifically inhibiting M-MDSC infiltration and immunosuppressive function through negative regulation of STING, which reduced M-MDSC expression of PD-L1 and CCR2. These findings identify NLRC3–STING–PD-L1/CCR2 as a mechanistic axis that could be therapeutically targeted to relieve M-MDSC–mediated immune suppression in cancer.

Fu Y, Zhan X, Liu S et al. · Cellular & molecular immunology · (2026) · View on PubMed ↗

IFN-α and IFN-β inhibit NLRP1-driven PANoptosis.

This study examined regulation of NLRP1-driven PANoptosis in innate immune signaling, testing how LPS and type I interferons affect NLRP1-mediated caspase activation and IL-18 release. LPS inhibited NLRP1-mediated caspase activation, IL-18 release, and inflammatory cell death in a TRIF-dependent (not MyD88-dependent) manner requiring IRF3, and exogenous IFN-α or IFN-β similarly suppressed NLRP1-driven PANoptosis. These results define a TRIF–IRF3–type I IFN pathway that restrains NLRP1 inflammasome/PANoptosis, suggesting potential therapeutic modulation of type I IFN signaling in NLRP1-associated inflammatory diseases.

Sharma BR, Mummareddy H, Chadchan SB et al. · EMBO reports · (2026) · View on PubMed ↗ · Free PDF ↗

cGAS-mediated type I IFN signaling contributes to disease progression in drug-refractory epilepsy.

The study investigated cGAS-mediated type I interferon (IFN) signaling in drug-refractory epilepsy (DRE) by analyzing human DRE brain tissue and microglia, and by testing cGAS pathway activation in Dravet syndrome mouse models. The key finding is that microglial cGAS–STING signaling is activated in DRE, with DNA released from hyperexcitable neurons able to trigger microglial cGAS, and that genetic reduction and pharmacologic intervention (as described in the abstract) implicate this pathway in disease progression. This identifies a potentially targetable innate immune signaling axis for treating drug-refractory epilepsy.

Huang Y, Fan L, Wong MY et al. · Nature neuroscience · (2026) · View on PubMed ↗ · Free PDF ↗

IL-27 shapes NK cell heterogeneity and function in colorectal cancer.

This study examined how interleukin-27 (IL-27) regulates natural killer (NK) cell heterogeneity and function in colorectal cancer (CRC). The authors focused on the problem that tumor-infiltrating NK cells in CRC often show defective maturation and impaired effector activity, and they investigated IL-27’s role in shaping NK differentiation and antitumor responses in intestinal tumors. The work is significant because it may support IL-27–based strategies to restore NK cell function and strengthen innate immune control in CRC.

Lucantonio L, Kosta A, Schiano L et al. · Journal for immunotherapy of cancer · (2026) · View on PubMed ↗ · Free PDF ↗

Gasdermin E couples viral pyroptosis to lethal hepatic lipid accumulation.

This study investigated tick-borne orthonairovirus infection (including wetland virus, WELV) and its hepatic pathogenesis in patients and experimental models, focusing on gasdermin E (GSDME)-mediated pyroptosis. WELV induced GSDME-dependent pyroptosis in hepatocytes through mitochondrial and Fas-mediated apoptotic pathways, with viral RNA activating RIG-I/CASP3-mediated GSDME cleavage and viral nucleoprotein undergoing CASP3-dependent processing that formed a negative feedback loop (abstract truncated before detailing downstream lipid effects). The work is significant because it mechanistically links viral pyroptosis to lethal hepatic lipid accumulation and hyperinflammation, identifying GSDME/CASP3 pathways as potential therapeutic targets.

Wang C, Zheng X, Zhang Y et al. · Cell · (2026) · View on PubMed ↗

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Aging and senescence biology (SASP/mitochondria/lysosomes/senotypes)

Atlas of lysosomal aging reveals a metabolite signature shared with lysosomal storage disorders.

The authors constructed a multitissue lysosomal aging metabolite atlas using rapid lysosome isolation to profile metabolite changes during aging. Aged lysosomes accumulated glycerophosphodiesters and cystine in brain, heart, muscle, and white adipose tissue, with levels increasing linearly with age and resembling metabolite signatures causally linked to lysosomal storage disorders such as Batten disease and cystinosis. They further found caloric restriction mitigated these lysosomal changes in heart and muscle but not brain, linking lysosomal storage-disorder pathways to normal aging and suggesting tissue-specific intervention windows.

Puszynska AM, Nguyen TP, Cangelosi AL et al. · Science (New York, N.Y.) · (2026) · View on PubMed ↗

Targeting chaperone-mediated autophagy by nutritional interventions mitigates age-related cardiac fibrosis and diastolic dysfunction.

This study investigated how chaperone-mediated autophagy (CMA) regulates age-related cardiac fibrosis and diastolic dysfunction, focusing on fibroblast collagen synthesis and identifying SHMT2 as a CMA substrate in aging models. CMA was suppressed in the aging heart, promoting collagen overproduction, while enhancing CMA activity ameliorated fibrosis and diastolic dysfunction. These findings suggest that therapeutically boosting CMA (via pathways controlling SHMT2 turnover) could be a mechanistic strategy to treat or prevent age-associated heart failure.

Wang Z, Zhang Z, Ping Z et al. · Autophagy · (2026) · View on PubMed ↗

Senotypes define the diverse landscape of senescent cells.

This Nature Aging article proposed a framework to classify senescent cells by “senotypes,” integrating inputs, molecular features, and functional effects across cell types, species, senescence-inducing stresses, tissue context, and time. It argues that senescent states are heterogeneous and that experimentally defined senotypes can serve as reference categories for organizing and comparing senescence biology. The significance is providing a practical conceptual and experimental taxonomy that can accelerate mechanistic studies and therapeutic targeting of specific senescent cell states.

Schafer MJ, Basisty N, Hertzel AV et al. · Nature aging · (2026) · View on PubMed ↗

The glycolytic enzyme PGAM1 functions as a metabolic-autophagy checkpoint to coordinate growth and stress tolerance.

This study identified the glycolytic enzyme PGAM1 as a metabolic–autophagy checkpoint that coordinates growth and stress tolerance, using complementary yeast and mammalian systems to dissect mechanism. It reports that PGAM1 functions as a scaffold that recruits PI3K complex I to the phagophore assembly site to license autophagosome biogenesis, and that this autophagy-regulatory role is genetically essential and evolutionarily conserved independent of PGAM1’s catalytic activity. The significance is that it links glycolysis to autophagy initiation via a defined molecular checkpoint, suggesting a targetable integration point for improving stress resilience.

Zhang Y, Zhao P, Liang H et al. · Nature cell biology · (2026) · View on PubMed ↗

Mitochondrial metabolism and epigenetic crosstalk drive SASP.

This study investigated how mitochondrial metabolism interfaces with epigenetic regulation to drive the senescence-associated secretory phenotype (SASP) in senescent cells. It showed that upregulation of the mitochondrial pyruvate–citrate–acetyl-CoA axis increases acetyl-CoA availability to support histone acetylation at SASP genes, while mitochondrial DNA-driven innate signaling activates inflammatory transcription factors but requires acetyl-CoA for robust SASP transcription. These results connect mitochondrial metabolic state to epigenetic control of inflammatory secretory programs, suggesting metabolic or acetyl-CoA–linked interventions to dampen SASP-driven tissue dysfunction.

Martini H, Birch J, Marques FDM et al. · Nature · (2026) · View on PubMed ↗ · Free PDF ↗

Genomic, epigenomic and transcriptomic regulation of cellular senescence.

The review summarizes how genomic, epigenomic, and transcriptomic regulation shapes cellular senescence, a stress-induced state with stable cell-cycle arrest and a senescence-associated secretory phenotype (SASP). The key finding is that emerging technologies—new genetic models, single-cell and spatial multi-omics, and machine learning—are enabling improved senescence phenotyping, lineage tracing, and manipulation. This provides a roadmap for mechanistic discovery and therapeutic targeting of senescence across cancer, regeneration, antiviral defense, and age-related diseases.

Salekeen R, Kieu TL, Robbins PD et al. · Nature reviews. Genetics · (2026) · View on PubMed ↗

CRISPR screens identify targets to rescue age-related T cell dysfunction in cancer.

This study used single-cell CRISPR screens to identify regulators of CD8+ T cell persistence and effector differentiation in aged tumors, focusing on immune aging–driven dysfunction in cancer. It identified Dusp5 and Zfp219 as key regulators: Dusp5 loss increased ERK phosphorylation and globally enhanced proliferation, while Zfp219 deletion caused epigenetic reprogramming with increased cytotoxic molecule expression and improved antitumor immunity in aging (abstract truncated before reporting in vivo validation details). The significance is that it pinpoints actionable targets (DUSP5/ZNF219) to rescue age-related T cell dysfunction and potentially improve immunotherapy outcomes in older patients.

Chen ACY, Ji KY, Yerinde C et al. · Cell · (2026) · View on PubMed ↗

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Stem cell fate, tissue development, and organogenesis (incl. kidney atlas; differentiation dynamics)

Single-cell spatial mapping of human kidney development implicates the microenvironment in guiding cell fate decisions.

This study used single-cell RNA sequencing and spatial transcriptomics to map over 700,000 cells during human kidney development. Spatial analysis revealed previously unrecognized plasticity in which early-established cell fates can be altered later in development, implicating the microenvironment in guiding fate decisions. These findings provide a high-resolution human atlas that can inform how tissue context regulates differentiation and may improve strategies for regenerative kidney engineering.

Levinsohn J, Grindel S, Dumoulin B et al. · Nature genetics · (2026) · View on PubMed ↗

Intestinal stem cells count self-renewal divisions to switch multipotency.

The study investigated how Drosophila intestinal stem cells (ISCs) maintain a constant enteroendocrine cell (EEC) to enterocyte (EC) ratio during repeated divisions by controlling multipotency switching. The key finding is that ISCs intrinsically count self-renewal divisions via an epigenetic mechanism, switching fate after a defined number of self-renewing divisions. This reveals a quantitative, division-counting logic for stem-cell fate control that can stabilize tissue homeostasis under rapid turnover.

Tong D, Li A, Jiang Q et al. · Nature · (2026) · 1 citations · View on PubMed ↗

Physiological re-replication during human stem cell differentiation.

The study investigated whether physiological re-replication occurs during human stem cell differentiation, analogous to developmental gene amplification/re-replication in Drosophila. Using Rerep-Seq and fiber-combing, it demonstrated re-replication during differentiation of human myoblasts into myotubes and during mesenchymal stem cell differentiation into adipocytes, osteoblasts, chondrocytes, and neurons. This reframes re-replication as a normal differentiation-associated process in humans, informing how genome duplication dynamics relate to development versus tumor-associated instability.

Minet M, Beganovic A, Rishik S et al. · Cell death discovery · (2026) · View on PubMed ↗ · Free PDF ↗

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Neurocritical care monitoring and brain injury management (EVD/SAH/ICH)

Early Prediction of External Ventricular Drain Weaning Trial Outcome in Patients with SAH Based on ICP Pulse Morphological Similarity: A Single-Center Retrospective Cohort Analysis.

This single-center retrospective cohort study examined whether early prediction of external ventricular drain (EVD) weaning trial outcomes in nontraumatic subarachnoid hemorrhage (SAH) can be achieved using intracranial pressure (ICP) pulse morphological similarity. It found that similarity in mean ICP conditions is associated with predictable pulse morphology and that acute ICP dynamics changes distinguish successful versus failed weaning attempts among 588 SAH patients. The significance is a more dynamic, physiology-informed approach to forecasting EVD weaning outcomes, potentially improving neurocritical care decision-making.

Dong K, Sadan O, Horton P et al. · Neurocritical care · (2026) · View on PubMed ↗

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Cardiometabolic risk and cardiovascular outcomes (Lp(a), cardiorenal syndromes, AKI prevention)

Dapagliflozin and Acute Kidney Injury Following Cardiac Surgery: A Randomized Clinical Trial.

This multicenter, double-blind, placebo-controlled randomized clinical trial studied whether initiating dapagliflozin 1 day before elective cardiac surgery reduces postoperative acute kidney injury (AKI) in adults undergoing cardiac surgery in the Netherlands. Dapagliflozin was tested as a preventive strategy for AKI measured at 7 days after surgery, compared with placebo. If effective, this would support perioperative use of the SGLT2 inhibitor dapagliflozin to reduce AKI risk after cardiac surgery, a common and clinically important complication.

Oosterom-Eijmael MJP, Hulst AH, de Oliveira NPM et al. · JAMA · (2026) · 1 citations · View on PubMed ↗

Glucagon-Like Peptide-1 Receptor Agonist Therapy and Neurocognitive Outcomes in Medically Managed Idiopathic Intracranial Hypertension: A Propensity Score-Matched Cohort Study.

The study evaluated whether glucagon-like peptide-1 receptor agonist (GLP-1RA) therapy is associated with neurocognitive outcomes in adults with medically managed idiopathic intracranial hypertension (IIH). Using the TriNetX US Collaborative Network, it conducted propensity score matching of adults with a first IIH diagnosis (2016–2025), comparing GLP-1RA initiation within 1 month before to 3 months after diagnosis versus non-users while excluding patients with CSF diversion, venous sinus stenting, or pre-existing cognitive/fatigue diagnoses (outcome results truncated). This addresses a key clinical uncertainty about cognitive effects of GLP-1RA use in IIH and can inform risk–benefit decisions for therapy selection.

Ahmed S, Dhaduk V, Kakadiya J et al. · AJNR. American journal of neuroradiology · (2026) · View on PubMed ↗ · Free PDF ↗

Lipoprotein(a) and aortic diseases: Epidemiological evidence from observation to causation.

This study analyzed whether genetically determined lipoprotein(a) [Lp(a)] is associated with and potentially causally related to aortic aneurysm and dissection (AA/AD) and its subtypes using UK Biobank participants. In a prospective cohort of 312,332 individuals, the authors used Kaplan–Meier curves, Cox regression, and Fine–Gray competing-risk models to evaluate incident AA/AD across Lp(a) levels and applied two-sample Mendelian randomization to assess causality. Clinically, establishing an Lp(a)–AA/AD causal link would support risk stratification and motivate targeted Lp(a)-lowering interventions to prevent fatal aortic events.

Xia D, Zhang L, Fang J et al. · Journal of clinical lipidology · (2026) · View on PubMed ↗

Acute cardio-renal and Reno-Cardiac syndromes in critical care.

This narrative review examined acute cardio-renal and reno-cardiac syndromes in critical care, focusing on the ICU-relevant cardiorenal syndrome types 1 and 3. It summarizes evidence from human and animal studies (2000–Oct 2025) to clarify mechanisms, clinical presentation, and management considerations, emphasizing that mortality exceeds 50% when renal replacement therapy is required. The review is clinically important because it consolidates current understanding to improve recognition and treatment decisions for high-risk CRS phenotypes in ICU patients.

Girombelli A, Longhitano Y, Vetrone F et al. · European journal of internal medicine · (2026) · View on PubMed ↗ · Free PDF ↗

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Clinical trial design, evidence synthesis, and treatment de-escalation (incl. network meta-analyses/consensus)

International advocacy for ketogenic diet research in schizophrenia: insights from a public petition.

This study analyzed an international Change.org public petition advocating for resumption of a halted randomized blinded inpatient ketogenic diet trial in people with schizophrenia, using quantitative signature/comment metrics and qualitative text mining. The petition garnered 21,637 signatures and 1,105 comments across 151 countries, with comments analyzed using top-down theme consensus coding and Latent Dirichlet Allocation (LDA) topic modeling. The findings highlight public demand and thematic priorities that could inform the design and ethical justification of future ketogenic diet research in schizophrenia.

Murray SL, Roche DJO, Palmer CM et al. · Frontiers in public health · (2026) · View on PubMed ↗ · Free PDF ↗

Efficacy of first-line treatment in driver gene-negative non-small cell lung cancer with liver metastases: a Bayesian network meta-analysis.

This Bayesian network meta-analysis studied first-line treatment efficacy and prognostic factors in driver gene-negative non-small cell lung cancer (NSCLC) patients with liver metastases by comparing chemotherapy, immunotherapy, and combination regimens across 20 randomized controlled trials. It used R (v4.2.3) and RevMan (v5.4) to rank relative treatment effectiveness and identify survival-associated factors in this specific molecularly defined population. Scientifically and clinically, the network approach aims to identify the most effective first-line strategy for driver gene-negative NSCLC with liver metastases where optimal sequencing remains uncertain.

Wu W, Guo X, Dong X et al. · Frontiers in immunology · (2026) · View on PubMed ↗ · Free PDF ↗

De-escalation trials in multiple myeloma: past, present and future.

The article reviewed de-escalation strategies in multiple myeloma, focusing on how to maintain durable disease control while reducing toxicity and treatment burden as effective agents and immunotherapies move earlier. The key finding is synthesis of emerging evidence for multiple de-escalation approaches, including dose/schedule modification, withdrawal of individual agents from multidrug regimens, and fixed-duration treatment concepts. This informs future trial design and clinical decision-making to balance efficacy and tolerability in MM treatment sequencing.

Mian H, Costa LJ, Mohty M et al. · Nature reviews. Clinical oncology · (2026) · View on PubMed ↗

Efficacy, acceptability, and related outcomes of pharmacological interventions for acute bipolar mania: a systematic review and dose-related network meta-analysis across different age groups.

This systematic review and dose-related network meta-analysis compared pharmacological interventions for acute bipolar mania across different age groups using randomized controlled trials and dose information. The key finding was the comparative efficacy/response/acceptability of treatments (and dose effects) for acute manic symptom change, alongside tolerability, remission, and adverse event rates. This is clinically significant because it can inform age- and dose-specific treatment selection for acute bipolar mania where comparative evidence is fragmented.

Fornaro M, Di Lorenzo C, Kishi T et al. · Journal of affective disorders · (2026) · View on PubMed ↗

Psoriasis.

This narrative review summarized psoriasis as a chronic immune-mediated disease with diverse clinical phenotypes and substantial comorbidity and psychosocial burden. The key finding is that psoriasis spans a spectrum of skin and musculoskeletal manifestations driven by shared genetic, environmental, and immunological mechanisms with psoriatic arthritis. This is clinically significant because it consolidates current understanding of phenotypes and associated risks to support more comprehensive patient management.

Eder L, Perez-Chada L, Liao W et al. · Lancet (London, England) · (2026) · View on PubMed ↗

Local management of second ipsilateral breast cancer events after primary breast-conserving therapy: an international Delphi consensus.

This international Delphi consensus project studied expert agreement on patient selection and local treatment strategies for second ipsilateral breast cancer events after primary breast-conserving therapy, using a two-round Delphi process with 36 panellists (radiation oncologists, breast surgeons, a plastic surgeon, and medical physicists). The key output was predefined consensus (≥75% agreement) on how to manage second iBCEs locally, collating existing evidence into guidance (abstract truncated before listing specific consensus recommendations). The consensus is significant because it standardises decision-making for a controversial clinical scenario where evidence is heterogeneous.

Hannoun-Levi JM, Margenthaler JA, Anderson B et al. · The Lancet. Oncology · (2026) · View on PubMed ↗

Cryobiopsy versus conventional bronchoscopic sampling for peripheral pulmonary lesions (Cryo-RCT): an open-label, parallel-group, randomised trial.

This open-label, parallel-group, randomised Cryo-RCT studied stand-alone cryobiopsy using single-use cryoprobes versus conventional bronchoscopic sampling for peripheral pulmonary lesions in adults (≥18 years) with lesions ≤30 mm visualised by radial endobronchial ultrasound across six Asian centres. The trial tested whether cryobiopsy improves diagnostic yield during bronchoscopy (abstract truncated before reporting the diagnostic-yield results). If cryobiopsy is superior, it could change diagnostic workflows for peripheral lung lesions by increasing tissue adequacy and reducing nondiagnostic procedures.

Matsumoto Y, Nakai T, Park D et al. · The Lancet. Respiratory medicine · (2026) · View on PubMed ↗

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Microbiome–immunity/metabolism interactions (bile acids, dysbiosis, microbiota effects)

Dietary arginine drives codon-dependent MHC class I translation and improves immunity in colon tumorigenesis and respiratory viral infection.

Researchers examined how dietary arginine availability affects colon tumorigenesis and antiviral immunity, focusing on arginine tRNA-dependent control of major histocompatibility complex class I (MHC-I) translation. Extracellular arginine restriction repressed specific arginine tRNAs, leading to codon-usage–dependent suppression of MHC-I translation and antigen presentation, which reduced anti-viral immunity against influenza and SARS-CoV-2 and increased colon tumorigenesis. The work suggests that manipulating arginine/codon translation could modulate immune surveillance and therapeutic responses in cancer and infection.

Wu Q, Seydlitz LM, Iakimov V et al. · Cell · (2026) · View on PubMed ↗

Gut microbiota restricts intestinal lipid uptake via modulation of bile phosphatidylcholine metabolism in mice.

This study used stable isotope-labeled tracers in gnotobiotic mouse models to determine how gut microbiota affects dietary intestinal lipid uptake and bile phosphatidylcholine metabolism. Microbial colonization restricted intestinal lipid absorption, with microbiota-colonized mice showing up to 12-fold higher labeled lipid content in gut contents than germ-free animals, and mechanistic modeling plus lipidomics/proteomics indicated that gut microbes activate Myd88 signaling to downregulate hepatic Cyp7b1 activity. These results clarify a microbiota–Myd88–Cyp7b1 regulatory pathway controlling bile lipid metabolism and intestinal lipid uptake, informing strategies to modulate metabolic disease risk.

Brunner S, Plagge J, Zimmermann-Kogadeeva M et al. · Nature microbiology · (2026) · View on PubMed ↗ · Free PDF ↗

Subclinical cholestasis is a hallmark of gut dysbiosis causing resistance to cancer immunotherapy.

This study investigated how gut dysbiosis and antibiotic-associated changes in bile acid metabolism affect cancer immunotherapy resistance in patients and mice, focusing on secondary bile acids and the ileal mucosal addressin cell adhesion molecule 1 (MAdCAM-1) axis. The authors found that antibiotics or Enterocloster-associated dysbiosis caused loss of secondary bile acids (including deoxycholic acid) and accumulation of tauro-conjugated primary bile acids, and that interventions such as fecal microbial transplantation (FMT), the ileum-specific FXR agonist fexaramine, or glycodeoxycholic acid (GDCA) could compensate (abstract truncated before detailing the immunotherapy outcome). The work is significant because it links subclinical cholestasis/gut dysbiosis to immunotherapy resistance and suggests bile-acid-targeted strategies to restore antitumor immunity.

Mallard de La Varende AL, Tian AL, Thomas S et al. · Cancer cell · (2026) · View on PubMed ↗ · Free PDF ↗

Bile acids in cancer: From metabolism to immunomodulation.

This article is a mechanistic review that studied (synthesised) how bile acids function as immunometabolic signals across cancer, integrating host metabolism, microbial ecology, and tumor immunity. It highlights that altered bile acid profiles correlate with tumor progression, immune tone, and immunotherapy responsiveness, and that bile acids can either support immune surveillance or drive immune escape by reshaping antigen priming, lymphocyte fitness, myeloid suppression, and immune cell trafficking depending on bile acid species and context (abstract truncated). The significance is that it frames bile acids as potential biomarkers and therapeutic targets to modulate tumor immune responses.

Fang Q, Schneider KM · Immunity · (2026) · View on PubMed ↗ · Free PDF ↗

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Microbial defense and phage biology (restriction/counter-defense/STAND NTPases)

Phage hijacks host phosphorothioate DNA modification machinery to circumvent bacterial Ssp defences.

This study characterized a phage counter-defense mechanism against the bacterial Ssp system by identifying PptA, a phage-encoded [4Fe-4S] cluster protein that hijacks host phosphorothioate (PT) DNA modification machinery. PptA hijacked cognate IscS homologues to assemble a streamlined PT modification system, and robust PptA expression during infection drove sufficient PT incorporation into the phage genome via sulfur transfer within the IscS–PptA complex, enabling molecular mimicry of host PT-modified DNA. The findings reveal how phages exploit host PT modification enzymes to evade Ssp restriction, providing mechanistic insight into bacterial defense and phage evasion strategies.

Wang Y, Yang H, Jiang L et al. · Nature microbiology · (2026) · View on PubMed ↗

Diverse bacterial pattern recognition receptors sense the core phage proteome.

This study performed a systematic phylogenetic and functional analysis of bacterial and archaeal STAND NTPases to determine how diverse pattern recognition receptors detect phage proteins. It identified at least 90 structurally distinct STAND families linked to antiviral defense and showed that the Avs7 family recognizes the major capsid protein (MCP) of tailed phages, supported by cryogenic electron microscopy structures of Salmonella STAND proteins bound to phage MCP. These findings expand the repertoire of intracellular bacterial antiviral sensors and provide structural targets for engineering or modulating bacterial immunity.

Lee H, Luengo-Woods S, Zhang J et al. · Nature · (2026) · View on PubMed ↗

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Protein engineering and computational biology (AI design; phosphorylation prediction; nanopore/proteomics methods)

Enabling sustainable supply of the essential cancer medicines etoposide and teniposide in yeast.

This work engineered yeast to biosynthesize podophyllotoxin-type aryltetralin lignan precursors for the anticancer drugs etoposide and teniposide. By identifying key glycosyltransferases and performing more than 60 genetic edits involving 45 heterologous enzymes, the authors enabled sustainable production of these drug precursors rather than relying on extraction from the endangered plant Sinopodophyllum hexandrum. The approach could reduce supply risk and environmental impact for essential chemotherapy medicines.

Shen S, Hu X, Li D et al. · Science (New York, N.Y.) · (2026) · View on PubMed ↗

A global view of human centromere variation and evolution.

This study assembled and analyzed 2,110 centromeres from diverse individuals spanning 5 continental and 28 population groups to map human centromere sequence variation and evolutionary patterns. The authors identified 226 centromere haplotypes and 1,870 α-satellite higher-order repeat variants, providing a global catalog of centromere diversity. This large-scale centromere variation map improves understanding of chromosome segregation evolution and supports more accurate genomic analyses in diverse human populations.

Gao S, Oshima KK, Chuang SC et al. · Nature · (2026) · View on PubMed ↗

Miniaturizing and modifying natural proteins with Raygun.

This study introduced Raygun, a generative AI framework, to miniaturize, modify, and augment natural proteins using probabilistic sequence encoding derived from protein language model embeddings. Raygun enables large-scale function-preserving protein sequence modifications by leveraging per-residue representations to generate new sequences from existing templates. The approach provides a practical computational route to engineer proteins beyond conventional design methods, accelerating protein engineering for research and biotechnology.

Devkota K, Shonai D, Mao J et al. · Nature · (2026) · 1 citations · View on PubMed ↗ · Free PDF ↗

Sequential reading of a stepwise-shortened peptide immobilized on nanopore.

The study developed a nanopore peptide sequencing method using transient pore analyte looping (tPAL) with an engineered Mycobacterium smegmatis porin A (MspA) nanopore dual-modified with nickel-ion-bound nitrilotriacetic acid (NTA) to enable sequential reading of stepwise-shortened immobilized peptides. The key finding is that tPAL generates narrowly distributed, sequence-dependent nanopore events that support accurate decoding of peptide sequences. This provides a scalable route to nanopore-based proteomics by improving event consistency for sequential peptide readout.

Chen J, Zhang H, Wang K et al. · Nature · (2026) · View on PubMed ↗

An AI-enabled structural atlas decodes kinase specificity across the human proteome.

The study developed KinoPlex, an AI-enabled computational framework integrating ~20,000 AlphaFold protein structure models with kinase recognition motifs to predict phosphorylation potential and kinase specificity across the human proteome. It identified ~567,000 serine/threonine/tyrosine residues as structurally phospho-competent and ~250,000 high-confidence kinase–substrate phosphorylation candidates using positive-unlabeled transfer learning and kinase position-specific scoring matrices. This provides a proteome-wide, structure-informed map of kinase specificity that can prioritize experimental phosphorylation targets and improve mechanistic interpretation of signaling networks.

Vanderwall DR, Huttlin EL, Mintseris J et al. · Nature biotechnology · (2026) · View on PubMed ↗

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Structural biology and imaging methods (cryo-EM/tomography/super-resolution/ExM)

Capless self-amplifying mRNA vaccine induces dose-sparing protective immunity against HPAI clade 2.3.4.4 H5 virus in mice.

This mouse study developed a capless self-amplifying mRNA (CLsamRNA) vaccine platform using a Coxsackievirus B5 replicon with IRES-mediated cap-independent translation to address 5’ capping manufacturing challenges. In mice, the CLsamRNA vaccine induced dose-sparing protective immunity against HPAI clade 2.3.4.4 H5 virus, with rapid early antigen expression and RNA amplification kinetics. The work supports capless samRNA as a potentially scalable, lower-dose vaccine strategy for emerging influenza threats.

Kim BK, Park JH, Choi WS et al. · Molecular therapy : the journal of the American Society of Gene Therapy · (2026) · View on PubMed ↗ · Free PDF ↗

In situ structure of the poxvirus portal complex.

This study determined the in situ structure of the poxvirus portal complex in vaccinia virus using cryo-electron tomography with subtomogram averaging and structure prediction. The hexameric portal complex was resolved as a pore spanning the core wall composed of E8, E6, and L3 proteins. This structural definition of a conserved poxvirus assembly component provides a foundation for mechanistic understanding of viral genome packaging and for antiviral target development.

Calcraft T, Hernandez-Gonzalez M, Way M et al. · Nature · (2026) · View on PubMed ↗ · Free PDF ↗

In situ structures of plant photosystem supercomplexes.

The study used in situ cryo-electron microscopy to image Oryza sativa (rice) chloroplasts and determine native structures of photosystem I/II supercomplexes in their thylakoid membrane environment. The key finding was resolution of a C2S2M2L4-type PSII–LHCII supercomplex containing four LHCII antenna trimers that were not retained in purified preparations. This advances understanding of how PSI and PSII are organized in vivo and how native antenna architecture shapes excitation energy transfer.

Li J, Elias E, Zhang K et al. · Nature · (2026) · View on PubMed ↗ · Free PDF ↗

Resolving endogenous protein organization in cells with nanometer resolution.

The study introduced an expansion microscopy (ExM) workflow using double-homogenized hydrogels to enable nanometer-resolution imaging of endogenous multiprotein organization with dSTORM (direct stochastic optical reconstruction microscopy). By increasing effective labeling density ~4-fold, it resolved ~8 nm spacing between neighboring α-tubulin molecules in microtubules and improved visualization of endogenous protein architectures (polyhedral lattice details truncated). This advances the ability to map endogenous protein complex organization at near-molecular resolution in cells, overcoming labeling constraints that limit super-resolution localization precision.

Eilts J, Jungblut M, Helmerich DA et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

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Reproductive biology and developmental genetics (oocyte/meiotic fidelity; plant chirality)

Supergene control of chiral development in mirror-image flowers.

Researchers investigated genetic control of chiral organ development in mirror-image butterfly lilies, identifying a hemizygous supergene containing two candidate causal loci, MIR156-R and YUCCA-R. They found that female and male organ orientation is governed by genetically controlled chirality combined with gravitropism, aligning left/right placement relative to an external reference axis. This provides a mechanistic framework for how supergenes coordinate complex, directional morphological traits in plants.

Xue H, Saltini M, Illing N et al. · Science (New York, N.Y.) · (2026) · View on PubMed ↗

Insufficiency of cohesin regulatory protein PDS5B triggers meiotic failure and aneuploidy in oocytes during advanced maternal aging.

The study examined how age-related insufficiency of the cohesin regulatory protein PDS5B affects oocyte meiotic maturation, focusing on meiotic failure and aneuploidy during advanced maternal aging. PDS5B declined with age and was found to localize to spindle poles during metaphase stages, where it promoted spindle pole formation through a noncanonical role independent of its cohesion function. These findings identify PDS5B as a mechanistic driver of age-associated chromosome segregation errors and potential target for improving reproductive health.

Zhang Y, Bai J, Li N et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗

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Oncology clinical therapeutics in specific cancers (breast/prostate/AML/NSCLC/HCC/RCC/UC/CRPC)

Phase I Trial of GPC3-Targeted TCR Fusion Construct, CT0180, in patients with Advanced Hepatocellular Carcinoma.

This phase I, open-label dose-escalation trial tested the GPC3-targeted TCR fusion construct CT0180 in patients with advanced GPC3-positive hepatocellular carcinoma after fludarabine/cyclophosphamide lymphodepletion. The study evaluated safety and preliminary efficacy of CT0180 designed to integrate into the native TCR complex via a GPC3-targeted single-chain variable fragment linked to CD3ε to trigger full TCR signaling upon GPC3 binding. If effective and tolerable, CT0180 would represent a tumor-specific T-cell therapy strategy for GPC3-high HCC with limited options after standard treatments.

Sun X, Gao W, Shou C et al. · Clinical cancer research : an official journal of the American Association for Cancer Research · (2026) · View on PubMed ↗

Transarterial Chemoembolization Plus Thermal Ablation in Unresectable Hepatocellular Carcinoma: The Phase 3 TORCH Randomized Clinical Trial.

In the open-label phase 3 TORCH randomized clinical trial, investigators compared transarterial chemoembolization (TACE) plus subsequent thermal ablation versus TACE alone in patients with liver-confined unresectable hepatocellular carcinoma (Barcelona Clinic Liver Cancer stage B). The trial was designed to test whether adding thermal ablation improves survival and clinical outcomes compared with standard TACE. If positive, this strategy could change standard-of-care for unresectable stage B HCC by improving outcomes beyond TACE alone.

Lyu N, Yi JZ, Wu XT et al. · JAMA oncology · (2026) · View on PubMed ↗

Cemiplimab and Fianlimab With Neoadjuvant Chemotherapy in Early-Stage High-Risk ERBB2-Negative Breast Cancer: The I-SPY2 Randomized Clinical Trial.

This randomized I-SPY2 platform trial evaluated whether adding dual immune checkpoint blockade—cemiplimab (anti–PD-1) and fianlimab (anti–LAG-3)—to neoadjuvant chemotherapy improves outcomes in early-stage high-risk ERBB2-negative breast cancer. The study tested the combination in a biomarker-driven adaptive neoadjuvant setting to enhance response rates beyond chemotherapy alone. Positive results would support a new immunotherapy regimen for ERBB2-negative patients at high risk of recurrence.

Isaacs C, Nanda R, Yau C et al. · JAMA oncology · (2026) · View on PubMed ↗

Efgartigimod in the treatment of immune checkpoint inhibitor-related myasthenia gravis -myositis overlap syndrome: a case report.

This case report described the use of efgartigimod, an FcRn blocker, for immune checkpoint inhibitor (ICI)-related myasthenia gravis (MG)–myositis overlap syndrome in a patient receiving PD-1/PD-L1 inhibitor therapy. The report addresses an investigational approach in a context where standard care typically involves IVIG, plasma exchange, and high-dose corticosteroids. If supported by additional cases, efgartigimod could become a targeted alternative for refractory ICI-related MG–myositis overlap syndromes.

Li K, Hu J, Gan Z et al. · Frontiers in immunology · (2026) · View on PubMed ↗ · Free PDF ↗

Genomic Determinants of Lethality and Therapeutic Vulnerability in Castration-Resistant Prostate Cancer.

This preprint study analyzed genomic determinants of lethality and therapeutic vulnerability in metastatic castration-resistant prostate cancer (mCRPC) using multi-institutional cohort data. It identified androgen-regulated MYC fusions as potent drivers of early progression and validated TP53, RB1, and CDKN1B alterations as the strongest genetic predictors of poor survival, with mechanistic links including CDKN1B loss promoting an AR-positive state. These results suggest that specific genomic alterations (MYC fusions, TP53/RB1/CDKN1B) could stratify prognosis and guide targeted therapeutic vulnerability discovery in mCRPC.

Rebernick RJ, Hammer L, Gondal M et al. · bioRxiv : the preprint server for biology · (2026) · View on PubMed ↗ · Free PDF ↗

Harnessing immunity against breast cancer: from checkpoints to cell therapies.

This review synthesizes evidence for immunotherapy in breast cancer, focusing on immune checkpoint inhibitors (PD-1/PD-L1) and multiple adoptive cell therapy platforms (e.g., CAR-T, CAR-NK, CAR-M, TIL, TCR-T, CIK) across patient populations with different breast cancer subtypes. It highlights that while PD-1/PD-L1 blockade can benefit certain triple-negative breast cancer subgroups, broader use is constrained by intrinsic resistance, an immunosuppressive tumor microenvironment, and treatment-related adverse effects. The review’s significance is in mapping current and emerging strategies to overcome resistance mechanisms and improve the clinical applicability of breast cancer immunotherapy.

Mussa A, Hamid M, Talib M et al. · Journal of translational medicine · (2026) · View on PubMed ↗ · Free PDF ↗

DLL3-Targeted Strategies in Advanced Prostate Cancer: Current Evidence and Future Perspectives.

This article reviews DLL3-targeted therapeutic strategies in advanced prostate cancer, particularly in aggressive-variant prostate cancer (AVPC) states that are neuroendocrine-like and often androgen receptor (AR)-indifferent or AR-independent. It summarizes current evidence and future directions for targeting DLL3 in contexts such as neuroendocrine prostate cancer (NEPC), including treatment-emergent NEPC (t-NEPC) and de novo NEPC. The clinical significance is that DLL3 may provide a actionable target for lethal AR-independent prostate cancer phenotypes where standard AR signaling inhibition fails.

Pecoraro G, De Giorgi A, Montelatici G et al. · Drugs · (2026) · View on PubMed ↗

Efficacy of Lenvatinib as Subsequent Therapy After Combination Immune Checkpoint Inhibitors for Unresectable Hepatocellular Carcinoma.

This multicenter study assessed whether lenvatinib (LEN) is effective as subsequent therapy after progression on durvalumab plus tremelimumab (DT) in unresectable hepatocellular carcinoma (u-HCC). Patients receiving LEN after DT progression (2nd-line LEN following DT) were compared with those receiving LEN as first-line therapy (1st-line LEN), with disease control rate (DCR) and objective response rate (ORR) as primary endpoints. The results are significant because they address an evidence gap for sequencing immunotherapy (DT) followed by VEGF-targeted therapy (LEN) in real-world u-HCC management.

Uchihara N, Tamaki N, Marusawa H et al. · Anticancer research · (2026) · View on PubMed ↗

Pembrolizumab Plus Lenvatinib in Metastatic Renal Cell Carcinoma: Real-world Prognostic Factors.

This retrospective Japanese multicenter cohort study evaluated real-world outcomes and prognostic factors for pembrolizumab plus lenvatinib in metastatic renal cell carcinoma (mRCC). Among 160 patients treated first-line with pembrolizumab plus lenvatinib, the authors measured objective response rate (ORR), disease control rate (DCR), progression-free survival (PFS), overall survival (OS), treatment exposure, and adverse events, and analyzed clinicopathological factors associated with PFS. Clinically, identifying predictors of PFS can help tailor first-line immunotherapy–TKI use and improve patient selection in mRCC.

Yamashita S, Yamasaki T, Ueda K et al. · Anticancer research · (2026) · View on PubMed ↗

Effectiveness and Safety of Enfortumab Vedotin Plus Pembrolizumab for Patients Aged 80 Years and Older With Metastatic Urothelial Carcinoma: A Multicenter Retrospective Study.

This multicenter retrospective study assessed the effectiveness and safety of enfortumab vedotin plus pembrolizumab (EVP) in very elderly patients with metastatic urothelial carcinoma (mUC). In 60 Japanese patients treated at six institutions, outcomes were compared between those aged ≥80 years and those <80 years, with progression-free survival (PFS) and overall survival (OS) as primary endpoints. The findings are important for guiding treatment decisions and expectations for EVP in patients who are often underrepresented in clinical trials.

Kobari Y, Nakajima N, Saito A et al. · Anticancer research · (2026) · View on PubMed ↗

Deramiocel heart-derived cellular therapy in advanced Duchenne muscular dystrophy (HOPE-3): a phase 3, randomised, double-blind, placebo-controlled trial.

This phase 3, multicentre, randomised, double-blind, placebo-controlled trial studied deramiocel (human allogeneic cardiosphere-derived cells) in participants aged ≥10 years with advanced Duchenne muscular dystrophy (DMD). Deramiocel infusion was assessed for efficacy and safety to determine whether it improves cardiac and skeletal muscle outcomes compared with placebo, building on prior HOPE-1/HOPE-2 signals (abstract truncated before reporting results). If effective, deramiocel would represent a clinically meaningful allogeneic cell therapy strategy for advanced DMD cardiomyopathy and myopathy.

McDonald CM, Villa C, Soslow JH et al. · Lancet (London, England) · (2026) · View on PubMed ↗ · Free PDF ↗

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Generated automatically on July 31, 2026 from PubMed’s trending articles. Summaries are AI-generated; always consult the original publication for clinical or research decisions.