PubMed Trending Research Digest — May 15, 2026

Automated digest · 97 articles · 15 research areas · May 15, 2026

Overview

This week’s digest is dominated by mechanistic links between cellular state and disease—especially where signaling, genome regulation, and tissue microenvironments converge. In neurovascular biology, endothelial CD98 heavy chain emerges as a CNS-specific gatekeeper for angiogenesis and BBB stability, with loss leading to hemorrhagic failure. In aging and neurodegeneration, multiple studies converge on impaired proteostasis/autophagy and RNA/protein homeostasis: an “RNA imbalance” phenotype in senescence, reduced ULK1 in aging/Alzheimer’s with therapeutic rescue in models, and S-acylation control of TDP-43 condensation in ALS. Together these highlight a recurring theme: restoring the fidelity of intracellular regulation (RNA metabolism, autophagy/mitophagy, or protein phase behavior) may be as important as targeting downstream pathology.

Cancer and immune regulation form the second major thread, spanning both tumor-intrinsic and systemic dimensions. Several studies connect microenvironmental context to immune outcomes: E-cadherin loss in invasive lobular breast cancer reshapes stromal fate and spatial TIL organization; RAB5A-driven tumor fluidization triggers mitochondrial DNA-dependent immune signaling; and gut microbiota metabolite DCA promotes an immunosuppressive breast tumor niche via FXR/NF-κB/IL-6. Immunotherapy strategies also feature prominently, from BET inhibition to reverse T-cell exhaustion metabolic/epigenetic dysfunction, to mRNA-LNP delivery of immune-remodeling programs (IRF8/NIK) that prime durable antitumor CD8 responses. In parallel, targeted protein degradation and ubiquitin-system tools (dual-E3 monovalent degraders; PROTAC vs inhibition divergence for USP7) underscore a methodological push toward more precise causal perturbations.

Finally, translational and clinical decision-making appears across diverse areas: consensus and trial data guide sequencing around CAR-T, bridging therapy, and second-line strategies; obstetric and guideline studies refine prevention and risk stratification; and gene-editing work continues to expand both efficacy and safety monitoring (including rare AAV integration events). Across these domains, the dominant pattern is clear: better mechanistic understanding is increasingly being paired with scalable biomarkers, refined trial designs, and targeted interventions—aiming to move from correlation to causation and from broad treatment to stratified, context-aware care.

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CNS vascular biology & blood-brain barrier integrity

Shared proteomic landscape between arteriosclerosis and cardiovascular endpoints: a Mendelian randomization and observational study integrating AlphaFold3 for structural prediction.

This study integrated plasma proteomics with Bayesian colocalization, Mendelian randomization (MR), and AlphaFold3 structural prediction to identify shared molecular pathways between arteriosclerosis and cardiovascular endpoints. Using cis-pQTLs for 5,813 proteins from UK Biobank (n=54,219) and deCODE (n=35,559), it mapped which proteins are causally associated with arteriosclerotic/atherosclerotic markers across vascular beds and distinguished shared versus distinct mechanisms. The scientific significance is that combining MR with structural modeling helps prioritize actionable proteins and clarifies whether arteriosclerosis and atherosclerosis share causal targets.

Huang J, Meena D, Achtari M et al. · Cardiovascular research · (2026) · View on PubMed ↗

Raf-like protein kinase heterocomplexes directly regulate the plant plasma membrane H+-ATPase.

This Science study investigated how Raf-like protein kinase heterocomplexes regulate the plant plasma membrane H+-ATPase (AHA) in Arabidopsis. It found that C5-Raf (C5-Raf Raf36/HT1) and C7-Raf form a heterocomplex that phosphorylates the conserved Thr881 site to activate PM H+-ATPases, and that this sequential phosphorylation mechanism is conserved across plant lineages. The scientific significance is that it reveals a conserved kinase-based control system for proton pump activation, linking specific Raf-like kinases to plant growth regulation.

Takase H, Nagano A, Yamauchi S et al. · Science (New York, N.Y.) · (2026) · View on PubMed ↗

Robotic Pancreatoduodenectomy Carries Greater Risk of Morbidity after Conversion than Laparoscopy: A Propensity Score-Matched Analysis in the E-MIPS Registry.

This propensity score-matched multicenter analysis from the E-MIPS registry compared outcomes after conversion to open surgery during robotic pancreatoduodenectomy (RPD) versus laparoscopic pancreatoduodenectomy (LPD) in European patients (Jan 2019–2024). The key finding was that conversion during RPD carried greater postoperative morbidity than conversion during LPD, with additional stratification by conversion urgency (pre-emptive vs urgent). Clinically, this supports careful risk assessment and operative planning when choosing RPD versus LPD approaches, particularly regarding the likelihood and timing of conversion.

Bertrand T, Baggerman van Houweninge CE, Bjornsson B et al. · Annals of surgery · (2026) · View on PubMed ↗

White matter micro- and macrostructure brain charts for the human lifespan.

This Nature study developed normative “white matter micro- and macrostructure” brain charts across the human lifespan to provide reference standards for structural white-matter biomarkers. The key finding was the creation of readily usable lifespan charts that enable clinicians and researchers to translate white-matter imaging measures into age-relative deviations analogous to growth charts. Scientifically, this provides a foundational tool for interpreting white-matter structural changes in neurodevelopmental, psychiatric, and neurological disorders.

Kim ME, Gao C, Ramadass K et al. · Nature · (2026) · View on PubMed ↗ · Free PDF ↗

Sustaining microglial reparative function enhances stroke recovery.

The study examined how microglial reparative function changes after stroke and identified molecular regulators in the post-stroke brain using cellular fate analysis. It found that reparative microglia persist after stroke but lose beneficial recovery-phase gene expression, with ZFP384 acting as a pivotal transcriptional regulator that drives this functional dysfunction. These findings suggest targeting ZFP384 to sustain reparative microglia and improve long-term stroke recovery outcomes.

Tsuyama J, Sakai S, Kurabayashi K et al. · Nature · (2026) · View on PubMed ↗ · Free PDF ↗

Endovascular Treatment of Medium-Vessel-Occlusion Strokes.

The study investigated whether endovascular thrombectomy improves functional outcomes in adults with acute ischemic stroke due to medium-vessel occlusion and moderate-to-severe deficits, using an open-label randomized design with blinded outcome assessment across 48 centers in China. It compared thrombectomy versus medical management within 24 hours of onset for patients with NIHSS ≥6. The trial’s results are clinically significant because they clarify whether thrombectomy should be standard for medium-vessel occlusion patients with substantial deficits.

Hu W, Jing X, Chen Z et al. · The New England journal of medicine · (2026) · 1 citations · View on PubMed ↗

Effectiveness and Safety of Early Rhythm Control in Patients With Atrial Fibrillation and Chronic Kidney Disease.

This predefined secondary analysis of the EAST-AFNET 4 randomized trial studied early rhythm control versus usual care in patients with recently diagnosed atrial fibrillation and chronic kidney disease stratified by estimated glomerular filtration rate (eGFR). The key finding was that early rhythm control’s effectiveness and safety could be assessed across CKD severity groups defined by Kidney Disease Improving Global Outcomes criteria. If consistent across CKD strata, ERC could broaden guideline-supported rhythm management for AF patients with renal impairment while maintaining acceptable safety.

Schenker N, Borof K, Goette A et al. · Journal of the American College of Cardiology · (2026) · View on PubMed ↗

ACKR1/Duffy-null genotype testing for clozapine: A guideline developed by the UK Centre of Excellence in Regulatory Science and Innovation in Pharmacogenomics (CERSI-PGx).

This scientific statement update from the American Heart Association reviewed evidence and advances in secondary prevention after coronary artery bypass graft (CABG) surgery. The key finding was a synthesis of emerging strategies to address ongoing post-CABG coronary disease progression, including long-term graft patency and prevention of further atherosclerotic events in the post-surgical population. Clinically, it supports updated, evidence-based management recommendations tailored to the unique risks and comorbidities of CABG patients.

Murtough S, Stellakis O, Mills D et al. · British journal of clinical pharmacology · (2026) · View on PubMed ↗ · Free PDF ↗

Melatonin, Caffeine, or Their Combination: Effects on Sleep, Performance, Perceived Exertion in a Placebo-Controlled Crossover Study.

This randomized double-blind placebo-controlled crossover study tested melatonin, caffeine, or their combination on sleep, performance, physiological/biochemical measures, and perceived exertion in 14 trained males. The key finding was the characterization of how melatonin and caffeine—alone and in combination—affect sleep and exercise-related outcomes under controlled conditions. These results are relevant for athletes and performance medicine by informing whether combining melatonin with caffeine produces additive, neutral, or interactive effects on recovery and performance.

Mahdi N, Delleli S, Maaoui KB et al. · Nutrients · (2026) · View on PubMed ↗ · Free PDF ↗

Brain endothelial cell-derived extracellular vesicles (c-BEEVs) as a promising biomarker for brain vascular pathology and cognitive decline.

This multicenter cohort study evaluated whether cerebrospinal fluid brain endothelial-derived small extracellular vesicles (c-BEEVs) can serve as biomarkers for brain vascular pathology and cognitive decline. c-BEEVs correlated with vascular risk factors and small-vessel disease severity, showed high diagnostic performance for vascular cognitive impairment, and when combined with p-tau181 distinguished vascular cognitive impairment from Alzheimer’s disease in mixed pathology cases. The biomarker approach could improve early identification and differential diagnosis of vascular contributions to cognitive impairment.

You T, Wang Y, Xu J et al. · Nature aging · (2026) · View on PubMed ↗

CD98hc controls CNS angiogenesis and blood-brain barrier integrity through localized regulation of the systemic integrin-FAK pathway.

This study examined the role of CD98 heavy chain (CD98hc/SLC3A2/4F2hc) in CNS endothelial cells of mice and humans, focusing on CNS angiogenesis and blood-brain barrier (BBB) integrity. Endothelial CD98hc ablation in mouse embryos caused aberrant CNS angiogenesis, defective BBB formation, and cerebral hemorrhage while leaving peripheral vasculature unaffected, and CD98hc was enriched in CNS endothelium versus peripheral endothelium. These findings identify CD98hc as a CNS-specific endothelial regulator that controls the systemic integrin–FAK signaling axis to maintain vascular homeostasis and prevent hemorrhagic BBB failure.

Hu X, Yu M, Yang S et al. · Nature cardiovascular research · (2026) · View on PubMed ↗

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Aging, senescence & RNA/proteostasis dysregulation

Reduced ULK1 links impaired autophagy and mitophagy to Alzheimer’s disease pathology.

The study examined ULK1 (Atg1) levels and function in aging and Alzheimer’s disease (AD) using serum/cerebrospinal fluid from cognitively unimpaired COGNORM participants (n=75) and AD patients (NorCog Memory Clinic cohort, n=316), plus AD mouse models. ULK1 was reduced during aging and in AD, while ULK1 overexpression increased autophagic flux and mitophagy, reduced amyloid-β and tau pathology, improved mitochondrial quality, and delayed cognitive decline. These findings implicate ULK1 as a mechanistic driver linking impaired autophagy/mitophagy to AD pathology and suggest ULK1-targeted strategies could be therapeutically relevant.

Pan JP, Wang PJ, Zhang J et al. · Nature aging · (2026) · View on PubMed ↗

Age-Dependent Interplay of Modifiable Risk Factors and Genetic Risk in Pancreatic Cancer.

This JAMA Oncology prospective cohort study tested whether the association between modifiable risk factors and pancreatic cancer risk differs by age and genetic risk, using UK Biobank participants enrolled 2006–2010 and followed for a median of 11.7 years. The key finding was that the impact of a modifiable risk score (MRS, including smoking, alcohol, diet, and physical inactivity) on pancreatic cancer risk varied across polygenic risk score (PRS) strata and across age. Clinically, this supports more tailored prevention strategies that incorporate both genetic susceptibility and age-dependent risk-factor effects.

Ding J, Edelmann D, Carlsson SV et al. · JAMA oncology · (2026) · View on PubMed ↗

Teriparatide Plus Zoledronic Acid for Osteogenesis Imperfecta: A Randomized Clinical Trial.

This multicenter open-label randomized clinical trial evaluated whether teriparatide followed by zoledronic acid reduces fracture risk in adults with osteogenesis imperfecta. The key finding (from the trial’s randomized comparison) was whether the sequential anabolic-to-antiresorptive regimen improved fracture outcomes relative to the control strategy, alongside effects on bone mineral density and bone turnover markers. The clinical significance is that it directly tests a practical, sequential osteoporosis-like treatment approach for adults with osteogenesis imperfecta, a population with high lifelong fracture burden.

Hald JD, Weir CJ, Keerie C et al. · JAMA · (2026) · View on PubMed ↗

Plasma Extracellular Vesicle Surface Marker Profiling Reveals Immune Cell-Associated Mitochondrial Membrane Potential Alterations in Long COVID and Myalgic Encephalomyelitis/Chronic Fatigue Syndrome.

This study profiled plasma extracellular vesicles (EVs) from 125 individuals—including long COVID (LC) and ME/CFS cohorts with overlapping phenotypes—to identify immune-cell-associated mitochondrial membrane potential alterations using EV surface marker profiling. The key finding was that EV-associated signals reflected mitochondrial membrane potential changes shared across long COVID and ME/CFS, supporting a common immune/mitochondrial dysregulation signature. These results suggest plasma EV profiling could provide biomarker candidates to distinguish or stratify LC and ME/CFS beyond subjective diagnostic criteria.

Ikeda G, Koike-Ieki M, Inoue H et al. · Open forum infectious diseases · (2026) · View on PubMed ↗ · Free PDF ↗

Sleep chart of biological ageing clocks in middle and late life.

This study proposed a “Sleep Chart” framework linking self-reported sleep duration to 23 biological ageing clocks derived from in vivo imaging, plasma proteomics, and metabolomics. The key finding was a systemic U-shaped relationship between sleep duration and biological age gaps, with the lowest age gaps occurring around 6.4–7.8 hours in UK Biobank participants (37–84 years), varying by organ and sex. This provides a quantitative, multi-omics method to relate sleep patterns to biological ageing trajectories and potential targets for healthy ageing interventions.

O’Toole CK, Song Z, Anagnostakis F et al. · Nature · (2026) · 1 citations · View on PubMed ↗ · Free PDF ↗

SNOR promotes translation restart after dormancy.

The study investigated how dormant eukaryotic ribosomes restart translation upon nutrient return in the fission yeast Schizosaccharomyces pombe using high-resolution in situ cryo-electron tomography. It identified SNOR, an SBDS domain-containing ribosome-associated factor that binds at the peptidyl transferase center and contacts the hypusinated loop of eIF5A during glucose-depletion dormancy, licensing rapid translational restart rather than acting as a canonical hibernation factor. This mechanistic insight links SNOR–eIF5A cooperation to efficient recovery from dormancy and may inform strategies to modulate translation in stress and disease.

Gluc M, Rosa H, Bozko M et al. · Nature · (2026) · View on PubMed ↗ · Free PDF ↗

Obesity rise plateaus in developed nations and accelerates in developing nations.

The study assessed global obesity dynamics from 1980 to 2024 using 4,050 population-based studies with measured height and weight data from 232 million participants. It found that obesity rise decelerated and plateaued in many high-income countries (including school-aged children and adolescents), while indications of continued acceleration persisted in developing nations. These results refine epidemiologic expectations for obesity trends and can guide timing and targeting of prevention and treatment strategies.

Nature · (2026) · 1 citations · View on PubMed ↗ · Free PDF ↗

Allelic variation in UVR8 modulates thermotolerance-yield tradeoffs in plants.

The study investigated how allelic variation in the rice photoreceptor UVR8b (OsUVR8b) affects thermotolerance–yield tradeoffs by identifying it as a substrate of SnRK1 and analyzing natural variation at a phosphorylation site. It found that a natural OsUVR8b variant (Ala177 at the SnRK1-mediated Ser177 site) correlates with adaptation to tropical climates and is enriched in low-latitude regions, linking energy signaling to heat-stress responses. This provides a mechanistic genetic explanation for climate adaptation and suggests targets for breeding heat-resilient crops.

Li Z, Zhang Y, Li S et al. · Cell research · (2026) · View on PubMed ↗

The evolving landscape of obesity pharmacotherapy.

This review summarized the evolving landscape of obesity pharmacotherapy, focusing on how incretin-based treatments expanded from GLP-1 receptor agonists to multi-receptor agonist peptides targeting GLP-1, GIP, glucagon, and amylin receptors. It highlights that these next-generation therapies have produced average human weight loss exceeding 20% and improvements in obesity-related comorbidities. The synthesis frames current clinical progress and outlines emerging strategies for future obesity drug development.

Petersen J, Finan B, Johansen VBI et al. · Nature reviews. Drug discovery · (2026) · View on PubMed ↗

S-acylation of TDP43 regulates its condensation in amyotrophic lateral sclerosis.

The study examined how S-acylation regulates TDP43 condensation in amyotrophic lateral sclerosis (ALS), focusing on TDP43 in the context of the S-acyltransferase zDHHC23 and the Cys244 residue. It found that zDHHC23 primarily S-acylates TDP43 at Cys244, which preserves liquid-like TDP43 behavior by reducing aberrant interactions with PARP1 and PARylated proteins and thereby countering pathological TDP43 condensation. This mechanistic link suggests that modulating TDP43 S-acylation could be a therapeutic strategy to prevent translational shutdown and neurodegeneration in ALS.

Xu W, Li H, Zhang W et al. · Molecular cell · (2026) · View on PubMed ↗

m6A RNA modification guides alternative polyadenylation to maintain T cell quiescence.

T cell post-transcriptional regulation was studied by examining how the m6A writer METTL3 coordinates with the alternative polyadenylation factor NUDT21 to maintain T cell quiescence, using T cells with Nudt21 deletion. METTL3 interacted with NUDT21 to guide poly(A) site selection, and loss of NUDT21 caused simultaneous T cell overactivation and accelerated apoptosis, leading to T cell loss and impaired adaptive immune function. These findings link m6A-dependent control of alternative polyadenylation to T cell quiescence, identifying METTL3–NUDT21 as a regulatory node with immunological significance.

Zhang X, Li H, Wang G et al. · Science advances · (2026) · View on PubMed ↗ · Free PDF ↗

The metabolomic signatures mediate associations between physical frailty and metabolic dysfunction-associated steatotic liver disease.

In a prospective analysis of 405,224 UK Biobank participants followed for 13.65 years, metabolomic signatures were used to study how physical frailty relates to metabolic dysfunction-associated steatotic liver disease (MASLD) and how frailty interacts with metabolic syndrome. Physical frailty was associated with increased risk of clinically diagnosed MASLD and intensified the adverse effect of metabolic syndrome on MASLD incidence. This suggests that metabolomic pathways may mediate frailty–MASLD risk and could help identify modifiable targets for prevention.

Jiang R, Rosenblatt M, Qi S et al. · Science advances · (2026) · View on PubMed ↗ · Free PDF ↗

Pragmatic Parental Support to Mitigate Burnout Among Pregnant and Postpartum Trainees: A Randomized Clinical Trial.

This pragmatic randomized clinical trial studied a parental support package designed to mitigate perinatal stressors and reduce burnout and distress among pregnant (≥12 weeks’ gestation) residents and fellows across 7 training institutions. The intervention was evaluated against usual training conditions to determine whether it lowers occupational burnout and related distress in childbearing physicians in training. If effective, this scalable workplace-and-family support strategy could improve physician well-being and retention while protecting care quality during pregnancy and the postpartum transition.

Rubio-Chavez A, Koelliker EL, Askew EA et al. · JAMA · (2026) · 1 citations · View on PubMed ↗

Atherosclerosis Profiling Reveals BHLHE40 as a Candidate Modulator of VSMC.

This guideline from the UK Centre of Excellence in Regulatory Science and Innovation in Pharmacogenomics (CERSI-PGx) assessed ACKR1/Duffy-null (T>C) genotype testing to inform clozapine management. The key finding was that identifying the ACKR1 homozygous Duffy-null genotype (ADAN/benign ethnic neutropenia) can justify adjusted ANC/WBC monitoring thresholds to reduce unnecessary interruption while maintaining safety. Clinically, this provides a pharmacogenomics-based pathway for safer clozapine use in patients with naturally low neutrophil counts.

Ibikunle CO, Garcia EJ, Xue C et al. · Circulation research · (2026) · View on PubMed ↗

Secondary Prevention After Coronary Artery Bypass Graft Surgery: 2026 Update: A Scientific Statement From the American Heart Association.

This Mendelian randomization and bioinformatics analysis studied plasma proteins causally linked to diabetic neuropathy (DN) using genome-wide association study data for 4,907 proteins and then validated biological relevance with differential expression and functional enrichment using GEO dataset GSE148061 (53 DN patients, 53 healthy donors). The key finding was identification of specific plasma proteins with causal associations to DN risk, suggesting protein-mediated mechanisms in DN pathogenesis. Scientifically, these proteins provide candidate targets for therapeutic development and biomarkers for DN risk stratification.

Ruel M, Sandner S, Ponnambalam M et al. · Circulation · (2026) · View on PubMed ↗

The 2024 Endocrine Society Guideline on Vitamin D: Comprehensive Summary and Critical Appraisal.

This guideline summary critically appraised the 2024 Endocrine Society Clinical Practice Guideline on vitamin D, focusing on people without established indications for vitamin D treatment or 25-hydroxyvitamin D (25(OH)D) testing. Using a GRADE/EtD framework and prioritizing randomized controlled trial evidence, it concluded that vitamin D supplementation reduces rickets and respiratory tract infections in children and lowers mortality in certain populations (with other outcomes assessed across the evidence base). Clinically, it supports evidence-based decisions about when to supplement vitamin D rather than routine testing/treatment in low-risk individuals.

Pilz S, Pludowski P, Kraus DA et al. · Nutrients · (2026) · View on PubMed ↗ · Free PDF ↗

Differential Acute Kidney Injury Profiles of GLP-1RAs and SGLT2is: A Network Meta-Analysis.

This network meta-analysis compared acute kidney injury (AKI) risk across individual drugs and doses within glucagon-like peptide-1 receptor agonists (GLP-1RAs) versus sodium-glucose co-transporter 2 inhibitors (SGLT2is) in patients treated for diabetes/renal outcomes. The key finding was that AKI risk should not be assumed equivalent across the drug classes because medication-specific effects may differ, motivating a dose- and agent-level comparison. Scientifically and clinically, it helps refine renoprotective assumptions and supports more accurate risk stratification when selecting GLP-1RAs versus SGLT2is.

Liang CS, Hsu CW, Chen JJ et al. · International journal of molecular sciences · (2026) · View on PubMed ↗ · Free PDF ↗

Glycaemic and Cardiometabolic Outcomes of Empagliflozin Versus Sitagliptin Added to Metformin in T2DM: Insights From a Systematic Review and Meta-Analysis.

This systematic review and meta-analysis compared empagliflozin versus sitagliptin when each was added to metformin in adults with type 2 diabetes mellitus (T2DM), assessing glycaemic and cardiometabolic outcomes and safety. The key finding was the pooled comparison of how these two add-on classes differ in metabolic effects and tolerability when used as combination therapy with metformin. The results can guide clinicians in selecting add-on therapy based on expected cardiometabolic benefits and risk profiles.

Ashraf S, Burhan M, Sarwar S et al. · Endocrinology, diabetes & metabolism · (2026) · View on PubMed ↗ · Free PDF ↗

Hypoxia-induced autophagic degradation of HIF-1α attenuates cellular aging and extends mammalian lifespan.

This research examined how hypoxia regulates aging in the intervertebral disc (IVD) and whether targeting HIF-1α degradation can extend lifespan in mammals. The authors linked slow IVD aging to persistently hypoxic conditions that enable optineurin-mediated selective autophagy to degrade HIF-1α in nucleus pulposus cells, limiting hypoxia-driven cellular stress, and they developed a small-molecule HIF-1α-targeting autophagy-tethering compound (HATC) to pharmacologically promote protective HIF-1α export. These results suggest a druggable hypoxia–HIF-1α–autophagy pathway for decelerating cellular aging and potentially extending mammalian lifespan.

Yang C, Xu Z, He ST et al. · Nature aging · (2026) · View on PubMed ↗

Pasteurized Akkermansia muciniphila MucT for weight loss maintenance in people with overweight and obesity: a controlled randomized trial.

This double-blind, placebo-controlled phase 3b ATTAIN-MAINTAIN trial studied orforglipron, a once-daily oral nonpeptide GLP-1 receptor agonist, for maintaining weight reduction in participants previously treated with tirzepatide or semaglutide in SURMOUNT-5. Participants were randomized to orforglipron versus placebo within two cohorts (tirzepatide-exposed: N=205; semaglutide-exposed: N=171), testing durability of weight loss after prior incretin therapy. If the trial confirms sustained benefit, orforglipron could offer an oral maintenance option to preserve cardiometabolic improvements after injectable incretin-induced weight loss.

Mount S, Canfora EE, Jocken JW et al. · Nature medicine · (2026) · View on PubMed ↗

Evidence-based clinical practice guidelines for metabolic dysfunction-associated steatotic liver disease (MASLD) 2026.

This 2026 evidence-based clinical practice guideline summarized recommendations for metabolic dysfunction-associated steatotic liver disease (MASLD), focusing on diagnosis, risk stratification, and management to prevent progression to cirrhosis and hepatocellular carcinoma (HCC). The guideline was developed via systematic literature review and expert consensus, emphasizing early identification of patients at high risk for advanced fibrosis using practical diagnostic approaches. Clinically, it provides an actionable framework for improving long-term outcomes in the most prevalent chronic liver disease worldwide.

Akuta N, Kogiso T, Ikejima K et al. · Journal of gastroenterology · (2026) · View on PubMed ↗ · Free PDF ↗

RNA imbalance as a hallmark of cellular ageing.

This article reviewed ageing-associated dysregulation across the mRNA life cycle, including transcription, splicing, and translation, in the context of cellular senescence. It reports that ageing shifts mRNA transcription toward shorter genes, increases alternative exon usage, and promotes ribosomal collisions, collectively creating an “RNA imbalance” phenotype. The work highlights RNA metabolism as a mechanistic hallmark of cellular ageing and a potential target for interventions aimed at restoring proteostasis and gene expression fidelity.

Sun P, Miller BA, Sakai AP et al. · Nature cell biology · (2026) · View on PubMed ↗

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Targeted protein degradation & ubiquitin/proteostasis tools

Dual E3 ligase recruitment by monovalent degraders for tunable SMARCA 2/4 degradation.

This study investigated how monovalent molecular glue degraders can recruit two E3 ligases to degrade SMARCA2/4, using orthogonal genetic screening, biophysical/structural methods, deep mutational scanning, and mass spectrometry. The authors found that a monovalent degrader can recruit CUL4DCAF16 and CRL1FBXO22 in parallel to drive SMARCA2/4 degradation, with DCAF16 residue C173 essential for activity and intact protein mass spectrometry confirming covalent modification. This provides a tunable strategy for PROTAC/MGD design that enables dual E3 engagement for selective degradation of SMARCA2/4 chromatin remodelers.

Spiteri VA, Segal D, Correa-Sáez A et al. · Nature chemical biology · (2026) · 1 citations · View on PubMed ↗ · Free PDF ↗

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Nanomedicine for inflammatory disease (RNA/ROS targeting)

Wolbachia-mediated viral transmission enhancement in insect vectors.

The mechanism of Wolbachia-mediated enhancement of viral transmission was investigated in insect vectors, focusing on white-backed planthopper (Sogatella furcifera) transmission of southern rice black-streaked dwarf virus (SRBSDV). High-transmission planthopper populations contained high Wolbachia levels, and thoracic injection experiments supported Wolbachia’s specific role in breaching the salivary gland barrier for SRBSDV. This mechanistic insight identifies Wolbachia as a driver of vector competence, with implications for controlling SRBSDV spread.

Wang Y, Zhou S, Li S et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗ · Free PDF ↗

Emerging and re-emerging vector-borne and other zoonotic RNA viruses: pathogenesis, climate-driven dynamics, and strategies for global control.

This review examined the pathogenesis and epidemiology of multiple vector-borne and zoonotic RNA viruses (including dengue, Zika, chikungunya, yellow fever, Japanese encephalitis, Crimean-Congo hemorrhagic fever, Nipah, Ebola, and hantaviruses) in the context of climate-driven changes to arthropod vector ecology and zoonotic spillover. It found that rising temperatures, altered precipitation patterns, and accelerated urbanization can reshape vector habitats and increase spillover dynamics, thereby driving emergence and re-emergence. The synthesis highlights climate and social determinants as actionable levers for global surveillance and control strategies against RNA zoonoses.

Farsiu N, Rezaie Zadeh Rukerd M, Khodadadpour Mahani F et al. · Frontiers in microbiology · (2026) · View on PubMed ↗ · Free PDF ↗

Acarbose redirects gut microbiome utilization of dietary carbohydrates to suppress anaphylaxis in mice.

This mouse study examined how the antidiabetic α-glucosidase inhibitor acarbose alters gut microbial carbohydrate utilization to suppress mast-cell-dependent anaphylaxis. Acarbose increased availability of microbiota-accessible carbohydrates, promoting Parabacteroides distasonis expansion, higher succinate abundance, and increased intracellular NAD+ levels, which reduced anaphylaxis independently of adaptive immunity. These findings suggest a microbiome-metabolic mechanism by which acarbose could be repurposed to mitigate severe allergic reactions.

Yakabe K, Inoue Y, Yanagisawa Y et al. · Nature microbiology · (2026) · View on PubMed ↗ · Free PDF ↗

Double-stranded RNA and ROS scavenging nanoplatform for modulating skin inflammation.

This study tested a cerium-doped polyoxometalate nanoplatform (Mo90Ce10) that scavenges both double-stranded RNA (dsRNA) and reactive oxygen species (ROS) to modulate skin inflammation in models relevant to psoriasis and atopic dermatitis. Mo90Ce10 directly binds dsRNA via an oxygen-rich hydrogen-bonding surface to suppress type I interferon responses while also scavenging ROS, and in vivo it reduced disease severity and dsRNA-induced inflammation. The results suggest a dual-target nanotherapeutic approach that neutralizes pathogenic dsRNA while mitigating oxidative amplification of inflammatory signaling.

Cui L, Lu H, Cai J et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

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Cancer microenvironment & stromal-immune interactions

Navigating the clinical progress of antibody-drug conjugates: Emerging opportunities and remaining challenges.

This Cell review synthesized current evidence on antibody-drug conjugates (ADCs) across hematologic and solid tumors, focusing on their biology and how they should be advanced into earlier lines and combination regimens. The key message is that ADCs can improve tumor-targeted delivery and safety, but success depends on careful patient selection and toxicity management as indications expand. Scientifically and clinically, it frames the remaining translational challenges—especially optimizing combinations and managing adverse effects—to guide future ADC development.

Conilh L, Metrangolo V, Crescioli S et al. · Cell · (2026) · View on PubMed ↗

Macrophage-to-Myofibroblast Transdifferentiation Contributes to Pulmonary Fibrosis via the MERTK-SPP1-SRC-TKS5 Signaling Axis.

This Advanced Science study examined macrophage-to-myofibroblast transdifferentiation (MMT) in human idiopathic pulmonary fibrosis (IPF) lungs and in a bleomycin-induced mouse model. Mechanistically, GAS6-driven activation of MERTK in macrophages initiated a signaling cascade through SPP1, SRC, and TKS5 that promoted MMT, and macrophage-specific MERTK knockout or AAV-mediated TKS5 knockdown disrupted this axis and suppressed MMT in vitro and in vivo. The significance is that it identifies the MERTK–SPP1–SRC–TKS5 signaling pathway as a potential therapeutic target to block fibrogenic transdifferentiation in pulmonary fibrosis.

Wei Y, Guo H, Yang X et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗

Integrated Single-Cell Atlas Reveals Cross-Subtype Heterogeneity in Human Pulmonary Hypertension.

This study integrated multiple human pulmonary hypertension (PH) single-cell RNA sequencing datasets to build a standardized, PH-specific cellular atlas using a core quantification and batch-correction pipeline and hierarchical cell-type/state annotation. The key finding was that cross-subtype cellular heterogeneity can be resolved into a core atlas while revealing PH-relevant cell states that were otherwise fragmented across individual studies and processing pipelines. This improves cross-study comparability and provides a unified framework for identifying candidate disease-driving cellular programs across PH subtypes.

Feng H, Lai J, Yang X et al. · Arteriosclerosis, thrombosis, and vascular biology · (2026) · View on PubMed ↗

Eosinophils drive intestinal remodelling and innate defence in reproduction.

This study investigated how eosinophils regulate intestinal barrier remodeling and innate defense across reproductive stages, from pregnancy through lactation, using mechanistic experiments in mammalian models. The key finding was that eosinophils are required for remodeling of the intestinal barrier during reproduction, with activity peaking during lactation. This advances understanding of tissue-specific immune adaptation in reproduction and identifies eosinophils as a functional driver of barrier defense during postpartum transition.

Huang C, Sun A, Reyes J et al. · Nature · (2026) · 1 citations · View on PubMed ↗ · Free PDF ↗

Ecotypes of triple-negative breast cancer in response to chemotherapy.

This study analyzed pretreatment tissue from 101 treatment-naive patients with triple-negative breast cancer (TNBC) who received neoadjuvant chemotherapy, using single-cell transcriptomics (427,857 cells) and spatial transcriptomics (44 patients). The key finding was identification of four patient-level TNBC ecotypes (archetypes) and 13 single-cell metaprograms capturing intra-tumor heterogeneity that likely underlie differential chemotherapy response. Clinically, these ecotypes could enable more precise prediction of treatment response and guide stratified therapeutic strategies in TNBC.

Yan Y, Lin Y, Kumar T et al. · Nature · (2026) · View on PubMed ↗ · Free PDF ↗

Long-term editing of brain circuits using an engineered electrical synapse.

This study engineered an electrical synapse for mammalian circuit modulation by combining connexin proteins (connexin 34.7 and connexin 35) and used mutagenesis, an in vitro hemichannel docking assay, and computational modeling to define structural requirements. The key finding was that an engineered connexin-based electrical synapse can be used to modulate long-term brain circuit activity with circuit-level specificity. This provides a platform for selectively tuning electrical coupling in neural circuits, advancing tools for studying and potentially treating circuit dysfunction.

Ransey E, Thomas GE, Wisdom EM et al. · Nature · (2026) · View on PubMed ↗ · Free PDF ↗

Nivolumab plus chemoradiotherapy followed by nivolumab with or without ipilimumab for untreated locally advanced stage III NSCLC: a randomized phase 3 trial.

The trial studied adults with untreated, unresectable stage III non-small cell lung cancer (NSCLC) randomized to nivolumab plus concurrent chemoradiotherapy (CCRT) followed by nivolumab with or without ipilimumab versus nivolumab alone versus standard CCRT followed by durvalumab, with progression-free survival (PFS) as the primary endpoint. At a median follow-up of 30.5 months, it reported no significant improvement in the primary comparison of nivolumab+CCRT→nivolumab+ipilimumab versus CCRT→durvalumab (with additional secondary outcomes including OS and PFS in the nivolumab-alone arm). Clinically, the findings inform whether adding nivolumab (and ipilimumab) to standard stage III NSCLC chemoradiotherapy consolidation improves outcomes beyond durvalumab.

Peters S, Tan DSW, Gerber DE et al. · Nature cancer · (2026) · View on PubMed ↗ · Free PDF ↗

Spatiotemporal brain transcriptomics reveal risk gene hot-spots in major neuropsychiatric disorders.

The study mapped spatiotemporal expression patterns of genome-wide neuropsychiatric disorder risk gene sets across 15 traits using bulk and single-cell transcriptomic data from the human brain. It identified trait-specific spatiotemporal enrichment “hot-spots,” indicating that risk genes act in distinct developmental and regional contexts rather than uniformly across the brain. This helps prioritize when and where genetic risk is most likely to influence disease biology, supporting more targeted mechanistic follow-up.

Liu W, Shimogori T · Communications biology · (2026) · View on PubMed ↗

Deep peptide recognition profiling decodes TCR specificity and enables disease-associated antigen discovery.

The study developed a system combining high-throughput yeast display with fine-tuned protein language models to generate deep peptide recognition profiles (PRPs) for individual T cell receptors (TCRs). Using a panel of HLA-B*27:05-restricted TCRs from people with ankylosing spondylitis and acute anterior uveitis, it showed that the TCRs almost exclusively recognize peptides through CDR3β and enabled peptide discovery by training pLMs on PRPs. This advances antigen discovery for HLA-restricted autoimmune disease and improves prediction of TCR specificity from functional recognition data.

Wang N, Yeh H, Lai B et al. · Nature biotechnology · (2026) · View on PubMed ↗ · Free PDF ↗

Immune-remodeling mRNAs expressing IRF8 or NIK generate durable antitumor immunity in multiple cancer models.

The study engineered tumor microenvironment immune remodeling by delivering lipid nanoparticle (LNP)-encapsulated immune-remodeling mRNAs (IR-mRNAs) encoding IRF8 or NF-κB-inducing kinase (NIK) across multiple cancer models. It found that IR-mRNAs activate antigen-presenting cells in tumors, increasing activated type 1 conventional dendritic cells, immunostimulatory cytokines, and priming antitumor CD8+ T cells to generate durable antitumor immunity. These results support IRF8/NIK mRNA-LNP approaches as a potentially broadly applicable strategy to overcome immunosuppressive tumor microenvironments.

Gupta A, Das R, Reed K et al. · Nature biotechnology · (2026) · View on PubMed ↗

Galvanin (TMEM154) is an electric-field sensor for directed cell migration.

The study investigated how single cells detect endogenous electric fields during directed migration, identifying Galvanin (TMEM154) as a required sensor in rapidly moving immune and epithelial cells. It found that Galvanin expression is sufficient to confer electric-field-guided migration and that electric-field exposure rapidly relocalizes Galvanin to the anodal side. This establishes TMEM154 as a mechanistic electric-field sensor and provides a target for understanding and potentially manipulating wound-directed cell migration.

Belliveau NM, Footer MJ, Platenkamp A et al. · Cell · (2026) · View on PubMed ↗ · Free PDF ↗

Gut microbiota-derived deoxycholic acid shapes an immunosuppressive tumor microenvironment and promotes breast cancer progression.

The study examined how gut microbiota-derived deoxycholic acid (DCA) shapes the tumor microenvironment and promotes breast cancer progression, focusing on Enteroclosterbolteae enrichment and signaling in tumor cells. It found that DCA accumulates in tumors, activates the farnesoid X receptor (FXR), induces interleukin-6 via NF-κB signaling, and drives recruitment of granulocytic myeloid-derived suppressor cells and T helper 17 cells to create an immunosuppressive microenvironment. This links a specific microbiota metabolite to defined immune pathways, suggesting FXR/IL-6 axis modulation as a potential strategy to slow breast cancer progression.

Li L, Yang C, Wang Z et al. · Cell metabolism · (2026) · View on PubMed ↗

Efficacy and Safety of Camrelizumab Plus Apatinib in Patients With Refractory Chordoma: A Phase II Clinical Trial.

This phase II clinical trial studied camrelizumab (PD-1 inhibitor) plus apatinib (VEGFR-targeting antiangiogenic drug) in patients with refractory chordoma, using an investigator-initiated single-center design. The key finding reported was the objective response rate (ORR) per RECIST 1.1 as the primary endpoint, along with secondary efficacy and safety outcomes for the combination regimen. Clinically, it evaluates whether combining PD-1 blockade with antiangiogenic therapy can provide meaningful activity in a cancer type with limited effective options.

Yang C, Jia Q, Zhao C et al. · Journal of clinical oncology : official journal of the American Society of Clinical Oncology · (2026) · View on PubMed ↗

Natural killer cell immunotherapy reverses lung fibrosis by eliminating senescent fibroblasts.

Natural killer (NK) cell immunotherapy was studied in fibrotic lung disease to determine how senescent fibroblasts evade immune clearance, using single-cell RNA sequencing and spectral flow cytometry in patient samples and mechanistic coculture experiments. The study identified NKG2A as the predominant inhibitory receptor on NK cells in fibrotic lungs and showed that senescent fibroblasts suppress NK cells via HLA-E expression, the high-affinity ligand for NKG2A. By reversing fibrosis through elimination of senescent fibroblasts, the work highlights an immune checkpoint axis (HLA-E/NKG2A) as a mechanistic target for antifibrotic therapies.

Merkt W, Rodon L, Deicher FS et al. · Science translational medicine · (2026) · View on PubMed ↗

Rural-Urban Disparities in Hepatocellular Carcinoma Incidence and Mortality.

Rural-urban differences in hepatocellular carcinoma (HCC) incidence and incidence-based mortality were studied using US cancer registry data (2001–2022 diagnoses) and SEER/SEER-21 mortality data (2007–2022), stratified by sex, race/ethnicity, and stage at diagnosis. The study assessed whether rural residents experienced similar trends to overall US declines in HCC incidence and mortality, using 2013 Rural-Urban Continuum Codes to define rurality. These findings are clinically important for identifying disparities in HCC prevention, detection, and outcomes across geographic settings.

Damgacioglu H, Uygun G, Deshmukh AA et al. · JAMA network open · (2026) · View on PubMed ↗ · Free PDF ↗

Single-cell transcriptomics reveals immune landscape dynamics in metastatic hormone receptor-positive breast cancer treated with abemaciclib and endocrine therapy.

This study used single-cell RNA-sequencing of CD45-enriched cells to map the baseline immune landscape and immunomodulatory effects of abemaciclib plus endocrine therapy in advanced estrogen receptor–positive, HER2-negative metastatic breast cancer. The key finding was that abemaciclib combined with endocrine therapy reshapes tumor immune microenvironment dynamics at single-cell resolution compared with baseline immune states. These results support CDK4/6 inhibitor–endocrine therapy as an immunomodulatory regimen and help identify immune features that may predict or explain response.

Strawser CH, Chakraborty B, Michaud D et al. · Clinical cancer research : an official journal of the American Association for Cancer Research · (2026) · View on PubMed ↗

A Spatial Atlas of Muscle-Invasive Bladder Cancer Reveals Lineage-Specific Vulnerabilities and Immune Architecture.

This study constructed a spatial atlas of muscle-invasive bladder cancer by integrating spatial transcriptomics from 22 tumors with matched bulk RNA sequencing and whole-exome sequencing to define spatially organized tumor states. It identified a continuous luminal-to-basal axis within individual tumors, with luminal cores enriched for FGFR3 and NECTIN4 and basal-like invasive-margin states associated with elevated EGFR signaling and greater chromosomal instability/plasticity. Scientifically, this reveals lineage-specific vulnerabilities tied to spatial immune architecture, potentially enabling more precise, location-aware therapeutic targeting in MIBC.

Yu K, Chen J, Chu YY et al. · Cancer discovery · (2026) · View on PubMed ↗ · Free PDF ↗

Targeting Cancer Cachexia: A Mechanistic Evaluation of Anti-GDF-15 Antibody-Based Combination Therapies.

This mechanistic preclinical study evaluated anti-GDF-15 antibody–based combination therapies for cancer cachexia, focusing on how ponsegromab (anti-GDF-15) could be integrated with muscle anabolic and appetite-stimulating agents. The key finding was that neutralizing the GDF-15 pathway can be combined with other interventions (including anti-myostatin and the ghrelin receptor agonist anamorelin) to further address the multifactorial cachexia syndrome. These results support GDF-15 as a therapeutic hub and guide rational combination strategies to improve weight, appetite, and muscle outcomes in cachexia.

Breen DM, Joaquim S, Paulhus BL et al. · Journal of cachexia, sarcopenia and muscle · (2026) · View on PubMed ↗ · Free PDF ↗

SRC as a Prognostic and Immunomodulatory Biomarker in Acute Myeloid Leukemia: A Multi-Omics Study.

This multi-omics study integrated bulk transcriptomic and single-cell RNA-sequencing datasets (TCGA, BeatAML, and GEO) to characterize the non-receptor tyrosine kinase SRC as a prognostic and immunomodulatory biomarker in acute myeloid leukemia (AML). Using xCell-based immune scoring, weighted gene co-expression network analysis (WGCNA), protein-protein interaction analysis, and multi-algorithm machine-learning screening, it identified SRC expression patterns linked to prognosis and immune regulation. If validated, SRC could serve as a biomarker and potential immunomodulatory target to improve risk stratification and therapeutic decision-making in AML.

Zhong J, Liu X, Gu X et al. · International journal of molecular sciences · (2026) · View on PubMed ↗ · Free PDF ↗

An inflammasome-driven differentiation program in intestinal stem cells protects against Salmonella infection.

This study investigated a stem cell-intrinsic defense mechanism in Lgr5+ intestinal stem cells (ISCs) against intracellular Salmonella enterica. Using fluorescent-labeled bacteria, single-cell transcriptomics, fate mapping, organoid models, and genetic perturbations, the authors found that invaded ISCs activate an inflammasome-dependent differentiation program via ASC (Pycard)-mediated inflammasome signaling, reprogramming toward antimicrobial peptide-enriched Paneth cells through apoptosis-associated pathways. The work identifies a specific inflammasome–ASC axis in ISCs that could be targeted to enhance intestinal barrier immunity against enteric pathogens.

Lebon S, Habshush Menachem A, Davidzohn N et al. · Nature immunology · (2026) · View on PubMed ↗ · Free PDF ↗

Epigenetic reprogramming of T cell metabolism restores function and enhances anti-tumor immunity in lung cancer.

This study tested whether epigenetic bromodomain and extra-terminal motif inhibitors (BETis) can restore function in terminally exhausted T cells (TEX) from lung cancer patients. In primary TEX cells from malignant pleural effusions, BETis reinvigorated effector function by activating polyamine biosynthesis, expanding intracellular polyamine pools, and changing chromatin accessibility as shown by transcriptomics, metabolomics, and ATAC-seq. Clinically, BETis may improve responsiveness to immune checkpoint blockade by reversing exhaustion-associated metabolic and epigenetic dysfunction in lung cancer.

Wu YC, Yang SF, Lee YT et al. · Nature immunology · (2026) · View on PubMed ↗

E-cadherin inactivation shapes tumor microenvironment specificities in invasive lobular breast cancer.

This study examined how E-cadherin (CDH1) inactivation shapes the tumor microenvironment in invasive lobular breast cancer (ILC) using single-cell analysis, immunohistochemistry, bulk RNA-seq deconvolution, and functional assays in a large female ILC cohort. CDH1 loss in ILC cells prevented differentiation of FAP+ inflammatory cancer-associated fibroblasts (iCAF) into FAP+ myofibroblastic CAF, leading to iCAF accumulation in ILC and promoting recruitment of tumor-infiltrating lymphocytes (TILs) into the tumor center. These findings link CDH1-driven stromal fate control to spatial TIL organization and provide a mechanistic explanation for ILC microenvironment-specific immune patterns.

Djerroudi L, Mhaidly R, Kieffer Y et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

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Cell division & kinetochore/meiotic regulation

Cruise ship outbreak spotlights a little-studied hantavirus.

This Science news piece highlights an Andes virus outbreak on a cruise ship as a real-world example of how a little-studied hantavirus can spread and trigger public-health response. The key finding is that the outbreak provided a stress test for global crisis-response systems and drew attention to the epidemiology and preparedness gaps for hantaviruses beyond well-known pathogens. Its significance lies in informing surveillance and response planning for emerging infectious threats in closed or high-contact settings.

Kupferschmidt K · Science (New York, N.Y.) · (2026) · View on PubMed ↗

Lineage and organ signals sequentially build organ intrinsic nervous systems.

The study analyzed how organ intrinsic nervous systems (OINSs) arise from neural crest cells across multiple organs by integrating lineage tracing, 3D imaging, single-cell transcriptomics, and genetic perturbations in heart, pancreas, intestine, and lungs. It found that differences in neural crest cell migratory trajectories prefigure the spatial architecture of OINSs, enabling organ-specific patterning. This provides a systems-level developmental framework for how distinct neural circuits are built from a common progenitor lineage.

Hsu IY, Zhao J, Lin Y et al. · Nature · (2026) · View on PubMed ↗ · Free PDF ↗

A divergent Plasmodium NEK4 acts as a key regulator driving the early events of meiosis.

This study investigated the Plasmodium berghei NIMA-related kinase NEK4 as a regulator coupling meiotic initiation to zygote morphogenesis during early meiosis after fertilization. Using ultrastructure expansion microscopy, the authors showed NEK4 accumulates at the microtubule-organising centre (MTOC) and the apical polar complex (APC) and identified it as a key driver of early meiotic events. The work clarifies how a divergent Plasmodium NEK4 coordinates meiotic and morphological transitions, informing understanding of malaria parasite sexual development control points.

Yanase R, Hair M, Zeeshan M et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Models for the architecture of the human inner kinetochore on centromeric α-satellite CENP-A nucleosome arrays.

This study determined the architecture of the human inner kinetochore assembled on centromeric α-satellite CENP-A nucleosome arrays using cryo-EM. It found that CCAN bound to free DNA and a monomeric CENP-A nucleosome engages ~70 bp of DNA containing an upstream α-satellite repeat, with upstream DNA interactions resembling nucleosome DNA wrapping via CENP-TWSX histone-fold subunits. These structural insights define how CCAN and CENP-A nucleosomes organize centromeric DNA at the molecular level to build the inner kinetochore.

Yu C, Muir KW, Yang J et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

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Hematology/oncology: CAR-T bridging & treatment sequencing

Addition of autologous stem-cell transplantation to an ibrutinib-containing first-line treatment in patients aged 18-65 years with mantle cell lymphoma (TRIANGLE): 4·5-year follow-up of a three-arm, randomised, open-label, phase 3 superiority trial of the European MCL Network.

This phase 3, three-arm randomized open-label TRIANGLE trial evaluated whether adding autologous stem-cell transplantation (ASCT) to an ibrutinib-containing first-line regimen improves outcomes in adults aged 18–65 years with mantle cell lymphoma (MCL). With extended follow-up, the trial assessed failure-free survival and overall survival across arms comparing ibrutinib plus standard immunochemotherapy with or without ASCT. The results are clinically significant because they test whether intensifying first-line therapy with ASCT can further improve long-term disease control when combined with ibrutinib.

Dreyling M, Doorduijn J, Giné E et al. · Lancet (London, England) · (2026) · View on PubMed ↗

Multicenter Cohort Study of Original or Substitute Systemic Therapy With or Without Brain Radiotherapy for Extensive-Stage Small Cell Lung Cancer With Brain-Only Progression After First-Line Treatment.

This multicenter cohort study investigated second-line treatment strategies for extensive-stage small cell lung cancer (ES-SCLC) patients who developed brain-only progression (BOP) after first-line therapy, using 889 screened patients and 203 assigned to three strategies. Compared across continuation of original systemic therapy plus brain radiotherapy (OTP+BRT), substitution therapy plus BRT (ST+BRT), and substitution therapy alone (ST), the study used inverse probability of treatment weighting to balance baseline differences and determine which approach best improves outcomes. The clinical significance is that it aims to define an evidence-based second-line standard for ES-SCLC with BOP, where optimal sequencing of systemic therapy and brain radiotherapy is currently unclear.

Lu S, Jia J, Ren K et al. · Journal of clinical oncology : official journal of the American Society of Clinical Oncology · (2026) · View on PubMed ↗

Glofitamab and epcoritamab for large B cell lymphoma: a real-world retrospective UK analysis of efficacy, tolerability, and impact of treatment sequencing.

This UK real-world retrospective study evaluated treatment efficacy and tolerability of the CD3xCD20 bispecific antibodies glofitamab versus epcoritamab in 332 patients with relapsed/refractory large B-cell lymphoma (RR LBCL) treated across 34 centers (Nov 2023–May 2025). In this high-risk cohort (median 2 prior lines; 55% primary refractory; 50% prior CAR T; 78% ineligible for pivotal trials), 28% developed cytokine release syndrome (CRS) mostly grade 1/2, with outcomes reported for overall response rate (truncated in abstract). These data support real-world feasibility and help inform sequencing decisions between glofitamab and epcoritamab in heavily pretreated RR LBCL patients who often differ from pivotal-trial populations.

Osborne W, Haynes E, Wilson W et al. · Haematologica · (2026) · View on PubMed ↗ · Free PDF ↗

Experiences and expert panel consensus on bridging therapy before anti-BCMA CAR-T cell therapy in multiple myeloma.

The study used qualitative interviews and an expert consensus workshop with 10 European clinicians to evaluate how to select bridging therapy (BT) before anti-BCMA CAR-T cell therapy in heavily pretreated patients with relapsed/refractory multiple myeloma. Experts agreed BT should reduce tumor burden and maintain or improve performance status, while emerging options such as bispecific T-cell engagers may be considered to optimize efficacy and safety after CAR-T. This consensus helps standardize BT decision-making to improve outcomes when transitioning patients to anti-BCMA CAR-T in real-world practice.

Rasche L, Krauth MT, Agis H et al. · Bone marrow transplantation · (2026) · View on PubMed ↗ · Free PDF ↗

Final overall survival analysis of the APPLE study: atezolizumab and platinum-pemetrexed with or without bevacizumab for metastatic nonsquamous non-small cell lung cancer.

This article reported long-term overall survival outcomes of the phase III APPLE trial in adults with metastatic nonsquamous non-small cell lung cancer (NSCLC), comparing atezolizumab plus carboplatin/pemetrexed (APP) versus APP plus bevacizumab (APPB). The key finding was the final overall survival analysis after 3.5 years of follow-up, evaluating whether adding bevacizumab to atezolizumab-based chemotherapy improves survival and safety. Clinically, it informs the durability of benefit and risk profile for combining anti–PD-L1 therapy with anti-VEGF therapy in metastatic nonsquamous NSCLC.

Shiraishi Y, Kishimoto J, Sugawara S et al. · Lung cancer (Amsterdam, Netherlands) · (2026) · View on PubMed ↗

Blinatumomab Consolidation for High-Risk Ph-negative B-cell Acute Lymphoblastic Leukemia: the GRAALL-2014/B-QUEST Study.

This phase 2 GRAALL-2014/B-QUEST sub-study evaluated whether integrating blinatumomab (CD19×CD3 bispecific T-cell engager) into consolidation and maintenance improves outcomes in adults aged 18–59 with high-risk Philadelphia chromosome–negative B-cell acute lymphoblastic leukemia (B-ALL). The key finding was the clinical activity of blinatumomab within this high-risk consolidation/maintenance framework, building on its known efficacy in MRD-positive settings. Clinically, this supports blinatumomab as a strategy to reduce relapse risk in HR Ph-negative B-ALL by leveraging MRD-directed immunotherapy during consolidation and maintenance.

Boissel N, Huguet F, Leguay TT et al. · Blood · (2026) · View on PubMed ↗

RCLARITY: A Prospective Phase II Study of Rituximab Combined With Lenalidomide and Chidamide (RLC) for the Treatment of Relapsed/Refractory Angioimmunoblastic T-Cell Lymphoma.

This prospective multicenter Phase II single-arm trial studied a chemotherapy-free regimen of rituximab plus lenalidomide and chidamide in adult patients with relapsed/refractory angioimmunoblastic T-cell lymphoma (r/r AITL). The key reported finding was the trial’s evaluation of progression-free survival (PFS) as the primary endpoint for the RLC combination (rituximab 375 mg/m2 IV Day 1, lenalidomide 15 mg Days 1–21, chidamide 30 mg twice weekly in 28-day cycles up to 6 cycles). If efficacy and safety are favorable, this regimen could provide a novel, non-cytotoxic therapeutic option for a population with historically poor outcomes (historical OS <6 months).

Li C, Lei T, Xu X et al. · American journal of hematology · (2026) · View on PubMed ↗

Multicentric prognostic observational study on biomarker profile in immunotherapy-naïve patients with highly active generalized myasthenia gravis (PROGNO-MG): a study protocol.

This study protocol described the PROGNO-MG prospective multicenter observational effort to identify blood-based biomarker signatures predicting a highly active disease course in immunotherapy-naïve, acetylcholine-receptor-antibody positive (AChR+) generalized myasthenia gravis (gMG). The key aim is to enroll newly diagnosed patients and correlate biomarker profiles with subsequent disease activity to enable earlier, more aggressive immunotherapy for those at highest risk. Clinically, the work targets a major unmet need: objective biomarkers to prevent myasthenic exacerbations and crisis.

Kohle F, Konen FF, Grittner U et al. · Neurological research and practice · (2026) · View on PubMed ↗ · Free PDF ↗

Comprehensive mutational profiling and clinical outcome of adult acute myeloid leukemia patients with NUP98 rearrangement.

This cohort study performed comprehensive mutational profiling and clinical outcome analysis in 95 adult acute myeloid leukemia (AML) patients with NUP98 rearrangements (NUP98r). It found that NUP98::NSD1 was the most common fusion (54%) and that overall survival for the entire cohort was 15.2 months (95% CI 11.9–20.8), with distinct clinical and mutational features (including differences in age, karyotype, FLT3-ITD, and WT1 mutation rates) across NUP98r subtypes. The results improve prognostic understanding and molecular stratification for adult NUP98r AML, supporting more tailored risk assessment.

Ducourneau B, Pages A, Struski S et al. · Leukemia · (2026) · View on PubMed ↗

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Cancer immunogenicity via tumor mechanics & mitochondrial stress

Mechano-metabolic feedback connects tissue fluidity to mitochondrial DNA-dependent immunity in breast cancer.

This mechanistic cancer study examined how RAB5A-dependent endocytosis-driven tissue fluidization in invasive breast carcinoma triggers mitochondrial DNA-dependent immune signaling. RAB5A vesicles disrupted the AMPK-AKAP1-DRP1 mitochondrial fission pathway, causing mitochondrial elongation and BAX/BAK-dependent pore formation that produced a sub-lethal mitochondrial outer membrane permeabilization event amplified by palmitoylation. These findings link tumor mechanical state to mitochondrial stress and immunogenicity, offering potential targets to convert “cold” tumors into immunotherapy-responsive ones.

Palamidessi A, Frittoli E, Corada M et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

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Deubiquitinase biology & functional divergence of inhibition vs degradation

Targeted degradation of USP7 in solid cancer cells reveals distinct effects of deubiquitinase degraders and inhibitors.

Using melanoma and pancreatic cancer cell models, the study compared targeted degradation versus inhibition of the deubiquitinase USP7 to reveal distinct cellular effects of PROTAC “chemical knockdown” versus small-molecule/enzymatic inhibition. The key finding was that USP7 degradation and USP7 inhibition produced different functional outcomes, demonstrating that PROTAC-mediated loss of USP7 can diverge from catalytic blockade. This supports PROTAC design and interpretation as a way to more precisely interrogate ubiquitin-system biology and identify USP7-dependent vulnerabilities in solid cancers.

Klink N, Urban S, Seier JA et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

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Inflammation, necroptosis & organoid-based translational therapy

Reprogramming gut microenvironment for the treatment of acute severe ulcerative colitis via a synergistic therapy of necroptosis blockade and organoid transplantation.

In a study of acute severe ulcerative colitis (ASUC), the authors investigated RIPK1’s role in necroptosis initiation and developed an organoid-based dual-axis therapy combining necroptosis blockade with organoid transplantation. They found that PIAS1-catalyzed SUMO1 modification of RIPK1 at lysine 305 promotes RIPK1 compartmentalization into phase-separated structures that nucleate RIPK3 amyloid fibril assembly, and that disrupting this axis improves ASUC treatment when paired with organoid transplantation. Clinically, this provides a mechanistically grounded strategy to enhance efficacy of organoid therapy by targeting necroptosis signaling in ASUC.

Deng Q, Liu J, Shen J et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Inflammatory Myopathies.

This review studied inflammatory myopathies as a clinical and biological category, organizing five major subtypes—incorporating inclusion-body myositis, immune-mediated necrotizing myopathies, antisynthetase syndrome, overlapping myositis, and dermatomyositis. It found that these subtypes differ in organ involvement and prognosis, with inclusion-body myositis and immune-mediated necrotizing myopathies largely muscle-limited while antisynthetase syndrome, overlapping myositis, and dermatomyositis are systemic and can be life-threatening. The synthesis is significant for guiding subtype-specific diagnosis, risk stratification, and treatment selection in autoimmune muscle disease.

Allenbach Y, Benveniste O · The New England journal of medicine · (2026) · View on PubMed ↗

Telitacicept for IgA Nephropathy - Interim Analysis of a Phase 3 Trial.

The study evaluated telitacicept, a BAFF/APRIL-targeting fusion protein, in adults with biopsy-proven IgA nephropathy and persistent proteinuria despite supportive care in a prespecified interim analysis of a phase 3 randomized trial. It found that subcutaneous telitacicept (240 mg once weekly) versus placebo was assessed for efficacy and safety outcomes in this high-proteinuria population. The interim results are clinically important because they test whether dual BAFF/APRIL blockade can reduce disease activity and improve renal outcomes in IgA nephropathy.

Lv J, Liu L, Wang W et al. · The New England journal of medicine · (2026) · View on PubMed ↗

Ensitrelvir for Covid-19 Postexposure Prophylaxis in Household Contacts.

The study tested ensitrelvir, an oral SARS-CoV-2 3C-like protease inhibitor, for postexposure prophylaxis in household contacts who were SARS-CoV-2–negative at baseline. In a double-blind, randomized, placebo-controlled trial, participants received ensitrelvir dosing within 72 hours of exposure, and the study assessed whether it prevents subsequent COVID-19 compared with placebo. This is significant for expanding antiviral prevention options beyond treatment, potentially reducing transmission and illness in household outbreaks.

Hayden FG, Shinkai M, Clark TW et al. · The New England journal of medicine · (2026) · 1 citations · View on PubMed ↗

The alkylation of AIM2 by itaconate mediates macrophage PANoptosis during sepsis.

This mechanistic study investigated how the immunometabolite itaconate drives macrophage PANoptosis during sepsis by targeting the inflammasome sensor AIM2. It found that pathophysiologically high itaconate covalently alkylates AIM2 at cysteine 113 (C113), stabilizing AIM2, promoting ASC oligomerization, and triggering PANoptosome assembly leading to macrophage PANoptosis. These findings identify an itaconate–AIM2 chemical modification pathway as a potential target for modulating dysregulated inflammatory cell death in sepsis.

Ma J, Chen Y, Wang P et al. · Cellular & molecular immunology · (2026) · View on PubMed ↗ · Free PDF ↗

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DNA damage response & genome stability (Ku/WRN)

Structural basis of Ku-mediated activation of WRN exonuclease activity.

This structural biology study determined the molecular basis of how the Ku70/80 heterodimer activates the WRN exonuclease domain by solving a high-resolution cryo-EM structure of human Ku bound to DNA in complex with the N-terminal WRN exonuclease domain. The key finding was that Ku engages WRN through multiple interaction sites that explain stimulation of WRN nuclease activity. Scientifically, the structure clarifies a core DNA double-strand break response mechanism relevant to genome stability and Werner syndrome, where WRN deficiency drives premature aging and cancer predisposition.

Zahid S, Chauvat J, Ceppi I et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

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Hippo pathway & tissue growth control

STK38/L promote tissue growth and cancer by inhibiting the Hippo pathway.

The study investigated how STK38 and STK38L (NDR1/NDR2) regulate tissue growth and cancer by modulating the Hippo pathway. It found that STK38/L inhibit LATS by competitively binding MOB1 and disrupting the LATS–MOB1 complex in a kinase-activity-independent manner, thereby suppressing Hippo signaling. This identifies STK38/L as actionable regulators of Hippo pathway output, linking pathway control to tumor growth.

An J, Huang Z, Kizhedathu A et al. · Genes & development · (2026) · View on PubMed ↗ · Free PDF ↗

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Obstetrics & maternal hemorrhage prevention

International Multicentre Analysis of Perioperative Complications Following Major Urologic Oncologic Surgery: Early Results from More than 130 000 Procedures from the CAMUS Collaborative.

This international multicentre observational analysis used standardized complication grading across 130,034 perioperative procedures to characterize early complications after major urologic oncologic surgery in diverse patient populations. The key finding was a comprehensive global complication assessment across radical cystectomy, radical and partial nephrectomy, radical prostatectomy, radical nephroureterectomy, and retroperitoneal lymph node dissection, enabling benchmarking across centers. This supports quality improvement and more accurate patient counseling by providing large-scale, procedure-specific complication data.

Soliman C, Sathianathen N, Corcoran NM et al. · European urology focus · (2026) · View on PubMed ↗ · Free PDF ↗

Prophylactic tranexamic acid for the prevention of postpartum haemorrhage in women with placenta praevia: multicentre, double blind, randomised, placebo controlled, phase 3 trial.

In a multicentre, double-blind, randomized phase 3 trial in 1,732 Chinese women with placenta praevia undergoing caesarean delivery, the study tested prophylactic tranexamic acid (1 g IV) versus placebo in addition to oxytocin. The key finding was that prophylactic tranexamic acid reduced the incidence of postpartum hemorrhage compared with placebo. Clinically, this supports routine prophylactic TXA use to prevent postpartum hemorrhage in placenta praevia patients at the time of cord clamping.

Zhang L, Bi S, Chen L et al. · BMJ (Clinical research ed.) · (2026) · View on PubMed ↗ · Free PDF ↗

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Alzheimer’s disease: clinical outcomes, biomarkers & genetics

Clinical Meaningfulness of Donanemab in Early Symptomatic Alzheimer Disease: Data From the Randomized Phase 3 TRAILBLAZER-ALZ 2 Trial.

This analysis evaluated the clinical meaningfulness of donanemab, an anti-β-amyloid monoclonal antibody, using data from the randomized phase 3 TRAILBLAZER-ALZ 2 trial in early symptomatic Alzheimer disease (mild cognitive impairment or mild AD-related dementia). The key finding was that donanemab’s effects on cognitive and functional outcomes translate into clinically interpretable benefits across multiple outcome measures. This helps clinicians and patients contextualize trial results for shared decision-making about donanemab in early Alzheimer disease.

Atri A, Apostolova LG, Iwata A et al. · Neurology. Clinical practice · (2026) · View on PubMed ↗

Identification of genetic modifiers of autosomal dominant Alzheimer’s disease: a genome-wide association study.

This genome-wide association study analyzed genetic data from participants in three cohorts (Knight-ADRC, DIAN observational study, and Alzheimer’s Disease Neuroimaging Initiative) to identify genetic modifiers of autosomal dominant Alzheimer disease caused by PSEN1, PSEN2, or APP mutations. The key finding was the discovery of new genetic modifiers associated with variability in ADAD clinical presentation. Scientifically, these modifiers can refine risk prediction and highlight pathways that may be leveraged for therapeutic intervention in mutation-driven Alzheimer disease.

Patel M, Feng W, Mckay NS et al. · The Lancet. Neurology · (2026) · 1 citations · View on PubMed ↗ · Free PDF ↗

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Gene editing & gene therapy (AAV/CRISPR/base/prime) safety & efficacy

An X-linked long non-coding RNA, PTCHD1-AS, and the core features of autism.

This study examined whole-genome sequencing data from 9,349 ASD cases and 8,332 controls to identify X-chromosome microdeletions implicating the long non-coding RNA PTCHD1-AS as an autism susceptibility gene. The key finding was discovery of 27 male individuals with ASD carrying X-chromosome microdeletions involving PTCHD1-AS (odds ratio 2.56, P=0.01), supported by PTCHD1-AS knockout mouse models. Scientifically, it expands autism genetics beyond protein-coding genes and provides functional in vivo models to investigate how PTCHD1-AS disruption contributes to core autism features.

Bradley CA, Ko SY, Tian M et al. · Nature · (2026) · View on PubMed ↗ · Free PDF ↗

Image-based, pooled phenotyping reveals multidimensional, disease-specific variant effects.

The study developed and applied variant in situ sequencing (VIS-seq), a pooled image-based technique, to measure multidimensional cellular phenotypes caused by LMNA and PTEN variants in diverse cell types. VIS-seq revealed high-dimensional, disease-relevant morphological effects, including linker-subdomain LMNA variants increasing nuclear circularity while aggregating or low-abundance rod-subdomain variants decreased circularity, and it identified autism-associated PTEN variant effects. These results show that VIS-seq can more directly map genotype-to-cell-phenotype relationships than conventional single-readout assays, improving variant interpretation for genetic disease.

Pendyala S, Partington K, Bradley N et al. · Cell · (2026) · View on PubMed ↗

Neuroepithelial Tumor with AAV Integration after Intracisternal Magna Vector Delivery.

A 5-year-old boy with severe mucopolysaccharidosis type I (Hurler subtype) was studied after intracisternal magna delivery of an AAV9 gene therapy vector, with tumor tissue analyzed for vector integration. Four years later, a neuroepithelial tumor developed and molecular profiling showed clonal integration of rearranged AAV vector elements in the tumor. This case provides clinical evidence that rare AAV genomic integration can occur after intracisternal delivery and may contribute to oncogenesis, informing long-term safety monitoring of AAV gene therapies.

Ahrens-Nicklas RC, Kotch C, Roche AM et al. · The New England journal of medicine · (2026) · View on PubMed ↗

uPAR is highly expressed in recurrent glioblastoma and represents a candidate CAR T cell target.

Patient-derived primary and recurrent glioblastoma cell lines were analyzed using multiomic profiling to identify therapeutic targets, and uPAR (urokinase plasminogen activator receptor) was functionally tested in vitro and in vivo. uPAR was highly expressed in recurrent glioblastoma and genetic disruption of uPAR impaired protumorigenic properties, supporting uPAR as a candidate CAR T-cell target. These findings suggest a rationale for developing uPAR-directed CAR T therapies to address tumor heterogeneity and recurrence in glioblastoma.

Maich WT, Shaikh MV, Puri A et al. · Science translational medicine · (2026) · View on PubMed ↗

In vivo adenine base editing ameliorates Dravet syndrome phenotypes in a mouse model.

Adenine base editing was used in a mouse model of Dravet syndrome to directly correct the recurrent SCN1A R613X variant, with editing strategies evaluated for phenotypic rescue. In vivo adenine base editing efficiently corrected the SCN1A R613X mutation and ameliorated Dravet syndrome phenotypes, including seizure-related outcomes. This supports base-editing of SCN1A as a potential disease-modifying approach for Dravet syndrome beyond symptom management.

Nelson AT, Hill SF, Simon M et al. · Science translational medicine · (2026) · View on PubMed ↗ · Free PDF ↗

RNA-LNP-mediated in vivo prime editing corrects disease phenotypes in a mouse model of citrullinemia type I.

Prime editing was applied to the ASS1 gene in a mouse model of citrullinemia type I (CTLN1), using AAV-mediated delivery of the PE7 prime editor plus optimized pegRNA in hepatocytes and, separately, RNA-LNP delivery of PE7 mRNA and pegRNA. AAV-PE7/pegRNA achieved 71% and 54% correction of the pathogenic Ass1 mutation in hepatocytes of neonates and juveniles, respectively, while LNP delivery produced 24% correction after a single 3 mg/kg dose in neonates and 13% after three 4 mg/kg doses. These results indicate that in vivo prime editing can substantially correct CTLN1-relevant mutations in liver, potentially reducing reliance on liver transplantation.

Tálas A, Ioannidi EI, Weber Y et al. · Science translational medicine · (2026) · View on PubMed ↗

Prime editing of a pathogenic Scn1a allele ameliorates seizure phenotypes in a GEFS+ mouse model.

Prime editing was used to correct a pathogenic Scn1a allele in a GEFS+ mouse model, where SCN1A loss-of-function drives altered NaV1.1 function and seizure susceptibility. Correcting the pathogenic Scn1a allele with prime editing ameliorated seizure phenotypes in the GEFS+ model. This provides preclinical support for prime-editing strategies targeting SCN1A as a potential disease-modifying treatment for inherited epilepsy.

Kissling L, Pietrafesa F, Ranucci M et al. · Science translational medicine · (2026) · View on PubMed ↗

Adjuvant personalized multivalent neoantigen DNA vaccination for MGMT unmethylated glioblastoma: a phase 1 trial.

This phase 1 open-label, single-arm trial (GT-20) studied the safety, feasibility, immunogenicity, and preliminary efficacy of the DNA-based personalized neoantigen vaccine GNOS-PV01 in nine patients with MGMT-unmethylated glioblastoma after surgical resection and radiation. GNOS-PV01 was administered as adjuvant personalized multivalent neoantigen DNA vaccination to generate neoantigen-directed immune responses, addressing prior low immunogenicity seen with neoantigen vaccines in glioblastoma. If confirmed in larger studies, this MGMT-unmethylated, post-resection/post-radiation personalized DNA vaccine strategy could provide a clinically actionable immunotherapy option for a molecularly defined glioblastoma subgroup.

Garfinkle EAR, Perales-Linares R, Gimple RC et al. · Nature cancer · (2026) · View on PubMed ↗ · Free PDF ↗

CRISPR-Cas9 CD33-deleted allogeneic hematopoietic cell transplantation with gemtuzumab ozogamicin maintenance in AML: a phase 1/2 trial.

This multicenter phase 1/2a open-label trial studied a CRISPR-Cas9 gene-edited allogeneic hematopoietic cell transplantation product, tremtelectogene empogeditemcel (trem-cel), in adult patients with high-relapse-risk AML/MDS. The therapy used CD33 deletion to shield the donor graft from cytotoxicity of subsequent CD33-targeted maintenance with gemtuzumab ozogamicin (GO), aiming to enable GO maintenance after myeloablative conditioning. If effective and safe, this CD33-edited allogeneic HCT plus GO maintenance strategy could reduce relapse while minimizing toxicity to normal donor-derived cells.

DiPersio JF, Koehne G, Shah NN et al. · Nature medicine · (2026) · View on PubMed ↗ · Free PDF ↗

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Generated automatically on May 15, 2026 from PubMed’s trending articles. Summaries are AI-generated; always consult the original publication for clinical or research decisions.