PubMed Trending Research Digest — June 13, 2026
A curated digest of 95 trending PubMed articles, automatically categorised and summarised across 15 research areas.
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PubMed Trending Research Digest — June 13, 2026
Automated digest · 95 articles · 15 research areas · June 13, 2026
Overview
This week’s digest is dominated by two converging trends: (1) precision, multi-omic stratification to identify who will benefit from therapies and (2) mechanistic links between immune state, metabolism, and disease progression. Across oncology and neurodegeneration, studies used single-cell/spatial multi-omics, proteomics, and AI-enabled spatial biomarker discovery to connect cellular programs (e.g., immune fitness, lipid–stemness pathways, senescence “senotypes,” and allele-specific regulatory dysregulation) to response, resistance, and survival. In parallel, multiple papers emphasized how metabolic context—obesity, fasting redox programs, amino-acid sensing, and diet-driven inflammatory signaling—reshapes inflammatory pathways and therapeutic effectiveness.
Immunotherapy and immune regulation also featured prominently, spanning solid-tumor strategies (armed/ex vivo expanded T cells, ECM remodeling CAR-T approaches, and NK-driven evolutionary trajectories) and immune-mediated disease frameworks (cGVHD biology, pulmonary antibody-mediated rejection definitions, and immune selection/immunoediting in tumors). Several clinical and consensus efforts aimed to standardize care and improve decision-making—ranging from prostate MRI screening standards and epilepsy surgery evaluation practices to HIV low-level viraemia definitions and ICU resuscitation guidance. Together, these articles suggest a field moving toward more standardized endpoints and more mechanistically grounded patient selection.
Finally, reproductive and developmental biology remained a key theme, with advances in placental metabolic sensing, trophoblast stem cell modeling for preeclampsia, and mechanistic identification of early embryonic arrest bottlenecks. Meanwhile, infectious disease surveillance and pediatric immune response characterization (e.g., tularemia cytokine dynamics; community spread of MDR Klebsiella via plasmids) highlight ongoing efforts to translate molecular epidemiology into practical public-health action.
HIV persistence, latency, and low-level viraemia
Guidance on the clinical management of HIV-1 persistent low-level viraemia on antiretroviral treatment: a scoping review and an international Delphi consensus.
This scoping review and modified Delphi consensus studied definitions and clinical management of HIV-1 persistent low-level viraemia (LLV) in people on antiretroviral treatment, synthesizing evidence across settings and expert panel recommendations. The key finding was that LLV definitions vary widely, most commonly using repeated viral loads of 50–1000 copies/mL, with heterogeneous outcomes and evidence linking LLV at 50–200 copies/mL to higher risk of virological failure (>1000 copies/mL). These consensus guidance efforts are clinically significant because they standardize how persistent LLV is defined and managed to improve decision-making and reduce inconsistent care.
Clemente T, Stam AJ, Elvstam O et al. · The lancet. HIV · (2026) · View on PubMed ↗
International Society for Heart and Lung Transplantation Scientific Statement on pulmonary antibody-mediated rejection and proposed graft, antibody, and pathology (GAP) definition.
This International Society for Heart and Lung Transplantation scientific statement reviewed evidence on pulmonary antibody-mediated rejection (AMR) and updated the proposed graft, antibody, and pathology (GAP) definition using a modified Delphi consensus process. It synthesizes current research and clinical experience to refine how pulmonary AMR is defined and diagnosed after lung transplantation. The updated GAP framework is intended to standardize diagnosis and improve comparability of studies and clinical decision-making in a setting with poor AMR outcomes.
Calabrese F, Levine DJ, Adam BA et al. · The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation · (2026) · View on PubMed ↗ · Free PDF ↗
Pharmacological and genetic modulation of IL-32 expression in intestinal epithelial cells does not impact HIV-1 outgrowth in co-cultured CD4+ T-cells.
This study examined whether pharmacological and genetic modulation of IL-32 expression in intestinal epithelial cells (IEC) affects HIV-1 outgrowth in co-cultured CD4+ T cells from ART-treated people with HIV-1. The authors found that altering IL-32 expression in IEC did not change HIV-1 outgrowth in the IEC–CD4+ T-cell co-culture system. These results suggest IL-32 is not a causal driver of HIV-1 reactivation/outgrowth in this gut-epithelial crosstalk model, refining targets for understanding latency versus reactivation in the intestinal mucosa.
Moreira Gabriel E, Moreaux J, Kaofai C et al. · Frontiers in immunology · (2026) · View on PubMed ↗ · Free PDF ↗
Immunotherapy for solid tumors (CAR-T/BATs/BsAbs and tumor microenvironment)
Natural killer cell-mediated immunosurveillance modulates liver cancer evolution through cancer stemness enhancement and lipid metabolism reprogramming.
In immune-humanized spatiotemporal liver cancer models, this study integrated single-cell and spatial transcriptomics with CRISPR/Cas9 screening to define how natural killer (NK) cells shape liver cancer evolution. It showed that early NK cell-mediated immunosurveillance promotes tumor state transitions, enhances cancer stemness, and reprograms lipid metabolism—particularly cholesterol accumulation—while impairing later adaptive immune responses. These findings suggest NK activity can drive pro-tumor evolutionary trajectories in liver cancer, highlighting lipid–stemness pathways as potential therapeutic targets.
Shi L, Liu B, Sun R et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗
Heparanase-Loaded CAR T Extracellular Vesicles Remodel the Colorectal Tumour Microenvironment and Boost T Cell Antitumor Immunity.
The study engineered mesothelin-targeted CAR T cells to display heparanase (HPSE) fused to the truncated hepatitis A virus pX domain (pX-Δ1-30) on extracellular vesicles to remodel the colorectal tumor microenvironment. HPSE-pX-Δ1-30 CAR T cells penetrated ECM mimics nearly fourfold more effectively than standard CAR T cells and increased pro-apoptotic signaling (including TRAIL) to enhance antitumor activity. This supports a strategy to improve solid-tumor CAR T efficacy by locally, pH-dependent ECM degradation while limiting systemic exposure.
Zhu S, Yin J, Yang W et al. · Journal of extracellular vesicles · (2026) · View on PubMed ↗ · Free PDF ↗
NIR-II Imaging-Guided Phototherapy-Induced Senescence Reprograms Immunosuppressive Tumor Microenvironment for Potent Cancer Immunotherapy.
This preclinical study developed an NIR-II imaging-guided phototherapy nanoplatform that induces reactive oxygen species–mediated cellular senescence in triple-negative breast cancer to reprogram the immunosuppressive tumor microenvironment. The approach promoted a senescence-associated secretory phenotype (SASP) that enhanced immune infiltration and improved anti-tumor immunotherapy potency. The work suggests a strategy to convert senescence from a tumor-permissive state into an immunostimulatory mechanism for cancer treatment.
Yang Z, Ou X, Tang Z et al. · ACS nano · (2026) · View on PubMed ↗
Beyond the chimeric antigen receptor T cells and bispecific antibody duopoly: ex vivo armed T cells for solid tumors.
This article reviewed and conceptually evaluated ex vivo armed T cells (EATs/BATs) for solid tumors as an alternative to the CAR-T and bispecific antibody (BsAb) “duopoly,” focusing on how antibody-mediated targeting can be combined with ex vivo expanded T-cell effector function. The key finding is that BATs/EATs can provide a “third way” to address limitations of CAR-T and BsAbs in solid tumors, including the need for more diversified targeting and effector strategies. Scientifically and clinically, this supports further development of armed T-cell platforms for solid tumor immunotherapy where tumor complexity and therapeutic resistance remain major barriers.
Park JA, Cheung NV · Frontiers in immunology · (2026) · View on PubMed ↗ · Free PDF ↗
Cancer genomics, biomarkers, and functional genomics (omics, imaging, AI)
Optimized post-GWAS analysis identifies therapeutic targets for essential thrombocythemia and polycythemia vera.
Using an optimized post-GWAS framework that combines omics-wide Bayesian colocalization with Mendelian randomization (MR), this study prioritized genetically supported molecular determinants and distinguished shared versus subtype-specific causal pathways for essential thrombocythemia (ET) and polycythemia vera (PV). The analysis identified therapeutic targets supported by genetic evidence that help clarify disease susceptibility and hematologic phenotype regulation. These results provide a prioritized target list to accelerate mechanism-driven therapeutic development for ET and PV.
Li X, An W, Wang X et al. · Communications medicine · (2026) · View on PubMed ↗ · Free PDF ↗
Large-scale, spatially resolved panoramic CRISPR screening in native tissue environments using Perturb-DBiT.
This study developed Perturb-DBiT, a spatially resolved CRISPR screening method that co-sequences total RNA whole transcriptomes and sgRNAs from the same tissue section in situ. In a human cancer metastatic colonization model, it applied 80,000+ sgRNA perturbations across tumor colonies and linked perturbation-driven changes in lncRNA covariation, microRNA–mRNA interactions, and amino-acid-specific tRNA alterations to tumor migration and growth. The technique enables large-scale, spatially contextual functional genomics in native tissue environments, improving discovery of regulators of metastasis and therapy-relevant phenotypes.
Baysoy A, Tian X, Renauer P et al. · Nature biotechnology · (2026) · 1 citations · View on PubMed ↗ · Free PDF ↗
SenCat: Cataloging human cell senescence through multi-omic profiling of multiple senescent primary cell types.
This study profiled transcriptomes and proteomes to build SenCat, a multi-omic catalog of human cell senescence across 14 primary human cell types subjected to 30+ senescence paradigms. The key finding was that senescent cells did not share a single unique marker but did converge on shared metabolic and damage-response pathways, and machine-learning-refined SenCat signatures enabled senescence scoring and cross-dataset identification in human and mouse data. This is scientifically significant because it provides a cell-type-resolved, multi-omic framework for quantifying senescence heterogeneity and comparing senescence states across experiments.
Anerillas C, Altés G, Gresova K et al. · Molecular cell · (2026) · View on PubMed ↗ · Free PDF ↗
Spatial biomarker discovery via interpretable semantic learning in histopathology.
This study developed PathPrism, an interpretable semantic-learning AI framework for discovering spatial biomarkers from histopathology whole-slide images. The key finding was that PathPrism encodes tissue architecture into pathologically informed spatial features and, when applied to 7,000 colorectal cancer patients across 11 cohorts, uncovered hundreds of interpretable biomarkers predicting survival and molecular alterations (including MSI, BRAF, and TP53) and stratifying chemotherapy benefit in stage II/III disease. This is significant for precision oncology because it enables transparent, spatially grounded biomarker discovery and “virtual experimentation” rather than relying on black-box models.
Liang J, Jiang X, Reitsam NG et al. · Cancer cell · (2026) · View on PubMed ↗ · Free PDF ↗
Mapping cell type-resolved transcriptomic profiles to patient survival in pancreatic cancer.
This study integrated single-nucleus RNA-seq with longitudinal clinical data to map cell type-resolved transcriptomic profiles to patient survival in 152 patients with pancreatic ductal adenocarcinoma (PDAC), profiling 1.2 million cells. The key finding was that the resulting prognostic map linked specific cell-type gene expression programs to overall survival, and spatial transcriptomic analysis using a single-cell-resolved platform (3.1 million cells) further associated spatial distribution with therapeutic response. This is clinically significant because it enables cell-type- and location-aware prognostic and treatment-response insights, packaged as the ctPANDA interactive platform.
Tang R, Jin L, Chen C et al. · Cancer cell · (2026) · View on PubMed ↗ · Free PDF ↗
Transposable element DNA and RNA: Drivers of gene expression, evolution, and disease.
This Cell review studied how transposable element (TE) DNA and TE-derived RNA regulate gene expression, genome evolution, and disease, focusing on locus-specific TE functions enabled by long-read sequencing and functional (epi)genomics. The key finding is that individual TE loci—rather than TE families—frequently act as alternative promoters, enhancers, splicing regulators, and 3D genome organizers even when most TEs are no longer mobilizable. This is significant for interpreting noncoding regulatory variation and for linking TE activity to human disease mechanisms and evolutionary change.
Ho JSY, Douse CH, Marazzi I · Cell · (2026) · View on PubMed ↗
Charting human cellular senescence in aging and disease.
This review studied how to map cellular senescence across human tissues in aging and disease by integrating single-cell and spatial multi-omics with AI-driven analyses to define senescent cell states (“senotypes”). The key finding is that these combined approaches reveal tissue-specific senescence programs and senescent cell–microenvironment interactions that can be used for biomarker discovery and development of senotherapeutic strategies. This is significant because it provides a scalable framework for identifying actionable senescence targets and improving precision interventions.
Suryadevara V, Farzad N, Yang M et al. · Cell · (2026) · View on PubMed ↗
Colocalization of eQTLs With Type 2 Diabetes and Glycemic Traits Using Whole-Genome Sequences in Diverse Populations From the NHLBI Trans-Omics in Precision Medicine (TOPMed) Program.
This TOPMed-based genetic study used whole-genome sequencing in diverse populations to colocalize expression quantitative trait loci (eQTLs) with type 2 diabetes and glycemic traits. The authors improved fine-mapping resolution and identified 80 regulatory colocalization signals in diabetes-relevant tissues, linking genetic variants to regulatory mechanisms. These results advance precision medicine by connecting GWAS signals to functional biology underlying type 2 diabetes.
Wang N, DiCorpo DA, Zhang Y et al. · Diabetes · (2026) · View on PubMed ↗
Hematologic malignancies (leukemia/lymphoma/myeloma) therapies and targets
Targeting SMC3 deacetylation synergizes with XPO1 inhibition to reprogram the epigenetic landscape and suppress NPM1-mutated acute myeloid leukemia.
This study investigated how targeting SMC3 deacetylation and inhibiting XPO1 affects NPM1-mutated acute myeloid leukemia (AML), using mechanistic experiments in NPM1c AML models and pharmacologic HDAC8 inhibition. The authors report that loss of ESCO2 destabilizes cohesin and the NuRD complex, promoting leukemia self-renewal, and that HDAC8 inhibition restores SMC3 binding to induce differentiation and apoptosis in NPM1-mutated AML, with synergy from XPO1 inhibition to reprogram the epigenetic landscape. Scientifically, it links cohesin/SMC3 acetylation control to NPM1c AML epigenetic regulation and suggests a combined therapeutic strategy (HDAC8/SMC3 axis plus XPO1 inhibition) for this genetic AML subtype.
Fu J, Xu H, Zhao X et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗
Early predictors of MR4.5 attainment and eligibility for TKI discontinuation in CML treated with second-generation TKIs.
This analysis studied early predictors of achieving and maintaining MR4.5 (BCR::ABL1 IS ≤ 0.0032%) and eligibility for tyrosine kinase inhibitor (TKI) discontinuation in chronic myeloid leukemia (CML) patients treated with second-generation TKIs. Using data from 431 patients in the phase III JALSG CML212 trial comparing nilotinib (300 mg twice daily) versus dasatinib (100 mg once daily), the authors identified clinical/laboratory factors associated with MR4.5 attainment and sustained deep molecular response. This is significant because it can refine patient selection for TKI discontinuation strategies and improve long-term management decisions in CML.
Ono T, Okada T, Takahashi N et al. · Blood advances · (2026) · View on PubMed ↗ · Free PDF ↗
Product-Intrinsic NF-κB-Driven Transcriptional Programs Connote Durability of CAR-T Response in Multiple Myeloma.
This study profiled 40 idecabtagene vicleucel (ide-cel) infusion products from relapsed/refractory multiple myeloma patients using single-cell RNA sequencing to identify transcriptional features linked to durable CAR-T response. A CD4 CAR-T intrinsic NF-κB-driven transcriptional program was associated with durability, distinguishing durable from non-durable responders at single-cell resolution. These product-intrinsic biomarkers could guide patient counseling and inform manufacturing or engineering strategies to increase long-term response rates.
Noble JD, Peixoto BC, Menges MA et al. · Blood · (2026) · View on PubMed ↗
A novel triple-knockout allogeneic BCMA CAR T cell therapy (CT0590) in multiple myeloma: preclinical and phase I study.
This preclinical and phase I study evaluated a novel allogeneic BCMA CAR T product (CT0590) in multiple myeloma, using an HLA-I-deficient BCMA CAR T armored with an NKG2A CAR to mitigate host-versus-graft NK-cell attack. The dual-targeting BCMA/NKG2A allogeneic CAR T cells resisted NK-mediated killing in vitro and showed robust antitumor activity in vivo, leading to first-in-human enrollment of five patients. The approach advances safer allogeneic CAR T design by reducing HvGR-related rejection while preserving antitumor function.
Jin S, Liao Z, Yan S et al. · Blood · (2026) · View on PubMed ↗
Indirect Comparison of the Efficacy of Zanubrutinib vs Ibrutinib and Acalabrutinib in Treatment-Naive Chronic Lymphocytic Leukemia: 6-Year Follow-Up.
This indirect treatment comparison evaluated long-term efficacy of zanubrutinib versus ibrutinib and versus acalabrutinib in treatment-naive chronic lymphocytic leukemia (CLL) using cross-trial naive comparisons aligned across SEQUOIA (zanubrutinib), ELEVATE-TN (acalabrutinib), and RESONATE-2 (ibrutinib). The analysis reported comparative progression-free survival and overall survival outcomes over a 6-year follow-up period, supporting relative efficacy differences among the BTK inhibitors. Clinically, the results help inform selection of first-line BTK inhibitor therapy in treatment-naive CLL in the absence of head-to-head trials.
Shadman M, Munir T, Xu S et al. · Advances in therapy · (2026) · View on PubMed ↗ · Free PDF ↗
Romosozumab for cancer treatment-induced bone loss in postmenopausal women with hormone receptor-positive breast cancer: a case series.
This retrospective case series studied romosozumab for cancer treatment-induced bone loss (CTIBL) in postmenopausal women with hormone receptor–positive breast cancer receiving aromatase inhibitor therapy. Romosozumab increased bone mineral density and showed no observed clinical signals of fracture occurrence or cancer recurrence in the small cohort. The results suggest a potential anabolic option for CTIBL, but they require confirmation in larger prospective studies.
Tsujino S, Koyanagi H, Sawamura C et al. · Archives of osteoporosis · (2026) · View on PubMed ↗
High-Dose Methotrexate as CNS Prophylaxis in Ultra High-Risk Large B-Cell Lymphoma: An International Multicenter Analysis.
This international multicenter analysis assessed whether high-dose methotrexate (HD-MTX) used as CNS prophylaxis affects outcomes in ultra high-risk (UHR) patients with large B-cell lymphoma (LBCL). By combining two prior retrospective datasets, the study compared UHR patients treated with versus without HD-MTX using UHR criteria such as CNS-IPI 5–6 and specific extranodal or organ involvement. The findings aim to clarify the clinical value of HD-MTX CNS prophylaxis in the subgroup where guidelines currently recommend it despite limited robust evidence.
Wilson MR, Lewis KL, Kirkwood AA et al. · Journal of clinical oncology : official journal of the American Society of Clinical Oncology · (2026) · 1 citations · View on PubMed ↗ · Free PDF ↗
Exa-cel in Children with Transfusion-Dependent β-Thalassemia or Sickle Cell Disease.
This phase 3 study evaluated exagamglogene autotemcel (exa-cel), an autologous CD34+ CRISPR-Cas9–edited cell therapy targeting the erythroid enhancer of BCL11, in children aged 5–11 years with transfusion-dependent β-thalassemia or sickle cell disease. Exa-cel eliminated vaso-occlusive crises and reduced/removed the need for red-cell transfusions in this pediatric population. These results support exa-cel as a potentially curative, gene-editing approach that can be extended to younger children with hemoglobinopathies by reactivating fetal hemoglobin through BCL11 editing.
Frangoul H, de la Fuente J, Chopra Y et al. · The New England journal of medicine · (2026) · View on PubMed ↗
Longitudinal mechanisms of response, resistance and relapse to teclistamab in multiple myeloma: results from MajesTEC-1.
This longitudinal analysis of MajesTEC-1 correlated peripheral blood and bone marrow tumor microenvironment immune profiles and BCMA antigen expression with clinical response, resistance, and relapse to teclistamab in triple-class-exposed relapsed/refractory multiple myeloma. The study found that immune fitness and specific T-cell/tumor microenvironment states tracked with response, while resistance/relapse were associated with immune dysfunction and altered BCMA-related features over time. These mechanistic insights can guide biomarker-driven patient selection and strategies to prevent or overcome teclistamab resistance.
Vishwamitra D, Skerget S, Cortes-Selva D et al. · Haematologica · (2026) · View on PubMed ↗ · Free PDF ↗
Cancer mechanisms: signaling, transcription factors, epigenetics, and condensates
TEAD1 condensates are transcriptionally inactive storage sites on the pericentromeric heterochromatin in cancer cells.
This study examined how TEA domain transcription factor 1 (TEAD1) organizes nuclear condensates in cancer cells, using high-resolution imaging, ChIP-seq, RNA sequencing, and proximity-based proteomics in patient-derived renal cell carcinoma cells. TEAD1 formed micrometre-sized condensates on pericentromeric heterochromatin that were transcriptionally inactive, seeded by TEAD-specific MCAT motifs via TEAD1’s DNA-binding domain. The discovery reframes TEAD1’s role in cancer biology from purely transcriptional regulation to nuclear condensate organization, suggesting new avenues for targeting TEAD1-associated chromatin states.
Wang Y, Liang J, Lange KS et al. · Nature cell biology · (2026) · View on PubMed ↗ · Free PDF ↗
Dynamic transitioning between MAPK-driven and WNT-driven cell states drives intestinal cancer and shapes therapy response.
Using an allele-specific mouse model of intestinal KRAS-driven MAPK hyperactivation, this work investigated how MAPK- and WNT-pathway states govern colorectal cancer initiation and therapy response. It showed that KRAS mutations drive a regenerative state that antagonizes Lgr5+ intestinal stem cells, but tumor initiation requires a WNT-driven stem-like state dependent on WNT pathway activation. The findings clarify a state-transition mechanism that could be exploited to improve therapeutic targeting of the stem-like WNT program in CRC.
Moore AR, Biehs B, Kljavin N et al. · Nature genetics · (2026) · View on PubMed ↗
FOXP4 promotes metastatic progression in colorectal cancer through transcriptional activation of BAG3.
This study investigated the role of the transcription factor FOXP4 in colorectal cancer (CRC) metastasis, integrating analyses across patient cohorts and single-cell transcriptomics with functional experiments. It found that FOXP4 is upregulated in malignant epithelial cells, correlates with poor survival, and that FOXP4 depletion reduces tumor growth, angiogenesis, and liver metastatic burden in vivo, via transcriptional activation of the co-chaperone BAG3. The significance is that FOXP4–BAG3 signaling may be a tractable driver of epithelial plasticity and metastatic progression in CRC.
Wang J, Yu T, Liu L et al. · Cell death & disease · (2026) · View on PubMed ↗ · Free PDF ↗
Immunoediting restricts clonal neoantigens in primary, treatment-naive human tumors.
This work examined immunoediting effects on the antigen landscape in primary, treatment-naive human tumors using cutaneous squamous cell carcinoma samples from immunocompetent versus immunosuppressed patients. The key finding was that high-immune-infiltrate tumors from immunocompetent patients had lower overall and clonal mutational burdens than low-infiltrate tumors from immunocompetent patients and tumors from immunosuppressed patients, consistent with immune selection of neoantigens. This is clinically significant because it supports immunoediting as a mechanism shaping which clonal neoantigens persist in human tumors, informing immunotherapy target selection.
Borden ES, Castellano D, Kantzos EA et al. · Immunity · (2026) · View on PubMed ↗
A protective role for APP in nuclear waste clearance via lysosomal exocytosis.
The study examined the physiological role of amyloid precursor protein (APP) in nuclear waste clearance under genotoxic stress in cultured cells and mouse models. Loss of APP caused nuclear-derived debris accumulation, increased inflammation, and cell death, whereas APP overexpression reduced these effects by promoting extracellular release of nuclear waste via lysosomal exocytosis. These results position full-length APP as a protective regulator of lysosomal exocytosis and nuclear waste disposal, extending APP biology beyond amyloid-β production.
Dougnon G, Otsuka T, Nakamura Y et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗ · Free PDF ↗
Chemically induced skin tumors arise from long-lived stem cells of the upper hair follicle.
The study used fluorescent lineage tracing, single-cell transcriptomics, and Duplex sequencing to identify the cell of origin of chemically induced skin tumors in mice. Tumors predominantly arose from long-lived Lgr6+ and/or Lrig1+ stem cells of the upper hair follicle, with initiated Lgr6+ cells showing clonal expansion after dimethylbenzanthracene initiation and tumor promoter treatment, including canonical Hras Q61L mutations. This pinpoints upper hair follicle stem cell subtypes as the main origins of these tumors and links initiation/promotion to specific oncogenic clonal trajectories.
Kandyba E, Jabouille A, Calvet F et al. · Science (New York, N.Y.) · (2026) · View on PubMed ↗
RNF138 promotes cisplatin resistance and PD-L1-mediated immune evasion via JAK2/STAT3 activation in nasopharyngeal carcinoma.
This study investigated the role of the E3 ubiquitin ligase RNF138 in nasopharyngeal carcinoma chemoresistance and immune evasion, focusing on RNF138-mediated signaling through JAK2/STAT3. RNF138 promoted K48-linked ubiquitination of hnRNPA0 at K133 to destabilize WWOX mRNA, which relieved inhibition of JAK2 self-phosphorylation and activated JAK2/STAT3, suppressing chemotherapy-induced apoptosis via reduced ROS and increasing PD-L1-mediated immune evasion. These findings identify RNF138–hnRNPA0–WWOX–JAK2/STAT3 as a mechanistic axis and potential therapeutic target to overcome cisplatin resistance and immune escape in NPC.
He C, Lou L, Lei Y et al. · Cell reports · (2026) · View on PubMed ↗ · Free PDF ↗
Microbiome and host–microbe interactions in disease
Intratumor Lactobacillus drives ferroptosis resistance via D-lactate-STAT3 K631 lactylation in esophageal squamous cell carcinoma.
This study investigated how intratumor Lactobacillus alters stress responses in esophageal squamous cell carcinoma (ESCC) by integrating 16S rRNA gene sequencing from 27 patients with multiregional tissue blocks with metabolomics, RNA sequencing, and mass spectrometry, followed by mechanistic testing in ESCC cell lines and nude-mouse xenografts. Tumor-enriched Lactobacillus (notably Lactobacillus reuteri) promoted ferroptosis resistance via D-lactate–STAT3 K631 lactylation, contrasting with host-derived L-lactate effects. The findings link a specific intratumor bacterial metabolite to a defined STAT3 post-translational modification that could be targeted to sensitize ESCC to ferroptosis-based therapies.
Wang D, Lu H, Li W et al. · Gut microbes · (2026) · View on PubMed ↗ · Free PDF ↗
Gardnerella enrichment in the vaginal microbiome of women with gestational diabetes mellitus is associated with lower fetal birthweight percentiles.
In a single-centre observational case-control study of diet-managed gestational diabetes mellitus (GDM) in pregnancy (n=60) versus healthy controls (n=119), late-pregnancy vaginal microbiota were characterized using full-length 16S rRNA gene sequencing of third-trimester vaginal swabs. Women with GDM showed enrichment of Gardnerella, which was associated with lower fetal birthweight percentiles (FBW%ile). These findings suggest that Gardnerella-associated vaginal microbiome shifts may contribute to impaired fetal growth in GDM and could inform microbiome-targeted risk stratification.
Fu Y, Long N, Sourn P et al. · Diabetologia · (2026) · View on PubMed ↗ · Free PDF ↗
Genomic landscape of the human vaginal microbiome is linked to host genetics and population of origin.
This study analyzed host–microbe relationships in the vaginal microbiome by building the Global Vaginal Metagenome-assembled Genomes (vMAG) catalog from 10,665 in-house Chinese metagenomes plus 2,967 public metagenomes and 1,433 bacterial isolates. It found that vaginal microbial genomic diversity is linked to host genetics and population of origin, and it mapped conserved virus–bacteria (phage–host) associations. The resulting catalog and host-genetic/population associations improve understanding of how host factors shape vaginal microbiome function and may guide personalized interventions.
Jie Z, Liang W, Ding Q et al. · Nature genetics · (2026) · View on PubMed ↗ · Free PDF ↗
Metabolic disease, obesity, and cardiometabolic risk
Nutrition-First Support for GLP-1 and Dual Incretin Therapy in Obesity: A Practical Framework for Dietary Management, Symptom Tolerability, and Long-Term Weight Maintenance.
This narrative review synthesized evidence to propose a “nutrition-first” practical framework for dietary management, symptom tolerability, and long-term weight maintenance in patients treated with GLP-1 receptor agonists and dual GIP/GLP-1 receptor agonists for obesity. It emphasizes that gastrointestinal adverse events, reduced intake, fat-free mass loss, and weight regain after discontinuation can limit real-world effectiveness and should be addressed through structured nutrition strategies. The framework is clinically significant for improving tolerability and preserving body composition during and after incretin-based therapy.
Zambrano-Villacres R, Campuzano-Donoso M, Reytor-González C et al. · Nutrients · (2026) · View on PubMed ↗ · Free PDF ↗
Plasma proteomics of sleep traits reveals systemic immune-metabolic pathways and genetically prioritized proteins.
In 43,709 predominantly European-ancestry UK Biobank participants, this study used plasma proteomics to associate protein levels with seven self-reported sleep traits and a derived sleep health score. It identified 935 proteins linked to at least one sleep trait, converging on immune/inflammation and lipid metabolism pathways, and used genomic structural equation modeling to prioritize genetically influenced proteins. These results provide a systems-level immune-metabolic framework for sleep biology and nominate proteins for causal prioritization in sleep-related risk.
Chen H, Wang X, Chen W et al. · Molecular psychiatry · (2026) · View on PubMed ↗
Cryo-EM structure of the LARS1:IARS1 complex reveals a nutrient-responsive switch controlling mTORC1 signaling.
This study used cryo-electron microscopy along with structural, biochemical, and cellular assays to determine the structure of the LARS1:IARS1 complex and define how leucine sensing by human cytosolic leucyl-tRNA synthetase 1 (LARS1) regulates mTORC1 signaling. The authors report a nutrient-responsive structural mechanism in which the LARS1:IARS1 complex acts as a switch controlling mTORC1 activation in response to leucine availability. Clinically and scientifically, this provides a molecular explanation for how amino-acid sensing couples translation machinery to mTORC1 metabolic control.
Kim Y, Kim JC, Kim DW et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗
Hepatic venous pressure gradient, non-invasive tests, and prognosis across the subtypes of advanced steatotic liver disease.
This multicenter study evaluated prognosis in compensated advanced chronic liver disease (cACLD) across steatotic liver disease (SLD) subtypes—MASLD, alcohol-related liver disease (ALD), and mixed type (MetALD)—and assessed the impact of clinically significant portal hypertension (CSPH) using hepatic venous pressure gradient (HVPG) plus non-invasive tests (NITs). It reports outcomes including first hepatic decompensation and liver-related mortality in 696 patients, stratifying risk by CSPH and NIT performance across SLD etiologies. The significance is that it informs non-invasive risk prediction and prognosis for advanced steatotic liver disease by linking HVPG-defined portal hypertension to clinically meaningful endpoints.
Hofer BS, Shalaby S, Kwanten W et al. · Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association · (2026) · View on PubMed ↗ · Free PDF ↗
A systemic role of macrophage-derived BMP2/4 homolog Dpp in inhibiting sterol hormone synthesis under dietary stress.
This study investigated how a macrophage-derived BMP2/4 homolog, Dpp, regulates sterol hormone synthesis under dietary stress, using mechanistic experiments in a model system of dietary stress. The key finding was that Dpp acts systemically to inhibit sterol hormone synthesis during dietary stress, linking macrophage signaling to endocrine disruption. This is significant for understanding how diet-driven inflammation can contribute to metabolic disease and developmental timing problems such as delayed pubertal onset.
Juarez-Carreño S, Milán M · Current biology : CB · (2026) · View on PubMed ↗
Whole goat milk versus cow milk formula and atopic dermatitis in infants: A randomized clinical trial.
This randomized, double-blind, controlled trial studied whether whole goat milk formula (WGF) versus cow milk formula (CF) affects the development of atopic dermatitis (AD) during the first year of life in healthy term infants up to 3 months old in Spain and Poland. The key finding was the comparative effect of WGF versus CF on AD incidence/diagnosis across scheduled visits using UK Working Party diagnostic criteria. This is clinically significant because it tests an early-life dietary exposure that could inform infant feeding recommendations to reduce AD risk.
Grote V, Schlosser L, Campoy C et al. · Clinical nutrition (Edinburgh, Scotland) · (2026) · View on PubMed ↗
High glucose impairs cognitive function by inducing lipid droplet accumulation through lactylation of HSD17B10 at K105.
This study tested whether high glucose impairs cognition by altering post-translational modifications in hippocampal neurons, using lactylome-guided analysis to identify lactylation targets. High glucose increased Aars1-driven lactylation of HSD17B10 at K105, reducing HSD17B10 activity, causing lipid droplet accumulation, neuronal apoptosis, and cognitive decline in diabetic mice, and a competitive peptide that inhibited HSD17B10 K105 lactylation mitigated impairment. The results link metabolic stress to specific lysine lactylation control of lipid metabolism and suggest a targeted therapeutic approach for diabetic cognitive dysfunction.
Xu J, Cao J, Yang X et al. · Cell reports · (2026) · View on PubMed ↗ · Free PDF ↗
GLP-1-based therapy and ICD-10-documented heart failure or respiratory failure events in non-diabetic adults with rheumatoid arthritis and obesity: a TriNetX federated cohort study.
This TriNetX federated retrospective cohort study examined whether GLP-1-based therapy was associated with first post-landmark ICD-10–documented heart failure or respiratory failure events in non-diabetic adults with rheumatoid arthritis (RA) and obesity (BMI ≥30 kg/m2) receiving baseline DMARD therapy. GLP-1-based therapy was associated with a change in the risk of subsequent heart failure or respiratory failure events compared with non-use (with diabetes and overlapping systemic autoimmune diseases excluded). The findings provide real-world safety signal guidance for GLP-1 use in a specific RA+obesity population where prospective outcomes data are limited.
Loizidis G, Summer R · Clinical rheumatology · (2026) · View on PubMed ↗
The Impact of Obesity on Airway Inflammation, Lung Function and Biologic Treatment in Asthma: A Narrative Review.
This narrative review studied how obesity influences airway inflammation, lung function, and response to biologic therapies in asthma, focusing on the “obese asthma phenotype” and its underlying mechanisms. The key finding is that obesity-associated mechanical effects, chronic low-grade systemic inflammation, and metabolic dysfunction can alter inflammatory pathways and thereby affect the effectiveness of biologics, especially in type-2–high versus other asthma endotypes. Scientifically and clinically, it highlights the need to consider obesity status and asthma endotype when selecting biologic treatments for severe asthma.
Hadžić B, Vasbinder EC, Lek RM et al. · Journal of inflammation research · (2026) · View on PubMed ↗ · Free PDF ↗
Inflammation, immune regulation, and cytokine biology
METTL3 loss exacerbates colitis via m6A-dependent Slc39a8 regulation and epithelial lineage depletion.
This study examined the role of the m6A RNA methyltransferase METTL3 in intestinal inflammation by using intestine-specific Mettl3 knockout mice challenged with DSS and analyzing human IBD relevance. METTL3 loss exacerbated colitis and was linked to m6A-dependent regulation of Slc39a8 and depletion of epithelial lineages, supported by single-cell transcriptomics of colonic tissue. The results identify an m6A–Slc39a8 axis controlled by METTL3 as a mechanistic driver of epithelial vulnerability in IBD.
Su H, Liu DH, Shang HY et al. · Acta pharmacologica Sinica · (2026) · View on PubMed ↗
Chronic graft-versus-host disease.
This article reviews chronic graft-versus-host disease (cGVHD) in recipients of allogeneic hematopoietic cell transplantation, focusing on immune dysregulation involving B cells, T cells, regulatory T cells, and fibrosis pathways driven by macrophages and fibroblasts. It highlights that cGVHD affects ~30–70% of patients, is a leading cause of non-relapse mortality, and is initially treated with glucocorticoids, but ~50% develop steroid-refractory or steroid-dependent disease requiring prolonged immunosuppression. The clinical significance is that understanding the heterogeneous immune-fibrotic biology is essential for improving risk stratification and developing steroid-sparing therapies.
Ye Y, Savani B, Malard F et al. · Nature reviews. Disease primers · (2026) · View on PubMed ↗
HnRNP A1 and A2B1 enforce Ezh2 mRNA splicing to promote germinal center B cell responses.
This work studied the physiological roles of the RNA-binding proteins hnRNP A1 and hnRNP A2B1 in mouse B cells by conditionally deleting Hnrnpa1 and Hnrnpa2b1 during T cell-dependent immune responses. It found that loss of hnRNP A1/A2B1 impairs germinal center B cell proliferation and high-affinity antibody production, mediated by reduced inclusion of Ezh2 exon 14 (via binding to UAG-rich motifs) leading to loss of EZH2 catalytic activity. The significance is that hnRNP A1/A2B1-dependent Ezh2 mRNA splicing is a key control point for effective humoral immunity and may inform strategies to modulate germinal center responses.
Zhu Z, Zhang R, Kang H et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗
French protocol for diagnosis and management (guidelines) of IgG4-related disease.
This guideline article reviews diagnosis and management of IgG4-related disease (IgG4-RD), a heterogeneous pseudo-tumoral/inflammatory condition characterized by characteristic histology (polyclonal lymphoplasmacytic infiltration, fibrosis, and IgG4+ plasma cells) and often elevated serum IgG4. It emphasizes that diagnosis relies on suggestive clinical/radiologic features across organ systems (e.g., pancreas, salivary/lacrimal glands, retroperitoneal fibrosis, cholangitis, aortitis) and that IgG4-RD typically responds well to glucocorticoids. The clinical significance is providing a standardized, multidisciplinary approach to improve recognition, diagnostic accuracy, and treatment selection for this systemic disease.
Schleinitz N, Audia S, Cohen F et al. · La Revue de medecine interne · (2026) · View on PubMed ↗ · Free PDF ↗
Progressive pulmonary fibrosis: a state-of-the-art review.
This state-of-the-art review summarizes mechanisms and management of progressive pulmonary fibrosis, including fibrosing interstitial lung diseases (ILDs) that develop a progressive phenotype similar to idiopathic pulmonary fibrosis (IPF). It reports that progression can occur despite conventional treatments (e.g., monitoring, antigen eviction, glucocorticoids, immunosuppression, pulmonary rehabilitation) and is associated with worsening lung function and increased risk of acute exacerbation and respiratory failure. The significance is that it frames current evidence-based strategies for identifying and treating the progressive fibrosing phenotype across ILD subtypes.
Cottin V, Brown K, Flaherty KR et al. · The European respiratory journal · (2026) · View on PubMed ↗
Macrophage-neutrophil crosstalk via the Selplg-Sell-YAP axis drives NETosis and MASH-associated liver fibrosis.
The study investigated myeloid-cell crosstalk in mouse models of metabolic dysfunction-associated steatohepatitis (MASH)–associated liver fibrosis, focusing on Selplg+ macrophages and their interaction with neutrophils via the Selplg–Sell axis using single-cell transcriptomics. The Selplg–Sell axis was activated across CDAHFD- and WD+CCl4-induced MASH fibrosis models and drove macrophage-neutrophil communication that promoted NETosis and fibrosis. These findings identify the Selplg–Sell signaling axis as a mechanistic immune target to potentially prevent or treat MASH-associated fibrotic progression.
Nian F, Wu C, Wu D et al. · Hepatology (Baltimore, Md.) · (2026) · View on PubMed ↗
Rapid Onset of Response in Adults with Dermatomyositis Receiving Dazukibart: A Phase 2, Double-Blind, Randomized, Placebo-Controlled Study.
This prespecified secondary analysis studied the rapidity of efficacy onset in adults with dermatomyositis (skin-predominant or muscle-predominant) treated with dazukibart, an anti–interferon-β (IFNβ) monoclonal antibody, in a phase 2 double-blind randomized placebo-controlled trial (NCT03181893). The key finding was that dazukibart produced measurable clinical improvements earlier than the original 12-week assessment time points (before Week 12), indicating a rapid onset of response. Clinically, this supports dazukibart as a potentially faster-acting IFNβ-targeted therapy for dermatomyositis, which may improve treatment decision-making and patient management.
Aggarwal R, Peeva E, Fiorentino DF et al. · Clinical, cosmetic and investigational dermatology · (2026) · View on PubMed ↗ · Free PDF ↗
Neurodegeneration and neuroinflammation (ALS/AD/microglia/brain aging)
Single-nucleus multiomic atlas of ALS primary motor cortex nominates neuroprotective WDR49-expressing astrocytes.
Using a single-nucleus multiomic atlas (single-nucleus RNA-seq and ATAC-seq) from 140 genetically characterized donors (778,330 nuclei) of ALS primary motor cortex, the study identified astrocyte subpopulations linked to disease pathology. ALS-associated transcriptional reprogramming highlighted a WDR49-expressing astrocyte subpopulation spatially associated with TDP-43 pathology, and genetic variants in WDR49 conferred ALS risk. These data nominate WDR49-expressing astrocytes as neuroprotective candidates and suggest a genetically supported target pathway for ALS therapeutic development.
Cooper-Knock J, Bonsall S, Kazu R et al. · Research square · (2026) · View on PubMed ↗ · Free PDF ↗
Single-cell proteome atlas of aging mouse microglia reveals subpopulation-specific phagoproteome.
This study used label-free single-cell proteomics with Orbitrap Astral mass spectrometry and FACS-sorted microglia to profile proteomic heterogeneity in the hippocampus and prefrontal cortex of young, middle-aged, and aged mice. The key finding was a large single-cell dataset (3,085 cells; ~1,153 protein groups/cell) revealing subpopulation-specific phagoproteome changes with aging. This is scientifically significant because it maps how microglial functional states shift at the protein level over the lifespan, which may help explain age-associated neuroinflammation.
Zhang H, Liu Z, Chen B et al. · Neuron · (2026) · View on PubMed ↗
Receptor and cell-type-specific mechanisms in mesocortical dopamine circuits gate chronic pain and comorbid anxiodepression.
This study used receptor- and circuit-specific manipulations in a trigeminal neuralgia (TN) mouse model to define how mesocortical dopamine pathways gate chronic pain and comorbid anxiodepression. The key finding was that orbitofrontal cortex (OFC) D1R- and D2R-expressing neurons independently mediated anxiodepression and allodynia, with TN inducing a hypodopaminergic state in the VTA–OFC circuit and pathway activation reversing symptoms that were abolished by selective D2R or D1R blockade. This is clinically significant because it identifies receptor-specific targets within a defined dopamine circuit for treating pain with comorbid affective symptoms.
Cai YQ, Hou XY, Wang GH et al. · Neuron · (2026) · View on PubMed ↗
Fatty acid amide hydrolase inhibition for treatment of amyotrophic lateral sclerosis.
This reverse translational study explored therapeutic targets for amyotrophic lateral sclerosis (ALS) based on systemic metabolic abnormalities observed in patients, emphasizing the expanded endocannabinoid system and fatty acid amide hydrolase (FAAH) biology. It investigated fatty acid amide hydrolase inhibition as a potential ALS treatment strategy informed by metabolite associations with disease progression. The work supports a metabolism-linked mechanism and provides rationale for FAAH-targeted interventions in ALS.
Ito D, Iida M, Iguchi Y et al. · JCI insight · (2026) · View on PubMed ↗ · Free PDF ↗
Allele specific expression in Alzheimer’s disease.
This genome-wide study characterized allele-specific expression (ASE) across seven brain regions in 2,231 Alzheimer’s disease (AD) and control samples from Mount Sinai Brain Bank and ROSMAP, using bulk and single-cell analyses to infer cell-type-specific regulatory activity. The authors identified tens of thousands of ASE variants enriched in imprinted regions (e.g., chr6, chr14q32, chr15q11) and observed ASE patterns in coding exons, indicating widespread allele-dependent dysregulation in AD. Scientifically, this supports ASE as a previously underexplored layer of AD genetics that may help pinpoint regulatory variants and cell types driving disease risk.
Wang Z, Hossain D, Wang JJ et al. · Alzheimer’s & dementia : the journal of the Alzheimer’s Association · (2026) · View on PubMed ↗ · Free PDF ↗
Donanemab treatment effect by baseline tau burden and disease severity: Observations from the TRAILBLAZER-ALZ 2 trial.
This observational analysis of the TRAILBLAZER-ALZ 2 trial assessed how baseline disease severity—defined by tau PET, plasma P-tau217, or predicted progression—modulated the treatment effect of donanemab on CDR-SB in Alzheimer’s disease. Donanemab slowed clinical decline across baseline tau PET and plasma P-tau217 strata, with greater benefit in participants with lower baseline tau burden and P-tau217. Clinically, the findings reinforce earlier intervention with donanemab and support using tau/P-tau biomarkers to identify patients most likely to benefit.
Raket LL, Lu M, Evans CD et al. · Alzheimer’s & dementia : the journal of the Alzheimer’s Association · (2026) · View on PubMed ↗ · Free PDF ↗
Neurodevelopment and pediatric neurology (epilepsy/spasms, brain development)
Nuclear proteome reveals microtubule-associated protein regulating fate and disease.
This study profiled nuclear and cytosolic proteomes in human and murine neural stem cells (NSCs) to identify cytoskeletal proteins that regulate nuclear programs, focusing on the microtubule-associated protein MAP1B. The key finding was that MAP1B shuttles to the nucleus, where it interacts with a BRG1-containing chromatin remodeling complex, and that nuclear enrichment of MAP1B promotes NSC fate (contrasting with cytosolic MAP1B promoting neuronal differentiation). This is clinically significant because it links microtubule-associated signaling to chromatin remodeling via MAP1B–BRG1 and provides a mechanistic basis for MAP1B’s role in fate decisions and disease.
Merino F, Miranda L, Kumar A et al. · Cell · (2026) · View on PubMed ↗ · Free PDF ↗
Childhood environments shape the brain.
This Science commentary/review studied how childhood environments influence brain structure and function, emphasizing socioeconomic factors as major determinants. The key finding highlighted is that socioeconomic influences are among the strongest drivers of variation in children’s brain development. This is significant because it frames environmental and policy-level targets as potential levers for reducing neurodevelopmental disparities.
Sisk LM, Satterthwaite TD · Science (New York, N.Y.) · (2026) · View on PubMed ↗
Patterns of brain-wide associations reflect socioeconomics.
The study mapped 649 variables to children’s brains using brain-wide association studies (BWAS) and compared the resulting association patterns with neurobiological reference maps. Socioeconomic status (SES) showed the strongest brain-wide associations, with the strongest effects in motor and sensory regions and a shared BWAS pattern across variables that best reflected children’s socioeconomics. This supports SES as a dominant driver of brain variability in BWAS and suggests that adjusting for SES can substantially alter apparent brain–cognition (e.g., IQ) relationships.
Marek S, Donohue MR, Karcher NR et al. · Science (New York, N.Y.) · (2026) · View on PubMed ↗
Biallelic inactivating variants in the chromatin remodeler DMAP1 cause a syndromic neurodevelopmental disorder.
This study identified biallelic inactivating variants in the chromatin remodeler DMAP1 in individuals with a syndromic neurodevelopmental disorder and tested functional consequences in model systems. Neural-specific knockdown of the Drosophila ortholog dDMAP1 caused pupal lethality, supporting a conserved requirement for DMAP1 in neural development. The findings establish DMAP1 as a human disease gene and provide a mechanistic entry point for understanding how chromatin remodeling defects drive neurodevelopmental pathology.
Wang Q, Sobering AK, Tirrito C et al. · The Journal of clinical investigation · (2026) · View on PubMed ↗ · Free PDF ↗
Diagnosis and management guidelines for infantile epileptic spasms syndrome around the world: A scoping review and comparative study of international approaches.
This scoping review and comparative study synthesized and compared international guidelines for diagnosis and management of infantile epileptic spasms syndrome (IESS) across regions worldwide. It evaluated how recommendations differ for rapid diagnosis and treatment strategies intended to optimize neurodevelopmental outcomes. The work highlights global variability and can guide harmonization of evidence-based IESS care pathways.
Erdemir G, Rao CK, Pino AF et al. · Epilepsia · (2026) · View on PubMed ↗ · Free PDF ↗
Pediatric epilepsy surgery: Global survey of invasive explorations.
This ILAE Pediatric Epilepsy Surgery Taskforce global survey characterized invasive presurgical evaluation practices in pediatric epilepsy surgery, focusing on MRI-negative cases where invasive exploration guides resective, disconnective, or ablative procedures. Data from 61 epilepsy surgery programs in 29 countries (children/adolescents undergoing presurgical evaluation and surgery in 2023) were analyzed to provide an updated global overview of current invasive evaluation approaches. The findings support benchmarking and international comparison to improve presurgical evaluation standards for children undergoing epilepsy surgery.
Ramantani G, Feucht M, Cserpan D et al. · Epilepsia · (2026) · View on PubMed ↗ · Free PDF ↗
Reproductive biology, pregnancy complications, and fetal development
Proteomics-based insights into mammalian oocyte and early embryo development.
This review summarizes proteomics methodologies and stage-specific proteome reprogramming during mammalian oocyte maturation and preimplantation embryo development in humans and mice. It highlights that proteomic profiling reveals distinct, time-resolved molecular changes underlying developmental competence across stages. The work supports proteomics as a translational tool for studying reproductive ageing and improving mechanistic understanding of early developmental failure.
Rong S, Liu Z, Zhu W et al. · Nature cell biology · (2026) · View on PubMed ↗
Two distinct causes contribute to the low efficiency of human pre-implantation development.
This study used live imaging of ~150 human and monkey fertilized eggs to determine causes of arrest during human pre-implantation development. The key finding was that second mitotic divisions were the most error-prone, driven by stochastic centriole overduplication that could be suppressed by transient PLK4 inhibitor centrinone, leading to fewer multipolar spindles, reduced chromosome missegregation, and fewer micronuclei. This is significant for assisted reproductive technology because it identifies a mechanistic bottleneck and a potential intervention point to improve early embryo viability.
Li Z, Leng L, Zhai J et al. · Cell · (2026) · View on PubMed ↗
Placental nicotinamide adenine dinucleotide modulates the timing of labor.
The study examined how placental nicotinamide adenine dinucleotide (NAD+) regulates gestational timing in mice. Placental NAD+ depletion triggered earlier labor by reducing NAD+-dependent activity of 15-hydroxyprostaglandin dehydrogenase, which normally suppresses prostaglandin accumulation, while increasing placental NAD+ prolonged gestation. These findings identify placental NAD+ as a metabolic sensor that tunes prostaglandin signaling and could inform strategies to manage preterm or delayed labor risk.
Ciampa EJ, Machado LM, Lee KJ et al. · Science (New York, N.Y.) · (2026) · 1 citations · View on PubMed ↗
Development of a robust method to derive human trophoblast stem cells from late-gestation placentas and its application to preeclampsia.
The study developed a robust method to derive human trophoblast stem cells (hTSCs) from late-gestation placentas and applied it to preeclampsia research. The key finding was that the new derivation technique enables generation of hTSCs from late-gestation tissue, overcoming prior limitations that restricted trophoblast modeling of late pregnancy complications. This provides a scalable human model system to investigate trophoblast dysfunction mechanisms and test potential interventions for preeclampsia.
Oike A, Kobayashi EH, Yamamoto Y et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗ · Free PDF ↗
Cardiovascular/critical care resuscitation and thrombosis
Distinct Clinical Phenotypes in Moyamoya Disease: A Multicenter Comparison of Ischemic and Hemorrhagic Presentations.
This multicenter retrospective cohort study compared perioperative complications and long-term stroke risk after revascularization surgery in 485 North American patients with ischemic-type versus hemorrhagic-type moyamoya disease (MMD). Ischemic and hemorrhagic phenotypes showed distinct clinical profiles with different perioperative safety and long-term stroke outcomes following surgical revascularization. These findings support phenotype-aware risk stratification and long-term management planning for MMD patients undergoing revascularization.
Gabriel El-Hajj V, Musmar B, Roy JM et al. · Neurosurgery · (2026) · View on PubMed ↗
Sodium Bicarbonate for Critically Ill Adults with Metabolic Acidosis and Shock.
In a pragmatic, adaptive, double-blind randomized trial, critically ill adults with metabolic acidosis receiving vasopressors in the ICU were assigned to sodium bicarbonate versus placebo (5% dextrose). Sodium bicarbonate did not provide clear clinical benefit over placebo for outcomes in this vasopressor-dependent population with acidemia. The results inform ICU practice by questioning routine bicarbonate use for metabolic acidosis in shock when patients are already receiving vasopressors.
Serpa Neto A, McNamara M, White K et al. · The New England journal of medicine · (2026) · View on PubMed ↗
Allosteric activation of Trx1 by antagonizing nitrative modification at tyrosine 49 confers neuroprotection against ischemic stroke.
This mechanistic study investigated how tetramethylpyrazine (TMP) protects against ischemic stroke by identifying its molecular target and mode of action in cells. Using a bifunctional photoaffinity TMP probe, SILAC-based activity-based protein profiling (SILAC-ABPP), and follow-up binding/modification assays, the authors found that TMP directly targets thioredoxin 1 (Trx1), binds specifically at tyrosine 49 (Y49), antagonizes nitrative modification at that residue, and allosterically activates Trx1. This is significant because it resolves TMP’s target mechanism and suggests Trx1 Y49 nitration as a therapeutic axis for ischemic stroke.
Guo M, Guo H, Ren W et al. · Redox biology · (2026) · View on PubMed ↗ · Free PDF ↗
Association of White Blood Cell Count with Treatment Response to Cefepime vs Piperacillin-Tazobactam.
This post-hoc analysis evaluated whether baseline white blood cell (WBC) count modifies the effect of empiric antibiotics on mortality by comparing cefepime versus piperacillin-tazobactam using data from the ACORN randomized trial and an instrumental variable (IV) study. The study assessed treatment-by-WBC interaction using regression modeling to determine if WBC levels stratify mortality benefit or harm from antibiotic choice. If confirmed, WBC-guided selection could improve sepsis antibiotic stewardship by tailoring empiric anti-pseudomonal therapy to patient risk profiles.
Rzewnicki DI, Chanderraj R, Qian ET et al. · American journal of respiratory and critical care medicine · (2026) · View on PubMed ↗
Real-World Safety Profile of Middle Meningeal Artery Embolization for Chronic Subdural Hematoma: a Multinational Multicenter Study.
This multinational multicenter retrospective study evaluated the real-world 30-day safety of middle meningeal artery embolization (MMAE) for chronic subdural hematoma (cSDH) in 1781 consecutive patients treated from 2019–2025. The 30-day procedure-related complication rate was 5.1%, and the analysis used inverse probability of treatment weighting (IPTW) to assess associations between technical success and complications. Scientifically and clinically, the study provides contemporary safety benchmarks for MMAE and informs risk–benefit discussions and quality improvement efforts.
DeMessie B, Karandish A, Essibayi MA et al. · Clinical neuroradiology · (2026) · View on PubMed ↗ · Free PDF ↗
Vasopressors or Fluids in Early Septic Shock.
This randomized emergency-department trial studied early resuscitation strategies in adult patients with septic shock, comparing restricted-volume intravenous fluids plus early vasopressor therapy versus higher-volume fluids with later vasopressor therapy. The key finding was that the vasopressor-first strategy (restricted fluids with early vasopressors) improved the primary outcome of days alive and out of the hospital compared with the fluids-first strategy. Clinically, this supports earlier vasopressor use with less fluid in early septic shock to optimize recovery and reduce harm from fluid overload.
Peake SL, Macdonald SPJ, Howe BD et al. · The New England journal of medicine · (2026) · View on PubMed ↗
Sodium Bicarbonate for In-Hospital Cardiac Arrest: A Randomized Clinical Trial.
This double-blind, placebo-controlled randomized clinical trial tested whether giving sodium bicarbonate during in-hospital cardiac arrest improves outcomes in adults who received at least one dose of epinephrine. Sodium bicarbonate did not increase the proportion of patients achieving return of spontaneous circulation compared with placebo. The trial’s results question a common practice and suggest bicarbonate should not be routinely used during in-hospital cardiac arrest.
Granfeldt A, Kirkegaard BL, Vallentin MF et al. · JAMA · (2026) · View on PubMed ↗
RND3 Enhances Cardiac Glucose Metabolism Through Inhibiting ACAT1-Dependent PDHA1 Acetylation and Protects Against Ischemia-Reperfusion Injury.
This mechanistic animal study investigated whether RND3 enhances cardiac glucose metabolism and protects against myocardial ischemia-reperfusion injury by inhibiting ACAT1-dependent PDHA1 acetylation. In mice with cardiomyocyte-specific Rnd3 knockout or overexpression, RND3 promoted metabolic protection by reducing ACAT1-dependent PDHA1 acetylation and improving glucose utilization, leading to less injury after ischemia-reperfusion. The findings identify a specific RND3–ACAT1–PDHA1 axis that could be targeted to mitigate I/R injury.
Xiong Z, Li Y, Zhang Y et al. · Circulation · (2026) · View on PubMed ↗ · Free PDF ↗
Platelet RIP2 Limits Dense Granule Release and Thrombosis via DOCK8-Cdc42.
This study examined how platelet RIP2 regulates dense granule release and thrombosis through a DOCK8–Cdc42 pathway, using in vitro platelet assays, ex vivo microfluidic whole-blood perfusion, and in vivo FeCl3-induced thrombosis and myocardial ischemia/reperfusion models. RIP2 deficiency reduced dense granule secretion and thrombus formation, and the effects were mediated via DOCK8–Cdc42 signaling rather than through upstream PRR pathways. These results position RIP2 as a potential therapeutic target to limit platelet-driven thrombosis and myocardial injury.
Zhang J, Zhang Z, Pan G et al. · Arteriosclerosis, thrombosis, and vascular biology · (2026) · View on PubMed ↗
Infectious disease surveillance and clinical case reports
Nationwide spread of multidrug resistant Klebsiella pneumoniae across US communities.
Using a nationwide genomic survey of 2,006 ceftriaxone-nonsusceptible outpatient Klebsiella pneumoniae isolates from 42 US states, this study mapped how multidrug resistance spread in community settings. It found that dissemination of the blaCTX-M-15 ESBL gene across diverse K. pneumoniae lineages—carried on IncFIB(Kpn3) plasmids—primarily drove the nationwide spread. The coupling of blaCTX-M-15 with plasmid-associated stress/metal tolerance traits suggests enhanced environmental survival and informs public-health surveillance of community MDR K. pneumoniae.
Jiang J, Terlecky AJ, Rome KJ et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗
Clinical Features, Treatment Outcomes, and Cytokine Levels in Pediatric Tularemia Patients in Türkiye.
This multicenter prospective study evaluated clinical features, treatment outcomes, and serum cytokine dynamics (including IL-6 and IL-2) in 40 laboratory-confirmed pediatric tularemia patients in Türkiye compared with nine matched healthy controls. The key finding was characterization of cytokine level changes associated with active disease and treatment response in children, alongside detailed clinical course data. These results are significant because they provide pediatric immune-response biomarkers and improve understanding of host-pathogen immunology in tularemia, a rare zoonosis with limited pediatric data.
Cakici O, Aykac K, Seyrek BE et al. · The American journal of tropical medicine and hygiene · (2026) · View on PubMed ↗
Plant biology and bioengineering (motility, metallomics, biosynthesis)
Molecular regulation and physiological role of GOLPH3-mediated Golgi retention.
This article examined the physiological role of GOLPH3 in mice and how it regulates Golgi retention of resident proteins, using depletion/functional studies to assess downstream cellular phenotypes. It reports that GOLPH3 depletion alters protein and lipid glycosylation, causes partially penetrant embryonic lethality, and severely impairs growth and bone mineralization, consistent with disrupted Golgi-resident protein sorting. The scientific significance is that GOLPH3 is positioned as a key component of the Golgi retention machinery with systemic developmental consequences.
Theodoropoulou A, Nasrallah A, Abriata LA et al. · Nature communications · (2026) · 3 citations · View on PubMed ↗ · Free PDF ↗
Complete biosynthesis of the anticancer cephalotaxinone and homoerythratine.
This study investigated the complete biosynthetic pathway for cephalotaxinone and homoerythratine-type alkaloids in the context of homoharringtonine (HHT) production, using comprehensive multi-omics analyses and chemically synthesized standards to identify missing enzymes. The authors report identification of previously unknown enzymes required to reconstruct these cephalotaxinone/homoerythratine biosynthetic steps, enabling a complete pathway description for these Cephalotaxus-derived alkaloids. This advances scalable, resource-independent biosynthesis of clinically important HHT-related compounds and clarifies the enzymology underlying cephalotaxine-type alkaloid diversification.
Tian R, Lin F, Guo N et al. · Cell · (2026) · View on PubMed ↗
Fasting requires Peroxiredoxin 2 and Peroxiredoxin 6 to coordinate redox dependent mitochondrial and lipid remodelling in Caenorhabditis elegans.
This study investigated how fasting triggers redox-dependent mitochondrial and lipid remodeling in Caenorhabditis elegans, focusing on the roles of peroxiredoxin 2 (PRX2) and peroxiredoxin 6 (PRX6). The key finding was that PRX2 and PRX6 are required to coordinate fasting-induced transient mitochondrial ROS changes, mitochondrial turnover, and reductions in age-related lipid accumulation/lipofuscin during the fasting/reweding regimen. This is significant because it links specific redox enzymes to conserved metabolic remodeling programs that influence stress resistance and longevity.
Li P, Zheng Y, Casas-Martinez JC et al. · Redox biology · (2026) · View on PubMed ↗ · Free PDF ↗
Fast cell wall softening causes Venus flytrap closure.
The study investigated the mechanism of rapid Venus flytrap (Dionaea muscipula) lobe closure using in situ hydraulic and mechanical measurements. Closure was driven by a nonhydraulic mechanism: about one-second rapid softening of the epidermal cell wall that releases elastic energy stored in the trap, too fast to be explained by water transport. This reveals a fastest-known mode of plant motility based on dynamic tuning of cell-wall mechanics.
Ryu J, Colombani M, Mollier C et al. · Science (New York, N.Y.) · (2026) · 2 citations · View on PubMed ↗
Subcellular metallomic networks orchestrate physiological outcomes: Single-cell mapping via an integrated SEM-FIB-TOF-SIMS platform.
The study created an integrated SEM-FIB-TOF-SIMS platform to map subcellular metallomic networks at single-cell resolution in plant cells. Using nanoscale coregistration of ultrastructure with metal(loid) distributions, it generated single-cell metallome maps across Arabidopsis, soybean, and wheat that reveal how metal(loid) organization evolves with cell state. This advances quantitative, subcellular metal(loid) imaging for linking metallomic architecture to physiological outcomes.
Cheng M, Wang L, Wang Z et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗ · Free PDF ↗
Glycosylation-independent functions for distinct glypican core proteins drive cell-specific responses in corticogenesis.
The study investigated how glycosylation-independent functions of distinct glypican core proteins regulate cell-specific responses during corticogenesis. It found that in the developing cerebral cortex, GPC4 (in cortical progenitors) promotes proliferation and intermediate progenitor generation, while neuronal GPC2 drives neuronal differentiation and maturation through mechanisms independent of glycosylation. These results clarify how specific glypican core proteins encode complementary developmental programs in a cell-type-specific manner.
Douceau S, Guerrero TD, Borowski C et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗ · Free PDF ↗
Protection and deprotection of the Rec8 cohesin complex during meiosis.
This fission yeast study examined how the Rec8 cohesin complex is protected or deprotected during meiosis, focusing on the roles of shugoshin (Sgo1) and meikin (Moa1) and their regulation by the APC/C-Slp1 pathway. Sgo1 and Moa1 were degraded during anaphase I via APC/C-Slp1, and ectopic stabilization of Sgo1 plus Moa1 non-degradability enabled protection-like phosphorylation states of Rec8 during meiosis II. The work clarifies how temporal control of meiotic regulators prevents inappropriate cohesin protection and ensures correct chromosome segregation.
Liu Y, Zhang K, Bai Z et al. · Cell reports · (2026) · View on PubMed ↗ · Free PDF ↗
Methods, imaging, and translational platforms (assays, imaging, consensus standards)
Standardized processing of explanted hearts after stereotactic arrhythmia radiotherapy (Bio-STAR): a STOPSTORM framework and first human findings.
The Bio-STAR study developed a STOPSTORM framework to standardize ex vivo processing of explanted hearts after stereotactic arrhythmia radiotherapy (STAR) and reported first human feasibility findings. STAR-treated myocardium could be sampled into non-irradiated control, minimally fibrotic irradiated, and fibrotic irradiated zones using electroanatomical mapping and radiotherapy dose overlays, enabling downstream ex vivo MRI and histologic analyses. This provides a reproducible translational pipeline to quantify human myocardial effects of STAR for refractory ventricular tachycardia.
Nedios S, Hüttemeister J, Heil E et al. · European heart journal open · (2026) · View on PubMed ↗ · Free PDF ↗
Risks Associated With Benzodiazepine Long-Term Use in Chronic Insomnia: A Systematic Review and (Network) Meta-Analysis.
This systematic review and network meta-analysis evaluated risks of benzodiazepines used for more than 3 months in adults with chronic insomnia, drawing on 27 studies published between 1987 and 2023. Longer-term benzodiazepine use was associated with concerns including dependence and negative long-term health/safety outcomes compared with shorter use or alternative approaches. The synthesis supports caution against prolonged benzodiazepine prescribing for chronic insomnia and informs safer long-term insomnia management decisions.
Riemann D, Baglioni C, Nissen C et al. · Journal of sleep research · (2026) · View on PubMed ↗ · Free PDF ↗
Clinical Profile and Genomic Characterization of the 2026 Bundibugyo Virus Index Case in Uganda.
This Nature Medicine case report described the 2026 Bundibugyo virus disease (BVD) index case in Uganda in a male patient who traveled from the Democratic Republic of the Congo and presented after more than two weeks of gastrointestinal symptoms. The patient rapidly deteriorated with multi-organ involvement including acute kidney injury, pulmonary edema, hepatic dysfunction, hypoxemia, delirium, atrial flutter, and possible disseminated intravascular coagulation. Clinically, the report highlights the diagnostic and surveillance challenges of BVD in settings with nonspecific early symptoms and delayed recognition.
Nsawotebba A, Ssewanyana I, Ayitewala A et al. · Nature medicine · (2026) · View on PubMed ↗ · Free PDF ↗
Skeletal-muscle-targeted non-viral delivery of full-length DMD mRNA for Duchenne muscular dystrophy.
This preclinical study in a murine model of Duchenne muscular dystrophy (DMD) tested systemic, skeletal-muscle-targeted delivery of full-length DMD mRNA using allogenically engineered targeting extracellular vesicles (DMD t-EVs). The approach enabled restoration of dystrophin expression from full-length DMD mRNA in skeletal muscle. The non-viral, transient mRNA strategy may reduce limitations of viral gene therapy (toxicity, immunogenicity, and packaging constraints) and supports further development for DMD.
Tian Y, Liu Y, Tong Y et al. · Nature biomedical engineering · (2026) · 1 citations · View on PubMed ↗
Low concentration atropine eye drops and progression of myopia in children: multicentre placebo controlled, double masked, randomised trial in the UK (CHAMP-UK).
This multicentre, placebo-controlled, double-masked randomized trial studied whether low-concentration atropine eye drops (0.01% once daily) slow myopia progression in UK children aged 6–12 years with baseline myopia between -0.50 and -10.0 dioptres. The key finding (from the trial’s primary outcome assessment using autoref-measured spherical equivalent refractive error over two years) is whether atropine reduces refractive error progression compared with placebo while maintaining safety. The clinical significance is that it directly tests a practical, low-dose atropine regimen for myopia control in a real-world UK pediatric population.
Azuara-Blanco A, Logan NS, McConnell E et al. · BMJ (Clinical research ed.) · (2026) · View on PubMed ↗ · Free PDF ↗
Family engagement in the management of breast cancer-related lymphedema: A qualitative study.
This qualitative study investigated patterns of family engagement in home-based management among patients with breast cancer-related lymphedema to derive patient personas for personalized support. The key finding was identification of distinct family engagement profiles (“personas”) that differ in how families facilitate long-term self-management behaviors. This is significant because it can guide tailored nursing interventions and improve adherence and outcomes in a chronic condition requiring sustained home care.
Wang L, Yan S, Xiao R et al. · International journal of nursing studies · (2026) · View on PubMed ↗
Strain-specific propagation of variant Creutzfeldt-Jakob disease prions in humanized neural cells.
The study developed and used a humanized neural cell system to test how variant Creutzfeldt-Jakob disease (CJD) prions propagate in vitro and whether they preserve strain-specific properties. The key finding was that humanized neural cells support strain-specific propagation of variant CJD prions, enabling mechanistic analysis of conformational templating in a mammalian cell context. This provides a tractable platform for studying human prion strain biology and for improving infectivity assays relevant to public-health surveillance.
Rayner MLD, Arora P, Linehan JM et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗ · Free PDF ↗
Laser phase plate improves structure determination of small proteins by cryo-EM.
The study evaluated whether a laser phase plate (LPP) improves structure determination of small proteins in cryo-electron microscopy (cryo-EM) on a Titan Krios microscope. The key finding was that LPP enhanced single-particle reconstruction resolution by improving specimen-motion correction, recovery of early-frame information, and downstream steps including particle visualization, 3D classification, and alignment. This demonstrates a practical hardware-and-processing advance that can surpass standard cryo-EM performance for small proteins.
Petrov PN, Zhang JT, Remis J et al. · Science (New York, N.Y.) · (2026) · 1 citations · View on PubMed ↗
Prostate Imaging Standards for Screening Magnetic Resonance Imaging (PRISM): International Consensus Recommendations.
This international consensus study synthesized evidence from randomized trials and prospective cohorts to develop PRISM (Prostate Imaging Standards for Screening MRI) recommendations for prostate MRI acquisition, interpretation, and reporting in population-level screening. The key outcome was standardized guidance intended to reduce uncertainty in how prostate MRI should be performed and used for screening. Implementing PRISM could improve consistency and diagnostic performance of MRI-based screening pathways for prostate cancer.
Mayor N, Light A, Gopalakrishnan A et al. · JAMA oncology · (2026) · View on PubMed ↗
Primary Aldosteronism: CXCR4- and FAP-Targeted PET/MR for Adrenal-Cardiac Axis.
This prospective imaging study evaluated the adrenal-cardiac axis in primary aldosteronism by integrating CXCR4-targeted 68Ga-Pentixafor PET/MR with FAP-targeted 68Ga-FAPI-04 PET/cardiac MRI in 82 participants (40 with primary aldosteronism, including aldosterone-producing adenoma and idiopathic hyperaldosteronism, and 42 with essential hypertension). The key finding was that CXCR4- and FAP-targeted tracer uptake reflected adrenocortical activity and myocardial fibroblast activation/remodeling differences associated with primary aldosteronism. This supports PET/MR-based molecular imaging as a noninvasive way to link aldosterone-driven adrenal signals to cardiac remodeling and cardiovascular risk.
Ding J, Wang K, Song J et al. · Circulation. Cardiovascular imaging · (2026) · View on PubMed ↗
Chinese expert consensus on conversion and perioperative therapy of primary liver cancer (2024 edition).
This 2024 Chinese expert consensus (updated for clinical use) studied and synthesized evidence to standardize conversion and perioperative therapy strategies for primary liver cancer patients, particularly those at intermediate-to-advanced stages who are often not initially eligible for curative surgery. The consensus key finding is that integrating modern systemic options (including immune checkpoint inhibitor combinations) with locoregional therapies can enable conversion to surgery and improve perioperative outcomes despite high recurrence rates. Clinically, it provides a structured framework to guide treatment selection and sequencing to improve prognosis in a high-risk Chinese primary liver cancer population.
Wang Z, Sun H, Zhou J et al. · Hepatobiliary surgery and nutrition · (2026) · 1 citations · View on PubMed ↗ · Free PDF ↗
Generated automatically on June 13, 2026 from PubMed’s trending articles. Summaries are AI-generated; always consult the original publication for clinical or research decisions.