PubMed Trending Research Digest — June 20, 2026

Automated digest · 100 articles · 15 research areas · June 20, 2026

Overview

Across this week’s papers, a dominant theme is how immune function is shaped by context—whether that context is the CNS–immune interface, the tumor microenvironment, or systemic metabolic and inflammatory states. Reviews and mechanistic studies link gut-derived metabolites (SCFAs, bile acids) and viral exposures to neuroimmune inflammation, while multiple cancer-focused studies show that immune escape and therapeutic resistance are driven by spatially organized microenvironments (e.g., CAF/TLS architecture), immune effector–tumor signaling loops (e.g., NK–glioblastoma TFPI2), and metabolism-linked pathways (including ferroptosis suppression and DDR-related resistance). Several studies also emphasize that immune modulation can carry long-term risks, particularly malignancy signals and infectious toxicities in T-cell–engaging therapies, underscoring the need for risk-aware patient selection and monitoring.

A second major thread is the move toward actionable biomarkers and personalized decision tools. Examples include DNA methylation episignatures for rare neurodevelopmental disorders, improved antibody assay workflows for NMOSD/MOGAD, AI-assisted imaging/diagnostics (e.g., HER2-LADDER, AI-derived bone mineral density), and multi-omics liquid biopsy frameworks for early breast cancer detection and lymph node risk. In parallel, clinical effectiveness and safety studies across non-oncology domains (obesity pharmacotherapy, ocular/respiratory safety signals of GLP-1 RAs, steroid use for long COVID prevention in children, and step-down antibiotic strategies) highlight heterogeneity in real-world outcomes and the importance of pragmatic, scalable monitoring.

Finally, several mechanistic studies connect physiology to disease progression through signaling and structural biology—ranging from endothelial KLF4 loss driving BBB dysfunction and cognitive decline, to hypoxia/lactate-driven signaling in TNBC, to cGAS nuclear signaling promoting metastasis, and to viral protease disruption of nuclear pore function in acute flaccid myelitis. Together, these findings reinforce a unifying message: understanding the molecular “wiring” of disease—often at the level of cell state, microenvironment architecture, and biomarker readouts—enables more precise therapies and better prognostic stratification.

---

Neuroimmune & CNS–Immune Crosstalk

An aminoacyl-tRNA synthetase governs dsRNA-mediated trade-off between longevity and innate immunity.

This study examined how endogenous double-stranded RNA (dsRNA) signaling affects organismal aging and innate immunity, focusing on the aminoacyl-tRNA synthetase FARS-1/FARSA and mitochondrial dsRNA homeostasis. The authors found that FARS-1/FARSA regulates mitochondrial dsRNA levels to balance longevity against activation of innate immune pathways. These findings link a translation-associated enzyme to dsRNA–mitochondria crosstalk, suggesting a new molecular lever for modulating aging and antiviral/inflammatory immunity.

Ozaki H, Sasaki N, Kitajima S · Molecular cell · (2026) · View on PubMed ↗

Maternal trans-vaccenic acid shapes neonatal T cell development and early-life immune imprinting.

This study examined whether maternal trans-vaccenic acid (TVA), a trans-fatty acid abundant in human breast milk, shapes neonatal T cell development and immune imprinting, using a mouse maternal supplementation model. TVA supplementation expanded naïve CD4+ T cells and enhanced adaptive immunity against infection, reprogramming neonatal naïve CD4+ T cells via a G protein-coupled receptor–CCCTC-binding factor (CTCF) axis and promoting Th1 skewing through cooperation with TBX21. These findings link a specific maternal dietary component to early-life immune programming, suggesting nutritional modulation as a lever for neonatal immune resilience.

Fan H, Zheng Z, Oliphant K et al. · Science (New York, N.Y.) · (2026) · View on PubMed ↗

Microglia-driven neuroinflammatory signaling in neurodegeneration: mechanisms and therapeutic opportunities.

This narrative review examined microglia-driven neuroinflammatory signaling mechanisms in neurodegeneration and discussed therapeutic opportunities across major diseases including Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, and Huntington’s disease. The key finding was synthesis of how persistent microglial and astrocytic activation and peripheral immune pathway signaling contribute to progressive neurodegeneration and synaptic loss (specific experimental results are not applicable because this is a review). Scientifically, it highlights actionable targets within neuroinflammatory pathways that could guide development of disease-modifying therapies.

Saini K, Dhiman P · Molecular biology reports · (2026) · View on PubMed ↗

From Marginal to Central: Marginal Zone-like B Cells as Critical Targets in Cladribine-Treated Multiple Sclerosis.

This Annals of Neurology study examined the longitudinal effects of cladribine on B-cell subsets in 36 people with relapsing-remitting multiple sclerosis over 48 months using high-parameter flow cytometry, with additional cross-sectional characterization of inflammatory properties. Cladribine produced durable, subset-specific reshaping of B-cell populations, identifying marginal zone-like B cells as critical targets. The scientific significance is that it links cladribine’s long-term immunomodulatory effects to specific B-cell phenotypes, potentially guiding more precise biomarker-driven MS treatment strategies.

Pirronello M, Picozza M, Guerrera G et al. · Annals of neurology · (2026) · View on PubMed ↗ · Free PDF ↗

Mechanisms and therapeutic advances of gut metabolites in the regulation of neuroimmune inflammatory diseases.

This review examined how gut-derived metabolites—especially short-chain fatty acids (SCFAs) and bile acids—regulate neuroimmune inflammatory diseases in the context of CNS–immune crosstalk. It reports that SCFAs can promote anti-inflammatory regulatory T-cell (Treg) differentiation via GPCR activation on immune cells and that bile acids can modulate immunity either by crossing the blood–brain barrier or by acting peripherally. These mechanistic links support metabolite-targeted strategies to prevent or treat neuroimmune inflammatory disorders by tuning systemic immunity and neural homeostasis.

Shen X, Zheng C, Lin R et al. · Frontiers in immunology · (2026) · View on PubMed ↗ · Free PDF ↗

Weight-loss dynamics with tirzepatide versus semaglutide.

This retrospective cohort study compared weight-loss dynamics in real-world patients treated with the GLP-1/GIP agonist tirzepatide versus the GLP-1 receptor agonist semaglutide using de-identified electronic health records with 1:1 propensity matching. Across 10,339 patients per group, it assessed maximum weight loss over 2 years and stratified outcomes into five response categories, with adverse events identified via AI-enabled curation of clinical notes. Clinically, the work characterizes heterogeneity in long-term weight-loss trajectories between tirzepatide and semaglutide, supporting more personalized expectations and monitoring in obesity/type 2 diabetes care.

Venkatakrishnan AJ, Murugadoss K, Soundararajan V · PNAS nexus · (2026) · View on PubMed ↗ · Free PDF ↗

Proinflammatory Epstein-Barr Virus Antibody Functions Track with Disease Activity in Multiple Sclerosis.

This study examined whether proinflammatory Epstein–Barr virus (EBV) antibody features track with disease activity in relapsing-onset multiple sclerosis (MS) by profiling virus-specific immune signatures over time. It found that EBNA1-specific IgG in MS patients shows a distinct proinflammatory Fc signature, including increased affinity for Fc gamma receptors (FcγRs), compared with EBV-seropositive healthy controls. Scientifically, it links EBV antibody functional properties to MS immunopathology and suggests a potential biomarker framework for monitoring disease activity.

Behrens M, Terroba-Navajas P, Willemse EAJ et al. · Annals of neurology · (2026) · View on PubMed ↗ · Free PDF ↗

---

Immunotherapy Safety, Malignancy Risk & Long-Term Outcomes

Beyond oncogenesis: the unexplored benefits of viruses in cancer immunity.

This review examined how viral exposures beyond classic oncogenic viruses (e.g., HBV, HCV, HPV, EBV, HTLV-1, KSHV, and Merkel cell polyomavirus) may shape antitumour immunity in humans. It argues that the traditional oncogenesis-focused paradigm has overshadowed evidence that some members of the human virome can enhance cancer immune surveillance through long-term coevolutionary effects. Clinically, reframing “viruses in cancer” to include immunostimulatory viral exposures could inform future cancer immunotherapy and biomarker strategies.

Wang XW, Day CP, Koonin EV · Nature reviews. Cancer · (2026) · View on PubMed ↗

Infectious toxicities associated with bispecific antibodies and CAR-T Cells in multiple myeloma: a systematic review.

This systematic review assessed infectious toxicities in relapsed/refractory multiple myeloma patients treated with BCMA-directed CAR-T cells or bispecific antibodies (BsAbs). Across 123 mostly early-phase non-comparative studies, infections were frequent (any-grade incidence ~40–80%) with the highest risk occurring early after therapy, and the review synthesized pathogens, timing, risk factors, and prevention strategies. The clinical significance is improved risk stratification and guidance for infection monitoring and prophylaxis in RRMM patients receiving CAR-T or BsAbs.

Benda M, Reimann P, Willenbacher W et al. · Annals of hematology · (2026) · View on PubMed ↗

Second Primary Malignant Neoplasms After T-Cell-Engaging Bispecific Antibody Therapy: A Systematic Review and Meta-Analysis.

This systematic review and meta-analysis synthesized published evidence on second primary malignant neoplasms (SPMs) occurring after treatment with T-cell–engaging bispecific antibodies (BsAbs) in B-cell non-Hodgkin lymphoma and multiple myeloma. The key finding was an effort to estimate the frequency of reported SPMs and to evaluate how study-level characteristics and differing definitions/reporting practices influence SPM estimates (quantitative results are truncated in the provided abstract). Scientifically and clinically, the work aims to clarify long-term malignancy risk signals for BsAbs as these therapies move earlier in treatment and broaden in use.

Tomasik J, Tix T, Alhomoud M et al. · JAMA oncology · (2026) · View on PubMed ↗

Is Kaposi’s sarcoma the end of the OX40/OX40L axis in atopic dermatitis?

This commentary reviewed the OX40/OX40L axis as a therapeutic target in atopic dermatitis and discussed emerging safety concerns involving Kaposi’s sarcoma. It highlights that rocatinlimab was discontinued after confirmed/suspected cutaneous Kaposi’s sarcoma cases and that additional cumulative cases occurred in the amlitelimab program among patients with known risk factors, shifting the discussion toward risk and strategy rather than early efficacy alone. The clinical significance is that OX40/OX40L modulation in atopic dermatitis may require careful patient selection and monitoring for herpesvirus-associated malignancy risk.

Salek-Ardakani S · Frontiers in immunology · (2026) · View on PubMed ↗ · Free PDF ↗

---

Cancer Immunotherapy Targets, Cell Therapies & Response Modulation

Teclistamab induces rapid clinical response and deep tissue depletion in refractory systemic sclerosis-a case series.

This case series investigated the effects of the BCMA×CD3 bispecific antibody teclistamab on clinical response, serologic changes, and immune-cell depletion in patients with severe, treatment-refractory systemic sclerosis (SSc). Patients received off-label teclistamab, and outcomes were assessed using the ACR-CRISS response index alongside immunologic profiling of blood and tissue (skin and bone marrow) via immunohistochemistry and flow cytometry, with antibody quantification by ELISA. The significance is early clinical and mechanistic evidence that teclistamab can rapidly modulate pathogenic immune compartments in SSc, informing future controlled studies.

Siegert E, Phithak E, Albach FN et al. · Annals of the rheumatic diseases · (2026) · View on PubMed ↗

TFPI2 promotes NK cell-mediated glioblastoma killing through adhesion and checkpoint control.

This study examined NK cell–glioblastoma cross-talk and identified TFPI2 as a central mediator of how NK attack shapes tumor responses. NK cell attack induced TFPI2 expression in glioblastoma cells via IL1β- and TNFα-driven NFκB signaling, and TFPI2 both restrained tumor proliferation (by suppressing the POU2F2–CCND1 axis) and enhanced NK cytotoxicity through complementary adhesion/checkpoint-related mechanisms. The results suggest TFPI2 could be leveraged to improve NK-cell-based glioblastoma immunotherapy by coordinating tumor susceptibility and immune effector function.

Zheng D, Li F, Zhang Z et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗

The first-in-human ENCIT01 trial comparing second- versus third-generation L1CAM-specific CAR T cells in patients with primary refractory or relapsed neuroblastoma.

The ENCIT-01 first-in-human trial studied L1CAM-specific CAR T cells in 22 treated children and adolescents with primary refractory or relapsed neuroblastoma, comparing three 4-1BB-based CAR constructs (2GS short spacer, 3GS short spacer with CD28, and 2GL long spacer). The study enrolled 36 patients and evaluated safety/efficacy across the three arms, with results reported for the treated cohorts (Arm A/2GS n=11 and Arm B/3GS truncated in the provided abstract). This head-to-head construct comparison is clinically significant because it informs which L1CAM CAR T design (spacer length and CD28 inclusion) may optimize outcomes while minimizing toxicity in pediatric neuroblastoma.

Pinto N, Künkele A, Albert CM et al. · Clinical cancer research : an official journal of the American Association for Cancer Research · (2026) · View on PubMed ↗

Teclistamab in relapsed/refractory light chain amyloidosis: A retrospective multicenter study by the German Society for Amyloid Diseases.

This retrospective multicenter study evaluated teclistamab, an anti–BCMA/CD3 bispecific T-cell engager, in 52 German patients with relapsed/refractory systemic light chain (AL) amyloidosis. It reports high hematologic response rates, with ≥very good partial response (VGPR) achieved in 81% of patients by Day 15 and rising to 95% at 3 months. The clinical significance is that teclistamab may offer an effective and tolerable option for relapsed/refractory AL amyloidosis where no approved regimens currently exist.

Carpinteiro A, Kimmich C, Trajanova D et al. · HemaSphere · (2026) · View on PubMed ↗ · Free PDF ↗

---

Tumor Microenvironment, Spatial Immunology & Immune Escape

The multi-omics landscape of lung adenocarcinoma evolution: deciphering metabolic reprogramming-driven immune escape and its implications in combined therapy.

This review integrated multi-omics data—including genomics, metabolomics, single-cell RNA sequencing, and spatial transcriptomics—to map how lung adenocarcinoma (LUAD) evolves from pre-invasive lesions to invasive disease and how metabolic reprogramming drives immune escape. It highlights metabolic pathways and tumor-immune microenvironment remodeling mechanisms that promote immune evasion and thereby influence response to combined therapies. Scientifically, it provides a framework for targeting metabolism-linked immune escape to improve selection and efficacy of combination treatment regimens in LUAD.

Liu N, Han G, Jia J et al. · Cell death discovery · (2026) · View on PubMed ↗

Macrophage-mediated brain-bone marrow crosstalk promotes chronic stress-induced glioma growth.

This study examined how chronic stress alters tumor progression by promoting macrophage–brain–bone marrow crosstalk in syngeneic glioma-bearing mice. It found that stress induces CD45+CD11b+C5aR1+ “stress-associated macrophages” (SAMs) derived from bone marrow monocytes via sympathetic nerve signaling through ADRB2, and that C5ar1 loss in macrophages or pharmacologic C5aR inhibition reduces this pro-tumor effect. These results identify a stress–C5aR1–macrophage pathway as a potential target to mitigate stress-driven glioma growth.

Yang Z, Zhou J, Fei F et al. · Cancer cell · (2026) · View on PubMed ↗

Aerobic Exercise Activates S1PR1 Signaling in Tumor Endothelial Cells to Promote Vascular Function in Pancreatic Cancer.

This study investigated how aerobic exercise alters pancreatic ductal adenocarcinoma (PDAC) tumor vasculature and function, using surgically resected PDAC from patients who exercised during neoadjuvant chemotherapy and mouse orthotopic PDAC models. The authors found that exercise activates S1PR1 signaling in tumor endothelial cells, remodeling vasculature and improving vascular function. These results support a mechanistic basis for combining exercise with therapy to enhance drug delivery in PDAC.

Ballarò R, Lam T, Pareek S et al. · Cancer research · (2026) · View on PubMed ↗

CD4+ T cells impair tumor growth through IL-3 and TNF-dependent vascular damage.

This study investigated how antigen-specific CD4+ T cells affect tumor growth through a stroma-targeting mechanism, using multiplex immunofluorescence and single-cell/tissue transcriptomics. The authors found that CD4+ T cells impair tumor growth via IL-3 and TNF-dependent vascular damage by inducing perivascular myeloid clusters of classically activated macrophages that produce TNF in response to T cell-derived IL-3. This provides a new immunotherapy concept that leverages CD4+ T cell–driven vascular disruption rather than solely direct tumor killing.

Lian Q, Nie J, Singh J et al. · Science (New York, N.Y.) · (2026) · View on PubMed ↗

Cancer-associated fibroblasts and tertiary lymphoid structure orchestrate the spatial architecture of tumor immunity.

This review article studied how the spatial organization of tumor microenvironment components shapes anti-tumor immunity, focusing on cancer-associated fibroblasts (CAFs) and tertiary lymphoid structures (TLS). It found that CAF heterogeneity can remodel extracellular matrix, limit lymphocyte infiltration, sustain chronic inflammation, and promote therapy resistance, while some CAF subsets can support antigen presentation and lymphoid organization; TLS act as ectopic immune hubs that further structure immune responses. The scientific significance is that it frames tumor immunity as a spatially orchestrated system, suggesting that targeting CAF–TLS architecture could improve immunotherapeutic outcomes.

Tang H, Shi Y, Ge Q et al. · Journal of hematology & oncology · (2026) · View on PubMed ↗ · Free PDF ↗

---

Cancer Metabolism & Ferroptosis/DDR/Resistance Mechanisms

Is achieving higher standards in real-world migraine care feasible with anti-CGRP monoclonal antibodies preventive therapies?: Insights from the EUREkA cohort.

This study used integrative multi-omics—including single-cell RNA-sequencing, bulk RNA-seq, and spatial transcriptomics—to analyze non-small cell lung cancer (NSCLC) tumors from patients treated with immune checkpoint blockade (ICB) and to identify mechanisms of immunotherapy resistance. GALNT7, a glycosyltransferase, was selectively upregulated in non-responders and enriched in malignant epithelial cells, and GALNT7-linked signaling suppressed ferroptosis-related pathways compared with responders. This mechanistic link suggests GALNT7-dependent ferroptosis suppression as a potential biomarker and therapeutic target to overcome ICB resistance in NSCLC.

Caronna E, Mas-de-Les-Valls R, Egeo G et al. · Cephalalgia : an international journal of headache · (2026) · View on PubMed ↗

TRIM21-mediated ubiquitination of PARP1 regulated by the PI3K/AKT-STAT5A axis suppresses small cell lung cancer.

This study investigated the mechanism by which the E3 ubiquitin ligase TRIM21 regulates PARP1 stability via the PI3K/AKT–STAT5A axis in small cell lung cancer (SCLC). TRIM21 binds PARP1, promotes polyubiquitination at PARP1 lysine 654 (K654) leading to PARP1 degradation, and TRIM21 downregulation in SCLC supports tumor progression and genomic instability. These findings position the TRIM21–PARP1 axis as a potential therapeutic vulnerability and mechanistic rationale for targeting PI3K/AKT–STAT5A signaling in SCLC.

Cao G, Li G, Wang X et al. · Nature communications · (2026) · View on PubMed ↗

Interleukin-19 ameliorates drug-induced liver injury by limiting proinflammatory macrophage infiltration via SUMOylation of C/EBPβ.

This preclinical study investigated whether interleukin-19 (IL-19) protects against acetaminophen (APAP)-induced drug-induced liver injury (AILI) in mice, using Il19-deficient mice and myeloid cell–specific Il20r2 knockout models. IL-19 ameliorated AILI by limiting proinflammatory macrophage infiltration through SUMOylation of C/EBPβ, as supported by single-cell RNA sequencing of liver macrophage subsets. These mechanistic data identify an IL-19–C/EBPβ SUMOylation axis as a potential therapeutic target for acute liver failure due to APAP overdose.

Xiao P, Zai Q, Ma N et al. · Journal of hepatology · (2026) · View on PubMed ↗

What Are HFpEF Mimics and What Are They Mimicking? Insights Into Our Conceptualization of Heart Failure With Preserved Ejection Fraction as a Disease.

This article is a conceptual review that examined common “HFpEF mimics” that must be excluded when evaluating patients with chronic heart failure with preserved ejection fraction (HFpEF), including cardiac amyloidosis, hypertrophic cardiomyopathy, infiltrative/restrictive/inflammatory cardiomyopathies (e.g., sarcoidosis, hemochromatosis, Fabry disease, radiation/chemotherapy-induced disorders), significant valvular disease, and pericardial diseases. The key message is that accurate diagnosis requires systematic identification of these alternative etiologies rather than assuming HFpEF based on left ventricular ejection fraction ≥50% alone. Clinically, this framework improves diagnostic precision and guides appropriate disease-specific management.

Packer M, Butler J, Ho JE et al. · Journal of cardiac failure · (2026) · View on PubMed ↗

Targeting TROP2 in drug-tolerant persister cells delays EGFR tyrosine kinase inhibitor resistance in non-small-cell lung cancer.

This study investigated mechanisms of resistance in EGFR-mutant non-small-cell lung cancer (NSCLC) by focusing on drug-tolerant persister (DTP) cells and the role of TROP2 during EGFR tyrosine kinase inhibitor (TKI) treatment. It found that TROP2 is dynamically upregulated during TKI-induced DTP formation and is required for DTP maintenance, with c-Myc acting as a transcriptional repressor of TROP2 and MAPK pathway inhibition lowering c-Myc. Combining the TROP2-targeting antibody-drug conjugate sacituzumab tirumotecan (sac-TMT) with osimertinib suppressed DTP emergence and delayed relapse in preclinical models, suggesting a strategy to prevent EGFR-TKI resistance.

Liao J, Yao W, Yu Y et al. · Cancer cell · (2026) · View on PubMed ↗

PKCα-mediated nuclear translocation of cGAS stabilizes β-catenin and drives metastasis.

This study explored how nuclear cyclic GMP-AMP synthase (cGAS) promotes metastasis in triple-negative breast cancer (TNBC), identifying a STING-independent pathway. It showed that protein kinase C alpha (PKCα) phosphorylates cGAS at Ser120 to drive nuclear translocation, where nuclear cGAS stabilizes β-catenin by disrupting the β-catenin–TRIM33 interaction and preventing β-catenin ubiquitination. The findings link PKCα–nuclear cGAS signaling to Wnt/β-catenin activation and metastasis, highlighting potential targets for anti-metastatic therapy.

Zhang Q, Tong C, Zhao M et al. · Molecular cell · (2026) · View on PubMed ↗

HSPA6 Confers Lenvatinib Resistance in Hepatocellular Carcinoma by Promoting Phase Separation-Mediated TXNRD1 Stabilization to Suppress Ferroptosis.

This study examined mechanisms of lenvatinib resistance in hepatocellular carcinoma (HCC) by integrating genome-wide CRISPR screening with transcriptomics and proteomics to identify resistance drivers. It found that HSPA6 promotes phase separation–mediated stabilization of TXNRD1 by recruiting the deubiquitinase USP9X, thereby suppressing lenvatinib-induced ferroptosis and correlating with poor response and survival. The work highlights HSPA6–TXNRD1 axis as a potential therapeutic target to overcome lenvatinib resistance in advanced HCC.

Zeng Y, Huang Z, Qiu J et al. · Cancer research · (2026) · View on PubMed ↗

PARG Governs a PARylation-Ubiquitination Toggle that Stabilizes RAD51AP1 to Drive Homologous Recombination-Mediated Chemoresistance.

This study investigated poly(ADP-ribose) glycohydrolase (PARG) as a DNA damage response factor in gastric cancer (GC) and its role in chemoresistance, using integrated analyses of multiple GC cohorts plus high-throughput screening of FDA-approved drugs. The authors found that PARG inhibition shows limited monotherapy efficacy but creates a synthetic lethal interaction with fluoropyrimidines such as 5-fluorouracil (5-FU), and mechanistically PARG binds the homologous recombination cofactor RAD51AP1 to stabilize it and drive homologous recombination–mediated chemoresistance. Clinically, this suggests a rational combination strategy pairing PARG inhibition with 5-FU to counter HR-dependent resistance in GC.

He H, Hu Y, Lu Y et al. · Cancer research · (2026) · View on PubMed ↗

Targeting the DNA methylation-H3K27me3 switch reverses castration resistance and immunosuppression via ADAMTS1-driven collagenolysis.

This study investigated epigenetic mechanisms of castration resistance in prostate cancer by analyzing how DNA methylation and H3K27me3 repression interact at the ADAMTS1 locus. DNMT inhibitors triggered EZH2-dependent H3K27me3 accumulation at ADAMTS1, sustaining a fibrotic ECM-remodeling niche via ADAMTS1-driven collagenolysis and promoting therapy resistance, while dual DNMT/EZH2 targeting disrupted this plasticity and reactivated ADAMTS1 to degrade collagen-rich stroma. The work supports a therapeutic approach that targets the DNA methylation–H3K27me3 switch to reverse CRPC resistance and immunosuppression.

Wu X, Song X, Li B et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗

rRNA intermediates associate with nucleolar reshaping in C. elegans.

This Nucleic Acids Research study in Caenorhabditis elegans investigated how ribosomal RNA (rRNA) processing and transcription events relate to nucleolar remodeling, focusing on rRNA intermediates and nucleolar architecture. Defects in pre-18S rRNA processing and rRNA transcription reorganized nucleolar structure, and depletion of class I ribosomal proteins (RPSs) produced a concentric three-layered nucleolus. The scientific significance is that it clarifies how specific rRNA biogenesis steps coordinate nucleolar organization, linking ribosome production dynamics to nuclear substructure changes.

Cheng J, Liu L, Xu D et al. · Nucleic acids research · (2026) · View on PubMed ↗ · Free PDF ↗

Dual CDK2 and CDK4/6 inhibition suppresses Rb/E2F signaling and enhances anti-leukemic activity in acute myeloid leukemia.

This Haematologica study evaluated a therapeutic strategy combining dual CDK2 and CDK4/6 inhibition to suppress Rb/E2F signaling and enhance anti-leukemic activity in acute myeloid leukemia (AML). The rationale builds on prior evidence that CDK4/6 inhibition (e.g., palbociclib) can improve outcomes in pediatric settings, and the authors sought to assess whether dual CDK2/CDK4/6 blockade increases AML sensitivity to standard-of-care and other regimens, but the provided abstract is truncated before reporting specific results. Scientifically, the work is significant because it targets cell-cycle control pathways (CDK2/CDK4/6–Rb/E2F) to overcome resistance in AML.

Weisberg E, Chowdhury B, Garg S et al. · Haematologica · (2026) · View on PubMed ↗ · Free PDF ↗

Hypoxia and lactate metabolism-related gene COL5A3 promotes triple negative breast cancer progression via DDR1/FAK/PI3K/AKT pathway.

This study investigated how hypoxia and lactate metabolism-related gene COL5A3 promotes triple-negative breast cancer (TNBC) progression through the DDR1/FAK/PI3K/AKT signaling pathway. It found that COL5A3 is associated with TNBC progression under hypoxic/lactate-rich conditions and drives pathway activation via DDR1/FAK/PI3K/AKT, supporting a mechanistic role in aggressive tumor behavior. The findings are significant because they identify COL5A3 and the DDR1/FAK/PI3K/AKT axis as potential targets for prognostic modeling and therapeutic intervention in TNBC.

Shao QF, Wang ZY, Liang W et al. · Biology direct · (2026) · View on PubMed ↗ · Free PDF ↗

---

Biomarkers, Omics Signatures & Diagnostic/Prognostic Tools

KMT2A and KMT2B episignatures address diagnostic challenges associated with rare neurodevelopmental disorders.

This study developed and validated DNA methylation (DNAm) episignatures for rare neurodevelopmental disorders caused by pathogenic variants in KMT2A (Wiedemann-Steiner syndrome, WDSTS) and KMT2B (Dystonia 28, DYT28). The KMT2A-WDSTS signature (264 CpG sites) and KMT2B-DYT28 signature (752 mostly hypermethylated CpG sites) achieved high sensitivity/specificity with >80% and >85% pathogenicity scores in validation, respectively, with limited overlap between signatures. These episignatures improve molecular diagnosis when variant interpretation is challenging, enabling more accurate clinical classification of KMT2A/KMT2B-related disorders.

Awamleh Z, Chen A, Choufani S et al. · Genetics in medicine : official journal of the American College of Medical Genetics · (2026) · View on PubMed ↗

Spatially interpretable artificial intelligence framework to tailored neoadjuvant dual HER2 blockade in HER2-positive breast cancer.

This study developed HER2-LADDER, a spatially interpretable AI framework to tailor neoadjuvant dual HER2 blockade using trastuzumab plus pertuzumab in HER2-positive breast cancer. By integrating clinicopathological and spatial topological features from routine H&E and HER2 IHC slides, the model aimed to predict heterogeneous treatment response and recommend therapy stratification. The clinical significance is a more practical, slide-based decision tool to personalize neoadjuvant dual HER2 blockade for improved outcomes.

Wu XR, Lv H, Zhao S et al. · Signal transduction and targeted therapy · (2026) · View on PubMed ↗

Quantitative Serological Detection of NELL1 Autoantibodies in Membranous Nephropathy.

This study developed and evaluated quantitative serologic assays for neural EGFL-like 1 (NELL1) autoantibodies in patients with membranous nephropathy (MN), aiming to replace or complement kidney biopsy–based diagnosis (mass spectrometry or immunostaining). The key finding was that high-throughput immunoassay approaches (including ELISA and related formats) can detect anti-NELL1 antibodies with sufficient performance characteristics to support research and potentially clinical diagnostic use. Reliable serologic testing for anti-NELL1 would enable less invasive diagnosis and monitoring of NELL1-associated MN.

Burbelo PD, Howard L, Caza TN et al. · Kidney international · (2026) · View on PubMed ↗

A practical alternative to live cell-based assay for AQP4 and MOG antibody detection.

This work studied diagnostic performance for aquaporin-4 (AQP4) and myelin oligodendrocyte glycoprotein (MOG) autoantibodies in neuromyelitis optica spectrum disorder (NMOSD) and MOG antibody-associated disorder (MOGAD), comparing fixed cell-based assay (FCBA) with a new serum-processing approach called AbFine. AbFine uses a high-performance untransfected vector cells lysate to pre-bind and deplete interferents before FCBA, improving practicality and standardizability while maintaining diagnostic accuracy in a multicenter, double-blind, prospective discovery study. Clinically, this provides a more scalable alternative to live cell-based assays (LCBA) for sensitive AQP4/MOG antibody detection.

Wang Q, Chen F, Tang Y et al. · EBioMedicine · (2026) · View on PubMed ↗

Age and early life adversity shape heterogeneity of the epigenome across tissues in macaques.

This study profiled DNA methylation (DNAm) across 14 tissues in 237 semi-free-ranging rhesus macaques to determine how age and early life adversity (ELA) shape epigenetic heterogeneity. It found that age-associated DNAm effects were largely tissue dependent, while tissue-specific epigenetic clocks were relatively consistent within individuals, and that ELA produced coordinated but adversity-specific effects across tissues with directions that differed from age. The results indicate that ELA does not simply accelerate epigenetic aging uniformly, refining how we interpret epigenetic biomarkers of life history.

Sadoughi B, Petersen RM, Patterson SK et al. · Science (New York, N.Y.) · (2026) · View on PubMed ↗

Nodular Fasciitis of the Vulva: Clinicopathologic Features and Diagnostic Pitfalls With Molecular Confirmation.

This 2026 case report and clinicopathologic analysis studied nodular fasciitis (NF) of the vulva in a 34-year-old woman, focusing on diagnostic pitfalls and confirming the diagnosis with molecular methods. The lesion was rapidly enlarging and histologically mimicked other entities, but molecular confirmation supported benign NF rather than malignancy. The clinical significance is that vulvar NF is rare and can be misdiagnosed, so combining careful histopathology with molecular confirmation can prevent inappropriate overtreatment.

Erbağci A, Ökten İN, Kir G · International journal of gynecological pathology : official journal of the International Society of Gynecological Pathologists · (2026) · View on PubMed ↗ · Free PDF ↗

Multimodality imaging characterization of Perugini scintigraphic grades in transthyretin amyloid cardiomyopathy: a single-center experience.

This single-center retrospective study evaluated multimodality imaging characteristics across Perugini scintigraphic grades in patients with transthyretin amyloid cardiomyopathy (ATTR-CM) undergoing technetium-99m pyrophosphate (99mTc-PYP) scintigraphy. The key finding was that Perugini grades 2 versus 3—both considered diagnostic—may show clinically and imaging-relevant phenotypic differences, with the study assessing diagnostic yield and cross-grade characteristics. Clinically, it helps refine interpretation of 99mTc-PYP grading by clarifying whether higher grades correspond to distinct ATTR-CM phenotypes.

Bucius P, Zarambaite E, Lusaite K et al. · Journal of cardiovascular imaging · (2026) · View on PubMed ↗ · Free PDF ↗

Plasma proteome-metabolome signatures enable non-invasive early detection and lymph node risk stratification in breast cancer.

This study investigated whether plasma proteome–metabolome multi-omics signatures can enable non-invasive early detection of breast cancer and stratify lymph node risk, particularly in Asian women with dense breast tissue. Using a registered multicenter prospective study (NCT06016790) plus an independent external validation cohort (662 participants across nine institutions), it evaluated a plasma-based multi-omics liquid-biopsy framework for early detection and lymph node risk stratification. Clinically, it aims to improve diagnostic accuracy beyond ultrasound and mammography by leveraging biologically informed circulating biomarkers.

Zhang W, Yao Y, Wang Y et al. · Molecular cancer · (2026) · View on PubMed ↗ · Free PDF ↗

---

Neurodegeneration, Neuroinflammation & Neuroimaging Biomarkers

Monocarboxylate transporter 2 regulates maintenance of myelin and axonal integrity by oligodendrocytes.

This study examined how monocarboxylate transporter 2 (MCT2, SLC16A7) supports myelin and axonal integrity in oligodendrocytes, particularly in the context of progressive multiple sclerosis (MS). MCT2 was downregulated in progressive MS, and oligodendrocyte-specific deletion of MCT2 in mouse spinal white matter using an oligodendrotropic AAV approach reduced lipid-synthesis enzymes and increased inflammatory signaling without affecting oligodendrocyte survival. These results identify MCT2-dependent metabolic maintenance as a potential target to preserve white matter integrity in progressive MS.

Izagirre-Urizar L, Mora-Huerta L, Soler-Saez I et al. · Nature communications · (2026) · View on PubMed ↗

Long-term prognosis of patients surviving progressive multifocal leukoencephalopathy.

This international multicenter retrospective study analyzed long-term (three-year) prognosis in patients with progressive multifocal leukoencephalopathy (PML) who survived at least one year, using data from 41 centers across 12 countries. The study characterized late mortality, favorable outcome factors, and recurrence rate among long-term survivors. Scientifically and clinically, it improves counseling and risk stratification for PML survivors beyond the first year despite improved overall survival.

Lambert N, El Moussaoui M, Le Guilloux A et al. · Brain : a journal of neurology · (2026) · View on PubMed ↗

Endothelial KLF4 depletion drives age-related neurovascular dysfunction and neuropsychiatric impairment.

This study used endothelial cell-specific Klf4 knockout mice (EC-K4KO) to test whether age-related declines in endothelial KLF4 drive blood-brain barrier (BBB) dysfunction, neurovascular uncoupling, and cognitive impairment. EC KLF4 loss accelerated multiple age-related brain pathologies, with middle-aged EC-K4KO mice showing pathological features consistent with impaired BBB and neuropsychiatric impairment. The findings identify endothelial KLF4 as a causal regulator of neurovascular health in aging and a potential target to prevent age-associated cognitive decline.

Dhar M, Vázquez-Rosa E, Chaubey K et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗

Obesity, White Matter Hyperintensities, and Cognitive Decline: Sex-Specific DTI-ALPS Index Mediation.

This study used UK Biobank data to examine sex-specific mediation pathways linking obesity metrics (BMI, waist-hip ratio, body fat percentage) to cognitive decline via glymphatic function measured by the DTI-ALPS index, and to relate these to white matter hyperintensity (WMH) volume using obesity trajectory modeling, genome-wide association studies, and 2-sample Mendelian randomization. The key finding was that the obesity→glymphatic dysfunction→WMH/cognitive decline pathway differed by sex, with DTI-ALPS (glymphatic function) acting as a mediator between obesity and downstream brain and cognitive outcomes. These results support a sex-dependent mechanistic role for glymphatic impairment in obesity-associated cognitive decline, informing risk stratification and potential targeting of glymphatic pathways.

Ran L, Huang H, He Y et al. · Stroke · (2026) · View on PubMed ↗

Affective and cognitive theory of mind and associated brain functional alterations in frontotemporal dementia.

This neuroimaging study examined theory of mind (ToM) deficits across the frontotemporal dementia spectrum and their neural correlates in 67 frontotemporal dementia patients using resting-state functional MRI. It found that ToM impairments in behavioural variant frontotemporal dementia extend beyond a single subtype and are associated with functional connectivity alterations across the brain network(s) supporting ToM. The clinical significance is that shared ToM-related network changes could improve understanding of diagnosis/prognosis across FTD variants and guide biomarker development.

Tripodi C, Canu E, Marangon A et al. · Brain communications · (2026) · View on PubMed ↗ · Free PDF ↗

---

Neuromuscular, Neurodevelopment & Circuit/Cell Biology

Pulmonary adverse events associated with GLP-1 receptor agonists: a systematic review of respiratory safety signals.

This study tested whether intrathecal delivery of (G4C2)149 repeats via an adeno-associated virus (AAV) in C9orf72-deficient mice would better model spinal involvement in ALS/FTD. Neonatal intrathecal AAV-(G4C2)149 produced widespread CNS expression with robust spinal cord targeting, and repeat expression primarily drove mild, progressive muscle weakness with ALS/FTD pathological hallmarks. The model helps disentangle gain- versus loss-of-function contributions of C9orf72 repeat biology and may improve preclinical relevance for spinal-region disease mechanisms.

Ahuja A, Prasad S, Manoharan S et al. · Cardiovascular diabetology. Endocrinology reports · (2026) · View on PubMed ↗

Multimodal imaging of gene expression, morphology, and activity of the same neuron.

This study developed a trimodal in vivo-to-ex vivo platform combining calcium (Ca2+) imaging, morphological reconstruction in cleared whole brains, and post hoc imaging-based in situ transcriptomic profiling to characterize the same neuron in mice. Applying the platform to mouse primary visual cortex (VISp), the authors generated trimodal profiles for 141 intratelencephalic (IT) and pyramidal tract (PT) neurons and linked neuronal activity and projection/morphology with gene-expression programs. The technique enables direct, cell-level mapping of how gene expression relates to neuronal structure and function, advancing circuit neuroscience.

Zhao Y, Shi Z, Liu X et al. · Cell · (2026) · View on PubMed ↗

Tracking mobilization uncovers an evolutionarily conserved mechanism in suppressing mobile genetic elements.

This study used spatiotemporal, single-cell–resolution monitoring of transposition events to identify mechanisms that suppress mobile genetic elements during somatic development in Drosophila and mice. It found that Cramp1 is a critical, evolutionarily conserved factor that silences transposon mobility during Drosophila hindgut regeneration and mouse embryonic erythropoiesis. By defining a conserved anti-transposition program, the work provides mechanistic insight relevant to diseases driven by aberrant transposon activation.

Luo YN, Liang Y, Wu S et al. · Molecular cell · (2026) · View on PubMed ↗

Lamprey 3D single-cell transcriptomics reveals ancestral and specialized features of the vertebrate brain.

This study used spatial transcriptomics and single-nucleus RNA sequencing to build a 3D molecular atlas of the lamprey brain across 14 regions, identifying 209 cell clusters. Cross-species comparisons showed conserved ancestral regional spatial architecture but substantial lineage-specific divergence with extensive neuronal specialization and regulatory shifts linked to spatial reorganization. These findings provide a vertebrate-evolution framework for how brain cell types and regulatory programs diversify while preserving core anatomical organization.

Wu H, Chen D, Li J et al. · Science (New York, N.Y.) · (2026) · View on PubMed ↗

Decoupling of global metabolic flux and proteome partitioning in bacteria.

This work compared how proteome allocation is regulated in Escherichia coli versus Bacillus subtilis, focusing on the roles of guanosine nucleotides (p)ppGpp versus GTP in coupling amino-acid supply to ribosome production. In Bacillus subtilis, GTP—not (p)ppGpp—controlled proteome partitioning, and translational inhibition depleted GTP and suppressed amino-acid biosynthesis via feedback without changing ribosome abundance, demonstrating a regulated decoupling between total amino-acid flux and proteome composition. The results revise how bacterial growth homeostasis can be modeled, showing that flux can diverge from proteome-based predictions depending on the nucleotide control architecture.

Thiermann R, Yang J, Zodage A et al. · Science (New York, N.Y.) · (2026) · View on PubMed ↗

Tmem67 Is Required for Spermiogenesis and Male Fertility in Mice.

This study generated germ cell-specific (Stra8-Tmem67f/f) and Sertoli cell-specific (Amh-Tmem67f/f) Tmem67 knockout mice to test TMEM67’s role in spermiogenesis and male fertility. Germ cell and Sertoli cell-specific loss of Tmem67 showed normal fertility and largely normal spermatogenesis, with no significant testicular histology differences reported in the excerpt. The findings indicate that despite TMEM67’s ciliary transition zone association, it is not essential in these specific mouse cell compartments for male reproductive function.

Wang B, Ling S, Sun W et al. · FASEB journal : official publication of the Federation of American Societies for Experimental Biology · (2026) · View on PubMed ↗

Evolutionarily conserved and divergent mechanisms of dual Ca2+ sensors in synaptic vesicle exocytosis.

This study analyzed dual Ca2+ sensor mechanisms at the C. elegans neuromuscular junction, focusing on SNT-1 and SNT-3 and their interactions with the SNARE complex and polybasic motifs. AlphaFold 3 modeling predicted a C2B–SNARE arrangement for SNT-1 and SNT-3 consistent with canonical synaptotagmin (Syt1) interfaces, supporting how the two sensors mediate fast versus slow neurotransmitter release. By linking conserved and divergent molecular architectures across species, the work clarifies how dual Ca2+ sensing can tune synaptic exocytosis kinetics.

Li L, Wang J, Xia J et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗

Structural basis for lysophosphatidic acid recognition and atypical Gαq coupling by LPAR5.

This study determined the cryo-EM structure of the lysophosphatidic acid receptor LPAR5 bound to 1-oleoyl-lysophosphatidic acid (LPA) in complex with Gq at 2.96 Å. The structure revealed a distinct activation/coupling mode in which the LPA phosphate headgroup interacts with extracellular loop 2 and TM5–TM7, while the lipid tail inserts into a deep hydrophobic cavity formed by TM3–TM5, and site-directed mutagenesis supported key functional residues. These structural insights explain how LPAR5 recognizes LPA and couples atypically to Gq, informing mechanistic targets for neuropathic pain, itch, and cancer pathways.

Li X, Wang K, Xing Z et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗

Sucrose and jasmonic acid positive feedback loop controls stem cell senescence in Arabidopsis.

This study investigated how sucrose and jasmonic acid (JA) regulate stem cell senescence and inflorescence meristem (IM) arrest in Arabidopsis, focusing on the JA–MYC2–WUSCHEL axis and sugar transporters. It found that JA accumulates in the aging IM and directly represses WUSCHEL and cytokinin accumulation via the transcription factor MYC2, while sucrose from siliques triggers local JA biosynthesis in the IM and increases SWEET transporter expression, driving stem cell senescence and meristem proliferation arrest. These findings define a sucrose–JA positive feedback mechanism that links nutrient signaling to meristem aging, offering a mechanistic framework for controlling plant developmental lifespan.

Chen YD, Zhang R, Yang J et al. · Molecular plant · (2026) · View on PubMed ↗

---

Infectious Disease Virology & Host–Virus Interactions

Enterovirus D68 2A protease causes nuclear pore complex dysfunction and independently contributes to motor neuron toxicity.

This eLife study investigated how enterovirus D68 (EV-D68) proteases, specifically 2A and 3C, affect nuclear pore complex (NPC) composition and function in the context of acute flaccid myelitis motor neuron toxicity. The authors found that EV-D68 2A and 3C proteases cause widespread NPC disruption, supporting a mechanistic link between viral protease activity and selective motor neuron injury. These findings are scientifically significant because they identify NPC dysfunction as an independent contributor to EV-D68 neurotoxicity, suggesting potential targets for therapeutic intervention in AFM.

Zinn KM, McLaren MW, Imai MT et al. · eLife · (2026) · View on PubMed ↗ · Free PDF ↗

Mapping the global distribution and spread of the Plasmodium vivax-associated virus MaRNAV-1.

This study mapped the global distribution and host associations of the Plasmodium vivax-associated virus MaRNAV-1 using primary and publicly available metatranscriptomic datasets. It detected MaRNAV-1 across Southeast Asia, parts of South America, and for the first time in Oceania, while finding it exclusively in metatranscriptomes containing P. vivax. Scientifically, it supports a specific virus–host relationship and provides a foundation for understanding MaRNAV-1 ecology and potential impacts on malaria transmission dynamics.

Petrone ME, Charon J, Parry RH et al. · Virus evolution · (2026) · View on PubMed ↗ · Free PDF ↗

---

Autoimmune/Inflammatory Disease Mechanisms & Clinical Management

Lung disease in rheumatoid arthritis.

This review summarized pulmonary disease manifestations in rheumatoid arthritis (RA), focusing on how systemic inflammation and shared risk factors (notably tobacco smoking) contribute to lung pathology. It highlights that RA is associated with airway obstructive disease, interstitial lung disease (ILD), and increased lung cancer prevalence, with pulmonary involvement contributing to reduced survival. The significance is that clinicians should more actively screen and manage lung complications in ACPA-positive RA, especially among smokers, to improve outcomes.

Bendstrup E, Dieude P, Kreuter M et al. · Nature reviews. Rheumatology · (2026) · View on PubMed ↗

Effects of Metabolic Dysregulation on Macrophage Polarization in Rheumatoid Arthritis.

This Arthritis & Rheumatology study investigated how metabolic dysregulation influences macrophage polarization in rheumatoid arthritis (RA), focusing on the balance between classically activated M1 and alternatively activated M2 macrophage states. The abstract frames macrophage polarization as a key driver of RA progression, with M1 macrophages promoting inflammation and M2 macrophages associated with resolution, but the provided text truncates before detailing the study’s specific experimental findings. The clinical significance is that metabolic pathways that shift macrophage polarization could become actionable targets to modulate inflammation and disease severity in RA.

Zhang X, Deng X, Wei S et al. · Arthritis & rheumatology (Hoboken, N.J.) · (2026) · View on PubMed ↗

ADA2 genotype and enzyme activity may predict vasculitic or hematologic DADA2 phenotype.

This genetic/clinical study analyzed 48 patients with DADA2 from Germany, Austria, and Switzerland to test whether ADA2 genotype and measured ADA2 enzyme activity predict vasculitic versus hematologic phenotypes. The key finding was that lower patient ADA2 activity predicted neutropenia and showed a trend toward higher decision probability for hematopoietic cell transplantation (HCT), while higher ADA2 activity correlated with different clinical features. Clinically, ADA2 activity could help refine phenotype prediction and treatment planning (including HCT consideration) in DADA2 patients.

Peters P, Schepp J, Albert MH et al. · Journal of human immunity · (2026) · View on PubMed ↗ · Free PDF ↗

Expert recommendations for the management of refractory gastroesophageal reflux disease in systemic sclerosis: A report from the World Scleroderma Foundation (WSF) Gastrointestinal “Ad hoc committee”.

This World Scleroderma Foundation (WSF) Gastrointestinal ad hoc committee report developed expert, consensus-based recommendations for managing refractory gastroesophageal reflux disease (GERD) in systemic sclerosis (SSc), including proposing practical definitions for refractory SSc-related GERD. The key finding was the committee’s structured, multidisciplinary consensus on how to define refractory disease and what management approaches to consider in SSc patients whose GERD does not respond to standard therapy. The significance is improved clinical guidance for a common SSc complication (~75% prevalence) where prior recommendations lacked operational depth.

Hughes M, Cricchio AL, De Santis MC et al. · Journal of scleroderma and related disorders · (2026) · View on PubMed ↗ · Free PDF ↗

An inverse probability of treatment weighted comparison between vedolizumab, ustekinumab, and tofacitinib in anti-TNF-experienced ulcerative colitis patients.

This multicenter retrospective observational cohort study used inverse probability of treatment weighting to compare effectiveness and safety among vedolizumab, ustekinumab, and tofacitinib in anti-TNF-experienced ulcerative colitis patients, assessing outcomes including partial Mayo score (pMayo), endoscopic remission, and biomarker response over 12, 24, and 52 weeks. The key finding was the comparative effectiveness/safety estimates derived from the weighted analysis across these three therapies in a real-world anti-TNF-exposed population. Clinically, the results aim to inform treatment selection when patients have failed anti-TNF therapy by providing comparative outcome data across biologic and small-molecule options.

Tursi A, Pasta A, Elisei W et al. · Therapeutic advances in gastroenterology · (2026) · View on PubMed ↗ · Free PDF ↗

Systemic Mastocytosis in Adults: 2026 Update on Diagnosis, Risk Stratification and Management.

This 2026 update reviewed the diagnosis, risk stratification, and management of systemic mastocytosis (SM) in adults, emphasizing the International Consensus Classification/WHO framework. It found that SM diagnosis hinges on multifocal mast cell clusters in bone marrow and/or extracutaneous organs (major criterion) plus minor criteria such as elevated serum tryptase, aberrant mast cell markers (CD25/CD2/CD30), and activating KIT mutations, with risk driven by SM subtype (indolent/smoldering vs advanced forms including aggressive SM and SM with associated myeloid neoplasm). Scientifically and clinically, it consolidates how KIT-driven clonal mast cell disease is categorized to guide prognosis and treatment selection.

Pardanani A · American journal of hematology · (2026) · View on PubMed ↗

Comparable Infection Risk of Ocrelizumab and Rituximab in Multiple Sclerosis in a Nationwide Swedish Cohort Study.

This nationwide Swedish cohort study compared infection risk and relapse outcomes among multiple sclerosis patients treated with anti-CD20 therapies—rituximab versus ocrelizumab versus other disease-modifying therapies (DMTs)—using 16,872 treatment episodes from 2014–2025. It found that both rituximab and ocrelizumab were associated with higher infection rates than other DMTs, while relapse rates were substantially lower with these therapies. The results are clinically significant because they quantify and contextualize the tradeoff between reduced MS relapse activity and increased infection risk for rituximab and ocrelizumab.

Frisell T, Hedberg S, Piehl F · Annals of neurology · (2026) · View on PubMed ↗ · Free PDF ↗

---

Respiratory Disease (Asthma/COPD/PAH) & Pulmonary Safety

Wearable-Derived Diurnal Alignment Between Physical Activity and Device Temperature Predicts Future Disease and Mortality Risk.

This systematic review synthesized evidence on pulmonary adverse events temporally associated with glucagon-like peptide-1 receptor agonists (GLP-1 RAs) in adults. Across published reports, the review characterized respiratory safety signals, described patterns and severity, and assessed risk of bias using validated tools. The findings address an evidence gap in GLP-1 RA respiratory safety and can inform clinicians and regulators when monitoring and interpreting pulmonary events.

Chen H, Wei J, Cedernaes J et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗

Clinical Features of Cellular Senescence Pathways in Severe Asthma.

This study evaluated whether cellular senescence pathways are enriched in the airways of patients with severe asthma by analyzing transcriptomic data from the U-BIOPRED cohort. Using gene set variation analysis, it assessed enrichment of p53 and senescence-associated secretory pathway (SASP) signatures across airway compartments and validated findings in the independent NOVA cohort, then related senescence enrichment to clinical severity and other asthma gene signatures. The significance is that senescence pathway activity could serve as a mechanistic biomarker and potential therapeutic target in severe asthma.

Song WJ, Kermani NZ, Versi A et al. · Allergy · (2026) · View on PubMed ↗

Apelin analog treatment reverses severe pulmonary arterial hypertension and right ventricular heart failure.

Using a sugen-hypoxia rat model of pulmonary arterial hypertension (PAH), the study tested a novel apelin analog engineered to resist native peptidase degradation for reversal of pulmonary vascular remodeling and right ventricular (RV) failure. Apelin analog therapy corrected lung vascular lesions, nearly normalized pulmonary arterial pressures, and improved RV dilation and dysfunction compared with untreated PAH controls (with additional mechanistic and functional outcomes truncated). These preclinical results support the apelinergic pathway as a therapeutic target and justify further development of apelin analogs for PAH with RV failure.

Vu J, Zhabyeyev P, Brown KJ et al. · JCI insight · (2026) · View on PubMed ↗

International consensus on airway clearance techniques for patients hospitalised with acute exacerbations of COPD: a European Delphi study.

This European Delphi study surveyed 162 experienced physiotherapists across 12 countries to reach international consensus on airway clearance techniques (ACTs) for patients hospitalized with acute exacerbations of COPD (AECOPD). The key finding was the identification of commonly used ACTs and the level of agreement on how to select airway clearance techniques for hospitalized AECOPD patients. The significance is standardized, evidence-informed guidance that can reduce variability in ACT selection and potentially improve care consistency during acute COPD exacerbations.

Schrøder C, Poncin W, Oliveira A et al. · ERJ open research · (2026) · View on PubMed ↗ · Free PDF ↗

---

Cardiovascular, Heart Failure & Vascular Aging

Single-Cell Reveal GALNT7-Dependent Ferroptosis Suppression as a Mechanism of Immunotherapy Resistance in Non-Small Cell Lung Cancer.

This narrative review synthesized evidence connecting dermatologic conditions and cardiovascular disease (CVD) risk, focusing on shared mechanisms such as chronic inflammation, oxidative stress, and endothelial dysfunction. It highlights that inflammatory and genetic skin diseases (e.g., psoriasis, atopic dermatitis, systemic lupus erythematosus) are associated with increased cardiovascular risk through overlapping systemic pathways. The review supports using skin findings as clinically relevant indicators for cardiovascular risk stratification and prevention.

Gan J, Zheng Q, Liu D et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗

Intrathecal (G4C2)149 delivery in C9orf72-deficient mice yields mild motor dysfunction and ALS/FTD pathological hallmarks.

This study investigated whether wearable-derived circadian alignment between physical activity and device temperature predicts future disease and mortality in free-living humans. Using week-long wrist-worn acceleration and device temperature data from ~90,000 UK Biobank participants (median age 63), the authors derived alignment features (including 24 h coupling strength and phase deviation) and tested their association with long-term health outcomes. The results support using noninvasive wearable circadian metrics to forecast disease and mortality risk beyond traditional clinical factors.

Russell KA, Shahrabi AA, Akerman SC et al. · Acta neuropathologica communications · (2026) · View on PubMed ↗

AI-derived bone mineral density from standard radiographs compared with DXA for fracture prediction in a 10-year real-world cohort study.

In a 10-year real-world cohort study, AI-derived bone mineral density (BMD) extracted from standard radiographs was compared with DXA measurements for agreement and for predicting incident fractures. The key finding was that AI-derived BMD showed strong agreement with DXA and comparable fracture-prediction performance, supporting an opportunistic screening approach without dedicated DXA scans (full metrics are truncated in the provided abstract). Clinically, this could expand osteoporosis risk identification in settings where DXA access is limited.

Tseng TH, Huang TT, Huang JE et al. · Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · (2026) · View on PubMed ↗

Cardiovascular Events in Patients With Acute Myeloid Leukemia Treated With Venetoclax: A Multicenter Cohort Study.

This multicenter retrospective cohort study evaluated major adverse cardiovascular events (MACE) in 1,012 adults with acute myeloid leukemia treated with hypomethylating agents plus venetoclax (HMA-VEN) across six U.S. health systems from 2017 to 2024. The study aimed to determine the incidence, risk factors, and prognostic significance of cardiovascular events and to identify clinical and genetic predictors, but the provided abstract truncates the key results. Clinically, defining MACE risk in HMA-VEN–treated AML patients is important for prevention, monitoring, and risk stratification during therapy.

Filimon S, Ghamari A, Vakilpour A et al. · JACC. Advances · (2026) · View on PubMed ↗ · Free PDF ↗

Strategies for Optimizing Heart Failure Care in the Older Adult: A Scientific Statement From the American Heart Association.

This American Heart Association scientific statement in Circulation reviewed evidence and strategies to optimize heart failure care specifically for older adults (≥65 years), addressing barriers to accessing guideline-directed, disease-modifying therapies. It emphasizes tailored, patient-centered approaches to overcome system- and patient-level obstacles that limit use of effective treatments in those at highest risk of cardiovascular death or worsening heart failure. The clinical significance is that it provides practical guidance for improving outcomes in an aging population with heart failure by translating evidence into age-appropriate care delivery.

Lewsey SC, Martyn T, Blumer V et al. · Circulation · (2026) · View on PubMed ↗

Cardiovascular-kidney-metabolic (CKM) syndrome.

This article reviewed and synthesized evidence on cardiovascular-kidney-metabolic (CKM) syndrome, focusing on how metabolic disorders (especially obesity, diabetes, and metabolic dysfunction–associated fatty liver disease) interact with chronic kidney disease and cardiovascular disease, including contributions from genetic/epigenetic predisposition and social determinants of health. The key finding is that CKM syndrome is driven mechanistically by insulin resistance, inflammation, oxidative stress, and vascular dysfunction, and that urinary albumin:creatinine ratio is a practical biomarker for identifying/monitoring CKM risk. Scientifically and clinically, framing these conditions as a unified syndrome supports earlier detection and integrated prevention strategies targeting shared metabolic and vascular pathways.

Dwyer KM, Figtree PE, Oetsch K et al. · Australian prescriber · (2026) · View on PubMed ↗ · Free PDF ↗

---

Metabolic Disease, Obesity/Diabetes & Liver Outcomes

Burden and Regional Disparities of MASH-Related Liver Cancer in the Asia-Pacific Region From 1990 to 2023.

This study quantified the burden and temporal trends of metabolic dysfunction-associated steatohepatitis (MASH)-related liver cancer across Asia-Pacific countries and subregions from 1990–2023 using the Global Burden of Disease (GBD) 2023 dataset. MASH-related liver cancer prevalence, deaths, and disability-adjusted life years (DALYs) showed substantial regional variation and were associated with Socio-demographic Index (SDI) patterns over time. These findings identify where MASH-driven liver cancer is rising fastest, supporting targeted prevention and surveillance strategies in Asia-Pacific health systems.

Zhou XD, Chen QF, Huang DQ et al. · Liver international : official journal of the International Association for the Study of the Liver · (2026) · View on PubMed ↗

Predictive significance of triglyceride-glucose index in forecasting adverse cardiovascular events among Type 2 diabetes mellitus patients with co-existing metabolic dysfunction-associated steatotic liver disease (MASLD): evidence from two cohort studies.

This retrospective cohort study evaluated whether the triglyceride-glucose (TyG) index predicts major adverse cardiovascular events (MACEs) in patients with co-existing type 2 diabetes mellitus (T2DM) and metabolic dysfunction-associated steatotic liver disease (MASLD). Among 1021 patients from Wenzhou Hospital (2019–2022), TyG was assessed for its association with incident MACEs, aiming to clarify prognostic value in this combined metabolic population. If validated, TyG could provide a simple, widely available risk stratification tool for cardiovascular outcomes in T2DM patients with MASLD.

Xu J, Zhao J, Dai Z et al. · Cardiovascular diabetology · (2026) · View on PubMed ↗

Adiponectin exerts sex-dependent effects on lipid, amino acid, and glucose metabolism during caloric restriction.

This study assessed sex-dependent metabolic effects of adiponectin during caloric restriction by using global adiponectin knockout (KO) male and female mice fed ad libitum or 30% caloric restriction from 9–13 weeks of age. Adiponectin KO did not change caloric restriction effects on body mass, body composition, or energy expenditure, but it decreased blood glucose levels during caloric restriction in the excerpted results. The findings indicate adiponectin modulates specific metabolic outputs during caloric restriction in a sex-dependent manner, refining how this hormone contributes to CR-associated cardiometabolic regulation.

Ikushima YM, Chen KC, Sulston RJ et al. · PLoS biology · (2026) · View on PubMed ↗

Glucagon-like peptide-1 receptor agonists and advanced liver outcomes in type 2 diabetes: a systematic review and exploratory meta-analysis.

This systematic review and exploratory meta-analysis evaluated real-world comparative cohort studies in adults with type 2 diabetes (T2D) to determine whether GLP-1 receptor agonists (GLP-1RAs) affect clinically advanced liver outcomes, using active-comparator designs and emphasizing limits of causal inference. The key finding was the pooled/structured evidence on associations between GLP-1RA use and advanced liver endpoints in T2D populations, addressing the gap that randomized trials have not been powered for these outcomes. The significance is that it helps clarify whether GLP-1RAs may provide liver-protective benefits in T2D beyond glycemic control, guiding future comparative-effectiveness research and clinical decision-making.

Hu JH, Chang ML, Huang TJ et al. · Frontiers in endocrinology · (2026) · View on PubMed ↗ · Free PDF ↗

Myostatin Inhibitory D‑Peptides Induce Skeletal Muscle Hypertrophy along with Alteration of Bioactive Sphingolipid Metabolism.

This study investigated whether intramuscular administration of the myostatin inhibitory D-peptide MID-35 induces skeletal muscle hypertrophy and whether it alters bioactive sphingolipid metabolism, with a focus on sphingosine-1-phosphate (S1P) pathways. The key finding was that MID-35 promotes muscle hypertrophy while also changing S1P-related sphingolipid metabolism, linking myostatin inhibition to downstream lipid signaling relevant to muscle mass regulation. These results support MID-35 as a potential therapeutic peptide modality and identify sphingolipid/S1P metabolism as a mechanistic axis for muscle growth.

Morito K, Nishikawa N, Hitachi K et al. · ACS pharmacology & translational science · (2026) · View on PubMed ↗ · Free PDF ↗

GLP-1 Receptor Agonists in Neurological Disorders: From Mechanisms to Clinical Translation.

This review summarized evidence for GLP-1 receptor agonists (GLP-1RAs) across neurological disorders, focusing on mechanistic pathways and translational hurdles. It reports that a leading neuroprotective mechanism involves activation of the cAMP/PKA/CREB signaling cascade to increase BDNF expression (as described in the abstract). The significance is that it frames how GLP-1RAs might be repurposed for CNS diseases while highlighting key barriers that must be addressed before clinical adoption.

Li P, Gao Y, Liu W · Drug design, development and therapy · (2026) · View on PubMed ↗ · Free PDF ↗

---

Endocrine/Thyroid & Iodine Metabolism

From bench to bedside: the evolving role of iodine in thyroid cancer management.

This review summarized how iodine metabolism shapes thyroid cancer biology and how molecular insights have changed management strategies. It emphasizes that iodide uptake enables radioactive iodine therapy in differentiated thyroid carcinomas, while loss of iodide-handling machinery contributes to refractoriness in advanced disease. The synthesis supports integrating iodine-metabolism genetics into routine clinical decision-making to guide therapy selection and improve outcomes.

Condello V, Nilsson JN, Zedenius J et al. · Nature reviews. Endocrinology · (2026) · View on PubMed ↗

---

Therapeutics Trials, Drug Safety & Clinical Effectiveness (Non-oncology)

The Changing Landscape of Maintenance Therapy in Newly Diagnosed Multiple Myeloma: A Systematic Review With Network Meta-Analysis of the European Myeloma Network (EMN).

This systematic review with network meta-analysis compared maintenance therapies in newly diagnosed multiple myeloma across treatment classes using European Myeloma Network (EMN) evidence. It found that lenalidomide, proteasome inhibitors, and CD38 antibodies improved progression-free survival (PFS), with overall survival (OS) benefit most clearly observed for lenalidomide in transplant-eligible patients, while network ranking suggested daratumumab-lenalidomide (DR) had the greatest PFS benefit. Clinically, these comparative effectiveness results support evidence-based selection of maintenance regimens by transplant eligibility and expected PFS/OS impact.

Ludwig H, Terpos E, Gay F et al. · American journal of hematology · (2026) · View on PubMed ↗

CNS target engagement of high-dose DHA supplementation in older adults at risk for dementia: a randomised, double-blind, placebo-controlled trial.

This phase IIa 24-month randomised, double-blind, placebo-controlled trial studied high-dose docosahexaenoic acid (DHA) supplementation in non-demented older adults (55–80 years) at risk for dementia, with stratification by APOE ε4 carrier status and low baseline dietary DHA intake (<200 mg/day). High-dose DHA produced CNS target engagement, shown by changes in cerebrospinal fluid (CSF) omega-3 measures in the trial’s APOE ε4–enriched prevention population. These findings support DHA as an early-intervention candidate for dementia risk reduction in APOE ε4 carriers by demonstrating brain-relevant pharmacodynamic effects.

Yassine HN, Pour SG, Juarez M et al. · EBioMedicine · (2026) · View on PubMed ↗

Stereotactic radiotherapy for neovascular age related macular degeneration: year 3 and 4 extended follow up results of a randomised, double masked, sham controlled, device trial (STAR).

This randomised, double-masked, sham-controlled device trial (STAR) evaluated one-off 16 Gray stereotactic radiotherapy (SRT) versus sham SRT in 411 UK participants aged ≥50 years with chronic, pretreated, active neovascular age-related macular degeneration (AMD). The year 3–4 extended follow-up assessed whether SRT benefits persisted beyond the original 2-year primary outcome, with outcomes compared against sham while participants reverted to routine care after the initial study period. If durable efficacy and safety are confirmed, SRT could become a non-anti-VEGF option to reduce treatment burden in neovascular AMD.

Jackson TL, Desai R, Wafa HA et al. · BMJ (Clinical research ed.) · (2026) · View on PubMed ↗

Association of Respiratory Syncytial Virus Vaccination During Pregnancy With Adverse Obstetric and Neonatal Outcomes.

This target trial emulation study assessed adverse obstetric and neonatal outcomes after bivalent prefusion F subunit-based respiratory syncytial virus vaccination (RSVpreF) during pregnancy among patients enrolled in the Vaccine Safety Datalink (VSD) across eight health systems in the United States. The key finding was the study’s evaluation of risk associated with RSVpreF given between 32 and <37 weeks’ gestation during the first season of availability. The results are important for informing maternal immunization safety guidance for RSVpreF in real-world pregnancy populations.

DeSilva M, Haapala J, Kharbanda EO et al. · Obstetrics and gynecology · (2026) · View on PubMed ↗

Genome-edited rice variety with low-cadmium accumulation in the grain.

This study used base-editing-mediated mutagenesis screening in rice to target OsNramp5, a transporter gene for Mn and Cd uptake, and identified an Ile-to-Thr substitution at position 441. The point mutation reduced cadmium accumulation in both shoots and grains without affecting accumulation of other essential metals, and functional analyses indicated the change did not alter gene expression or protein function in the excerpted portion. This provides a precise, gene-edited strategy to lower dietary Cd exposure while maintaining agronomic performance.

Huang S, Konishi N, Chen W et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗

Evaluation of steroids for acute COVID in the prevention of long COVID in children: An EHR and pediatric cohort study from the RECOVER Initiative.

This retrospective pediatric cohort study from the RECOVER Initiative used target trial emulation to compare children and youth who received acute-phase corticosteroids (dexamethasone, prednisone, prednisolone, or methylprednisolone within 12 days of SARS-CoV-2 infection) versus no steroids for prevention of long COVID. The key finding was that the abstracted results did not show a clear reduction in long COVID risk with early steroid use after balancing with inverse propensity of treatment weighting (details truncated in the provided abstract). If confirmed in full, these findings would inform whether routine steroid treatment during acute COVID should be used to prevent post-acute sequelae in children.

Hirabayashi K, Lorman V, Wuller S et al. · PloS one · (2026) · View on PubMed ↗

A Randomized Controlled Phase 3 Trial of Oral Prednisolone Administration Versus Local Triamcinolone Injection Therapy for Esophageal Stricture Prevention After Extensive Endoscopic Submucosal Dissection (JCOG1217).

In a phase 3 open-label multicenter randomized trial in patients with extensive superficial esophageal squamous cell carcinoma undergoing extensive endoscopic submucosal dissection (ESD), oral prednisolone was compared with standard local triamcinolone injection to prevent esophageal stricture. The primary endpoint was stricture-free survival (SFS), testing whether oral prednisolone is superior to local triamcinolone (full outcome data are truncated in the provided abstract). Clinically, this trial directly targets a less invasive alternative to endoscopic steroid injections to reduce post-ESD stricture burden.

Tanaka M, Ono H, Takizawa K et al. · Digestive endoscopy : official journal of the Japan Gastroenterological Endoscopy Society · (2026) · View on PubMed ↗

Real-world effectiveness of cenobamate in drug-resistant and ultra-refractory epilepsy: A multicenter study.

In a retrospective multicenter real-world study of 500 Czech adults with drug-resistant epilepsy (DRE)—including 83.4% with ultra-refractory epilepsy (URE)—the effectiveness and safety of cenobamate (CNB) were assessed, stratified by treatment duration and cumulative antiseizure medication (ASM) exposure. The key finding was that CNB effectiveness, retention, and adverse events were characterized across heavily pretreated populations (full seizure-outcome and retention results are truncated in the provided abstract). This supports evidence-based expectations for CNB performance in routine care for patients with high seizure burden and extensive prior ASM exposure.

Strýček O, Amlerová J, Pail M et al. · Epilepsia open · (2026) · View on PubMed ↗ · Free PDF ↗

Fosfomycin as Oral Transition Therapy Versus Continued Intravenous β-Lactams for Complicated Urinary Tract Infections Caused by Extended-Spectrum β-Lactamase-Producing Enterobacterales: A Multicenter, Open-Label, Randomized Controlled Trial.

This multicenter, open-label, randomized noninferiority trial in South Korea enrolled adults hospitalized with complicated urinary tract infections due to ESBL-producing Enterobacterales who improved after 3–7 days of intravenous therapy, comparing continued IV carbapenem-based treatment versus oral fosfomycin transition therapy. The key finding was the evaluation of whether oral fosfomycin is noninferior to continued IV β-lactams for clinical outcomes after initial IV improvement (primary outcome details are truncated in the provided abstract). If noninferiority is demonstrated, it would provide an oral carbapenem-sparing step-down option to reduce resistance pressure and healthcare burden.

Seo JW, Kim DY, Yoon Y et al. · Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · (2026) · 1 citations · View on PubMed ↗

Single-Fraction Stereotactic Body Radiotherapy for Localized Prostate Cancer: A Nonrandomized Clinical Trial.

This multicenter single-arm prospective phase 1/2 nonrandomized clinical trial studied single-fraction stereotactic body radiotherapy (SBRT) in men with low- or intermediate-risk localized prostate cancer to determine whether a one-session high-dose approach can achieve biochemical control with acceptable safety. The key finding was the assessment of biochemical disease control and toxicity as a potential alternative to the standard 5-fraction SBRT regimen (outcome results are truncated in the provided abstract). If effective and safe, single-fraction SBRT could simplify treatment logistics and improve patient convenience while maintaining cancer control.

Zilli T, Franzese C, Guckenberger M et al. · JAMA oncology · (2026) · View on PubMed ↗

Letrozole and Infertility Among Males With Spermatogenic Failure: A Randomized Clinical Trial.

In a multicenter open-label assessor-blinded randomized clinical trial in China, men with spermatogenic failure (nonobstructive azoospermia, cryptozoospermia, or severe oligozoospermia) were randomized to receive letrozole versus control to improve sperm concentration categories. The key finding was the trial’s evaluation of letrozole’s efficacy and safety for improving sperm concentration outcomes in this population (primary outcome results are truncated in the provided abstract). This could establish an evidence-based medical option for male infertility due to spermatogenic failure where current treatments are limited.

Sun Y, Yao C, Liu G et al. · JAMA network open · (2026) · View on PubMed ↗ · Free PDF ↗

FGF13 Deficiency Ameliorates Paclitaxel-Induced Neuropathic Pain by Inhibiting VASH1-Mediated Microtubule Detyrosination to Promote Mitophagy.

This Advanced Science study tested whether fibroblast growth factor 13 (FGF13) regulates paclitaxel-induced peripheral neuropathic pain (PIPNP) in mice, using conditional knockout of Fgf13 in dorsal root ganglion (DRG) neurons. FGF13 deficiency alleviated paclitaxel-induced mitochondrial damage and neuropathic pain, and RNA-seq supported a mitophagy-mediated mechanism involving inhibition of vasohibin 1 (VASH1)-mediated microtubule detyrosination. The clinical significance is that targeting the FGF13–VASH1 axis could represent a mechanistically grounded strategy to prevent or treat chemotherapy-induced neuropathy.

Dong Y, Wang Y, Lv S et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗ · Free PDF ↗

Study of Antithrombotic Treatment After Intracerebral Hemorrhage-Antiplatelets: A Randomized Trial.

This randomized, multicenter, open-label/blinded-endpoint trial (STATICH Antiplatelets; EudraCT 2014-002636-13, NCT03186729) studied adults with spontaneous intracerebral hemorrhage (ICH) who had an indication for antiplatelet therapy, comparing starting versus avoiding long-term antiplatelets. The key finding was the trial’s assessment of the safety/efficacy balance of antiplatelet therapy after ICH, focusing on recurrent hemorrhagic and ischemic outcomes over follow-up. Clinically, the results are intended to guide antithrombotic decision-making in ICH survivors by clarifying whether antiplatelets reduce ischemic risk without unacceptable hemorrhagic harm.

Eilertsen H, Larsen KT, Forfang E et al. · Stroke · (2026) · View on PubMed ↗

Modulation of corneal sensory processing and pain responses by dry eye and corneal wounding.

This preclinical study examined how dry eye disease and corneal wounding modulate corneal sensory processing and pain behaviors in female C57BL/6J wild-type mice and Mmp9KO mice, with attention to TRPV1- and TRPM8-mediated stimulus-specific pathways. The key finding was that ocular surface stress models (acute/chronic dry eye and corneal injury) produce distinct changes in sensory responses and pain-related behaviors that map onto TRPV1/TRPM8-associated mechanisms. Scientifically, it clarifies how different corneal insults reprogram sensory pathways, supporting more targeted approaches to treating ocular pain in dry eye and injury contexts.

Yaman E, Qu Y, Arpaia KC et al. · Frontiers in cellular neuroscience · (2026) · View on PubMed ↗ · Free PDF ↗

Current status and trends of immune-related adverse events in lung cancer treated with immune checkpoint inhibitors: a bibliometric analysis of the past decade (2016-2025).

This experimental study investigated how phosphorylation affects bacterial cell division in Streptococcus pneumoniae, focusing on the serine/threonine kinase StkP and the tubulin-like division protein FtsZ. It found that StkP phosphorylates FtsZ in vivo at six threonine residues in the C-terminal linker (CTL), and that CTL phosphorylation status alters pneumococcal cell morphogenesis based on mutational analyses. Scientifically, it identifies a specific post-translational regulatory mechanism controlling FtsZ-driven division, informing potential antibacterial strategies targeting phosphorylation-dependent cell-cycle control.

Guo B, Zhang G, Sang S et al. · Frontiers in immunology · (2026) · View on PubMed ↗ · Free PDF ↗

Ocular disorders during treatment with GLP-1 receptor agonists: a systematic review and meta-analysis of observational studies.

This systematic review and meta-analysis assessed ocular adverse events associated with GLP-1 receptor agonists in observational studies of people with diabetes and/or obesity/overweight. It synthesized evidence from PubMed, Embase, and Web of Science (2006–2025) to evaluate risks of retinopathy, glaucoma, and non-arteritic anterior ischemic optic neuropathy (NAION). The significance is that it aims to clarify whether GLP-1RAs increase ocular risk, informing ophthalmic screening and risk mitigation in routine clinical use.

Anatriello A, Liguori V, Cagnotta C et al. · Frontiers in pharmacology · (2026) · View on PubMed ↗ · Free PDF ↗

Laparoscopic management of Mirizzi syndrome type IV: a case report and review of minimal access surgery.

This case report studied a 44-year-old woman with Mirizzi syndrome type IV to evaluate whether laparoscopic surgery could replace traditional open management. The key finding was that a minimally invasive laparoscopic approach achieved successful treatment with rapid, complication-free recovery and no biliary stricture on 6-month follow-up. Clinically, it supports laparoscopic management as a feasible and effective option in carefully selected Mirizzi type IV patients.

Nguyen NBM, Pham TH, Pham TQ et al. · Journal of minimally invasive surgery · (2026) · View on PubMed ↗ · Free PDF ↗

Consensus on the Clinical Use of Pregabalin in Peripheral Neuropathic Pain.

This article synthesized evidence to develop expert consensus recommendations for using pregabalin in peripheral neuropathic pain (pNP) across diverse clinical conditions. The key finding was that pregabalin, a second-generation calcium channel regulator, has broad efficacy and an acceptable safety profile across multiple pNP etiologies based on a multidisciplinary Chinese expert panel’s literature review and consensus process. Clinically, it provides standardized guidance for pregabalin prescribing in pNP where treatment options vary in effectiveness and tolerability.

Lu H, Rao Y, Wang J et al. · CNS neuroscience & therapeutics · (2026) · View on PubMed ↗ · Free PDF ↗

---

---

Generated automatically on June 20, 2026 from PubMed’s trending articles. Summaries are AI-generated; always consult the original publication for clinical or research decisions.