PubMed Trending Research Digest — July 13, 2026

Automated digest · 99 articles · 15 research areas · July 13, 2026

Overview

This week’s digest is dominated by mechanistic, precision-oriented approaches that connect molecular targets to clinical translation. In oncology, multiple studies emphasize how treatment outcomes depend on biological context—ranging from tumor microenvironment remodeling that drives acquired resistance to sequencing-dependent strategies in stage III EGFR-mutated NSCLC and neoadjuvant regimens in muscle-invasive bladder cancer. Complementing this, several biomarker-focused efforts (HRD assay frameworks, ctDNA interpretation beyond VAF, imaging-based AI stratification for HCC, and immunopeptidomic discovery of transposable element antigens) reflect a broader push toward more reliable, multi-assay ways to predict response and guide therapy.

Outside cancer, a parallel theme is immune and inflammation biology as a therapeutic lever across organ systems. Studies span B-cell/plasma-cell survival pathways (TACI and mitochondrial ROS), neuroinflammation after brain injury (STING-driven microglial pyroptosis; RIPK3 silencing via neuron-targeted exosomes), and cardio-oncology/atherosclerosis links through shared immune mechanisms and inflammatory cell programs. Metabolic and aging-related work also converges on actionable mechanisms and risk stratification: proteomic insulin-resistance signatures, incretin-associated musculoskeletal safety, bile-acid and thyroid–liver axis effects on steatotic liver disease, and biological age acceleration in Hashimoto’s thyroiditis.

Finally, infectious disease and microbiome studies highlight how host–pathogen interactions can be mapped at high resolution and exploited therapeutically. Examples include structure-guided inhibition of the LolDF transporter in carbapenem-resistant Acinetobacter, phage counteraction of bacterial stringent response, vancomycin-stressed MRSA extracellular vesicles hijacking macrophage autophagy, and single-cell/spatial atlases that clarify parasite development or allergic rhinitis cellular circuitry. Together, these findings reinforce a unifying message: combining high-dimensional profiling (single-cell, proteomics, imaging, liquid biopsy) with mechanism-defined targets is increasingly central to both disease understanding and intervention design.

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Precision/Targeted Antimicrobials & Resistance Mechanisms

Conformational hijacking of lipoprotein transporter LolDF enables precision antimicrobial activity against Acinetobacter baumannii.

This study investigated the mechanism of the narrow-spectrum antibiotic abaucin against Acinetobacter baumannii, focusing on inhibition of the essential lipoprotein transporter LolDF in clinically relevant CRAB strains and in a murine pneumonia model. Cryo-EM showed that abaucin binds symmetrically to two sites in the LolDF cavity, locking LolDF in a non-productive outward-open conformation and thereby selectively impairing A. baumannii growth. These findings provide a structure-guided, transporter-targeted strategy for precision antimicrobials against carbapenem-resistant A. baumannii.

Pang J, Chen Y, Zhou D et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

A novel lncRNA HUDRPC suppresses ferroptosis via the DDX5/DDIT3 pathway to promote docetaxel resistance in prostate cancer.

This study investigated a novel long non-coding RNA (lncRNA) named HUDRPC in prostate cancer models of acquired docetaxel resistance. Using comparative transcriptome sequencing of isogenic docetaxel-sensitive versus resistant prostate cancer cell lines and validation in patient-derived tissues, it reports that HUDRPC is upregulated in resistant settings and suppresses ferroptosis through the DDX5/DDIT3 pathway, promoting docetaxel resistance. The clinical significance is that the HUDRPC–DDX5/DDIT3–ferroptosis axis may represent a drug-resistance mechanism and a potential therapeutic target to restore docetaxel sensitivity.

Liang S, Zheng Y, Wu X et al. · Cancer letters · (2026) · View on PubMed ↗

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Psychiatric–Cardiovascular Genetic Pleiotropy & Risk Stratification

Atherosclerotic Cardiovascular Disease and Cancer.

This immunology review examined how shared immune mechanisms link atherosclerotic cardiovascular disease (ASCVD) and cancer across exposures such as smoking, obesity, diabetes, dyslipidemia, aging, and clonal hematopoiesis of indeterminate potential (CHIP). It highlights a chronic inflammatory milieu driven by coordinated reprogramming of myeloid and lymphoid compartments and proposes a forward cardio-oncology axis in which cancer therapies (chemotherapy, radiation, immune checkpoint inhibitors) can induce cardiovascular injury. The synthesis is clinically significant because it frames ASCVD risk and treatment-related cardiotoxicity as immune-mediated processes that may be targeted to improve outcomes in cancer patients.

Amend A, Horstmann H, Lavine KJ et al. · Immunological reviews · (2026) · View on PubMed ↗

Macrophage extracellular traps accelerate atherosclerosis progression via Rap1 pathway-mediated necroptosis and phenotypic switching in vascular smooth muscle cells.

This translational medicine study examined how macrophage extracellular traps (METs) influence vascular smooth muscle cell (VSMC) fate and atherosclerosis progression using an ApoE−/− mouse model and complementary in vitro experiments. The key finding was that exogenous METs accelerated atherosclerosis by triggering Rap1 pathway-mediated necroptosis and driving VSMC phenotypic switching, with associated increases in inflammatory and necrotic markers. Scientifically and clinically, the work implicates the MET–Rap1–necroptosis axis as a mechanistic driver of plaque progression and a potential therapeutic target to improve plaque stability.

Wang S, Tang Y, Yu X et al. · Journal of translational medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Calcium signaling pathway implicates a shared genetic basis between psychiatric and cardiovascular diseases.

This study examined shared genetic architecture between psychiatric disorders (schizophrenia, bipolar disorder, major depressive disorder) and cardiovascular traits in East Asian populations using a genome-wide pairwise trait pleiotropy approach based on GWAS data. The analysis identified genetic overlaps across seven disease pairs (e.g., schizophrenia with coronary artery disease) and reported multiple pleiotropic loci contributing to comorbidity. The results support a common calcium-signaling-related genetic basis for brain-heart disease links and motivate pathway-focused risk stratification.

Zhu Y, Zhao G, Zhang Y et al. · Translational psychiatry · (2026) · View on PubMed ↗ · Free PDF ↗

Implementing a Multi-Ancestry Polygenic Risk Score for Coronary Heart Disease in a Diverse Cohort.

This prospective phase IV eMERGE Network cohort study implemented a multi-ancestry coronary heart disease polygenic risk score (PRS; PGS004696) and assessed outcomes after return of results in a diverse population (NCT05277116). The key finding was that PRSCHD was incorporated into a Genome Informed Risk Assessment (GIRA) report alongside family history and monogenic familial hypercholesterolemia risk, with high-PRS (top 5th percentile) and FH participants receiving results from study personnel. This is significant because it evaluates real-world feasibility and impact of multi-ancestry PRS-based risk stratification for CHD in a clinically actionable setting.

Hamed M, Naderian M, Bangash H et al. · Genetics in medicine : official journal of the American College of Medical Genetics · (2026) · View on PubMed ↗

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Systems Proteomics & Multimodal Biomarker Mapping

Plasma proteomic profiling deciphers molecular dynamics linking insulin resistance to multiple chronic diseases and mortality.

This UK Biobank plasma proteomics study analyzed 19,556 individuals with 2,920 plasma proteins to define insulin resistance (IR)-related proteomic signatures and their links to multiple chronic diseases and mortality. Using an elastic net model to derive IR-associated protein signature scores and Cox proportional hazards models for longitudinal outcomes, it reported that distinct IR indicators map to specific proteomic patterns associated with higher risk of chronic disease and death, with mediation analyses implicating individual proteins in these relationships. The work is scientifically significant because it provides proteome-based biomarkers and mechanistic candidates connecting insulin resistance to broad multimorbidity and mortality risk.

Zhou ZL, Zhou LG, Qu CH et al. · Cardiovascular diabetology · (2026) · View on PubMed ↗

The landscape of plasma proteomic links to human organ imaging.

This study integrated large-scale plasma proteomics with organ imaging in UK Biobank participants to map phenotypic and genetic links across 2923 proteins and 1051 imaging traits. It found thousands of protein–imaging associations (including organ-specific and shared patterns) and highlighted enriched protein–protein interaction networks and biological pathways. These multimodal maps improve mechanistic interpretation of circulating biomarkers for organ-level phenotypes and disease biology.

Fan Z, Chirinos J, Yang X et al. · Nature communications · (2026) · View on PubMed ↗

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Immunology of B Cells, Plasma Cells & Humoral Immunity

Inhibition of mitochondrial ROS by TACI sustains bone marrow plasma cells.

This study used plasma cell–specific conditional knockout mice to test how niche-factor receptors regulate survival of bone marrow long-lived plasma cells (LLPCs), focusing on the cytokine receptor TACI (TNFRSF13B). Loss of TACI reduced polyclonal plasma cell numbers and abrogated LLPCs induced by both T cell–dependent and T cell–independent antigens, severely compromising humoral protection. The work identifies TACI-mediated mitochondrial ROS control as a key survival mechanism for LLPCs, informing strategies to enhance vaccine durability or treat antibody-mediated disease.

Zhu Y, Chen J, Lv H et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

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Cancer Microenvironment & Cellular State Mapping (CAFs/EMT/TME)

Tumor heterogeneity: development, mechanisms, and therapeutic implications.

This review article examined the development and mechanisms of tumor heterogeneity and how it drives progression, metastasis, and therapeutic resistance. It emphasizes that heterogeneity arises from genomic instability, dynamic clonal evolution, and cancer stem cell plasticity, and that residual resistant subclones after conventional therapy can cause relapse, while tumor microenvironment crosstalk further amplifies diversity. The clinical significance is that it outlines how single-cell multi-omics, spatial transcriptomics, and liquid biopsy can enable multidimensional characterization to inform more effective, heterogeneity-aware therapies.

Zhang J, Li H, Ru S et al. · Signal transduction and targeted therapy · (2026) · View on PubMed ↗

INHBA secreted by cancer-associated fibroblasts promotes cisplatin resistance and malignant progression of ovarian cancer via ENG-mediated suppression of apoptosis and induction of EMT.

This study investigated how inhibin subunit beta A (INHBA) secreted by cancer-associated fibroblasts (CAFs) promotes cisplatin resistance and malignant progression in ovarian cancer via endoglin (ENG)-mediated apoptosis suppression and epithelial–mesenchymal transition (EMT). Using single-cell RNA sequencing (scRNA-seq) to define CAF subsets and expression of INHBA/ENG, along with immunohistochemistry and immunofluorescence on ovarian cancer tissue microarrays, the authors report that INHBA–ENG signaling drives pro-resistance and pro-EMT phenotypes. Clinically, targeting the INHBA/ENG axis could help overcome platinum resistance and limit ovarian cancer progression.

Liu X, Han Y, Qin Z et al. · Journal of translational medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Mesenchymal stem cell-induced metabolic reprogramming of EGFR-wild-type tumor cells drives therapeutic resistance in EGFR-mutant non-small cell lung cancer.

This study examined how mesenchymal stem cells (MSCs) induce metabolic reprogramming in EGFR-wild-type (EGFR-wt) tumor cells to drive therapeutic resistance in EGFR-mutant (EGFR-mt) non-small cell lung cancer (NSCLC). Using MSCs isolated from paired tumor and non-tumor lungs of EGFR-mt and EGFR-wt patients, integrated RNA sequencing with targeted free fatty acid and energy metabolomics, and spatial validation by immunohistochemistry/multiplex immunofluorescence, the key finding is that MSC–EGFR-wt tumor cell interactions within EGFR-mt tumors promote metabolic pathways linked to TKI resistance. Scientifically, this identifies a microenvironment-driven metabolic mechanism that could be targeted to prevent or reverse TKI resistance in EGFR-mutant NSCLC.

Bie H, Li J, Liu J et al. · Journal of experimental & clinical cancer research : CR · (2026) · View on PubMed ↗ · Free PDF ↗

TBL1XR1 mutations promoted tumor progression in diffuse large B-cell lymphoma through impairing nature killer cytotoxicity via the MYC-CD47/PD-L1 axis.

This molecular cancer study analyzed TBL1XR1 mutations in 1,842 newly diagnosed diffuse large B-cell lymphoma (DLBCL) patients and investigated how TBL1XR1-driven tumor biology affects the tumor microenvironment. The key finding was that TBL1XR1 mutations (present in 9.4% of cases) promoted aggressive disease by increasing H3K27ac at the MYC promoter, elevating MYC expression, and upregulating the immune-regulatory axis MYC–CD47/PD-L1, alongside impaired natural killer (NK) cytotoxicity. Clinically, identifying TBL1XR1-mutant DLBCL as a MYC–CD47/PD-L1–linked immune-evasion subtype may inform prognosis and rational combination strategies with immune checkpoint approaches.

Zhu Y, Shen YG, Tang W et al. · Molecular cancer · (2026) · View on PubMed ↗ · Free PDF ↗

Integrative single-cell and spatial transcriptomic analysis reveals a lactate-driven crosstalk between NFATc4⁺ tumor cells and SPP1⁺ macrophages in glioblastoma.

This Journal of Translational Medicine study integrated single-cell RNA sequencing (scRNA-seq), spatial transcriptomics, and machine learning to define lactate-driven interactions in glioblastoma (GBM), using scRNA-seq data from GSE138794. The key finding was that GBM neoplastic cells segregated into high- and low-lactate subgroups, with NFATc4 identified as a key transcription factor linked to elevated lactate metabolism and associated with crosstalk to SPP1+ macrophages. The scientific significance is that it connects lactate metabolism to NFATc4-dependent tumor–immune communication, suggesting metabolic-immune targeting strategies for GBM.

Wang R, Wu W, Wu X et al. · Journal of translational medicine · (2026) · View on PubMed ↗ · Free PDF ↗

CDK8 remodels the tumor microenvironment and promotes resistance to KRASG12D inhibitors and daraxonrasib in PDAC.

This EMBO Journal study used integrated spatial transcriptomics, single-cell RNA sequencing, and CODEX-based spatial proteomics in KRASG12D PDAC mouse models to determine how the tumor microenvironment affects resistance to KRASG12D inhibition. The key finding was that although KRASG12D inhibition with MRTX1133 initially increased CD11c+ cells and T-cell infiltration near cancer cells, long-term treatment remodeled the tumor microenvironment in ways that promoted resistance to KRASG12D inhibitors and to daraxonrasib. Clinically, it highlights specific TME remodeling as a mechanism of acquired resistance, supporting combination strategies that target microenvironmental pathways alongside KRASG12D inhibition.

McAndrews KM, Mahadevan KK, Li B et al. · The EMBO journal · (2026) · View on PubMed ↗ · Free PDF ↗

AURKA regulates LGR5 in response to Helicobacter Pylori infection by modulating its deubiquitination.

This study examined how Aurora kinase A (AURKA) regulates the gastric stem-cell marker LGR5 during Helicobacter pylori infection using analyses of public datasets, gastric cancer cell lines, patient-derived organoids and xenografts (PDOs/PDXs), mouse models, and human tissue samples. AURKA expression strongly associated with LGR5 levels, and AURKA promoted LGR5 upregulation in response to H. pylori by modulating LGR5 deubiquitination. These findings link AURKA to H. pylori–driven gastric tumorigenesis and suggest AURKA–LGR5 axis components as potential therapeutic targets in gastric cancer.

Gomaa A, Maacha S, Soutto M et al. · Cell death and differentiation · (2026) · View on PubMed ↗ · Free PDF ↗

Human ZBP1 is a potent inducer of cell death through mechanisms divergent from mouse ZBP1.

This study compared human ZBP1 (hZBP1) and mouse ZBP1 (mZBP1) in cells and in vivo models to define how ZBP1 triggers cell death upon sensing Z-form nucleic acids via RHIM-mediated signaling to RIPK1/RIPK3. hZBP1 induced cell death with heightened sensitivity across species and showed potent tumor-killing in vivo, but unlike mZBP1 it depended on RIPK1 in a RIPK3-independent manner, requiring RIPK1 scaffold function for apoptosis and RIPK1 kinase activity for necroptosis. The results highlight species-specific ZBP1–RIPK1/RIPK3 wiring and support hZBP1 as a potentially powerful, mechanism-defined cancer cell-death inducer.

Lu F, Tang L, Tian Z et al. · EMBO reports · (2026) · View on PubMed ↗ · Free PDF ↗

Single cell multiomics unravel the transcription networks controlling the different EMT tumor states.

This study used single-cell multiomics combining single-cell RNA-seq and single-cell ATAC-seq in a mouse skin model to map transcriptional and chromatin landscapes across EMT tumor states. It delineated distinct EMT states as a spectrum rather than a binary switch and aimed to define the transcriptional regulatory programs controlling transitions between EMT states. By linking EMT state-specific gene regulation to chromatin accessibility, the work provides a framework for identifying transcription factors and regulatory mechanisms driving metastasis and therapy resistance.

Pérez-González A, Windels G, Bévant K et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Single-cell multi-omics deciphers the myofibro-inflammatory program of cancer-associated fibroblasts in triple-negative breast cancer.

This study applied single-cell RNA sequencing and single-cell ATAC sequencing to decode the myofibro-inflammatory program and heterogeneity of cancer-associated fibroblasts (CAFs) in triple-negative breast cancer (TNBC) and compared them with HR+/HER2− breast cancers. It identified a distinct CAF subpopulation (my_iCAF) and validated a signaling axis that regulates both TNBC progression and CAF subtype switching. The findings provide a single-cell regulatory framework for targeting CAF states to modulate TNBC tumor microenvironment and progression.

Li M, Lin J, Yang C et al. · Cell death discovery · (2026) · View on PubMed ↗ · Free PDF ↗

Psychological Stress Associated Bile Acid Reprogramming Promotes Hepatocellular Carcinoma Progression.

This study examined whether psychological stress (especially depression) is associated with hepatocellular carcinoma (HCC) risk and whether stress-linked bile acid changes drive tumor progression in humans and models. Across three prospective cohorts (CHARLS, NHANES, UK Biobank; n=492,501), depression was associated with higher HCC risk (CHARLS HR 2.28; NHANES OR 5.95; UK Biobank HR 1.39), and multi-omics plus social isolation models identified taurocholate as a key metabolite elevated in stress-associated HCC. These findings suggest a non-genetic stress–bile acid axis (taurocholate) that could be targeted to slow HCC progression in patients experiencing depression.

Zeng R, Wang M, Wang K et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗ · Free PDF ↗

The use of antibiotic, probiotic, and FMT in modulating Immunotherapy Efficacy and Survival: a systematic review and meta-analysis of clinical outcomes.

This systematic review and meta-analysis evaluated whether microbiota-modulating interventions—antibiotics, probiotics, and fecal microbiota transplantation (FMT)—improve immunotherapy efficacy and survival in cancer patients receiving immune checkpoint inhibitors (ICIs). The key finding was that the authors synthesized clinical outcome evidence across these microbiota interventions to assess their impact on ICI response and survival. This is significant because it informs whether manipulating gut microbiota can be used as an adjunct strategy to overcome limited ICI efficacy in advanced malignancies.

Zhai Z, Ma S, Shang S et al. · The oncologist · (2026) · View on PubMed ↗ · Free PDF ↗

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Cancer Treatment Strategies & Trial Evidence (Neoadjuvant/Consolidation/Sequencing)

YEARS Algorithm for Diagnosis of Suspected Pulmonary Embolism in Patients With Cancer: A Randomized Clinical Trial.

This randomized clinical trial (Hydra study) evaluated the YEARS algorithm versus computed tomographic pulmonary angiography (CTPA) only to rule out acute pulmonary embolism (PE) in patients with active cancer. The key finding was that the YEARS strategy was noninferior in safety and efficiency compared with CTPA-only approaches, with blinded central adjudication of outcomes. The clinical significance is that it supports a cancer-specific diagnostic pathway that can reduce unnecessary imaging while maintaining safe PE exclusion.

Akerboom B, Martens ESL, Stals MAM et al. · JAMA · (2026) · 1 citations · View on PubMed ↗

Randomized, multicenter phase 3 study evaluating radiotherapy versus concurrent chemoradiotherapy in nasopharyngeal carcinoma patients achieving CR/PR after induction chemotherapy.

This multicenter randomized phase 3 noninferiority trial studied newly diagnosed stage III–IVb nasopharyngeal carcinoma (NPC) patients in China who achieved complete or partial response (CR/PR) after induction chemotherapy, comparing induction chemotherapy plus radiotherapy (IC+RT) versus induction chemotherapy plus concurrent chemoradiotherapy (IC+CCRT). The key finding was that adding concurrent chemotherapy to radiotherapy did not improve progression-free survival compared with radiotherapy alone in this CR/PR post-induction population (with safety assessed as part of the comparison). Clinically, the results support RT-only consolidation after induction response as a potentially less toxic standard option for stage III–IVb NPC patients who respond to induction chemotherapy.

Jin T, Jiang F, Jin QF et al. · BMC medicine · (2026) · View on PubMed ↗ · Free PDF ↗

AI in predicting the macrotrabecular-massive subtype of HCC and informing treatment selection: a multi-center and prospective validation study.

This multi-center prospective validation study developed and tested a CT-based artificial intelligence model (DeepCT-MTM) to predict the macrotrabecular-massive (MTM) subtype of hepatocellular carcinoma (HCC) and inform treatment selection. DeepCT-MTM was trained/validated in 832 early-stage resection patients and extrapolated to 2,286 intermediate/advanced-stage patients receiving IATs, including 480 prospectively collected cases, and demonstrated predictive performance for MTM-HCC (with downstream prognostic and biological utility). The approach supports noninvasive, imaging-based MTM stratification to guide clinical decision-making in aggressive HCC.

Wei R, Jiang H, Zuo M et al. · NPJ precision oncology · (2026) · View on PubMed ↗ · Free PDF ↗

Enfortumab vedotin monotherapy, enfortumab vedotin plus pembrolizumab, and immune checkpoint inhibitor-based neoadjuvant therapy for muscle-invasive bladder cancer: A systematic review and meta-analysis.

This systematic review and meta-analysis compared neoadjuvant enfortumab vedotin (EV) monotherapy, EV plus pembrolizumab (EV+P), and immune checkpoint inhibitor–based regimens for muscle-invasive bladder cancer using prospective Phase II+ trials. The primary endpoint was pathological complete response (ypT0N0), synthesized across 15 eligible trials using random-effects meta-analysis. The comparative efficacy results inform selection of neoadjuvant strategies to maximize pCR and potentially improve survival outcomes in MIBC.

Yajima S, Yoshida S, Imasato N et al. · Urologic oncology · (2026) · View on PubMed ↗

International consensus on mesopancreas and total mesopancreas excision (MESODELPHI).

This consensus study used a modified Delphi process with 43 pancreatic surgery experts from 20 countries to standardize the anatomical definition, surgical boundaries, and clinical role of the mesopancreas for total mesopancreas excision (TMpE). It achieved consensus on 19 of 27 statements in Round 1 and aimed to enable consistent reporting and comparison across pancreatic cancer surgery studies. The resulting MESODELPHI framework supports harmonized surgical practice and more interpretable evidence for TMpE in pancreatic cancer management.

Leite LF, Belotto M, Sá de Araújo M et al. · HPB : the official journal of the International Hepato Pancreato Biliary Association · (2026) · View on PubMed ↗

Single, early intravesical instillation of pirarubicin in the prevention of bladder recurrence after radical nephroureterectomy for upper tract urothelial carcinoma (JCOG1403): a multicentre, open-label, randomised, phase 3 trial.

This multicentre, open-label, randomized phase 3 trial (JCOG1403) studied whether a single early intravesical instillation of pirarubicin after radical nephroureterectomy reduces bladder recurrence in patients with upper tract urothelial carcinoma. It compares pirarubicin instillation versus no intravesical instillation in eligible adults aged 20–80 years with clinical stage 0a–III disease. The significance is that if effective, this simple perioperative intravesical chemotherapy strategy could improve recurrence prevention while informing standard-of-care practice.

Ito A, Arai Y, Kakehi Y et al. · The Lancet. Oncology · (2026) · View on PubMed ↗

Neuroprotection and prevention of oxaliplatin-induced neuropathy with Huangqi Guizhi Wuwu Decoction: a 12-center randomized, double-blind trial with mechanistic validation.

This multicenter, randomized, double-blind, placebo-controlled trial studied whether Huangqi Guizhi Wuwu Decoction (HQGZWWD) prevents oxaliplatin-induced peripheral neuropathy (OIPN) and explored underlying mechanisms. Across 12 tertiary hospitals in China, adults with colorectal cancer receiving oxaliplatin-based chemotherapy were randomized to HQGZWWD versus placebo, and the study evaluated efficacy/safety alongside mechanistic validation (details truncated). If effective, HQGZWWD would provide a clinically supported prophylactic option for OIPN and a mechanistic rationale for its neuroprotective use in chemotherapy patients.

Sun X, Fang Y, Yang X et al. · Phytomedicine : international journal of phytotherapy and phytopharmacology · (2026) · View on PubMed ↗

Optimal treatment strategies for unresectable stage III EGFR-mutated non-small cell lung cancer: a systematic review and Bayesian network meta-analysis.

This systematic review and Bayesian network meta-analysis synthesized randomized controlled trials to determine optimal treatment strategies for unresectable stage III EGFR-mutated non-small cell lung cancer (NSCLC), comparing PACIFIC-style durvalumab consolidation with sequential targeted-therapy approaches after chemoradiotherapy. The key finding was that the best regimen depended on the specific sequence and toxicity profile, with evidence supporting concurrent chemoradiotherapy followed by sequential EGFR tyrosine kinase inhibitor (TKI) therapy as a recommended approach in EGFR-mutated disease. Scientifically and clinically, the analysis helps refine regimen selection beyond PACIFIC for EGFR-mutated stage III NSCLC where optimal sequencing remains uncertain.

Yang Y, Sun J, Luo T et al. · Frontiers in oncology · (2026) · View on PubMed ↗ · Free PDF ↗

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Cancer Biomarkers, Genomics & Liquid Biopsy (including HRD/ctDNA/Immunopeptidomics)

ESR1 and PIK3CA circulating tumor DNA (ctDNA) mutation status as predictive biomarkers beyond variant allele fraction (VAF) in metastatic breast cancer.

This study evaluated whether circulating tumor DNA (ctDNA) mutation status for ESR1 and PIK3CA can predict outcomes in hormone receptor–positive/HER2-negative metastatic breast cancer beyond variant allele fraction (VAF), using plasma ctDNA testing. The authors conclude that VAF is affected by multiple biological and technical factors (e.g., tumor fraction, metastatic shedding, clonal architecture, copy-number state, assay sensitivity, and sampling timing), so mutation status may provide additional predictive value when interpreted beyond VAF alone. Clinically, this supports more robust ctDNA biomarker interpretation for guiding management of metastatic breast cancer patients with actionable ESR1/PIK3CA alterations.

Fusco N, Malapelle U · The journal of liquid biopsy · (2026) · View on PubMed ↗ · Free PDF ↗

TIPs: a deep learning-guided proteogenomic framework to expand the landscape of transposable element-derived antigens with immunopeptidomics.

This study developed TIPs (TE-derived Immunopeptidomic Search), a deep learning–guided proteogenomic framework to expand the repertoire of transposable element (TE)-derived antigens using immunopeptidomics. Across multiple cell lines and cancer types, TIPs identified on average 20-fold more TE-derived peptides than conventional approaches and revealed recurrent tumor-specific TE antigens, including candidates potentially induced by epigenetic therapy. The scientific significance is that TIPs improves discovery of HLA-presented TE antigens, supporting development of TE-targeted cancer immunotherapies and better interpretation of immunopeptidomic datasets.

Wu Q, Zhou X, Feng Q et al. · Genome biology · (2026) · View on PubMed ↗ · Free PDF ↗

Advancing genomics and integration of multi-omics for precision oncology using quantum machine learning.

This Perspective evaluated how quantum machine learning algorithms (e.g., quantum support vector machines, quantum principal component analysis, and quantum generative models) could improve multi-omics integration for precision oncology, including spatial transcriptomics and neoantigen prediction. It argues that quantum approaches may more efficiently search complex, heterogeneous multi-omics solution spaces and thereby enhance variant interpretation, tumor classification, and modeling of cancer evolution. If technical barriers such as qubit noise and limited scale are overcome, quantum genomics could accelerate clinically actionable multi-omics biomarker discovery.

Sung JY, Cheong JH · NPJ digital medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Comprehensive clinical cancer analysis of homologous recombination deficiency biomarkers in an academic molecular profiling program.

This academic molecular profiling study assessed strategies to detect and longitudinally monitor homologous recombination deficiency (HRD) biomarkers across >500 tumor samples and >20 paired liquid biopsies, integrating genetic, genomic, and functional readouts to guide PARP inhibitor (PARPi) relevance. HRD frequency differed by cancer type (highest in high-grade ovarian cancer at 52% versus 12% in metastatic breast and 20% in metastatic prostate), and assay concordance was low-to-moderate, indicating complementary HRD detection. Clinically, the work supports using multiple HRD assays—including RAD51 testing and a genomic instability score—to better capture intrinsic PARPi sensitivity and resistance that may be missed by mutation-only testing.

Domènech H, Simonetti S, Romero-Lozano P et al. · NPJ precision oncology · (2026) · View on PubMed ↗ · Free PDF ↗

Cancer history and second cancer risk in polycythemia vera and essential thrombocythemia.

This retrospective cohort study analyzed 1968 patients with polycythemia vera (PV) or essential thrombocythemia (ET) to identify predictors of second cancer risk using competing-risk cumulative incidence and Fine-Gray regression. Second cancers occurred in 404 patients (20%), with non-melanoma skin cancer the most frequent subtype, and prior cancer emerged as a significant predictor (sHR ~2.02). Clinically, the results help stratify PV/ET patients by second-cancer risk to guide surveillance intensity and follow-up planning.

Loscocco GG, Aperna F, Iftikhar M et al. · Blood cancer journal · (2026) · View on PubMed ↗ · Free PDF ↗

TROP-2 in Solid Tumors: From Oncogenic Driver to Therapeutic Target with Antibody-Drug Conjugates.

This critical review focuses on TROP-2 (trophoblast cell surface antigen 2) as an oncogenic driver and therapeutic target for antibody-drug conjugates (ADCs) across solid tumors. It identifies TROP-2’s mechanistic links to calcium signaling, MAPK, and PI3K/AKT pathways as the biological rationale for ADC development. The significance is that TROP-2-directed ADCs are positioned as a broadly applicable targeted therapy strategy given frequent TROP-2 overexpression in epithelial malignancies.

Liu J, Zhang M, Liu J et al. · Critical reviews in oncology/hematology · (2026) · View on PubMed ↗

Shiyiwei Shenqi Pian-derived quercetin reactivates apoptosis in clear cell renal cell carcinoma by destabilizing survivin and x-linked inhibitor of apoptosis protein.

This study examined how quercetin, derived from the herbal mixture Shiyiwei Shenqi Pian (SSP), induces apoptosis in clear cell renal cell carcinoma (ccRCC) by disrupting the oncogenic survivin–XIAP anti-apoptotic axis. Using integrative network pharmacology, transcriptomic profiling, machine learning, and structural dynamics simulations, the authors proposed and characterized quercetin’s mechanism as destabilization of the BIRC5 (survivin)–XIAP complex, thereby reactivating apoptosis in ccRCC. The findings are significant because they identify a specific SSP-derived compound and a defined molecular target (BIRC5–XIAP destabilization) that could support mechanism-based ccRCC therapeutics.

Zhang D, Li S, Zhang X et al. · Phytomedicine : international journal of phytotherapy and phytopharmacology · (2026) · View on PubMed ↗

Prediction and mechanistic insights into drug-induced reproductive toxicity through integrated machine learning, FAERS-based signal comparison, and network toxicology analyses.

This study developed and evaluated a machine-learning framework for predicting drug-induced reproductive toxicity by integrating FAERS signal comparison with network toxicology, molecular docking, and molecular dynamics simulations. LightGBM performed best among tested algorithms (F1-score 0.854) and the integrated analyses provided mechanistic hypotheses for post-marketing reproductive toxicity risk across evaluated drugs. The approach is significant for improving pharmacovigilance-driven, mechanism-informed reproductive safety screening without relying solely on costly long experimental pipelines.

Yan J, Zhou Y, Zhao Y et al. · Molecular diversity · (2026) · View on PubMed ↗

High Throughput Evidence Generation to Support Tentative Gene Disease Relationship from A Cohort Enriched for Autozygosity and Founder Effect.

This study investigated whether a high-throughput human genetics approach using a cohort enriched for autozygosity and founder effects can accelerate gene–disease relationship (GDR) evidence generation. By analyzing Lifera Omics Database (LODB) data, the authors aimed to identify homozygous loss-of-function variants and obtain strong segregation evidence at scale. The scientific significance is that it could substantially speed up validation of candidate GDRs for monogenic diagnostics compared with single-variant, single-publication approaches.

Bakur K, Alhaddad B, Balubaid A et al. · Genetics in medicine : official journal of the American College of Medical Genetics · (2026) · View on PubMed ↗

LSD1-based dual-target inhibitors as emerging anticancer agents: pharmacological perspectives and SAR exploration.

This review examined LSD1 (lysine-specific demethylase 1)-based dual-target inhibitors as emerging anticancer agents, focusing on structure–activity relationship (SAR) and pharmacological strategies. It found that dual inhibition partners (e.g., HDAC, EGFR, EZH2, tubulin, ERα, G9a/JmjC-related targets, DCN1, and SMOX) are being pursued to address limitations of LSD1 inhibitor monotherapy such as low selectivity, toxicity, and drug resistance. This is clinically significant because it frames how rational combination targeting of epigenetic and oncogenic pathways may improve efficacy and overcome resistance in cancers including acute myeloid leukemia.

Ghosh P, Dhir R, Sharma D et al. · Future medicinal chemistry · (2026) · View on PubMed ↗

Does lung adenocarcinoma subtyping offer clinical benefits?-a retrospective population-based cohort study from Sweden.

This retrospective, population-based cohort study used Swedish Cancer Registry data (2005–2021) to evaluate whether lung adenocarcinoma subtyping improves survival outcomes in an unselected European patient population. The key finding was that the clinical benefit of adenocarcinoma subtyping for survival was limited/inconsistent in this large real-world cohort. These results suggest that routine lung adenocarcinoma subtyping may not reliably translate into improved outcomes without additional actionable biomarkers or treatment stratification.

Zitricky F, Sundquist K, Sundquist J et al. · Annals of translational medicine · (2026) · View on PubMed ↗ · Free PDF ↗

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Hematologic Malignancies (CAR-T/FLT3/BCMA/CHIP/Leukemia)

Metabolic and functional analysis including repetitive antigen stimulation provides a more accurate assessment for CAR-T cell product quality and long-term functionality.

This Journal of Translational Medicine study developed and compared analytical workflows to better assess quality and long-term functionality of BCMA-directed CAR-T cell products, comparing two academic versions of CARTemis-1 that differ only in costimulatory domains (4-1BB vs CD28). The key finding was that incorporating metabolic and functional readouts plus repetitive antigen stimulation provided a more accurate characterization of CAR-T product quality and predicted long-term functionality than immunophenotyping alone. Scientifically, it offers a more robust framework for standardizing CAR-T release/monitoring assays and improving the ability to forecast clinical durability.

Guijarro-Albaladejo B, Sierro-Martínez B, Carrasco-Brocal I et al. · Journal of translational medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Dual-targeting LILRB3/LILRB4 CAR-T cells for the treatment of monocytic acute myeloid leukemia.

This preclinical study evaluated dual-targeting LILRB3/LILRB4 CAR-T cells for monocytic acute myeloid leukemia (AML). It found frequent co-expression of LILRB3 and LILRB4 in monocytic AML patient samples, leukemic stem cell-enriched populations, and AML cell lines, and engineered CAR-T cells using a dual-recognizing scFv derived from a humanized antibody. The significance is that targeting both inhibitory receptors may enhance CAR-T efficacy against monocytic AML compared with single-target approaches.

Chen X, Guo C, Tu Y et al. · Biochemical pharmacology · (2026) · View on PubMed ↗

iPSC-derived NK cell therapy induces durable responses in glioblastoma and overcomes resistance via a B7-H3-targeted tri-specific killer engager.

This preclinical study evaluated iPSC-derived NK cell therapy (FT538) in glioblastoma models and tested whether it overcomes resistance via a B7-H3-targeted tri-specific killer engager. Using in vitro assays against 13 patient-derived glioblastoma stem-like cells and orthotopic xenograft models, the authors found durable responses with improved efficacy, along with assessments of intracranial persistence and neurotoxicity in mice. The significance is that B7-H3-targeted tri-specific engager–equipped FT538 may represent a promising strategy to treat resistant glioblastoma with sustained in vivo activity.

Ning JF, Davis ZB, Zeb Q et al. · Neuro-oncology · (2026) · View on PubMed ↗

Potential of new BCMA-targeting therapies in overcoming resistance in multiple myeloma.

This review evaluated BCMA-targeted therapies in multiple myeloma, focusing on mechanisms of resistance across modalities including BCMA CAR-T cells, BCMA bispecific T-cell engagers, and BCMA antibody–drug conjugates. It found that resistance is multifactorial and includes antigen escape driven by TNFRSF17 (BCMA) biallelic loss, non-truncating extracellular-domain mutations, and γ-secretase–mediated BCMA shedding. These insights are clinically significant because they suggest modality-specific strategies to overcome BCMA antigen loss and improve durability of response in relapsed/refractory disease.

Sra MS, Kumar S · Expert opinion on biological therapy · (2026) · View on PubMed ↗

QuANTUM-Wild: a Phase III, randomized trial of quizartinib in newly diagnosed FLT3-ITD-negative acute myeloid leukemia.

This Phase III, double-blind, randomized, placebo-controlled trial (QuANTUM-Wild) studied quizartinib, a type II FLT3 inhibitor, in adult patients with newly diagnosed FLT3-ITD–negative acute myeloid leukemia (AML). The study design aims to confirm efficacy and safety of quizartinib plus standard induction/consolidation chemotherapy and as maintenance monotherapy, with patients randomized to three arms (including ~280 in Arm A). If successful, the trial could expand quizartinib’s clinical use beyond FLT3-ITD–positive settings by targeting FLT3-driven biology in FLT3-ITD–negative AML.

Montesinos P, Altman JK, Bullinger L et al. · Future oncology (London, England) · (2026) · View on PubMed ↗ · Free PDF ↗

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Neuroinflammation, Neurodegeneration & CNS Delivery (exosomes/nanoparticles/biomarkers)

Cardiomyocyte-enriched OTUD5 alleviates septic cardiomyopathy by promoting NLRP3 deubiquitination and inhibiting NLRP3 inflammasome activation.

This experimental study investigated whether cardiomyocyte-enriched OTUD5 protects against septic cardiomyopathy in primary neonatal rat cardiomyocytes and related in vitro/in vivo models of sepsis using lipopolysaccharide (LPS) and nigericin to induce pyroptosis. The authors found that OTUD5 promotes NLRP3 deubiquitination and inhibits NLRP3 inflammasome activation, with pyroptosis readouts including IL-1β ELISA, Western blot, PI staining, CCK-8, and LDH, and they used co-immunoprecipitation to identify OTUD5 substrates. These findings are significant because they implicate OTUD5–NLRP3 signaling as a mechanistic target to reduce inflammasome-driven cardiomyocyte injury during sepsis.

Jiang Y, Jia Z, Zheng Z et al. · Clinical and translational medicine · (2026) · View on PubMed ↗

Clinicopathologic Evaluation of Amyloid Clearance in Alzheimer Disease.

This JAMA clinicopathologic case report studied a male Alzheimer disease patient who was a carrier of the p.R47H TREM2 variant and received aducanumab, focusing on how amyloid clearance relates to downstream tau pathology and neurodegeneration. In the context of patchy areas with minimal residual amyloid after treatment, the report assessed postmortem and in vivo amyloid levels alongside neuropathologic outcomes. The significance lies in providing rare human evidence that informs whether amyloid-targeting therapies translate into slowed downstream neurodegenerative pathology.

Brown CA, Robinson JL, Das SR et al. · JAMA · (2026) · View on PubMed ↗

Regulation of AQP4 Expression and Investigation of the Underlying Mechanisms by HIV-1 Tat Through the NMDAR/cAMP/PKA Signaling Pathway in Astrocytes.

This mechanistic cell-based study examined how HIV-1 Tat regulates aquaporin-4 (AQP4) expression in astrocytes via the NMDAR/cAMP/PKA signaling pathway. It reported that Tat modulates AQP4 through NMDAR-dependent signaling (including Ca2+ dynamics and downstream components such as CaMKII/AC/cAMP/PKA), linking viral protein neurotoxicity to astrocytic water-channel regulation. The significance is that it clarifies a pathway potentially contributing to HIV-associated neurocognitive disorder (HAND) and identifies signaling nodes that could be targeted to mitigate neurotoxicity.

Li C, Duan R, Fu C · Iranian journal of allergy, asthma, and immunology · (2026) · View on PubMed ↗ · Free PDF ↗

Postoperative gabapentinoid use is associated with improved survival in glioblastoma: A nationwide population-based study.

This nationwide population-based retrospective study analyzed postoperative gabapentinoid use and overall survival in adult patients with pathology-confirmed glioblastoma (GBM) undergoing surgery in Turkey from 2016 to 2024. Using stabilized inverse probability of treatment weighting (sIPTW) to adjust for confounders, the study found that postoperative gabapentinoid use was associated with improved overall survival. If validated prospectively, this suggests gabapentinoids may influence GBM progression or treatment response and could represent a modifiable adjunctive factor after surgery.

Hanalioglu S, Cekic E, Gok E et al. · Neuro-oncology advances · (2026) · View on PubMed ↗ · Free PDF ↗

Analytical and clinical validation of a novel proximity extension assay-based plasma biomarker panel in a cohort of prevalent neurodegenerative dementias.

This study analytically and clinically validated the Olink Target 48 Neurodegeneration proximity extension assay (PEA) plasma biomarker panel in a retrospective cohort of 238 patients with prevalent neurodegenerative dementias, including Alzheimer’s disease (AD), dementia with Lewy bodies, frontotemporal dementia, progressive supranuclear palsy, and corticobasal degeneration. The key finding was that the panel demonstrated acceptable analytical performance and showed clinical utility by distinguishing dementia subtypes and/or reflecting disease-related proteomic differences across the clinically diverse cohort. Scientifically, it provides a validated, minimally invasive blood-based multiplex proteomics tool that could support diagnosis and monitoring in neurodegenerative dementia trials and practice.

Bentivenga GM, Mammana A, Baiardi S et al. · Alzheimer’s research & therapy · (2026) · View on PubMed ↗ · Free PDF ↗

Plasma exosomal HERV-K transcripts are increased in amyotrophic lateral sclerosis.

This BMC Neuroscience study investigated whether human endogenous retrovirus-K (HERV-K) transcripts are increased in amyotrophic lateral sclerosis (ALS) and whether exosomes carry this signal in peripheral blood. The key finding was that plasma-derived exosomes from ALS patients (n=21) showed increased exosomal HERV-K gag, env, and pol transcripts compared with healthy controls (n=16). Clinically and scientifically, it supports exosomal HERV-K transcripts as minimally invasive biomarker candidates and strengthens the rationale for antiretroviral strategies targeting HERV-K reactivation in ALS.

Roy T, Ramesh M, Nizam NAA et al. · BMC neuroscience · (2026) · View on PubMed ↗ · Free PDF ↗

Single-nucleus transcriptomics-based drug screening platform for focal cortical dysplasia.

This study used single-nucleus RNA sequencing on 49 human neocortical specimens spanning focal cortical dysplasia (FCD) types I–III to build a drug-screening platform based on cell-type–specific transcriptional programs. It identified prominent alterations in non-neuronal populations, especially astrocytes and vascular cells, with endothelial/smooth muscle dysfunction signatures, while neuronal populations showed additional subtype-specific heterogeneity. The consistent vascular-associated signatures across FCD subtypes suggest convergent therapeutic targets and provide a transcriptomic framework for prioritizing candidate antiseizure interventions.

Fang C, Meng G, Yang L et al. · Molecular psychiatry · (2026) · View on PubMed ↗

Targeting DNA mismatch repair in Huntington’s disease.

This review synthesizes evidence on how DNA mismatch repair (MMR) enzymes influence somatic expansion of the HTT CAG repeat in Huntington’s disease across post-mortem human brain tissue, cell systems, and mouse models. It highlights that MMR-driven erroneous repair promotes HTT CAG repeat expansion in a cell-type- and threshold-dependent manner, aligning with selective vulnerability of medium spiny neurons and distinct stages of cellular pathogenesis. Targeting MMR-linked mechanisms may therefore offer a gene-informed strategy to slow or prevent HTT repeat expansion and disease progression in HD.

Bunting EL, Panhale A, McColgan P et al. · Trends in neurosciences · (2026) · View on PubMed ↗

Targeting the APOE4-driven peripheral-central immune axis: a new frontier for Alzheimer’s disease therapy.

This review examines the APOE4 allele’s role in the peripheral-central immune axis and how it may drive neuroimmune dysfunction in Alzheimer’s disease. It concludes that APOE4 links CNS lipid metabolism with peripheral immune homeostasis, creating a therapeutic opportunity beyond amyloid- or tau-only approaches. Clinically, modulating APOE4-associated immune crosstalk could improve disease-modifying strategies for sporadic AD, where APOE4 is the strongest genetic risk factor.

Shang Y, Zhai Z, Cong L et al. · Pharmacological research · (2026) · View on PubMed ↗

Neuron-Targeted Exosomal Delivery of siRNA Against RIPK3 Slows Neurodegenerative Progression in Alzheimer’s Disease.

This study developed and tested a neuron-targeted exosomal delivery system for siRNA against RIPK3 to slow neurodegenerative progression in an Alzheimer’s disease context. Using engineered exosomes derived from an immortalized mouse hippocampal neuronal cell line and surface functionalization with a rabies virus glycoprotein-derived peptide to enable receptor-mediated BBB transcytosis, the platform improved neuronal uptake and intracellular siRNA delivery and inhibited RIPK3-driven neurodegeneration. The approach supports a cell-type-specific RNA therapeutic strategy for CNS disorders by combining BBB crossing with neuron-targeted delivery and RIPK3 silencing.

Zhang C, Zhang J, Wang Y et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗ · Free PDF ↗

Melatonin reprograms antioxidant defenses to suppress ferroptosis via Homer1a/mGluR1-Nrf2/xCT signaling after retinal ischemia-reperfusion.

This study investigated how melatonin modulates antioxidant defenses and ferroptosis in retinal ischemia-reperfusion (I/R) injury, focusing on Homer1a/mGluR1–Nrf2–xCT signaling. After retinal I/R, bulk RNA sequencing showed downregulation of melatonin receptors (Mt1/Mt2) and ferroptosis/iron-redox regulators (Gpx4, Fth1, xCT), while melatonin improved retinal structure and function and reprogrammed antioxidant/anti-ferroptotic pathways via mGluR1-dependent activation of Nrf2 and xCT. These results position melatonin as a mechanistically defined anti-ferroptosis therapy for retinal I/R injury through Homer1a/mGluR1–Nrf2–xCT signaling.

Dou YN, Wen Y, Huang Y et al. · Redox biology · (2026) · View on PubMed ↗ · Free PDF ↗

Precision therapeutics and innovative clinical trial design in neurodegenerative diseases.

This review studied how precision therapeutics and modern clinical trial designs are being developed for biologically heterogeneous neurodegenerative diseases across conditions such as Parkinson’s disease, Alzheimer’s disease, frontotemporal dementia, ALS, and Huntington’s disease. It highlights advances in biomarkers, molecular staging, and precision medicine that are reshaping therapeutic selection and trial endpoints, including approaches like monoclonal antibodies for protein aggregation, immune-modulating/metabolic interventions, antisense oligonucleotides, and gene replacement. The synthesis is significant because it frames how next-generation trials can better match patient subtypes to disease mechanisms to improve disease-modifying development.

Domínguez-García A, Delgado-Uriarte JC, Cervantes-Arriaga A · Revista de investigacion clinica; organo del Hospital de Enfermedades de la Nutricion · (2026) · View on PubMed ↗ · Free PDF ↗

CSF and plasma tau biomarkers in the Down syndrome-Alzheimer’s disease continuum.

This cross-sectional study examined how cerebrospinal fluid (CSF) and plasma tau species change across the Down syndrome–Alzheimer’s disease (DS-AD) continuum compared with sporadic Alzheimer’s disease. Using 461 samples from the DABNI and SPIN cohorts (DS, cognitively normal euploid controls, and sporadic AD), the authors assessed tau biomarker differences with regression and LOESS modeling to characterize species-specific trajectories. The findings are clinically important because they clarify which tau measures in CSF and blood best track AD progression in DS, supporting earlier and more accurate biomarker-based staging.

Arranz J, Lantero-Rodríguez J, Braun-Wohlfahrt LS et al. · EBioMedicine · (2026) · View on PubMed ↗ · Free PDF ↗

Targeted Degradation of STING by a Neutrophil Membrane-Coated Nanoplatform Suppresses Microglial Pyroptosis After Subarachnoid Hemorrhage.

The study investigated whether aberrant STING activation drives microglial pyroptosis after subarachnoid hemorrhage (SAH) and tested a STING-targeted degradation strategy in a SAH brain injury model. Using transcriptomic/biochemical analyses and MAPK pathway interrogation, the authors found STING signaling is closely linked to microglial pyroptosis and post-SAH injury, and they engineered MG1 peptide-functionalized, neutrophil membrane-coated STING-PROTAC nanoparticles (MG1@NM-Px) to penetrate the blood–brain barrier, target microglia, and efficiently degrade STING. This suggests a mechanistically grounded, nanoparticle-delivered STING-PROTAC approach to suppress neuroinflammation and pyroptosis as a potential therapeutic direction for SAH.

Zhang R, Yuan K, Zou H et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗ · Free PDF ↗

Brain targeting and trafficking of extracellular vesicles in central nervous system diseases: a therapeutic roadmap.

This therapeutic roadmap review studied how extracellular vesicles (EVs) can be targeted to the brain in central nervous system diseases by controlling EV brain trafficking. It concluded that effective brain delivery depends on a linked sequence—EV ligands and protein corona engagement of receptor modules, selection of endocytic routes, and determination of intracellular fate (e.g., lysosomal degradation, recycling, rare cytosolic delivery, or blood–brain barrier transport). The significance is that mapping these mechanisms can guide EV engineering to improve therapeutic delivery while also accounting for disease-related risks such as dissemination of proteopathic seeds and neuroinflammation.

Baker B, Emerson S, Tran T et al. · Nanomedicine (London, England) · (2026) · View on PubMed ↗ · Free PDF ↗

Light therapy in medicine: where do we stand?

This review studied the current status of light therapy across medical disciplines, distinguishing validated clinical uses from exploratory and preclinical applications. It found that light therapy’s biological effects vary by wavelength and delivery route, with bright light acting mainly via circadian pathways for mood and sleep, while peripheral photobiomodulation (PBM) and ultraviolet (UV) phototherapy act locally on tissues. The significance is that it provides a mechanistic and translational framework to guide appropriate clinical adoption and future research directions.

Oyama Y, Witowski A, Adamzik M et al. · Annals of translational medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Spinal cord tissueoid transplantation combined with tail nerve electrical stimulation promotes the voluntary movement of paralyzed hindlimbs in rats with transected spinal cord injury.

This preclinical rat study investigated whether biomimetic spinal cord tissueoid (SCToid) transplantation into a transected spinal cord injury cavity combined with tail nerve electrical stimulation (TNES) can restore voluntary hindlimb movement. The key finding was that the combined SCToid + TNES therapy promoted regeneration of the corticospinal tract and improved functional recovery compared with approaches lacking one of the components. This supports a translational strategy that couples structural neural pathway reconstruction with electrical reactivation of sensorimotor circuits after complete spinal cord injury.

Lai BQ, Wu CR, Yang SB et al. · Materials today. Bio · (2026) · View on PubMed ↗ · Free PDF ↗

MicroRNA-mediated regulation of hair follicle regeneration: mechanisms, delivery strategies, and translational perspectives.

This 2026 review summarized how microRNAs (miRNAs) regulate hair follicle regeneration by controlling hair follicle stem cell activation, dermal papilla inductive capacity, and immune microenvironment homeostasis via the RNA-induced silencing complex (RISC). The key finding was that miRNA-mediated post-transcriptional regulation can influence cell fate transitions, paracrine signaling, inflammatory thresholds, and fibrosis, making miRNAs promising therapeutic targets. Translationally, the review highlights delivery strategies and mechanistic rationale needed to move miRNA-based hair regenerative therapies toward clinical use.

Deng Y, Hong K, Xiong M et al. · Frontiers in cell and developmental biology · (2026) · View on PubMed ↗ · Free PDF ↗

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Neurodevelopmental & Pediatric Neuropsychiatric Care

Brexpiprazole Treatment in a Child With Autism Spectrum Disorder, Attention-Deficit/Hyperactivity Disorder (ADHD), and Trauma-Associated Hoarding Symptoms: A Case Report.

This 2026 case report described a child with autism spectrum disorder (ASD), attention-deficit/hyperactivity disorder (ADHD), and trauma-associated hoarding symptoms who had minimal response to psychotherapy and conventional pharmacologic interventions. The key finding was that treatment with the approved medication (brexpiprazole) was used in this complex comorbidity context after persistent severe emotional outbursts and irritability. Clinically, the report suggests brexpiprazole may be a potential option for severe behavioral dysregulation in pediatric patients with overlapping ASD/ADHD and trauma-related hoarding symptoms, though evidence remains anecdotal.

Ikeda M, Takaki M · Cureus · (2026) · View on PubMed ↗ · Free PDF ↗

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Endocrine/Metabolic Disease Mechanisms & Therapeutics (T2D/obesity/MASLD/GDM/thyroid)

Thyroid-Liver Axis: Mechanistic Insights and Clinical Implications.

This narrative review summarized the bidirectional thyroid–liver axis, focusing on how thyroid hormones regulate hepatic lipid handling, glucose metabolism, mitochondrial function, and energy balance while the liver controls thyroid hormone transport, activation, metabolism, and clearance. It highlights clinical links between thyroid dysfunction and metabolic dysfunction–associated steatotic liver disease (MASLD), fibrosis progression, and adverse metabolic outcomes. The significance is that it consolidates mechanistic and clinical implications to guide evaluation and therapeutic considerations for patients with coexisting thyroid and liver/metabolic disorders.

Parveen N, Chittawar S, Khandelwal D et al. · Cureus · (2026) · View on PubMed ↗ · Free PDF ↗

Impact of SGLT2 inhibitors in cardiac amyloidosis: A systematic review and meta-analysis.

This systematic review and meta-analysis assessed outcomes of sodium-glucose cotransporter-2 inhibitors (SGLT2i) in patients with cardiac amyloidosis (CA), including transthyretin (ATTR) and light-chain (AL) subtypes, using seven observational studies totaling 13,303 participants. It pooled comparative effectiveness against matched controls for endpoints including mortality, heart failure (HF) exacerbations, estimated glomerular filtration rate (eGFR), and NT-proBNP using random-effects models. The clinical significance is that it evaluates whether SGLT2i—proven in broader HF populations—may improve prognosis and surrogate markers in CA, informing future management and trial design.

Nandyal S, Vij A, Varma R et al. · American heart journal plus : cardiology research and practice · (2026) · View on PubMed ↗ · Free PDF ↗

Understanding reasons for initiation and experience with tirzepatide among individuals with obesity or overweight: Results from the PERCEPTIONS survey.

This real-world observational PERCEPTIONS survey studied reasons for initiation and experiences with tirzepatide among obesity medication–eligible adults with obesity (BMI ≥30 kg/m2) or overweight (BMI ≥27 kg/m2 with ≥1 obesity-related complication) without type 2 diabetes mellitus in the US (June–November 2025). The key finding is that baseline data from this cohort characterize real-world motivations and early experiences with tirzepatide initiation outside the controlled SURMOUNT trial setting. Scientifically and clinically, these findings help contextualize how patients translate trial-proven benefits of tirzepatide into real-world use and inform patient-centered adoption and adherence.

Gibble TH, Makin H, Gerber C et al. · Obesity pillars · (2026) · View on PubMed ↗ · Free PDF ↗

Primary Cilia as Integrative Hubs of Metabolic Signaling in Type 2 Diabetes: Inter-Organ Evidence From Central, Peripheral, and Pancreatic Islet Tissues.

This article is a systematic review describing how primary cilia function as integrative hubs for metabolic signaling pathways relevant to type 2 diabetes (T2D) across central nervous system, peripheral tissues, and pancreatic islets. The key finding is that primary cilia regulate multiple signaling axes implicated in metabolic dysregulation—specifically Hedgehog (Hh), Wnt, GPCR, and mTOR—and the review compiles evidence linking ciliary dysfunction to T2D pathogenesis. Scientifically, it consolidates methodological approaches and mechanistic targets (e.g., cilia-linked appetite/energy pathways) that could guide future therapeutic strategies for T2D.

Liang M, Wen C, Deng L et al. · Journal of cellular physiology · (2026) · View on PubMed ↗

Frailty may confound the association between MASLD and cardiovascular mortality in people with cardiometabolic risk factors.

This Cardiovascular Diabetology study assessed whether frailty confounds the association between metabolic dysfunction–associated steatotic liver disease (MASLD) and cardiovascular mortality in adults with cardiometabolic risk factors using 10,413 participants from the US NHANES III cohort. The key finding was that frailty—quantified with a 49-item frailty index (FI)—may distort or explain part of the observed MASLD–cardiovascular mortality relationship. Clinically, it emphasizes that frailty should be considered as an important effect modifier/confounder when interpreting MASLD-related cardiovascular risk in high-risk populations.

Wang R, Li W, Lazarus JV et al. · Cardiovascular diabetology · (2026) · View on PubMed ↗ · Free PDF ↗

Spalt-related is an inhibitor of mTORC1-mediated growth activated by the integrated stress response.

This EMBO Journal study identified Spalt-related (Salr), a transcription factor in Drosophila melanogaster, as a negative regulator of mTORC1-mediated growth. The key finding was that Salr activates catabolic gene expression and restricts mTORC1-driven cell growth in the Drosophila fat body, with Salr functioning downstream of the integrated stress response. Scientifically, it clarifies how stress-responsive transcriptional programs can suppress nutrient-sensing growth pathways, informing conserved mechanisms linking stress signaling to mTORC1 regulation.

Deniz O, Liu Y, Kirkinen T et al. · The EMBO journal · (2026) · View on PubMed ↗ · Free PDF ↗

The Use of FGF21 Analogues in MASH and MASH Cirrhosis - Metabolic Master Regulators or Liver-Specific Mechanisms? ☆.

This article reviews whether fibroblast growth factor 21 (FGF21) analogues act as metabolic master regulators or via liver-specific mechanisms in metabolic dysfunction-associated steatotic liver disease (MASH) and MASH cirrhosis. It reports that native FGF21 signaling is blunted due to FGF21 resistance (including reduced β-Klotho co-receptor availability), and that engineered FGF21 analogues are designed to sustain target engagement at the FGFR1c/β-klotho complex to restore downstream effects. The significance is that properly targeted FGF21-analogue therapy may overcome FGF21 resistance and provide a rational pharmacologic approach for advanced MASH.

Holleboom AG, Schattenberg JM · JHEP reports : innovation in hepatology · (2026) · View on PubMed ↗ · Free PDF ↗

Identification of anti-fibrotic components of Bofutsushosan under conditions of age-associated obesity in mice.

This study investigated whether the traditional herbal formula Bofutsushosan (BTS) has anti-fibrotic effects under age-associated obesity conditions and sought to identify responsible components. In an aged diet-induced obese mouse model combined with an in vitro TGFβ-induced fibrosis model in 3T3-L1 preadipocytes (and related systems, as described), the authors characterized BTS’s ability to counter pro-fibrotic changes and used component-focused approaches to pinpoint active constituents. The work is significant because it addresses a key translational gap—whether anti-fibrotic efficacy of BTS persists in aged, metabolically compromised settings relevant to MASH and other comorbidities.

Onishi A, Onodera T, Sugaya S et al. · Phytomedicine : international journal of phytotherapy and phytopharmacology · (2026) · View on PubMed ↗ · Free PDF ↗

Omnivorous and plant-based dietary patterns: a comparative analysis using data-driven and index-based approaches.

This cross-sectional study examined dietary profiles of plant-based diet (PBD) patterns compared with an omnivorous (OMN) reference using 760 participants classified as vegan, ovo-lacto-vegetarian, or pesco-vegetarian. Using food-frequency questionnaire data for 175 foods and energy-adjusted comparisons of 32 food groups, the authors assessed adherence to established index-based patterns (Pro-vegetarian, Mediterranean, and EAT-Lancet) alongside data-driven dietary pattern analyses. The findings are significant for characterizing how different PBD subtypes map onto measurable dietary components and established dietary indices.

Casas-Albertos E, Rodríguez-Martín NM, Alcalá-Santiago Á et al. · European journal of nutrition · (2026) · View on PubMed ↗ · Free PDF ↗

Lower fall and femoral fracture risks with semaglutide and tirzepatide compared with DPP-4 inhibitors in older adults with type 2 diabetes.

This retrospective cohort study evaluated whether semaglutide or tirzepatide reduces fall and femoral fracture risk compared with DPP-4 inhibitors in older adults (≥65 years) with type 2 diabetes and BMI ≥25 kg/m2 using the TriNetX database (2018–2025). The key finding was that semaglutide and tirzepatide were associated with significantly lower risks of both falls and femoral fractures versus DPP-4 inhibitors. This is clinically important because it suggests incretin-based therapies may confer musculoskeletal safety benefits in an at-risk geriatric T2DM population.

Chen HY, Wu JY, Chu YH 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 ↗ · Free PDF ↗

Clinical Characteristics, Treatment Patterns, and Complications in Permanent Hypoparathyroidism: A Large Retrospective Cross-Sectional Study.

This large retrospective cross-sectional study investigated clinical characteristics, treatment patterns, and complications in 958 adults with permanent hypoparathyroidism, stratifying patients by etiology (postsurgical vs nonsurgical) and further by thyroid histopathology type in the surgical subgroup. The authors assessed risk factors for hypoparathyroidism-related complications using regression analyses and reported treatment use across calcium, calcitriol, thiazide diuretics, cholecalciferol, teriparatide, and palopegteriparatide. The significance lies in identifying complication risk factors and real-world management patterns that can inform individualized care to reduce morbidity in permanent HypoPT.

Soyer AK, Polat ŞB, İnönü G et al. · Calcified tissue international · (2026) · View on PubMed ↗

Integrative multi-omics identifies CYP1B1 as a candidate molecular link between toxicant exposure and ferroptosis-related epithelial stress in COPD.

This integrative multi-omics study investigated COPD-associated epithelial stress pathways linking toxicant exposure (e.g., cigarette smoke) to ferroptosis-related injury, focusing on CYP1B1 as a candidate molecular link. By combining bulk transcriptomics, single-cell RNA sequencing, machine-learning analysis, and experimental validation, the authors identified CYP1B1 as connected to ferroptosis-related epithelial stress programs in COPD. Scientifically, it highlights CYP1B1-centered mechanisms that could be targeted to modulate ferroptosis and epithelial remodeling in COPD.

Liu L, Jiang M, Lei M et al. · Inflammation research : official journal of the European Histamine Research Society … [et al.] · (2026) · View on PubMed ↗ · Free PDF ↗

Tirzepatide compared with semaglutide in obesity disease: a subpopulation analysis applying Japan Society for the Study of Obesity criteria in the global SURMOUNT-5 trial.

This subpopulation analysis studied tirzepatide versus semaglutide for obesity disease in participants meeting Japan Society for the Study of Obesity criteria within the global SURMOUNT-5 trial (NCT05822830). In the eligible subgroup, outcomes through Week 72 included percent body-weight change and proportions achieving weight-loss thresholds, along with measures such as waist circumference change and safety endpoints. Clinically, it helps determine whether tirzepatide’s efficacy and tolerability observed in SURMOUNT-5 extend to patients defined by Japan’s national insurance obesity criteria.

Kitamoto T, Yoshino M, Shingaki T et al. · Current medical research and opinion · (2026) · View on PubMed ↗

Advances and challenges in the mechanistic understanding of beta-cell dysfunction in gestational diabetes mellitus.

This review studied the mechanistic basis of beta-cell dysfunction in gestational diabetes mellitus (GDM), focusing on how pregnancy-induced insulin resistance is normally compensated by increased beta-cell mass and function. It found that in GDM, hyperglycemia occurs when beta-cells fail to compensate, and that GDM is heterogeneous with subtypes involving defects in insulin sensitivity, secretion, or both. The significance is that clarifying these mechanisms can support more precise, subtype-informed interventions to prevent or treat GDM.

Pszczolkowski VL, Youn YJ, Her TK et al. · Journal of animal science · (2026) · View on PubMed ↗

Integrative oncology in colorectal cancer: evidence-based strategies from prevention through survivorship.

This narrative review integrated evidence across the colorectal cancer (CRC) care continuum—prevention through survivorship—summarizing lifestyle and supplement interventions and their trial/cohort support. The key finding was that high-fiber diets, Mediterranean dietary patterns, calcium supplementation, regular physical activity, healthy weight maintenance, and berberine each show reproducible CRC risk reduction in large prospective cohorts and multicenter randomized trials. These findings support incorporating evidence-based integrative oncology strategies into routine CRC prevention and survivorship care.

Shen C, Lou R, Bai F et al. · Frontiers in oncology · (2026) · View on PubMed ↗ · Free PDF ↗

Educational attainment and diabetes risk: triangulation evidence from UK Biobank prospective cohort, NHANES 2011-2018, and cross-trait genomics analyses.

This study triangulated evidence on educational attainment and diabetes risk using UK Biobank prospective data (n≈500k at baseline), NHANES 2011–2018 validation, and cross-trait genomics analyses. The key finding was that higher educational attainment was associated with lower prevalent and incident type 2 diabetes risk, with mediation patterns implicating adiposity, health behaviors, and cardiometabolic biomarkers, and genetic analyses supporting a causal/robust relationship. Scientifically and clinically, the integrated approach strengthens the case that educational attainment is a meaningful, partly modifiable determinant of diabetes risk.

Geng G, Qiu S, Zhang Z et al. · Frontiers in endocrinology · (2026) · View on PubMed ↗ · Free PDF ↗

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Aging, Biological Age & CHIP/Inflammaging

Clonal hematopoiesis of indeterminate potential (CHIP)-a pivotal contributor of aging and related disorders.

This review studied clonal hematopoiesis of indeterminate potential (CHIP) as a contributor to aging-related disorders by focusing on age-associated somatic mutations in leukemia driver genes. It found that mutations such as DNMT3A, TET2, ASXL1, TP53, PPM1D, SF3B1, SRSF2, and IDH1/2 confer growth advantage to mutated hematopoietic stem cell clones and that an altered bone marrow microenvironment with increased inflammation accelerates disease risk. The significance is that CHIP provides a mechanistic link between accumulated DNA damage, clonal expansion, and increased morbidity/mortality with aging.

Dhenge A, Kulkarni R · Annals of translational medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Metabolic dysregulation and biological age acceleration in Hashimoto’s thyroiditis: a cross-sectional study based on clinical biomarker aging indices and metabolomics.

This cross-sectional study assessed metabolic dysregulation and biological age acceleration in people with Hashimoto’s thyroiditis (HT) using clinical biomarker aging indices and metabolomics across discovery cohorts, an NHANES 2007–2012 validation cohort, and a metabolomics cohort. The key finding was that HT was associated with measurable biological age acceleration (via Klemera-Doubal and Phenotypic Age metrics) alongside metabolic alterations consistent with age-related remodeling. These results support a link between HT-related chronic inflammation and accelerated biological aging, with potential implications for risk stratification and metabolic monitoring.

Zhao X, Li Q, Luo T et al. · Frontiers in endocrinology · (2026) · View on PubMed ↗ · Free PDF ↗

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Autoimmune/Inflammatory Disorders (IBD/eczema/CIDP/Behçet/thyroid-related)

Glycocholic acid inhibits TRIB3-ID1 axis to acelerate colitis progression via suppressing intestinal stem cell renewal.

This study tested how glycocholic acid (a primary bile acid elevated in inflammatory bowel disease) affects intestinal stem cell renewal and colitis progression by targeting the TRIB3–ID1 axis. Glycocholic acid accelerated colitis progression by downregulating TRIB3, which disrupted intestinal stem cell renewal, thereby impairing mucosal healing capacity. The results implicate bile-acid–TRIB3 signaling as a mechanistic driver of IBD worsening and a potential therapeutic target to preserve intestinal stem cell function.

Shang S, Liu J, Dai SY et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Surveillance of patients at risk of liver cancer: Expert opinions.

This expert-opinion article reviewed the evidence base for liver cancer surveillance, emphasizing that randomized trial data are lacking and that many current practices rely on observational evidence. It highlighted limitations of screening in low-prevalence populations and the imperfect performance of surveillance tests, leading to high false-positive rates, while noting ongoing evaluation of novel modalities beyond ultrasound. The review provides guidance for clinicians and policymakers on how to interpret current surveillance recommendations and where stronger evidence is needed.

Yip TC, Innes H, Wong GL et al. · Journal of hepatology · (2026) · View on PubMed ↗ · Free PDF ↗

Diagnosis, treatment and monitoring of pediatric Behçet’s disease: Systematic literature review informing the ISSAID/PRES recommendations.

This systematic literature review evaluated evidence on diagnosis, treatment, and monitoring of pediatric Behçet’s disease (onset <16 years) to inform ISSAID/PReS recommendations. It summarizes population-level clinical features, diagnostic criteria, management strategies, and outcomes drawn from observational studies identified via PRISMA-guided searches. The significance is that it consolidates age-specific evidence to standardize care pathways and improve clinical decision-making in pediatric BD.

Mastrolia MV, Romano M, Piskin D et al. · Autoimmunity reviews · (2026) · View on PubMed ↗

Epidemiology of Alcohol-Associated Hepatitis: A Systematic Review of Population-Based Studies.

This systematic review studied the epidemiology of alcohol-associated hepatitis (AH) by compiling population-based incidence and point prevalence estimates from 2000 to 2025. It reports that reliable estimates are limited and synthesizes available data using MEDLINE/PubMed, Scopus, and Cochrane Library searches with risk-of-bias assessment via Joanna Briggs Institute tools. The significance is improved understanding of AH burden across fibrosis stages to guide public health planning and future clinical trial design.

Gazda J, Koky T, Robinska A et al. · Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association · (2026) · View on PubMed ↗

Decoding the epithelial-stromal interactome in allergic rhinitis through single-cell multi-omics integration.

This study used single-cell RNA sequencing and single-cell ATAC sequencing to build a cellular atlas of nasal mucosa and define transcriptional/epigenetic changes in allergic rhinitis (AR) versus non-allergic rhinitis (NAR). In 39 subjects (AR n=24, NAR n=15), it applied differential gene/peak analyses, cell-cell communication inference, trajectory inference, and gene regulatory network reconstruction to map disease-associated epithelial-stromal interactome alterations. The significance is that multi-omics single-cell integration can identify actionable pathways and cell interactions underlying AR pathogenesis.

Liu Z, Wu Y, Han S et al. · The Journal of allergy and clinical immunology · (2026) · View on PubMed ↗ · Free PDF ↗

Clinical phenotyping of asthma patients with elevated sputum eosinophils and low blood eosinophils: a post-hoc analysis of the multicentre ATLANTIS cohort.

This post-hoc analysis studied the clinical phenotype of asthma patients with isolated sputum eosinophilia—elevated sputum eosinophils with low blood eosinophils—within the multicentre ATLANTIS cohort. Using patients with available blood and/or sputum data, the analysis aimed to determine how this discordant eosinophil pattern relates to asthma characteristics and likely treatment responsiveness. The results are significant for refining eosinophil-based stratification and guiding biologic or corticosteroid decisions when blood eosinophils underestimate airway eosinophilia.

Kuks PJM, Aabed AMA, Premereur LCA et al. · EBioMedicine · (2026) · View on PubMed ↗ · Free PDF ↗

Epidemiology of primary sclerosing cholangitis in general and IBD populations: a systematic review and meta-analysis.

This systematic review and meta-analysis studied the prevalence and incidence of primary sclerosing cholangitis (PSC) in the general population and in inflammatory bowel disease (IBD) populations. The authors synthesized population- or cohort-based studies to generate updated PSC prevalence estimates in general and IBD groups and PSC incidence estimates in the general population. Clinically, these pooled epidemiologic estimates help refine risk stratification and screening priorities for PSC among IBD patients and in broader populations.

Ho GJK, Selvakumar A, Yeo LYY et al. · Hepatology international · (2026) · View on PubMed ↗ · Free PDF ↗

A Practical Guide to Management of Chronic Inflammatory Demyelinating Polyradiculoneuropathy.

This article studied the evidence base and practical management strategies for chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) in clinical practice. It summarizes current diagnostic and treatment approaches, emphasizing immunomodulatory therapies such as intravenous immunoglobulin, corticosteroids, and plasma exchange in the context of the 2021 European Academy of Neurology/Peripheral Nerve Society guideline. The significance is providing clinicians with an actionable management guide to standardize CIDP care and improve outcomes for patients with this immune-mediated demyelinating neuropathy.

Jakobsen J, Karam C, Kuitwaard K et al. · Neurology and therapy · (2026) · View on PubMed ↗ · Free PDF ↗

Chronic eczematous eruptions of aging: a clinical practice review.

This 2026 clinical practice review examined chronic eczematous eruptions of aging (CEEsA) as an umbrella diagnosis in older adults, focusing on epidemiology, causes, presentation, and management. The review found that CEEsA commonly presents as intensely pruritic, ill-defined trunk/extensor-limb eruptions that are often refractory to standard topical therapies and may be triggered by medications such as calcium channel blockers and thiazides. Clinically, adopting consistent terminology and targeted management strategies for CEEsA could improve recognition and treatment of a poorly characterized condition in later life.

Westerdahl JS, Sontheimer RD · Annals of translational medicine · (2026) · View on PubMed ↗ · Free PDF ↗

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Reproductive Health, Pregnancy/ART & Placental Biology

Inhibition of p65 nuclear translocation in decidual stromal cells underlies COS-induced supraphysiologic estrogen impairment of uNK cell function which drives placental abnormalities.

This mouse study examined how inhibition of p65 nuclear translocation in decidual stromal cells affects controlled ovarian stimulation (COS)-driven supraphysiologic estrogen impairment of uterine natural killer (uNK) cell function and placental outcomes. The key finding is that blocking p65 nuclear translocation in decidual stromal cells underlies the mechanism by which COS-level estrogen disrupts uNK cell function, leading to placental abnormalities. Clinically, it identifies a potential molecular intervention point (p65 signaling in decidual stromal cells) to mitigate estrogen-related placental dysfunction in ART settings.

Yu H, Mu H, Xiong Y et al. · Journal of translational medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Mesenchymal stem cells reverse ovarian dysfunction by inhibiting autophagy in polycystic ovary syndrome mice.

This study tested whether human umbilical cord mesenchymal stromal cells (Huc-MSCs) reverse ovarian dysfunction in a dehydroepiandrosterone (DHEA)-induced polycystic ovary syndrome (PCOS) mouse model by inhibiting autophagy. The key finding is that MSC treatment improved ovarian function and modulated sex hormone/estrous cycle outcomes in association with suppression of autophagy-related processes. Scientifically and therapeutically, it supports autophagy inhibition as a mechanism by which MSCs may restore reproductive function in PCOS.

Liu Q, Zhan L, Kong L et al. · Stem cell research & therapy · (2026) · View on PubMed ↗ · Free PDF ↗

Role of the trophoblastic BMP7-TGM2 axis in the pathogenesis and prevention of preeclampsia.

This study investigated the BMP7–TGM2 axis in preeclampsia by examining how bone morphogenetic protein 7 (BMP7) regulates tissue transglutaminase 2 (TGM2) and trophoblast behavior in the context of abnormal placental development. It reported that the BMP7–TGM2 pathway contributes to trophoblast invasion/differentiation defects characteristic of preeclampsia and that modulating this axis can prevent or ameliorate disease-relevant phenotypes. These mechanistic insights position BMP7–TGM2 signaling as a potential therapeutic target for preventing preeclampsia.

Ding Q, Liu M, Zhao B et al. · Cell death & disease · (2026) · View on PubMed ↗ · Free PDF ↗

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Infectious Disease Biology (viruses/parasites/bacteria/phage)

Vancomycin-stressed Staphylococcus aureus extracellular vesicles hijack macrophage autophagy to enhance bacterial intracellular survival.

This study investigated how vancomycin-stressed Staphylococcus aureus extracellular vesicles affect host defenses by hijacking macrophage autophagy to enhance intracellular bacterial survival in MRSA infection models. The authors found that subinhibitory vancomycin promotes S. aureus survival within macrophages by exacerbating autophagic flux blockade, using both in vitro and in vivo models to demonstrate the mechanism. This is clinically significant because it suggests a potential reason for vancomycin treatment failure in MRSA bloodstream infections and identifies host autophagy as a therapeutic intervention point.

Lu B, Chang W, Liu X et al. · Autophagy · (2026) · View on PubMed ↗

Enhanced EBNA2-dependent activity in EBV-transformed B cells from patients with multiple sclerosis.

This preprint investigated Epstein–Barr virus (EBV) effects on gene expression, chromatin accessibility, and transcription factor binding in EBV-transformed B cells derived from patients with multiple sclerosis (MS) versus healthy controls, compared with primary B cells. RNA-seq and ATAC-seq showed extensive MS-dependent transcriptional and chromatin accessibility differences in EBV-transformed B cells but not in primary B cells, indicating enhanced EBNA2-dependent activity in the transformed context. These results support a mechanistic role for EBV-driven transcriptional programs in MS pathobiology and identify EBV-transformed B cells as a relevant target for further study.

Granitto M, Kim E, Forney C et al. · medRxiv : the preprint server for health sciences · (2026) · View on PubMed ↗ · Free PDF ↗

Phage portal proteins counteract stringent-response-mediated restriction.

This study investigated how bacteriophage T7 infection is restricted by the bacterial stringent response alarmones ppGpp and pppGpp and how the phage portal protein Gp8 counteracts this barrier. It found that alarmone signaling constrains T7 infection and that Gp8 inhibits RelA and SpoT by engaging them to suppress their synthetase activities, thereby reducing alarmone accumulation. These mechanistic insights explain how phages overcome host resource-limiting states and identify a specific Gp8–RelA/SpoT interaction as a key determinant of infection success.

Kronborg K, Wang L, Schicketanz ML et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Lactiplantibacillus plantarum promotes intestinal goblet cell differentiation via indole-3-lactic acid-AHR signaling in pigs.

This study examined whether Lactiplantibacillus plantarum influences intestinal epithelial development in pigs by promoting goblet cell differentiation, using longitudinal metagenomics, dietary supplementation, and porcine ileum organoid co-culture. L. plantarum was transiently enriched in nursery-stage piglets and was associated with increased goblet cells and higher MUC2 expression, and its cell-free supernatant promoted goblet differentiation via indole-3-lactic acid–AHR signaling. The findings connect a specific developmental microbiome shift to host epithelial differentiation through a defined metabolite–receptor pathway, suggesting probiotic/metabolite strategies for gut health.

Liu Z, Wu H, Howe S et al. · NPJ biofilms and microbiomes · (2026) · View on PubMed ↗ · Free PDF ↗

Single-Cell and Spatial Transcriptomics Unveil Key Regulators Governing Cell Differentiation for Schistosoma japonicum Sexual Development.

This study mapped the cellular and regulatory programs underlying Schistosoma japonicum sexual development and egg production using single-cell and spatial transcriptomics across developmental stages. By building a dynamic single-cell atlas and integrating it with spatial transcriptomics to define tissue-resolved niches, the authors identified critical cell populations and regulatory networks that govern parasite maturation and egg production. The work provides a stage-resolved molecular blueprint that could inform targeted interventions against schistosomiasis by disrupting sexual development.

Lu Z, Wang X, Li S et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗ · Free PDF ↗

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Generated automatically on July 13, 2026 from PubMed’s trending articles. Summaries are AI-generated; always consult the original publication for clinical or research decisions.