PubMed Trending Research Digest — October 07, 2026

Automated digest · 96 articles · 21 research areas · October 07, 2026

Overview

This week’s digest is dominated by precision medicine themes: tailoring therapy based on biology, biomarkers, and patient subgroups. In oncology, long-term follow-up strengthens the clinical case for adding PD-1 blockade to chemotherapy in esophageal squamous cell carcinoma, while multiple studies probe why responses vary—through tumor immune microenvironment remodeling, transporter- and EV-mediated resistance, sex-biased signaling, and exhaustion states in tumor-infiltrating lymphocytes. Across cancers, mechanistic targets (e.g., macrophage polarization programs, CXCL9 inactivation, ferroptosis regulators, and RAS pathway targeting) are increasingly linked to actionable biomarkers that could guide treatment selection and combination strategies.

Outside cancer, the same “stratify and personalize” logic appears in cardiovascular–kidney–metabolic care (CKM staging and event-linked kidney trajectories), osteoporosis (mechanism-based subtypes and bone marrow adipose involvement), and neurodegeneration (cell-type-specific degeneration and proteostasis pathways). Several studies also emphasize the translational pipeline from bench to bedside: new imaging/radiomics and cfDNA signatures, spatial and multi-omics atlases, and improved computational frameworks for interpreting complex biological data. In parallel, clinical guidance updates (e.g., menopausal VMS pharmacologic recommendations and SLIT consensus) and real-world effectiveness/safety studies (e.g., MS anti-CD20 use in older adults, cGVHD after steroid/ruxolitinib failure) highlight how evidence is being operationalized for practice.

Finally, a cross-cutting thread is the role of the environment—dietary processing, microbiota, and immune priming—in shaping disease risk and treatment response. Studies range from ultraprocessed food effects on metabolic and brain responses to microbiome-dependent NK-cell protection in aging lungs and microbiota-driven amplification of genetically increased MASLD risk. Together, these findings reinforce a modern view of health and disease as systems-level phenomena, where genetics, immune state, and ecological exposures interact to determine outcomes.

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Bipolar disorder & nutraceutical/phytoceutical interventions

Microbiota-host genetic interactions modulate MASLD risk in PNPLA3I148M carriers via ceramides and are reversible by targeted microbial interventions.

This study investigated how intestinal host–microbiota interactions modify metabolic dysfunction–associated steatotic liver disease (MASLD) risk in PNPLA3 I148M carriers, focusing on ceramide-mediated mechanisms and reversibility by targeted microbial interventions. Using a dual-hit mouse model (hepatic Pnpla3I148M expression plus Nlrp6 deficiency) and multi-omics integration (metagenomics, metabolomics, transcriptomics) with human data, it identified microbiota-driven ceramide pathways that amplify PNPLA3-associated hepatic injury. The findings suggest that manipulating the gut microbiome could mitigate genetically increased MASLD risk in PNPLA3 I148M carriers.

Haque M, Lesker TR, Rolle-Kampczyk U et al. · Gut · (2026) · View on PubMed ↗ · Free PDF ↗

Sotatercept in Pediatric Pulmonary Hypertension: Experience from the Pediatric Pulmonary Hypertension Network.

This multicenter retrospective study assessed safety and efficacy of sotatercept, a TGF-β superfamily ligand trap, as add-on therapy in children and young adults ≤21 years with pediatric pulmonary hypertension using Pediatric Pulmonary Hypertension Network and institutional registry data. The analysis compared clinical characteristics before and after sotatercept to evaluate changes in outcomes such as exercise capacity and pulmonary vascular resistance. These real-world pediatric data help define whether adult efficacy signals for sotatercept extend to younger patients and inform risk–benefit considerations for clinical use.

Critser PJ, Krishnan US, Avitabile CM et al. · Chest · (2026) · View on PubMed ↗ · Free PDF ↗

Nutraceuticals and phytoceuticals in the treatment of bipolar disorder: A systematic review and network meta-analysis.

This systematic review and network meta-analysis evaluated randomized controlled trials of nutraceuticals and phytoceuticals for bipolar disorder in participants across 28 RCTs (n=2,222), comparing 22 treatments using standardized mean differences for depressive/manic symptoms and risk ratios for response/acceptability, with heterogeneity and bias assessed via CINeMA. The analysis found comparative effects across multiple nutraceutical/phytoceutical options on depressive and manic outcomes, treatment response, and acceptability, while also emphasizing limitations from small-study effects and risk of bias (details truncated in the provided abstract). These findings support further evidence-based consideration of specific nutraceutical/phytoceutical candidates as adjunctive or alternative strategies for bipolar disorder, but they require confirmation in larger, higher-quality trials.

Fornaro M, Nunez NA, Di Lorenzo C et al. · European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology · (2026) · View on PubMed ↗ · Free PDF ↗

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Menopausal vasomotor symptoms (VMS) guidelines & pharmacologic comparative effectiveness

Pharmacologic Treatments for Females With Menopausal Vasomotor Symptoms: A Clinical Guideline From the American College of Physicians.

This American College of Physicians (ACP) clinical guideline synthesized evidence from systematic reviews to inform pharmacologic treatment decisions for females with menopausal vasomotor symptoms in outpatient clinical practice using the GRADE framework. The guideline provides recommendations on which medication classes to use for VMS based on benefits, harms, patient values/preferences, and cost-effectiveness (the specific drug recommendations are truncated in the provided abstract). Clinically, it standardizes evidence-based prescribing for menopausal VMS to improve symptom control while balancing safety and patient-centered outcomes.

Qaseem A, Mackey K, Yost J et al. · Annals of internal medicine · (2026) · 1 citations · View on PubMed ↗

Pharmacologic Treatments for Female Menopausal Vasomotor Symptoms: A Systematic Review and Meta-analysis for the American College of Physicians.

This systematic review and meta-analysis for the ACP evaluated randomized trials (≥8 weeks) of pharmacologic medications for vasomotor symptoms in perimenopausal and postmenopausal females, assessing benefits, harms, patient-reported outcomes (including menopause-related quality of life and sleep), endometrial hyperplasia/cancer risk, and serious adverse events using searches through 3 March 2026. The study synthesized comparative effectiveness and safety across eligible drug options (specific effect estimates are truncated in the provided abstract). The results directly inform guideline recommendations for selecting VMS therapies that optimize symptom relief and quality of life while minimizing clinically important risks.

Diem S, Landsteiner A, Langsetmo L et al. · Annals of internal medicine · (2026) · 2 citations · View on PubMed ↗

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Multiple sclerosis (MS) anti-CD20 therapy comparative effectiveness

Risk of infection in ocrelizumab-treated adults with multiple sclerosis aged 55 years and older: a retrospective cohort study.

This retrospective cohort study compared infection risk and infection-related hospitalization in ocrelizumab-treated adults with multiple sclerosis aged >55 years versus older adults with MS who had never received B-cell–depleting therapies, using electronic medical records from Massachusetts General Hospital (June 2017–January 2026). The key finding was the modeled difference in infection and hospitalization rates between the ocrelizumab-exposed and unexposed groups using inverse probability of treatment weighting and negative binomial regression. Scientifically and clinically, it addresses an evidence gap because pivotal ocrelizumab trials excluded patients >55, informing real-world safety expectations in older MS populations.

Lee S, Scheu R, Enkhtsetseg N et al. · Lancet regional health. Americas · (2026) · 1 citations · View on PubMed ↗ · Free PDF ↗

Long-term comparative outcomes in relapse activity and disability progression among anti-CD20 therapies in relapsing multiple sclerosis: An unanchored matching-adjusted indirect comparison.

This unanchored matching-adjusted indirect comparison compared long-term relapse activity and disability progression among anti-CD20 therapies in relapsing multiple sclerosis using individual patient data from ULTIMATE I/II reweighted to match OPERA I/II and ASCLEPIOS I/II baseline characteristics. The analysis estimated five-year comparative outcomes for annualized relapse rate (ARR) and 24-week confirmed disability progression (CDP24) across ublituximab, ocrelizumab, and ofatumumab. Scientifically and clinically, it provides a framework for longer-term comparative effectiveness when head-to-head randomized trials are unavailable.

Gold R, Ansaripour A, Schmierer K et al. · Multiple sclerosis and related disorders · (2026) · View on PubMed ↗ · Free PDF ↗

Ofatumumab vs Ocrelizumab in Relapsing-Remitting Multiple Sclerosis: A Nationwide Cohort Study.

This nationwide observational cohort study used the Danish Multiple Sclerosis Registry to compare effectiveness of the anti-CD20 monoclonal antibodies ofatumumab versus ocrelizumab in patients with relapsing-remitting multiple sclerosis (RRMS) initiating therapy between January 2022 and November 2025. The primary outcome was the annualized relapse rate (ARR) rate ratio between ofatumumab and ocrelizumab (full results are truncated in the provided abstract). The findings are significant for real-world comparative effectiveness of anti-CD20 therapies in RRMS, supporting treatment selection beyond randomized trial data.

El Mahdaoui S, Pontieri L, Romme Christensen J et al. · Neurology · (2026) · 1 citations · View on PubMed ↗

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Genitourinary syndrome of menopause (GSM) & vaginal estrogen safety

Use of Vaginal Estrogen in Breast and Gynecologic Cancer Survivors.

This narrative review assessed the safety and efficacy of vaginal estrogen therapy for genitourinary syndrome of menopause (GSM) in breast and gynecologic cancer survivors, focusing on cancer recurrence and mortality risk and on dosing/formulation considerations. The review reports that vaginal estrogen is consistently associated with significant improvement in GSM symptoms and quality of life, with low-dose formulations showing minimal systemic absorption and serum estradiol levels remaining within postmenopausal ranges (recurrence/mortality quantitative findings are truncated). Clinically, it supports careful use of low-dose vaginal estrogen to treat GSM in cancer survivors when nonhormonal measures are insufficient, while monitoring for oncologic safety.

Burns JB, AlHilli MM, Ali A et al. · JCO oncology practice · (2026) · View on PubMed ↗

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Cancer immunotherapy: PD-1/immune checkpoint and CAR-T (clinical trials & biomarkers)

Extended follow-up of in vivo BCMA CAR-T therapy in relapsed/refractory multiple myeloma.

This Nature Medicine report presented extended in vivo follow-up of the BCMA-targeted CAR-T therapy ESO-T01 in four patients with relapsed/refractory multiple myeloma, using a regimen designed to avoid leukapheresis and lymphodepletion. All patients developed dual-phase cytokine release syndrome (grades 1–3) and grade ≥3 hematotoxicities, with one patient experiencing grade 1 immune effector cell-associated neurotoxicity syndrome, and the study extended safety/efficacy assessment beyond the earlier 3-month window. The long-term characterization of ESO-T01 informs the clinical risk–benefit profile and durability considerations for leukapheresis-free, lymphodepletion-free in vivo BCMA CAR-T approaches.

Xu J, Liu L, Xie W et al. · Nature medicine · (2026) · View on PubMed ↗

First-line durvalumab and tremelimumab in poor-prognosis unresectable hepatocellular carcinoma: Phase IIIb single-arm SIERRA study.

This phase IIIb single-arm SIERRA study evaluated first-line STRIDE (durvalumab plus tremelimumab) in adults with poor-prognosis unresectable hepatocellular carcinoma (uHCC), including cohorts with Child-Pugh B7/B8 liver function and other poor prognostic features. The primary analysis reported safety and efficacy outcomes for this poor-prognosis population receiving STRIDE as first-line therapy. These data extend the clinical applicability of dual immune checkpoint blockade to uHCC patients often excluded from earlier trials due to impaired liver function or other high-risk criteria.

Chan SL, Kudo M, Sangro B et al. · Journal of hepatology · (2026) · View on PubMed ↗

A multicenter phase II study of glofitamab plus polatuzumab-R-CHP for patients with diffuse large B-cell lymphoma.

This multicenter phase II study evaluated adding the CD3xCD20 bispecific antibody glofitamab to polatuzumab-R-CHP in patients with newly diagnosed diffuse large B-cell lymphoma (DLBCL) with IPI ≥2. The trial tested a regimen where glofitamab was incorporated during cycles 3–6 with polatuzumab-R-CHP and then used as monotherapy for cycles 7–8, with primary assessment of best complete response (CR) rate. The clinical significance is that it tests whether intensifying standard chemoimmunotherapy with a bispecific T-cell engager improves deep responses in a defined high-risk DLBCL population.

Crombie JL, Redd R, Phinney C et al. · Blood · (2026) · View on PubMed ↗

Pharmacologic HIF-2α inhibition preserves T cell effector function in clear cell renal cell carcinoma.

The study tested whether pharmacologic HIF-2α inhibition affects human T cell effector biology in clear cell renal cell carcinoma (ccRCC), focusing on the EPAS1/HIF-2α axis and the drug belzutifan. Using CRISPR/Cas9 deletion of HIF-2α in primary human T cells and pharmacologic HIF-2α inhibition, it found no notable transcriptional effects from EPAS1 perturbation and assessed whether belzutifan preserves T cell effector function. This is clinically important because it addresses a key concern that HIF-2α blockade in ccRCC could blunt antitumor immunity.

Madsen KN, Kashima S, Soulati H et al. · The Journal of clinical investigation · (2026) · View on PubMed ↗

Abundant CD8+ tumor-infiltrating lymphocytes in glioblastoma harbor distinct exhaustion signatures in potentially reactive subsets.

In 56 patients with newly diagnosed IDH-wildtype glioblastoma, investigators sorted abundant CD3+CD8+CD4− tumor-infiltrating lymphocytes from cases with prominent intratumoral T-cell infiltration for single-cell RNA sequencing and T-cell receptor (TCR) sequencing. They reported that these CD8+ TILs contain distinct exhaustion signatures within potentially reactive subsets. This supports the feasibility of identifying antigen-specific or less-exhausted T-cell populations for glioblastoma immunotherapy development.

Okamoto T, Mizuta R, Demachi-Okamura A et al. · British journal of cancer · (2026) · View on PubMed ↗

Extracellular vesicle proteins monitor and interfere with CLDN18.2-targeted CAR-T cell and antibody therapies against gastrointestinal cancers.

This study investigated whether extracellular vesicle (EV) proteins can both monitor and modulate responses to CLDN18.2-targeted CAR-T and antibody therapies in gastrointestinal cancers. By profiling serial plasma samples from the CT041-CG4006 CLDN18.2 CAR-T trial and the GLOW zolbetuximab trial, it identified EV-associated CLDN18.2, PD1, and PD-L2 as therapeutic markers and incorporated them into a CPP-score for improved prediction, while also showing mechanistic interference by specific EV proteins. These findings support EV protein signatures as biomarkers and potential therapeutic sensitization targets for CLDN18.2-directed treatment.

Qi C, Ma M, Liang K et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

First-line tislelizumab plus chemotherapy versus placebo plus chemotherapy in unresectable advanced/metastatic esophageal squamous cell carcinoma: minimum 3-year survival follow-up of a randomized phase 3 trial (RATIONALE-306).

This randomized phase 3 trial studied first-line tislelizumab 200 mg plus investigator-chosen chemotherapy versus placebo plus chemotherapy in 649 patients with unresectable advanced/metastatic esophageal squamous cell carcinoma. After a minimum 36.0-month follow-up, tislelizumab plus chemotherapy improved overall survival versus placebo plus chemotherapy (17.2 vs 10.6 months; hazard ratio 0.70). These long-term results support durable clinical benefit of adding the anti–PD-1 antibody tislelizumab to chemotherapy in this patient population.

Yoon HH, Kato K, Raymond E et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Early Changes in Lymphocyte Counts Predict Clinical Outcomes in Hepatocellular Carcinoma Treated With Durvalumab Plus Tremelimumab.

In a multicenter retrospective cohort of 299 patients with advanced hepatocellular carcinoma (HCC) treated with durvalumab plus tremelimumab (Dur/Tre), the study tested whether early changes in peripheral blood lymphocyte counts at 2 weeks (2w-Δlymphocyte) predict outcomes. Patients with favorable early lymphocyte changes had better objective response rate and progression-free survival during Dur/Tre therapy. If validated prospectively, 2-week lymphocyte dynamics could serve as an accessible biomarker to stratify advanced HCC patients for immunotherapy benefit.

Honma Y, Shimose S, Ito T et al. · Journal of gastroenterology and hepatology · (2026) · View on PubMed ↗ · Free PDF ↗

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Cancer targeted therapy & precision oncology (non-immunotherapy; e.g., PARP, RAS, TKIs, ADCs)

Pancreatic Cancer KRAS Breakthrough: Drug Graveyard No More.

This article reviewed the clinical shift toward direct RAS targeting in pancreatic ductal adenocarcinoma (PDAC), focusing on FDA-approved daraxonrasib (Rasonque) for adults with metastatic PDAC after prior systemic therapy. The key finding is that daraxonrasib represents a breakthrough that moves RAS from an undruggable concept to an actionable targeted therapy, alongside a wave of ongoing RAS-focused clinical trials. Clinically, this reframes PDAC treatment beyond “drug graveyard” strategies and may enable more effective, mechanism-based options for metastatic disease.

Yu PY, Oberstein PE, Maitra A et al. · Clinical cancer research : an official journal of the American Association for Cancer Research · (2026) · View on PubMed ↗

Efficacy and Safety of Olaparib plus Abiraterone Versus Placebo plus Abiraterone in the Non-BRCA Mutation Subgroup of Patients with Metastatic Castration-resistant Prostate Cancer in the PROpel Trial.

This analysis of the phase 3 PROpel trial evaluated olaparib plus abiraterone versus placebo plus abiraterone in the non–BRCA1/2 mutation subgroup of patients with metastatic castration-resistant prostate cancer. The study reports subgroup efficacy and safety outcomes to inform treatment decisions beyond the BRCA-mutant population. Clinically, it addresses whether PARP inhibition with olaparib adds benefit to androgen-receptor pathway blockade with abiraterone for non-BRCAm mCRPC patients.

Mehra N, Clarke NW, Armstrong AJ et al. · European urology oncology · (2026) · View on PubMed ↗ · Free PDF ↗

Testosterone breakthrough and outcomes during intensified therapy in metastatic hormone-sensitive prostate cancer: the ARASENS and LATITUDE trials.

This post hoc analysis assessed whether testosterone breakthrough (>35 ng/dL) during intensified therapy predicts outcomes in metastatic hormone-sensitive prostate cancer using the ARASENS and LATITUDE phase III trial experimental arms. Landmark analyses classified breakthrough based on serum testosterone measurements after treatment initiation through Day 147 (LATITUDE) or Day 266 (ARASENS) and related it to clinical endpoints. The work clarifies whether inadequate androgen suppression during therapy is associated with worse outcomes, informing monitoring and potential treatment optimization.

Xiao X, Ni X, Zhao Y et al. · BJU international · (2026) · View on PubMed ↗ · Free PDF ↗

Combined amivantamab, lazertinib, and bevacizumab in patients with EGFR-mutant advanced non-small-cell lung cancer with acquired resistance to a third-generation EGFR tyrosine-kinase inhibitor (ETOP 18-21 AMAZE-lung): a prospective, international, multicentre, single-arm, phase 2 trial.

This prospective, international, multicentre phase 2 trial studied combined amivantamab (EGFR/MET bispecific), lazertinib (third-generation EGFR TKI), and bevacizumab in adults with EGFR-mutant advanced non-small-cell lung cancer (NSCLC) who developed acquired resistance to a third-generation EGFR TKI. The regimen demonstrated clinically meaningful antitumor activity with a safety profile characterized in the trial cohort. The results provide a chemotherapy-sparing strategy targeting EGFR, MET, and angiogenesis pathways in a specific post–third-generation TKI resistance setting.

Soo RA, Popat S, Dafni U et al. · The Lancet. Respiratory medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Farletuzumab ecteribulin, a folate receptor alpha (FRα) antibody-drug conjugate, in select advanced cancers: An open-label, multicenter, phase 1/2 dose-finding study.

This open-label multicenter phase 1/2 dose-finding study evaluated farletuzumab ecteribulin (FZEC), a folate receptor alpha (FRα) antibody-drug conjugate, in adults with pretreated advanced solid tumors including ovarian cancer, endometrial cancer, triple-negative breast cancer, and NSCLC. The trial reported safety and antitumor activity across multiple dosing regimens (dose escalation and dose confirmation/optimization cohorts). Clinically, it supports further development of FRα-targeted antibody-drug conjugation in selected advanced cancers.

Wenham RM, Ray-Coquard I, Kristeleit R et al. · Gynecologic oncology · (2026) · View on PubMed ↗ · Free PDF ↗

MuSK agonistic antibody has therapeutic potential for MuSK antibody-positive myasthenia gravis.

This study investigated the therapeutic potential of a muscle-specific tyrosine kinase (MuSK) agonistic antibody in MuSK antibody-positive myasthenia gravis (MuSK-MG). The authors generated MuSK agonistic antibodies binding the Fz domain and showed they can recover MuSK signaling across varying levels of MuSK autoantibodies. These preclinical findings support MuSK agonism as a targeted strategy to counteract autoantibody-mediated disruption of neuromuscular junction function in MuSK-MG.

Yamamoto K, Uzawa A, Narazaki G et al. · Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · (2026) · View on PubMed ↗ · Free PDF ↗

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Cancer microenvironment, immune evasion & tumor resistance mechanisms

A non-canonical function of glutathione to suppress ferroptosis via FSP1.

This Cell study investigated how glutathione (GSH) suppresses ferroptosis independently of the canonical GPX4 pathway. Using genome-wide CRISPR-Cas9 screening, the authors identified ferroptosis suppressor protein 1 (FSP1) as the key mediator, showing that GSH enables FSP1 to generate reduced ubiquinone that scavenges oxidized lipids and blocks ferroptosis even in GPX4 knockout cells. The work reveals a non-canonical GSH–FSP1 axis that expands mechanistic targets for ferroptosis modulation.

Han J, Zhang YD, Liu S et al. · Cell · (2026) · View on PubMed ↗

Cancer competition for vitamin B2 creates metabolic checkpoint for T cell ferroptosis.

The study used the CareSLCs platform to define how tumor–T cell metabolic competition for vitamin B2 (VB2) regulates ferroptosis, focusing on the VB2 transporters SLC52A3 in T cells and SLC52A2 in tumors. It found that SLC52A3-mediated VB2 uptake is required for T cell antitumor immunity, and VB2 deficiency impairs mitochondrial respiration and glutathione regeneration, causing mitophagy, labile iron accumulation, lipid peroxidation, and T cell ferroptosis. The results identify a metabolic checkpoint in which tumors preferentially use SLC52A2 to outcompete T cells, suggesting transporter-targeted strategies to enhance immunotherapy.

Chen H, Li C, Ke Y et al. · Cell · (2026) · View on PubMed ↗

STING reprogramming by estrogen promotes neutrophil extracellular trap formation and sex-biased resistance to ADC therapy.

The study analyzed sex-biased responses to the CLDN18.2-targeted antibody-drug conjugate (ADC) in a phase II-like preclinical trial across 55 CLDN18.2+ pancreatic cancer patient-derived xenografts, testing estrogen signaling mechanisms. It found that estrogen acting through GPER1 reprograms tumor-intrinsic STING signaling from IRF3-driven interferon toward NF-κB activation, leading to CXCL1 secretion, neutrophil recruitment, and NET formation that restricts ADC access and drives female-biased resistance. This mechanistically links estrogen–GPER1–STING/NF-κB signaling to NET-mediated therapeutic resistance, highlighting sex-specific biology for ADC efficacy.

Yan J, Zhou T, Shi S et al. · Cell · (2026) · View on PubMed ↗

Biventricular vs conduction system pacing after atrioventricular node ablation for heart failure with atrial fibrillation: the CONDUCT-AF trial.

The CONDUCT-AF trial randomized patients with refractory atrial fibrillation and heart failure (LVEF <50%, QRS ≤120 ms, and elevated NT-proBNP) after atrioventricular node ablation to conduction system pacing (left bundle branch area pacing) versus biventricular pacing. The key finding was whether conduction system pacing was non-inferior to biventricular pacing for the trial’s primary outcome in this specific HF/AF population. Scientifically and clinically, it provides randomized evidence to guide device-pacing strategy after AV node ablation in patients with narrow QRS and reduced ejection fraction.

Žižek D, Ivanovski M, Mrak M et al. · European heart journal · (2026) · View on PubMed ↗

Multi-cell death gene signature predicts lung adenocarcinoma prognosis and reveals FURIN regulates ferroptosis via NRF2-xCT-GPX4 axis.

This study investigated lung adenocarcinoma (LUAD) prognosis using multi-cell death gene signatures derived from TCGA-LUAD, CPTAC, and GEO datasets and explored the mechanistic role of the proprotein convertase FURIN in ferroptosis regulation. The key finding was that FURIN promotes LUAD progression by regulating ferroptosis through the NRF2–xCT–GPX4 axis, supported by FURIN knockdown experiments in LUAD cell lines (HCC827, PC9, H460) with ferroptosis modulation using Ferrostatin-1. Scientifically, it identifies a prognostic gene signature and a FURIN–NRF2–xCT–GPX4 pathway that could be targeted to induce ferroptosis in LUAD.

Ning J, Xiao G, Wen S et al. · Respiratory research · (2026) · View on PubMed ↗ · Free PDF ↗

Global and specific mechanisms stimulate mistranslation in cancer.

The study investigated genetic control of tryptophan codon-specific mistranslation in cancer by screening for genes that regulate W>F codon reassignment (substitutants) under interferon-γ-mediated tryptophan shortage. The screen identified ADAR1 and FTSJ1 as key regulators of W>F substitutants, connecting RNA editing and tRNA anticodon methylation to cancer-associated mistranslation. This mechanistic link between immune-induced tryptophan limitation and specific translation errors may reveal new targets to modulate tumor proteostasis and immune escape.

Wernaart D, Fumagalli A, Adhikary M et al. · Nature cell biology · (2026) · View on PubMed ↗ · Free PDF ↗

Spit it out: rhoptry organelles in Plasmodium sporozoites.

This review examined rhoptry organelles in Plasmodium sporozoites, the malaria parasite stage transmitted from Anopheles mosquitoes to vertebrate hosts. It summarizes how genetic and imaging approaches have revealed rhoptry functions in host-cell invasion and the coordinated secretion of apical secretory organelles (micronemes and rhoptries). By clarifying rhoptry biology, the work informs future strategies to block sporozoite invasion and malaria transmission.

Bernard T, Silvie O, Marinach C · Trends in parasitology · (2026) · View on PubMed ↗

Preclinical and clinical outcomes in patients with high rheumatoid factor levels treated with TNF inhibitors:a systematic review.

This systematic review studied how rheumatoid factor (RF) binding to immunoglobulin Fc regions affects pharmacokinetics and clinical outcomes of tumor necrosis factor inhibitors (TNFis) in patients with rheumatoid arthritis. It evaluated RF binding mechanisms and the impact of RF levels on drug concentration and therapeutic response across TNFis with and without an Fc portion. The results are clinically significant for optimizing TNFi selection and anticipating reduced efficacy in RA patients with high RF.

Smolen J, Nikiphorou E, Pope J et al. · Annals of the rheumatic diseases · (2026) · View on PubMed ↗

PRTN3 drives immunosuppression in KRAS-mutant lung adenocarcinoma through proteolytic inactivation of CXCL9.

This study examined how PRTN3 promotes immunosuppression in KRAS-mutant lung adenocarcinoma by proteolytically inactivating CXCL9. Using integrated analyses of human LUAD cohorts, genetically engineered mouse models, tumor cell models, and patient-derived organoids, the authors used transcriptional profiling, chromatin immunoprecipitation, biochemical cleavage assays, and immune assays to define the PRTN3–CXCL9 axis. The results provide a mechanistic explanation for resistance to immune checkpoint blockade in KRAS-mutant LUAD and identify PRTN3 as a potential therapeutic target to restore antitumor immunity.

Liu Y, Zhang C, Li J et al. · Journal for immunotherapy of cancer · (2026) · View on PubMed ↗ · Free PDF ↗

Metabolic reprogramming and plasticity in breast Cancer: Mechanisms driving tumor progression, metastasis, and therapeutic resistance.

This narrative review synthesized evidence on metabolic reprogramming and plasticity in breast cancer, focusing on mechanisms that drive tumor progression, metastasis, and therapeutic resistance across major treatment modalities (endocrine therapy, HER2-targeted therapy, chemotherapy, and immunotherapy). It emphasizes that breast cancer cells adapt to nutrient limitation, hypoxia, oxidative stress, and drug pressure through dynamic metabolic switching beyond the classical Warburg effect. By mapping these pathways, the review supports metabolic vulnerabilities as potential targets to overcome resistance and limit metastatic progression.

Yuan J, Zhang H, Huang J et al. · Biochimica et biophysica acta. Reviews on cancer · (2026) · View on PubMed ↗

PLA1A Inhibition Enhances Chemoimmunotherapy Efficacy by Blocking Immunosuppressive Macrophage Polarization in Colorectal Cancer.

This colorectal cancer study investigated whether PLA1A inhibition can enhance neoadjuvant chemotherapy (NAC)-based chemoimmunotherapy by blocking immunosuppressive macrophage polarization, using paired tumor samples analyzed by single-cell RNA sequencing before and after NAC. The authors found that NAC reshaped the tumor immune microenvironment, with non-responders showing increased infiltration of immunosuppressive M2-like macrophages, and that PLA1A inhibition improved chemoimmunotherapy efficacy by interfering with this macrophage polarization program (key mechanistic and outcome details are truncated in the provided abstract). Scientifically, it identifies PLA1A as a potential therapeutic target to overcome NAC resistance by reprogramming the tumor immune microenvironment.

Wang TT, Kong WS, Li JJ et al. · Cancer research · (2026) · View on PubMed ↗

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Epigenetics, chromatin regulation & multi-omics atlases (incl. spatial/multi-omics methods)

Longer lipids mark aging and constrain lifespan.

This study used cross-species, multi-tissue lipidomics to examine how lipid remodeling changes with aging in mice, Caenorhabditis elegans, Drosophila, and humans. The authors found a conserved aging hallmark characterized by elongation of lipid acyl chains and depletion of shorter lipid species, with dietary restriction shortening cardiac lipids in mice. These results link ratiometric lipid remodeling to aging biology and suggest lipid-length trajectories as potential biomarkers and mechanistic constraints on lifespan.

Li W, Schomakers BV, Trętowicz MM et al. · Nature aging · (2026) · View on PubMed ↗

Chromatin accessibility trajectories reveal pre-cancerous epigenetic priming and an acid-driven immunotherapy-resistant gastric cancer subtype.

This Cancer Cell study used a large-scale chromatin accessibility atlas (650 multistage samples from 439 gastric cancer patients) to map epigenetic priming and define immunotherapy-relevant gastric cancer subtypes. The authors identified an epigenetically primed state in intestinal metaplasia that licenses later tumor initiation and stratified advanced cancers into three epigenomic subtypes, where proliferative and mesenchymal-inflammatory states were sensitive to neoadjuvant immunotherapy while a pseudo-gastric subtype was intrinsically resistant. These chromatin accessibility trajectories provide a framework for predicting immunotherapy response and for understanding stepwise gastric tumorigenesis.

Wang T, Xiang J, Tian S et al. · Cancer cell · (2026) · View on PubMed ↗

A spatiotemporal lifecycle atlas decodes spatial coordination in rice.

This Cell study constructed a spatiotemporal lifecycle atlas of rice by integrating high-resolution spatial transcriptomics, single-nucleus RNA sequencing, and a gap-free reference genome across 10 organs and 61 developmental stages. The atlas profiled 851,725 nuclei and 347,640 spatial bins, defining 119 cell types and 133 subtypes and reconstructing developmental trajectory graphs that link cell states from proembryo to mature organs. By identifying trajectory-associated regulators, the study provides a resource for deciphering how gene expression programs are coordinated across space and time during plant development.

Jing Y, Chen Q, Chen Y et al. · Cell · (2026) · View on PubMed ↗

Distinct chromatin landscapes dictate resident cardiac macrophage lifecycles and functions.

This study investigated how epigenetic regulation shapes resident cardiac macrophage subset lifecycles and functions in mice by mapping chromatin accessibility with bulk and single-cell ATAC-seq and integrating it with RNA-seq. The key finding was that two primary chromatin-accessibility-based cell states correspond to tissue residency, including a CCR2− macrophage chromatin-based state (and related subset-specific programs). These results provide mechanistic insight into how chromatin landscapes govern macrophage heterogeneity, informing potential epigenetic therapeutic targeting in cardiac disease.

Wong A, Vohra S, Ellis K et al. · Cardiovascular research · (2026) · View on PubMed ↗ · Free PDF ↗

Decline of chaperone-mediated autophagy in aging impairs macrophage clearance of senescent cells.

This work examined how age-related decline of chaperone-mediated autophagy (CMA) affects senescent cell properties and immune clearance by macrophages, using CMA-deficient cellular models. CMA deficiency promoted senescence with an aged-like secretory phenotype that inhibited macrophage CMA and impaired engulfment of senescent cells. The findings link reduced CMA to defective clearance of senescent cells during aging, suggesting CMA restoration as a potential anti-aging or senolytic-adjacent therapeutic direction.

Sereda R, Lindenau K, Diaz A et al. · Nature aging · (2026) · 1 citations · View on PubMed ↗ · Free PDF ↗

Decoding epithelial-mesenchymal transitions with multi-omics.

This review studied epithelial–mesenchymal transition (EMT) as a dynamic, heterogeneous cellular program across regulatory layers (transcriptome, epigenome, proteome, metabolome) using recent high-throughput single-cell and spatial multi-omics approaches in development, repair, ageing, cancer, and fibrosis. It finds that single-cell and spatially resolved multi-omics can systematically decode intermediate EMT states and cell-type-specific regulatory programs that were previously obscured by bulk averaging. These advances provide a scientific framework for mapping EMT trajectories and identifying actionable molecular drivers of EMT-associated disease.

Narwade N, Nieto MA · Nature reviews. Genetics · (2026) · View on PubMed ↗

Spatial transcriptomics reveals laminar and cell-type-specific A-to-I RNA editing signatures in the macaque cortex.

This study developed SRDRE, an analysis framework for calling ADAR-mediated A-to-I RNA editing sites in spatial transcriptomics, and applied it to over 40 million cells across 142 spatially annotated regions of the adult macaque cortex. It found laminar- and cell-type-specific RNA editing landscapes, with neuronal editing levels correlating with cortical hierarchy and parvalbumin neurons showing the highest editing activity in most regions. These findings provide a spatially resolved map of primate RNA editing that can inform how ADAR activity supports neuronal circuit function.

Chen C, Yang J, Zhu Z et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

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Cardiovascular–kidney–metabolic (CKM) syndrome & biological aging tools

A machine learning-derived aging index for risk stratification and mortality prediction in cardiovascular-kidney-metabolic syndrome: A retrospective cohort study.

The study developed a machine learning-derived aging index (CKMAI) tailored to cardiovascular–kidney–metabolic (CKM) syndrome pathways and evaluated it for mortality prediction and risk stratification. Using a retrospective NHANES cohort of 6,896 adults (2005–2018), it trained and selected among over 100 survival models using two-stage machine learning and Pareto front optimization. This provides a CKM-specific “biological age” tool that could improve identification of high-risk patients beyond existing generic aging indices.

Zhu Z, Ren K, Wang D et al. · PLoS medicine · (2026) · View on PubMed ↗

Adults with congenital heart disease: the growing impact of acquired cardiovascular risk factors on late mortality.

This retrospective analysis of 9,826 adults with congenital heart disease (ACHD) evaluated how acquired cardiovascular risk factors contribute to late all-cause mortality using Cox proportional hazards models. The key finding was that acquired cardiovascular risk factors were associated with increased late mortality risk in ACHD patients over the 2000–2024 follow-up period. Clinically, it supports aggressive management of modifiable risk factors in ACHD to improve long-term survival as these patients live longer.

Umei M, Diller GP, Brida M et al. · European heart journal · (2026) · View on PubMed ↗

Integrative characterization of human hepatocellular carcinoma-derived organoids and their HBV-associated biology.

This study established 20 patient-derived hepatocellular carcinoma (HCC) organoids and 12 patient-derived cell lines from 20 individuals and characterized them for HBV-associated biology using whole-exome sequencing, RNA sequencing, drug screening, and HBV-targeting PCR. The key finding was that transcriptomic and genomic profiling defined HBV-associated HCC features and molecular subgroups with distinct drug-response patterns across the organoid/cell-line models. Clinically, these HBV-focused organoid platforms can support mechanism-driven therapeutic testing and improved stratification of HBV-related HCC patients.

Kim SH, Choi YR, Choi EW et al. · Clinical and translational medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Kidney function decline, heart failure hospitalization, and the effect of empagliflozin in heart failure: an EMPEROR-pooled analysis.

This EMPEROR-pooled analysis examined longitudinal estimated glomerular filtration rate (eGFR) trajectories around heart failure (HF) events and tested whether empagliflozin modifies these changes in pooled data from EMPEROR-Reduced and EMPEROR-Preserved. The key finding was the temporal pattern of kidney function decline around HF-related events and the extent to which empagliflozin attenuated these eGFR changes. Clinically, it strengthens the mechanistic rationale for SGLT2 inhibition by linking event-related renal deterioration with treatment benefit in HF across preserved and reduced ejection fraction.

Kobayashi M, Duarte K, Baudry G et al. · European journal of heart failure · (2026) · View on PubMed ↗

Innovative holistic treatment for CKM: what lies ahead?

This article reviewed the cardiovascular-kidney-metabolic (CKM) syndrome framework and prevention strategy in humans, focusing on the AHA-defined five-stage model and the role of albuminuria and eGFR across stages. It highlights that visceral adiposity and insulin resistance accelerate CKM progression through interconnected inflammatory, oxidative, hemodynamic, and neurohormonal pathways, with albuminuria serving as both a kidney damage marker and an independent cardiovascular risk factor. The synthesis supports stage-specific, personalized prevention and treatment approaches for CKM syndrome rather than one-size-fits-all care.

Balfanz P, Marx N · European journal of internal medicine · (2026) · View on PubMed ↗ · Free PDF ↗

The Comorbidity-Driven Interleukin-6-Mediated Systemic Inflammation Hypothesis of Heart Failure With Preserved Ejection Fraction: A Decade of Testing Ends in Disappointment.

This article reviews and critically evaluates the comorbidity-driven interleukin-6 (IL-6) systemic inflammation hypothesis for heart failure with preserved ejection fraction (HFpEF) that was proposed in 2013, including proposed links to coronary microvascular disease and impaired NO–cGMP signaling. Across a decade of randomized controlled trials targeting the IL-6 pathway, the hypothesis has not translated into improved clinical outcomes, leading to a conclusion of “disappointment.” The negative trial record indicates that IL-6–mediated inflammation, as framed by the original causal model, is unlikely to be a sufficient therapeutic lever for HFpEF.

Packer M, Butler J, Zannad F et al. · Journal of cardiac failure · (2026) · View on PubMed ↗ · Free PDF ↗

Accelerated Biological Aging and Risk of Early-Onset Colorectal Cancer: Findings from a Large Prospective East Asian Cohort.

Using a large prospective East Asian cohort of 198,491 Korean adults under 50 years, this study estimated accelerated biological aging with Phenotypic Age (PhenoAge) derived from nine routine blood biomarkers and tested its association with early-onset colorectal adenocarcinoma (EOCRC-AC). Accelerated biological aging was linked to increased risk of EOCRC-AC compared with less accelerated aging. The findings suggest that blood-based biological age metrics could improve risk stratification for young-onset colorectal cancer beyond chronological age.

Chang Y, Kim K, Wild SH et al. · Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association · (2026) · View on PubMed ↗ · Free PDF ↗

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Vascular calcification & kidney/vascular mechanistic genetics

Transcription factor TBX2 is a key regulator of vascular calcification.

This study investigated TBX2 as a regulator of vascular calcification by combining cross-trait GWAS/phenome-wide association analyses with single-cell RNA-seq and ATAC-seq from human kidneys and coronary arteries, and validating direct transcriptional control using chromatin immunoprecipitation sequencing. TBX2 was identified as an upstream transcription factor driving vascular calcification programs, with functional relevance demonstrated in multiple gene-edited mouse models. The findings position TBX2 as a mechanistic target for preventing or treating vascular calcification, particularly in chronic kidney disease where risk is highest.

Li S, Liu H, Lee S et al. · European heart journal · (2026) · View on PubMed ↗

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Osteoporosis pathogenesis & personalized treatment (mechanism-based)

New insights into the pathogenesis of osteoporosis and the translational approach to personalized therapy.

This translational review analyzed osteoporosis pathogenesis as a heterogeneous syndrome and discussed how distinct subtypes (e.g., postmenopausal estrogen deficiency, age-related bone loss, anorexia nervosa, and GLP-1 receptor agonist-associated weight loss) show different bone turnover, fracture patterns, and treatment responses. It emphasizes bone marrow adipose tissue (BMAT) as a key regulator of the marrow microenvironment and links weight-loss states (including GLP-1 agonist–associated weight loss) to impaired bone via reduced mechanical loading and hormonal changes. The article supports personalized osteoporosis therapy based on underlying mechanism rather than treating osteoporosis as a single uniform disease.

Li B, Liu L, Luo E et al. · Best practice & research. Clinical rheumatology · (2026) · View on PubMed ↗

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Liver disease (MASLD/MASH/HCC/HDV/HBV) mechanisms & therapeutics

Intestinal epithelial GSK3β governs fumarate-dependent neutrophil reprogramming to promote colorectal cancer.

This Nature Cancer study investigated how intestinal epithelial glycogen synthase kinase-3β (GSK3β) regulates fumarate-dependent tumor-infiltrating neutrophil (TIN) reprogramming in mouse models of colorectal cancer using multiomics profiling. Intestinal epithelial GSK3β promoted polarization toward T3 neutrophils that express FTH1 and PD-L1, conferring ferroptosis resistance and immune evasion through a nuclear GSK3β–H1FX–USP43 axis that increases chromatin accessibility for glycolytic gene transcription. The work identifies an intestinal epithelial GSK3β–fumarate–neutrophil pathway as a mechanistic driver of colorectal cancer progression and therapeutic resistance.

He XS, Yang XQ, Wan S et al. · Nature cancer · (2026) · View on PubMed ↗

Trends in Hepatitis D Virus Prevalence Among HBsAg-Positive Individuals With and Without HIV in Italy: A Converging Epidemiology.

This study assessed trends in hepatitis D virus (HDV) prevalence among HBsAg-positive individuals in Italy by comparing anti-HDV prevalence in people with HIV (PWH) from the ICONA cohort (2009–2012 vs 2019–2023) with HIV-negative HBsAg-positive individuals from the MASTER and PITER cohorts. The key finding was a decline in anti-HDV prevalence among PWH over time, converging toward the prevalence observed in HIV-negative individuals, alongside marked reductions in injection drug use among PWH. Epidemiologically, it suggests that HIV status is no longer as strong a marker of HDV risk in contemporary Italy, informing targeted screening policies.

Puoti M, Tavelli A, Brancaccio G et al. · Liver international : official journal of the International Association for the Study of the Liver · (2026) · View on PubMed ↗ · Free PDF ↗

Effects of MASH risk genotypes on resmetirom efficacy in patients with MASH and fibrosis.

This study evaluated whether MASLD risk genotypes in PNPLA3, HSD17B13, TM6SF2, MTARC1, MBOAT7, and SERPINA1 modify baseline features and treatment response to resmetirom versus placebo in patients with non-cirrhotic MASH and fibrosis. Resmetirom improved MASH and liver fibrosis outcomes measured with MRI-proton density fat fraction (MRI-PDFF) and other biomarkers, with genotype-associated differences in efficacy signals across risk groups. These findings support using MASLD genetic risk stratification to refine expectations for resmetirom benefit in genetically heterogeneous MASH populations.

Chalasani NP, Taub R, Mogg R et al. · Journal of hepatology · (2026) · View on PubMed ↗ · Free PDF ↗

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Autoimmunity & immune modulation (incl. transplant, cGVHD, SLE, autoimmune CAR-T)

EFFICACY AND SAFETY OF ADVANCED THERAPIES AS INDUCTION THERAPY FOR ULCERATIVE COLITIS: AN UPDATED SYSTEMATIC REVIEW AND NETWORK META-ANALYSIS.

This updated systematic review and network meta-analysis compared advanced therapies (ATs) used as induction treatment for moderate-to-severe ulcerative colitis in phase 3 randomized controlled trials. Across included late-stage agents, the network meta-analysis synthesized relative efficacy and safety using frequentist random-effects models, enabling indirect comparisons among multiple ATs. Clinically, the results help rank induction options for UC when head-to-head trials are limited, supporting evidence-based selection of therapies.

Olivera PA, Lasa JS, Singh S et al. · Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association · (2026) · View on PubMed ↗

Induced regulatory B cells stably expressing interleukin-10 reverse central nervous system autoimmunity by targeting myeloid cells.

This Immunity study screened pharmacological compounds to induce IL-10 expression in B cells and identified compound N6 as a driver of stable IL-10+ B cell generation in vitro. Transfer of N6-induced IL-10+ B cells induced remission of experimental autoimmune encephalomyelitis and promoted CNS accumulation and differentiation into IL-10+ plasma cells that reshaped myeloid-cell transcriptional and phenotypic programs. The findings provide a tractable strategy to generate regulatory B cells at high frequency and demonstrate a mechanistic route to reverse central nervous system autoimmunity via IL-10–mediated myeloid targeting.

Manfroi B, Dang VD, Cuc BT et al. · Immunity · (2026) · View on PubMed ↗

Sitagliptin for Acute Graft-Versus-Host Disease Prevention in Alternative Donor Transplantation: A Randomized Phase III Trial.

This randomized phase III trial studied whether adding sitagliptin to antithymocyte globulin (ATG)-based prophylaxis reduces acute graft-versus-host disease (aGVHD) in adults (18–60 years) with hematologic malignancies undergoing myeloablative haploidentical or unrelated donor hematopoietic stem-cell transplantation. The intervention compared ATG + calcineurin inhibitor + methotrexate + mycophenolate mofetil with or without sitagliptin 600 mg orally every 12 hours from days -1 to +14. If effective, this would support a readily available pharmacologic strategy to improve outcomes after alternative donor transplantation.

Qiao M, Zhou B, Chen Y et al. · Journal of clinical oncology : official journal of the American Society of Clinical Oncology · (2026) · View on PubMed ↗

Delisting Strategies in Highly Sensitised Kidney Transplant Candidates.

This review evaluated HLA antigen delisting strategies in highly sensitised kidney transplant candidates, focusing on removing selected HLA antigens from the unacceptable antigen list to increase transplant opportunities. The key finding is that delisting—targeting less immunogenic antigens and lower-risk donor-specific antibodies (DSA) in a stepwise manner—can expand access for patients with poor allocation prospects. Clinically, it supports an emerging approach to improve transplant feasibility while managing immunologic risk in broadly sensitised patients.

D’Angelo M, Zahradka I, Jaklova K et al. · Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · (2026) · View on PubMed ↗ · Free PDF ↗

Efficacy and safety of the ROCK2-inhibitor belumosudil for chronic GVHD: results from a multicenter retrospective analysis of a large German-Austrian cohort of the belumosudil MAP.

This multicenter retrospective analysis studied the efficacy and safety of the selective ROCK2 inhibitor belumosudil in 144 German/Austrian patients with predominantly severe chronic graft-versus-host disease (cGVHD) after failure of corticosteroids and ruxolitinib, treated via a belumosudil managed-access program (MAP). The key finding was that belumosudil showed clinically meaningful outcomes in this heavily pretreated cohort (median of four prior therapies), supporting its real-world effectiveness and tolerability. Clinically, the results help define the post–steroid/ruxolitinib treatment role of ROCK2 inhibition for cGVHD in European practice.

Holtick U, Sala E, Egger-Heidrich K et al. · Bone marrow transplantation · (2026) · View on PubMed ↗

Belimumab prevention against organ damage over 8 years and safety up to 13 years: three pooled open-label, long-term extension SLE studies.

This post hoc pooled analysis evaluated long-term glucocorticoid use, safety, and organ damage accrual in 1304 patients with systemic lupus erythematosus (SLE) treated with open-label belimumab 10 mg/kg IV every 28 days plus standard therapy across three long-term extension studies (BEL112233, BEL112234, BEL112626). Belimumab treatment was associated with reduced long-term organ damage accrual over up to 8 years and acceptable safety through up to 13 years, with effects assessed alongside cumulative medication use including glucocorticoids. These findings support belimumab as a long-term disease-modifying option in SLE with potential to limit organ damage while maintaining a manageable safety profile.

Touma Z, Arriens C, Tektonidou MG et al. · Lupus science & medicine · (2026) · View on PubMed ↗ · Free PDF ↗

TDP-43 and ALS - what’s wrong with my membranes?

This mechanistic review focused on how dysfunction of the TDP-43 RNA/DNA-binding protein relates to amyotrophic lateral sclerosis (ALS), where ~97% of patients show TDP-43 abnormalities in affected neurons. It highlights that loss of nuclear TDP-43 can lead to organelle membrane defects (e.g., Golgi apparatus abnormalities) rather than cytosolic TDP-43 aggregation in certain vulnerable neurons such as Betz cells. The work reframes ALS pathology toward membrane/organellar dysfunction downstream of TDP-43 mislocalization, suggesting new targets beyond classical aggregation-centric models.

Dahlhaus R, Yalcin I, Tischer J et al. · Neurobiology of disease · (2026) · View on PubMed ↗ · Free PDF ↗

Induction of mucosal healing by biologics is topographically comparable in proximal and distal small bowel Crohn’s disease.

This pooled analysis compared biologic treatment responses in proximal versus distal small bowel Crohn’s disease by using video capsule endoscopy (VCE) to map mucosal inflammation topography. Across three prospective cohorts of patients initiating or optimizing biologic therapy, induction mucosal healing measured by Lewis score (LS≥135) was broadly comparable between proximal and distal small bowel segments at end-of-induction (14–26 weeks) and at 1 year. Clinically, this supports that biologic efficacy for mucosal healing is not strongly dependent on whether inflammation predominates proximally or distally within the small intestine.

Ukashi O, Kopylov U, Ungar B et al. · Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association · (2026) · View on PubMed ↗

CAR T cells for autoimmune diseases: 2026 update of the EBMT-ISCT-JACIE practice harmonisation and consensus recommendations.

This 2026 EBMT-ISCT-JACIE practice harmonisation and consensus update reviewed evidence and produced recommendations on using chimeric antigen receptor (CAR) T cells for patients with severe, refractory autoimmune diseases. The key conclusion was that CAR T-cell therapy can be considered for selected autoimmune indications with standardized patient selection, manufacturing/quality, and toxicity management frameworks. Clinically, the consensus aims to improve safety and consistency of CAR T-cell delivery across centers treating autoimmune disease.

Greco R, Müller F, Haghikia A et al. · The Lancet. Rheumatology · (2026) · View on PubMed ↗

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Neurodegeneration & neurobiology (ALS/TDP-43, Parkinson, Alzheimer, glioblastoma, pain circuits)

SOD1 co-pathologies in the brain: insights from neuropathological evidence and implications.

This review synthesized neuropathological evidence on SOD1 (superoxide dismutase 1) co-pathologies across human brain neurodegenerative diseases. It emphasized associations between pathological SOD1 species and other aggregation-prone proteins including TDP-43, tau, alpha-synuclein, and amyloid-β, summarizing how SOD1 pathology distributes across conditions. The significance is that it reframes SOD1 as a broader co-pathology contributor beyond ALS and supports more integrated models of protein aggregation in neurodegeneration.

de Azevedo EM, Bernardo VS, Lima MMS et al. · Acta neuropathologica · (2026) · View on PubMed ↗

Cognitive impairment in Parkinson disease correlates with loss of cholinergic axon projections to cortex in an autopsy study.

This autopsy study examined 37 Parkinson disease cases to test whether cognitive impairment correlates with loss of cholinergic axon projections from the nucleus basalis of Meynert to neocortical regions, using choline acetyltransferase (ChAT) levels as a marker. Mean neocortical ChAT levels measured by sandwich ELISA showed a positive correlation with global cognitive impairment (Mini-Mental State Examination score). The results support a mechanistic link between cortical cholinergic degeneration and dementia severity in Parkinson disease, informing biomarker and therapeutic targeting of the cholinergic system.

Miller R, O’Shea J, Rosok LM et al. · Alzheimer’s & dementia : the journal of the Alzheimer’s Association · (2026) · View on PubMed ↗ · Free PDF ↗

Clusterin is enriched in plaque-associated astrocytes and localizes to synapses in Alzheimer’s disease.

This study investigated the cellular and synaptic localization of the Alzheimer’s disease risk gene clusterin (CLU) in human brain, using newly generated monoclonal antibodies that distinguish secreted versus intracellular clusterin. The key finding was that clusterin is enriched in plaque-associated astrocytes and localizes to synapses in Alzheimer’s disease. Scientifically, this provides improved tools and evidence that clusterin may participate in AD synapse and plaque biology, supporting its continued development as a biomarker and therapeutic target.

Byrne RAJ, Veteleanu A, Cramp HL et al. · Alzheimer’s & dementia : the journal of the Alzheimer’s Association · (2026) · View on PubMed ↗ · Free PDF ↗

TBK1 eliminates aggregation-prone monomeric TDP-43 through an IFNβ-immunoproteasome pathway in ALS models.

The authors studied how TBK1 (TANK-binding kinase 1) clears aggregation-prone monomeric TDP-43 in ALS models via an IFNβ-immunoproteasome pathway. TBK1 was activated by physical association with aggregation-prone monomeric TDP-43, induced IFNβ expression, and upregulated the immunoproteasome to promote degradation of TDP-43, alleviating TDP-43 pathology in neuronal cells. This identifies a TBK1–IFNβ–immunoproteasome proteostatic axis as a potential therapeutic target for TDP-43 proteinopathies.

Sakai S, Oiwa K, Iguchi Y et al. · EMBO reports · (2026) · View on PubMed ↗ · Free PDF ↗

Sensory plasticity of dorsal horn silent neurons as a critical mechanism for neuropathic pain.

This study used two-photon calcium imaging in mice to test how spinal cord dorsal horn (DH) sensory processing reorganizes after nerve injury or disinhibition to produce neuropathic touch-evoked pain. It found that disinhibition/nerve injury converts most DH excitatory neurons into highly polymodal cells and unmasks a previously uncharacterized sensory-to-nociceptive circuit mechanism. The work identifies a cellular basis for neuropathic pain and highlights DH excitatory plasticity as a critical therapeutic target.

Negm A, Gabrielli F, Zbili M et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Astrocytic PI3Kα controls synaptic plasticity and cognitive function via serine metabolism.

This study examined how astrocytic PI3Kα (p110α) regulates synaptic plasticity and cognition through serine metabolism by deleting the p110α isoform in hippocampal astrocytes. It found that p110α deletion impairs NMDA receptor activation during hippocampal long-term potentiation (LTP), and that the deficit is rescued by D-serine or L-serine, indicating PI3K controls synaptic plasticity via serine availability. Scientifically, it links astrocytic PI3K signaling to neurotransmitter co-agonist metabolism as a mechanism for learning and memory.

Fernández-Rodrigo A, García-Vilela C, Eraso-Pichot A et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

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Infectious disease & host–pathogen interactions (malaria, TB, microbiome, CRISPR in bacteria, pneumococcal carriage)

Acquisition of novel arrays via horizontal gene transfer rewires CRISPR-mediated defense in Pseudomonas aeruginosa.

This study investigated the type I-F CRISPR-Cas system in the bacterium Pseudomonas aeruginosa ATCC 10145 and characterized its CRISPR arrays, including a novel isolated array (CRISPR3) located ~1.3 million bp from the cas operon. The authors found that acquisition of a horizontally transferred CRISPR array can rewire CRISPR-mediated defense by changing how the cas system and multiple arrays function together for adaptive immunity. These findings expand mechanistic understanding of how horizontal gene transfer can rapidly reshape bacterial CRISPR immunity and influence the evolution of phage resistance in P. aeruginosa.

Malaluan RPP, Dy RLV · Journal of bacteriology · (2026) · View on PubMed ↗ · Free PDF ↗

Hidden burden of pneumococcal colonization in adults with viral respiratory infections: the role of influenza and RSV.

This prospective emergency-department study investigated pneumococcal colonization frequency, associated factors, and serotype distribution in adults with confirmed viral respiratory infections—influenza A virus (IAV), SARS-CoV-2, or respiratory syncytial virus (RSV)—using nasopharyngeal RT-PCR targeting the lytA and piaB genes. The key finding was that pneumococcal colonization burden increased in the setting of specific viral infections compared with virus-negative controls, with a distinct serotype distribution. Clinically, it highlights a hidden reservoir of pneumococcal carriage during influenza/RSV/SARS-CoV-2 seasons that may influence secondary bacterial infection risk and prevention strategies.

España-Bonilla R, Calvo-Silveria S, González-Díaz A et al. · Frontiers in cellular and infection microbiology · (2026) · View on PubMed ↗ · Free PDF ↗

Source-specific priming of lung NK cells by Pseudomonas LPS enhances resistance to bacterial pneumonia.

This study examined how age-associated mucosal innate immunity changes by testing whether source-specific priming of lung NK cells by Pseudomonas LPS enhances resistance to bacterial pneumonia in murine models. It found that intratracheal low-dose Pseudomonas aeruginosa LPS protected against bacterial pneumonia via a microbiota-dependent mechanism, whereas E. coli LPS did not, and that the protective effect involved innate immune priming rather than adaptive immunity. Scientifically and potentially clinically, it suggests a pathway by which specific microbial components can tune NK-cell–mediated defense in the aging lung.

Yang X, Liu H, Xu Q et al. · Signal transduction and targeted therapy · (2026) · View on PubMed ↗ · Free PDF ↗

Mycobacterium tuberculosis gene expression dynamics in host environments with single-cell resolution.

This study developed a dual-fluorophore Mycobacterium tuberculosis (Mtb) reporter system to visualize spatiotemporal Mtb gene expression in infected human macrophages at single-cell resolution. Using reporters for ESX-1 secretion system components, the authors found substantial heterogeneity in Mtb promoter activity within and between macrophages, and linked altered expression patterns to PDIM deficiency and macrophage loss of ATG14. Scientifically, the approach enables mechanistic mapping of how host environments regulate specific Mtb gene programs, informing targets for tuberculosis intervention.

Aylan B, Botella L, Santucci P et al. · Cell reports methods · (2026) · View on PubMed ↗ · Free PDF ↗

Within-host evolution and transmission of a human gut symbiont across ecological scales.

This study quantified within-host evolution and between-host transmission of a human gut symbiont by tracking ~70,000 genomically barcoded lineages of Bacteroides thetaiotaomicron across co-housed mice. Adaptive mutations spread between hosts despite colonization resistance from resident Bt strains, and daily transmission rates varied by more than 10-fold across hosts while shared selection pressures drove predictable engraftment. The results clarify how ecological context and dispersal shape microbial evolution and transmission dynamics relevant to microbiome stability.

Vasquez KS, Wong DPGH, Kotaka K et al. · Cell host & microbe · (2026) · View on PubMed ↗

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Metabolism, diet, microbiome & obesity/diabetes interventions

Ebselen restores mitochondrial function through metabolic rewiring in Barth syndrome and related mitochondrial diseases.

This study evaluated ebselen (EBS) as a therapeutic candidate for Barth syndrome and related mitochondrial diseases, beginning with a phenotypic drug screen in a yeast model of cardiolipin-maturation deficiency. Ebselen improved oxidative phosphorylation-dependent growth across multiple mitochondrial disease models and was validated in patient-derived fibroblasts, iPSC-derived cardiomyocytes, and a cardiolipin-deficient mouse model (details truncated in the abstract). If translatable, ebselen could represent a repurposable small molecule to restore mitochondrial function in cardiolipin-related disorders.

Almyre C, Cayer AL, Bounaix N et al. · EMBO molecular medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Metabolic and neural responses to ultraprocessed foods: a randomized, controlled, crossover study.

In a randomized, controlled, crossover study of 57 healthy-weight adults, participants consumed nutritionally matched ultraprocessed food (UPF) versus non-UPF meals to assess post-ingestive metabolic and brain responses. UPF meals produced greater insulinaemic and energetic responses with attenuated carbohydrate oxidation compared with non-UPF meals. These findings support a processing-dependent mechanism for UPF-associated metabolic risk that could inform dietary guidance and mechanistic research.

Hutelin Z, Ahrens M, Baugh ME et al. · Nature metabolism · (2026) · 1 citations · View on PubMed ↗ · Free PDF ↗

Bidirectional Pharmacology of GIP Receptor Targeting in Obesity: Historical Foundations, Mechanistic Divergence, and Translational Boundaries.

This structured narrative review examined the “bidirectional pharmacology” of glucose-dependent insulinotropic polypeptide receptor (GIPR) targeting in obesity, contrasting GIPR agonism versus GIPR antagonism and their ability to lower body weight and interact with GLP-1 receptor (GLP-1R) agonism. It summarizes mechanistic divergence across preclinical and translational studies and delineates translational boundaries relevant to clinical development. The review frames how different GIPR modulation strategies can converge on weight loss, guiding rational selection and interpretation of next-generation anti-obesity therapies.

Liu C, Wang Y, Liu J et al. · Peptides · (2026) · View on PubMed ↗

Caloric restriction mimetics rewire the AMPK-mTOR-ULK1 signaling nexus to restore autophagic proteostasis in the aging brain.

This preclinical study investigated how caloric restriction mimetics (CRMs)—including rapamycin, metformin, resveratrol, and spermidine—affect the AMPK–mTOR–ULK1 signaling axis to restore autophagic proteostasis in the aging brain. The CRMs were reported to activate AMPK while suppressing mTORC1, thereby relieving ULK1 inhibition and promoting autophagosome nucleation to improve proteostasis. These findings support CRMs as mechanistically grounded candidates for mitigating age-related neurodegenerative protein accumulation via autophagy pathway reprogramming.

Al-Jehani H, Al-Kuraishy HM, Abdelaziz AM et al. · Molecular and cellular neurosciences · (2026) · View on PubMed ↗

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Respiratory/allergy & airway immunity (OSA, NK priming, SLIT)

Efficacy of acupuncture for tinnitus with anxiety: a systematic review and meta-analysis.

This systematic review and meta-analysis evaluated acupuncture for tinnitus with anxiety in human participants across randomized studies identified from nine databases up to January 15, 2026. Acupuncture was reported to improve tinnitus symptoms and reduce tinnitus-associated anxiety, with the analysis synthesizing comparative effect sizes across included trials. These findings support acupuncture as a potential non-pharmacologic option for patients with tinnitus complicated by anxiety, while also motivating better-designed trials to clarify the relationship between symptom and anxiety improvements.

Peiyun W, Shuaihui Q, Yi C et al. · Frontiers in neurology · (2026) · View on PubMed ↗

World Allergy Organization Sublingual Immunotherapy Position Paper: 2026 update: Global expert consensus on efficacy, safety, disease modification, and implementation.

This World Allergy Organization (WAO) position paper updated global consensus on sublingual immunotherapy (SLIT) using a structured Delphi methodology with an international expert panel. The key finding is an evidence-based, harmonized framework for SLIT efficacy, safety, disease modification, and implementation across healthcare settings. Clinically, it standardizes guidance for appropriate SLIT use in IgE-mediated allergic diseases such as allergic rhinitis and allergic asthma.

Canonica GW, Morais-Almeida M, Di Bona D et al. · The World Allergy Organization journal · (2026) · 1 citations · View on PubMed ↗ · Free PDF ↗

Associations between obstructive sleep apnea and Alzheimer’s disease-related biomarkers (amyloid-β and tau) in blood and cerebrospinal fluid: a systematic review and meta-analysis.

This systematic review and meta-analysis assessed whether obstructive sleep apnea (OSA) is associated with Alzheimer’s disease biomarkers—amyloid-β (Aβ40/Aβ42/total Aβ) and tau (total tau and phosphorylated tau)—measured in blood and cerebrospinal fluid in OSA versus non-OSA adults. Across included studies, the key finding was the pooled relationship between OSA status and AD-related biomarker levels in both peripheral blood and CSF using random-effects models. Scientifically, it clarifies whether OSA may contribute to AD pathophysiology detectable via Aβ/tau biology, informing risk stratification and potential biomarker-guided interventions.

Wang J, Che L, Su R et al. · Frontiers in neurology · (2026) · View on PubMed ↗ · Free PDF ↗

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Reproductive biology & germline development

DND1-NANOS3 shapes the PGC transcriptome via a heptanucleotide sequence in mRNA 3’ UTRs.

This work investigated how the RNA-binding proteins DND1 and NANOS3 cooperate to shape the primordial germ-cell (PGC) transcriptome by repressing mRNAs through a specific heptanucleotide motif in 3’ UTRs. The authors showed that a DND1–NANOS3 complex jointly represses dozens of epigenome and cell-cycle regulator mRNAs by recognizing the AUGAAUU heptamer, and that genome editing of this element relieved repression of CDK1 in vivo. These findings define a “two-factor authorization” mechanism that explains how DND1 and NANOS3 coordinate PGC survival and cell-cycle control.

Suzawa M, Qiu C, Polash AH et al. · Molecular cell · (2026) · View on PubMed ↗ · Free PDF ↗

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Translational methods & computational biology/biomarkers (imaging, radiomics, cfDNA, variant prioritization, CRISPR screens)

SPARCS enables scalable recovery of complex image-based phenotypes for genetic screening.

The study developed SPARCS, a spatially resolved CRISPR screening platform using automated laser microdissection to perform genome-wide CRISPR knockout screens in single-cell image phenotypes in cultured cells. SPARCS physically isolates mutant cells in situ and enables scalable multimodal hit phenotyping, demonstrated for autophagosome formation screens. This provides a practical route to connect genotype to complex, microscopy-derived phenotypes at genome scale, supporting discovery of genes controlling cellular image-based processes.

Schmacke NA, Mädler SC, Wallmann G et al. · Cell · (2026) · View on PubMed ↗

Global Disparities in the Availability and Reimbursement of Systemic Therapies for Renal Cell Carcinoma: Results of the International ARON-AID Survey.

This cross-sectional international survey assessed availability and reimbursement of 20 innovative systemic therapies for renal cell carcinoma (RCC) across 58 countries, based on responses from 144 clinicians. The key finding was that systemic therapy access and reimbursement are uneven globally and are associated with national economic indicators such as income level and GDP. This highlights a real-world barrier to equitable RCC care and can guide policy and funding strategies to reduce disparities in access to new treatments.

Urun Y, Sridharan K, Zgura A et al. · The oncologist · (2026) · View on PubMed ↗ · Free PDF ↗

Lipid Burden and Efficacy of Preventive PCI of Vulnerable Atherosclerotic Coronary Plaques: Post Hoc Analysis From the PREVENT Trial.

This post hoc analysis of the PREVENT trial evaluated whether near-infrared spectroscopy (NIRS)-derived lipid core burden index identifies high-risk atherosclerotic plaques that benefit from preventive percutaneous coronary intervention (PCI) versus optimal medical therapy. The key finding was that plaque lipid burden (via the lipid core burden index) can stratify which non-flow-limiting, functionally insignificant lesions (FFR >0.80) are more likely to derive benefit from preventive PCI. Scientifically and clinically, it supports using NIRS lipid metrics to personalize preventive PCI decisions and improve event reduction strategies.

Wee SB, Ahn JM, Kang DY et al. · Circulation · (2026) · View on PubMed ↗

Chemical synchronization using household bleach can affect development, behavior and lifespan in Caenorhabditis elegans.

This experimental study tested whether chemical synchronization using household bleach affects development, behavior, and lifespan in the nematode Caenorhabditis elegans compared with worms obtained by picking laid eggs. The key finding was that bleach-based chemical synchronization altered phenotypes, including reductions in at least some measured traits (with effects extending beyond embryonic stages). This is significant for experimental design because it shows that a commonly used synchronization method can introduce biological differences that may confound “unbiased” phenotype comparisons.

Kim SH, Ahnn J, Kim HS et al. · Animal cells and systems · (2026) · View on PubMed ↗ · Free PDF ↗

Oral small-molecule GLP-1RA safiglipron versus dapagliflozin in type 2 diabetes: a randomized, double-blind, active-comparator-controlled phase 3 trial.

This phase 3 randomized, double-blind, double-dummy trial in 810 Chinese adults with type 2 diabetes compared oral small-molecule GLP-1 receptor agonist safiglipron (30/60/90 mg) versus the active comparator dapagliflozin 10 mg over 32 weeks, with a 20-week active-treatment extension. Safiglipron was evaluated for efficacy and safety versus dapagliflozin on the primary endpoint (treatment differences versus dapagliflozin were reported but truncated in the abstract). If safiglipron demonstrates superior or non-inferior glycemic efficacy with acceptable tolerability, it would support an oral GLP-1RA alternative to SGLT2 inhibition for type 2 diabetes management.

Guo L, Yu D, Xu Y et al. · Nature medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Global and regional reference curves for pain across the lifespan in 6.1 million individuals in 118 countries.

This study harmonized self-reported pain data from 6,125,459 participants across 902 population-based sources in 118 countries to generate global and regional pain reference curves across the lifespan. Pain prevalence varied widely by site (e.g., ~2% for facial pain to ~40% for back pain) and was consistently higher in women across 11 anatomical sites. These reference trajectories enable standardized benchmarking of external datasets and improve comparability of pain burden estimates across regions, sexes, and ages.

Fillingim M, Tanguay-Sabourin C, Neuert L et al. · Nature medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Discovery and engineering of avian R2 retrotransposons for all-RNA-mediated targeted DNA integration in human cells.

Researchers discovered and engineered avian R2 retrotransposons to enable all-RNA-mediated targeted DNA integration in human cells, starting from 1,139 avian genomes and characterizing 159 R2 elements. Engineered R2 variants achieved up to ~60% site-specific gene integration in human primary cells. This expands the R2 toolkit and provides a new all-RNA genome-editing strategy that could simplify targeted DNA insertion in therapeutic research.

Chen Y, Hu Y, Luo S et al. · Nature biotechnology · (2026) · View on PubMed ↗

A heritability-optimized method for functional prioritization of rare coding variants in complex traits.

The authors developed RovHer, a heritability-optimized computational method to prioritize rare coding variants by estimating each variant’s probability of being functional using exome-wide association statistics across 4,927,334 rare variants. In UK Biobank European individuals (up to 357,086) across 21 complex traits, RovHer integrated 75 variant- and gene-level features using multivariate adaptive regression splines to improve functional inference (details truncated in the abstract). This provides a more trait-relevant way to prioritize rare missense variants for downstream biology and variant interpretation in complex diseases.

Pang K, Pathan N, Le A et al. · Nature genetics · (2026) · View on PubMed ↗ · Free PDF ↗

Multimodal radiopathomics model predicts postoperative metachronous liver metastasis in gastric cancer.

This study developed and validated the Radiopathomics-Clinical Stratification Assessment (RCSA) model to predict postoperative metachronous liver metastasis in patients with locally advanced gastric cancer using preoperative CT radiomics, routine H&E pathomics, and clinical variables. The key finding was that RCSA consistently stratified risk across multiple validation settings (internal, external, public, and a prospective trial cohort, NCT02555358). Clinically, it offers an interpretable, multimodal tool to identify patients at high risk for later liver metastasis after apparently curative surgery.

Ding P, Yang J, Guo H et al. · Nature communications · (2026) · 1 citations · View on PubMed ↗ · Free PDF ↗

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Musculoskeletal pain & rehabilitation personalization

Personalizing rehabilitation approaches: Moderator analyses of manual therapy and exercise effectiveness in individuals with chronic neck pain: Secondary analysis of the SS-MECH trial.

This secondary analysis of the SS-MECH trial studied whether baseline characteristics moderated differential improvement with manual therapy (MT) versus exercise (EX) in 124 individuals with chronic neck pain at 4 weeks and 6 months. Using linear regression product-term interaction models and the Johnson–Newman technique, the authors tested 18 candidate moderators for pain interference and pain outcomes. The goal is to personalize rehabilitation by identifying which patients are more likely to benefit from MT versus EX.

Cook CE, McDevitt A, Clewley D et al. · Musculoskeletal science & practice · (2026) · View on PubMed ↗

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Hematology/oncology supportive care & device/clinical management (GVHD prophylaxis, pacing, reirradiation, ciliary assembly)

DNAAF19-RUVBL1/2 complex recruits multiple adaptors to promote dynein arm assembly.

The study investigated how the DNAAF19–RUVBL1/2 complex recruits multiple adaptor proteins to promote dynein arm assembly in motile cilia, aiming to clarify a molecular step in the dynein axonemal assembly pathway relevant to primary ciliary dyskinesia. It found that DNAAF19-RUVBL1/2 functions as a hub that coordinates adaptor recruitment to enable timely, ordered dynein arm assembly. These mechanistic insights advance understanding of ciliary biogenesis defects and can inform targeted approaches for primary ciliary dyskinesia.

de Almeida Gomes M, Wood E, Burgoyne T et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗

Clinical Implications of Preoperative Thoracic Spine Magnetic Resonance Imaging for Percutaneous Spinal Cord Stimulation Procedures: A Large Retrospective Cohort Study.

This large retrospective cohort study assessed the clinical implications of preoperative thoracic spine MRI for percutaneous spinal cord stimulation (SCS) lead placement in patients with persistent spinal pain syndrome (PSPS) type II. It examined how routine MRI findings influenced procedural planning and outcomes in patients scheduled for thoracic percutaneous SCS lead placement at a single center between January 2020 and March 2023. The significance is that it evaluates whether preoperative imaging meaningfully changes clinical decision-making and safety for thoracic SCS implantation.

Oldenbeuving G, Schel-Huisman MCM, Vos JS et al. · Pain practice : the official journal of World Institute of Pain · (2026) · View on PubMed ↗

Reirradiation of recurrent brain tumors: a review by the ESTRO CNS Focus Group.

This non-systematic ESTRO CNS Focus Group review evaluated evidence for reirradiation in patients with recurrent CNS tumors excluding gliomas, including meningiomas, ependymomas, brain metastases, and pituitary neuroendocrine tumors, and addressed radiation necrosis management and safety considerations. The review synthesizes available data on patient selection, fractionation, and technical approaches to support pragmatic clinical decision-making for CNS reirradiation. Clinically, it helps standardize how to choose candidates and plan reirradiation to balance tumor control against toxicity risk in neuro-oncology.

De Pietro R, Clerici E, Harat M et al. · Clinical and translational radiation oncology · (2027) · View on PubMed ↗ · Free PDF ↗

Fragmentation patterns of human telomeric chromatin in plasma cfDNA.

This study examined how telomeric chromatin is represented in circulating plasma cell-free DNA (cfDNA) by mapping telomeric 6-mer (TTAGGG/CCCTAA) fragmentation patterns and subnucleosomal footprints. It found that cfDNA telomeric sequences carry distinct cleavage-derived footprints from the C-rich strand and show a telomeric nucleosome repeat length of ~145 bp (vs ~170 bp genome-wide), with telomeric footprint abundance decreasing with age. Scientifically, the work establishes telomere-specific cfDNA fragmentation signatures as a potential noninvasive readout of telomeric chromatin structure and age-associated changes.

Buck B, Weirich A, Eramo S et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Multiple overlapping SNARE complexes drive endosome maturation in Drosophila nephrocytes.

This in vivo study in Drosophila nephrocytes investigated how early endosome maturation is controlled by SNARE complexes rather than a single linear Rab5-to-Rab7 pathway. It identified a Syx12L–Snap29–Ykt6 SNARE complex for homotypic early endosomal fusion and showed that related assemblies (Syx7L–Snap29–Ykt6 and Syx7L–Snap29–Vamp7) promote later endosomal and lysosomal fusion with distinct Rab requirements. The results clarify the mechanistic logic of endosomal trafficking and SNARE specificity for cargo sorting decisions.

Hargitai D, Molnár M, Rubics A et al. · Nature communications · (2026) · 1 citations · View on PubMed ↗ · Free PDF ↗

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Generated automatically on October 07, 2026 from PubMed’s trending articles. Summaries are AI-generated; always consult the original publication for clinical or research decisions.