PubMed Trending Research Digest — October 02, 2026

Automated digest · 97 articles · 15 research areas · October 02, 2026

Overview

Across this week’s digest, a dominant theme is mechanistic precision—linking molecular regulators to disease behavior and using that knowledge to design safer, more targeted interventions. In gene and genome regulation, prime editing in patient-derived hematopoietic stem/progenitor cells for GATA2 deficiency highlights the move toward direct, potentially curative repair with improved safety versus nuclease-based editing. In parallel, multiple studies dissect how chromatin and transcriptional control shape mutagenesis and immune diversification (AID targeting via MLLT1/MLLT3 and transcription pause/elongation dynamics), and how higher-order regulatory architecture (ecDNA, immune multiome atlases, APA changes in aging/AD) can explain rapid adaptation and disease risk.

A second major thread is immune modulation—both to treat and to understand failure. Several cancer-focused papers converge on immune resistance mechanisms: CAR-T dysfunction in lymphoma via an IFN-γ→iNOS macrophage axis, and tumor immune evasion driven by senescence-associated neutrophil programs in glucose-deprived metastatic environments. Outside cancer, studies emphasize immune training and tolerance (lung macrophage “trained” tolerance after type 2 inflammation; macrophage/lysosomal stress–TFEB signaling) and clarify how immune cell origins (cranial bone marrow-derived monocytes) can sustain chronic neuroinflammation after traumatic brain injury. Together, these works suggest that future therapies will increasingly target not just immune activation, but the specific cellular states, niches, and regulatory circuits that govern outcomes.

Finally, the digest reflects a broad clinical translation push alongside lifestyle and systems-level risk modeling. Multiple trials and reviews address practical decision-making: optimizing incretin-based and GLP-1–pathway therapies for obesity/diabetes, refining cardiovascular and renal risk stratification (including continuous creatinine trajectories after thrombectomy), and updating infectious disease and oncology treatment pathways (hepatitis B elimination strategies; HCV shorter regimens; ADC–radiation safety; multiple myeloma living guidelines). Complementing these are real-world and modifiable factors—diet during antibiotic exposure, exercise effects on tumor stroma via the microbiome, and occupational risk stratification—underscoring that outcomes are shaped by both biology and context.

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Genome editing and DNA repair

Histone readers MLLT1 and MLLT3 concentrate AID to confer locus specificity.

The study investigated how the histone readers MLLT1 and MLLT3 regulate activation-induced deaminase (AID) targeting in B cells, using combined loss-of-function approaches to assess AID-dependent mutagenic processes. It found that combined loss of MLLT1 and MLLT3 abolishes AID-dependent mutagenesis, recapitulating AID deficiency, and identifies these readers as determinants of selective AID activity at immunoglobulin and off-target loci. This clarifies the chromatin logic that confers locus specificity for AID and suggests strategies to reduce off-target mutagenesis while preserving antibody diversification.

Seija N, Gannon S, Häfner KA et al. · Nature · (2026) · 1 citations · View on PubMed ↗

Transcription pause and elongation regulators mediate somatic hypermutation.

The study investigated molecular regulators of somatic hypermutation (SHM) by focusing on how transcription pause and elongation factors generate the substrate needed for activation-induced deaminase (AID) activity in activated B cells. It found that negative elongation factor (NELF) stabilizes RNA polymerase II (Pol II) in a paused state near transcription start sites and that release of NELF and Pol II elongation-versus-pause dynamics mediate AID chromatin recruitment and SHM. This links specific transcriptional pausing/elongation control to AID targeting, providing mechanistic targets to modulate antibody diversification and reduce off-target mutagenesis.

Wu L, Yadavalli AD, McAuliffe CC et al. · Nature · (2026) · 1 citations · View on PubMed ↗ · Free PDF ↗

The Fanconi anemia pathway restrains MLL-rearranged leukemogenesis through suppressing non-homologous end joining-mediated genomic instability.

This study examined how the Fanconi anemia (FA) DNA repair pathway affects MLL-rearranged leukemia using murine models and human MLL-r leukemia cells. FA pathway loss accelerated leukemogenesis by increasing error-prone non-homologous end joining (NHEJ)-mediated genomic instability, promoting leukemic stem cell expansion and elevated DNA damage. The work links FA-mediated DDR control to suppression of NHEJ-driven instability in MLL-r cancers, suggesting DDR pathway modulation as a therapeutic angle.

Xu J, Sund LM, Wolff EV et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Submolecular video-imaging of the Smc5/6 complex topologically bound to DNA.

This study used high-speed atomic force microscopy to directly visualize the eukaryotic Smc5/6 complex bound to DNA at submolecular resolution. Smc5/6 adopted an “I”-shaped conformation that transitioned to an “O”-shaped open ring upon ATP binding, with ATP-bound Smc5/6 stably associating with DNA and ATP hydrolysis promoting DNA entrapment within the SMC compartment. These mechanistic imaging results clarify how ATP state controls Smc5/6 DNA engagement and processing, advancing understanding of SMC-driven genome organization.

Umeda K, Kurokawa Y, Kodera N et al. · Nature communications · (2026) · 2 citations · View on PubMed ↗ · Free PDF ↗

Retatrutide, a Triple Hormone Receptor Agonist, for Treatment of Obesity.

This phase 3 randomized, double-blind trial studied retatrutide—a triple agonist of GIP, GLP-1, and glucagon receptors—in adults with obesity without diabetes, including a subgroup with knee osteoarthritis and another with sleep apnea. Retatrutide given once weekly at 4 mg, 9 mg, or 12 mg for 80 weeks produced dose-dependent improvements, with primary endpoints including greater percent body-weight reduction and improved WOMAC pain scores in the knee osteoarthritis subgroup and reductions in apnea-hypopnea measures in the sleep apnea subgroup. These results support retatrutide as an effective multi-receptor incretin/glucagon-based therapy for obesity with clinically meaningful benefits on weight and obesity-related symptoms.

Jastreboff AM, Kaplan LM, Davies MJ et al. · The New England journal of medicine · (2026) · View on PubMed ↗

Prime editing of human hematopoietic stem cells for correction of GATA2 deficiency.

The study investigated prime editing in a patient-derived ex vivo setting using human CD34+ hematopoietic stem and progenitor cells (HSPCs) to correct heterozygous GATA2 deficiency caused by a GATA2 c.956_962d variant. Prime editing achieved efficient correction with a safety profile characterized by favorable off-target and genotoxicity properties compared with nuclease-dependent approaches. This provides a potential curative, safer gene-editing strategy for GATA2-deficient immunodeficiency by directly repairing the transcription factor gene in autologous HSPCs.

Wolff JH, Skov TW, Dorset SR et al. · Science translational medicine · (2026) · View on PubMed ↗

A Giant Cystic Ectopic Parathyroid Adenoma of the Anterior Mediastinum Mimicking a Mediastinal Tumor: A Diagnostic Challenge.

This report described a 63-year-old man with primary hyperparathyroidism due to a giant cystic ectopic parathyroid adenoma located in the anterior mediastinum that mimicked a mediastinal tumor. Despite multinodular goiter on ultrasound and misleading localization challenges using dual-tracer technetium-99m imaging, the case highlights diagnostic pitfalls in mediastinal ectopic parathyroid disease. Clinically, it underscores the need for careful interpretation of nuclear localization studies when thyroid pathology is present to avoid misdiagnosis and guide appropriate surgical management.

Pano I, Leivaditis V, Andrikopoulou C et al. · Chirurgia (Bucharest, Romania : 1990) · (2026) · View on PubMed ↗ · Free PDF ↗

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Cancer immunotherapy and CAR-T mechanisms

The role of CHIP and pre-treatment neutropenia in patients treated with chimeric antigen receptor T cells for hematological malignancies.

This retrospective study evaluated whether clonal hematopoiesis of indeterminate potential (CHIP) and pretreatment neutropenia influence outcomes in 113 patients treated with CAR-T cells for B-cell hematologic malignancies. The key finding was that CHIP was present in 30.8% of patients and was assessed for associations with CAR-T–related toxicities and clinical outcomes (quantitative associations truncated). Scientifically and clinically, it suggests that baseline clonal immune risk factors may modulate inflammatory toxicity risk in CAR-T therapy.

Riedel A, Weiß-Haug A, Merz B et al. · Haematologica · (2026) · View on PubMed ↗ · Free PDF ↗

IFN-γ-driven iNOS induction in macrophages mediates CAR T cell resistance in B cell lymphoma.

This study investigated why CAR T cells fail in B cell lymphoma by analyzing pre-infusion tumor biopsies and testing mechanisms in murine models. It found that CAR T cell–produced interferon-gamma (IFN-γ) induces inducible nitric oxide synthase (iNOS/NOS2) in immunoregulatory macrophages, and iNOS-expressing macrophages suppress CAR T function via apoptosis and cell-cycle arrest. Clinically, it identifies an IFN-γ→iNOS macrophage axis as a resistance mechanism that could be targeted to improve CAR T efficacy in large B cell lymphoma.

Lee SB, Pavy A, Beatty N et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Forimtamig, a GPRC5DxCD3 bispecific antibody with a novel 2:1 format, in relapsed/refractory multiple myeloma.

This Phase 1 study evaluated forimtamig, a GPRC5DxCD3 bispecific antibody in a novel 2:1 format, in relapsed/refractory multiple myeloma (RRMM) using subcutaneous dosing (NCT04557150). The trial used dose escalation followed by backfilling at optimized target doses with step-up and condensed step-up schedules to determine safety/tolerability, maximum tolerated dose (MTD), and recommended Phase 2 dose/schedule, alongside pharmacokinetics, immunogenicity, and anti-tumor activity. If tolerable and active, forimtamig could expand bispecific antibody options for RRMM with a dosing strategy designed to improve benefit–risk.

Hasselbalch AC, Harrison SJ, Manier S et al. · Blood advances · (2026) · View on PubMed ↗ · Free PDF ↗

Functional evaluation of CAR-T anti-CD123 from immune-mediated inflammatory diseases patients for novel pDCs-targeted immunotherapy.

This study assessed the functional capacity of CAR-T cells targeting CD123 (CD123 CAR-T) to eliminate plasmacytoid dendritic cells (pDCs) derived from patients with immune-mediated inflammatory diseases (IMIDs). In the CARDA2I study, patients with psoriasis, hidradenitis suppurativa, systemic lupus erythematosus, or systemic sclerosis were enrolled, and the work focused on pDC targeting given high CD123 expression and pDC roles in type I interferon biology. The scientific significance is that it tests whether CD123 CAR-T could serve as a pDC-directed immunotherapy strategy across multiple IMIDs.

Caël B, Bôle-Richard E, Belakri I et al. · The Journal of allergy and clinical immunology · (2026) · View on PubMed ↗

Immunotherapy refractoriness and early post-alloHCT relapse define ultra-high-risk B-ALL after CD19 CAR T-cell therapy.

This study defined ultra-high-risk B-ALL after CD19 CAR T-cell therapy by examining immunotherapy refractoriness and early relapse after prior alloHCT. In a retrospective EBMT registry analysis of 345 patients with relapsed/refractory B-ALL treated with CAR T (2016–2023), the authors stratified patients by prior alloHCT exposure and categorized prior blinatumomab and inotuzumab ozogamicin as naïve, responder (CR/CRi), or refractory to determine how these factors predicted outcomes. The findings refine risk stratification for CAR T recipients by identifying immunotherapy refractoriness and early post-alloHCT relapse as defining features of an ultra-high-risk group.

Ortiz-Maldonado V, Galimard JE, Ottaviano G et al. · Blood advances · (2026) · View on PubMed ↗ · Free PDF ↗

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Targeted cancer therapies and resistance

BTK/BCL2 dual targeting enhances apoptosis in marginal zone lymphoma: preclinical activity of tacabrutideg (BGB-16673) and sonrotoclax.

This preclinical study tested BTK/BCL2 dual targeting in marginal zone lymphoma (MZL) using the BTK degrader tacabrutideg (BGB-16673) and the BCL2 inhibitor sonrotoclax, including models with acquired resistance to BTK, BCL2, and PI3K inhibitors. The key finding was that tacabrutideg showed single-agent activity and that combination regimens (including sonrotoclax and other agents such as venetoclax, bendamustine, and rituximab) enhanced apoptosis and antitumor effects in MZL models and primary samples (full results truncated). The significance is a rationale for combination strategies that overcome resistance mechanisms in MZL by simultaneously degrading BTK and inhibiting BCL2.

Arribas AJ, Zadro A, Civanelli E et al. · Haematologica · (2026) · View on PubMed ↗ · Free PDF ↗

GPCR antagonism via rewiring of receptor trafficking and degradation.

The study examined a bispecific antibody strategy for functional GPCR antagonism in which GPCR–TfR1 targeting chimeras (GTACs) are used to drive receptor endocytosis and lysosomal degradation. It found that GTACs downregulate multiple GPCRs—including BILF1, RXFP1, and CCR6—achieving complete inhibition of receptor signaling (including constitutive signaling) with 10–100× greater potency than conventional antibody antagonists. This provides a generalizable approach to drug previously difficult GPCR targets by forcing receptor trafficking to lysosomal degradation rather than blocking ligand binding.

Rhee K, Shue L, Adachi A et al. · Nature · (2026) · View on PubMed ↗ · Free PDF ↗

Lineage identity governs oncogene dependence in mouse NSCLC models of KRAS inhibitor resistance.

This study used genetically engineered mouse models of Kras-driven lung adenocarcinoma to test how lineage identity shapes dependence on oncogenic KRAS during KRAS inhibitor treatment and acquired resistance. With continued KRAS inhibitor exposure, tumors invariably developed genetic Kras amplification, and residual disease after initial dosing showed transcriptional similarity to alveolar epithelial cells, with CRISPR functional approaches used to model oncogene-independent resistance mechanisms. These findings suggest that KRAS inhibitor durability depends on tumor lineage programs and that Kras amplification is a key, targetable resistance route in KRAS inhibitor–resistant NSCLC.

Mathey-Andrews N, Rodriguez CL, Shui B et al. · Nature genetics · (2026) · View on PubMed ↗

Allele-Specific Mechanisms Guide Salvage Therapy to Overcome Daraxonrasib Resistance in Pancreatic Cancer.

This cancer research study investigated allele-specific resistance mechanisms to daraxonrasib (RMC-6236), a multiselective RAS(ON) inhibitor, in pancreatic ductal adenocarcinoma (PDAC) models harboring KRASG12D versus KRASG12R. The key finding was that daraxonrasib inhibited KRASG12D primarily via steric occlusion of effector binding with modest engagement of wild-type RAS (RASWT), whereas KRASG12R resistance involved altered signaling that leveraged EGFR/RASWT-GTP signaling (as truncated). Scientifically and therapeutically, it suggests that KRAS allele identity can determine adaptive resistance pathways and thereby guide salvage therapy selection.

Dorbin D, Herrera J, Davidson R et al. · Cancer research · (2026) · View on PubMed ↗

Systematic identification of p11 as a signaling modulator across the GPCRome.

This study examined the microprotein p11 (S100A10) as a signaling modulator across the GPCRome by mapping GPCR–p11 interactions and testing how receptor conformation affects p11 recruitment. The key finding was that p11 recruitment is promoted by an active GPCR conformation and that multiplexed suspension bead array (SBA) screening across 211 receptors identified more than two dozen high-confidence GPCR physical interactors. The significance is that it expands the mechanistic framework for p11-dependent GPCR signaling and provides a scalable interactome map for future functional targeting.

Saarinen M, Kotliar IB, Höffkes I et al. · Science advances · (2026) · View on PubMed ↗ · Free PDF ↗

Sensitizing tumor response to topoisomerase I antibody-drug conjugate by selective CDK7 inhibition.

This preclinical study investigated how selective CDK7 inhibition with Q901 sensitizes tumors to topoisomerase I (TOP1) antibody-drug conjugates by altering transcriptional programs. The key finding was that Q901 disrupted MYC- and E2F-dependent transcription, down-regulated cell-cycle and DNA damage repair pathways, and stabilized CDK7 binding at promoter-proximal regions to reduce MYC/E2F/RNAPII occupancy, thereby increasing susceptibility to TOP1-DNA-protein cross-links. The significance is a proposed combination strategy—CDK7 inhibition plus TOP1-targeted therapy—to overcome or prevent resistance driven by DNA repair activation.

Jung H, Lee Y, Yu D et al. · Science advances · (2026) · View on PubMed ↗ · Free PDF ↗

FAK inhibitor and RAF/MEK clamp avutometinib enhance KRAS G12C inhibitor efficacy in preclinical models of non-small cell lung cancer.

The study tested whether combining the RAF/MEK clamp avutometinib with the focal adhesion kinase (FAK) inhibitor defactinib improves the efficacy of KRAS G12C inhibitors in preclinical non-small cell lung cancer (NSCLC) models. The triplet regimen deepened MAPK pathway suppression and blocked adaptive resistance signaling (including FAK and PI3K pathways) induced by KRAS G12C inhibition and avutometinib. This supports a rational combination strategy to overcome resistance and improve outcomes for KRAS G12C-mutant NSCLC.

Coma S, Musteanu M, Malvezzi CC et al. · Science translational medicine · (2026) · View on PubMed ↗

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Oncology clinical trials and treatment strategies

Felzartamab plus lenalidomide-dexamethasone versus lenalidomide-dexamethasone for relapsed or refractory multiple myeloma: an open-label, parallel-controlled, randomised, phase 3 trial.

This open-label, parallel-controlled randomized phase 3 trial studied felzartamab (an anti-CD38 monoclonal antibody with attenuated complement-dependent cytotoxicity) plus lenalidomide-dexamethasone versus lenalidomide-dexamethasone alone in Chinese patients with relapsed or refractory multiple myeloma, with particular attention to the 1q21+ subgroup. Felzartamab-based therapy improved efficacy while aiming to mitigate CDC-associated infusion reactions and reduced activity seen with CDC-reliant CD38 antibodies. The trial is significant for optimizing CD38-targeted immunotherapy in relapsed/refractory multiple myeloma, especially in genetically defined high-risk disease (1q21+).

He H, Shang J, Wang Y et al. · The Lancet. Haematology · (2026) · View on PubMed ↗

Serial ctDNA Analysis for Monitoring Molecular Response and Acquired Resistance in Metastatic NSCLC and HR+/HER2-Negative Breast Cancer: A Real-World Study.

This real-world longitudinal study assessed serial circulating tumor DNA (ctDNA) monitoring using droplet digital PCR (ddPCR) to track molecular response and acquired resistance in 48 metastatic patients—42 with EGFR-mutant metastatic NSCLC and 6 with HR+/HER2-negative metastatic breast cancer. In the NSCLC cohort, ddPCR detected acquired resistance mutations such as EGFR T790M and enabled monitoring at specific time points (full performance metrics truncated). The significance is that ddPCR-based serial ctDNA profiling may improve detection of resistance and guide treatment decisions in routine oncology care.

Knebel FH, Ribeiro MFSA, Linck RDM et al. · Cancer medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Metastatic metaplastic triple negative breast cancer response to sacituzumab govitecan and biomarker targetability.

This retrospective clinical study investigated metastatic metaplastic triple-negative breast cancer (MpBC) responses to the antibody-drug conjugate sacituzumab govitecan (SG) and assessed biomarker targetability in patients treated at Massachusetts General Hospital Cancer Center (2000–2025). It found that MpBC cases treated with SG could be stratified by actionable biomarkers, including HER2-low status (IHC 1+/2+) and other targetable features, to inform future targeted therapy development. The clinical significance is that it links real-world SG outcomes in MpBC with biomarker-defined opportunities for precision oncology trials.

Maheswaran S, Dedeoglu AS, Niemierko A et al. · Breast cancer research and treatment · (2026) · View on PubMed ↗

Intravenous hyaluronidase-expressing oncolytic adenovirus with chemotherapy in metastatic pancreatic cancer: a randomized phase 2b trial.

This randomized phase 2b trial evaluated intravenous hyaluronidase-expressing oncolytic adenovirus Zabilugene almadenorepvec (VCN-01; VCN-01) plus gemcitabine and nab-paclitaxel (GnP) versus GnP alone as first-line therapy in patients with metastatic pancreatic ductal adenocarcinoma. The study compared overall survival and safety/tolerability across intent-to-treat and safety populations for two VCN-01 dosing arms, building on prior evidence of VCN-01 safety and antitumor activity. Clinically, it tests whether combining VCN-01’s hyaluronidase-enabled tumor penetration with GnP improves outcomes in a high-fatality metastatic setting.

Garcia-Carbonero R, Pazo Cid R, Macarulla T et al. · Nature medicine · (2026) · View on PubMed ↗

Phase II Study of Cisplatin/Gemcitabine Plus Necitumumab for Squamous NSCLC After ICI-Platinum Therapy (WJOG14120L).

This open-label, multicenter single-arm Phase II study evaluated cisplatin/gemcitabine plus the anti-EGFR antibody necitumumab (CGN) as second-line treatment in patients with unresectable/advanced lung squamous cell carcinoma (LSqCC) after immune checkpoint inhibitor (ICI) plus platinum therapy. The trial’s primary endpoint was objective response rate (ORR), testing a null hypothesis of 23% versus an alternative of 40%, with secondary endpoints including disease control (details truncated in the abstract). If effective, CGN could provide a prospective post-ICI chemotherapy-based option for LSqCC where treatment choices are currently limited.

Yoshioka H, Mori K, Ishikawa N et al. · Cancer science · (2026) · View on PubMed ↗ · Free PDF ↗

Retained epcoritamab activity despite routine CD20 assay negativity approximately one terminal half-life after mosunetuzumab in B-cell lymphoma.

This case report studied a patient with multiply relapsed B-cell lymphoma who had mosunetuzumab treatment and then showed retained anti-tumor activity despite routine CD20 assay negativity about one terminal half-life later. Immunohistochemistry using the CD20 clone L26 and flow cytometry using the CD20 clone L27 both showed undetectable CD20, while PAX5 and CD79a remained positive and the relapse specimen was characterized as diffuse large B-cell lymphoma (germinal center B-cell subtype). The finding is clinically significant because it suggests that CD20 negativity on routine assays shortly after CD20-directed therapy may not reflect loss of therapeutic activity, informing interpretation of post-treatment biopsies.

Kakiuchi S, Akiyama H, Tomigaki N et al. · Journal of clinical and experimental hematopathology : JCEH · (2026) · View on PubMed ↗ · Free PDF ↗

Safety of combining radiation therapy and antibody-drug conjugates in patients with breast cancer: a systematic review and meta-analysis.

This systematic review and meta-analysis evaluated the safety of combining radiation therapy with antibody-drug conjugates (ADCs) in patients with early and metastatic breast cancer. Across included studies, it summarizes available evidence to update the ESTRO consensus on whether concurrent/sequential RT plus ADCs increases treatment-related toxicity. The findings are important for clinical decision-making because they guide safe integration of modern ADC therapies with radiotherapy in breast cancer care.

Visani L, Becherini C, Kubeczko M et al. · Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology · (2026) · View on PubMed ↗ · Free PDF ↗

Abemaciclib plus endocrine therapy in HR-positive, HER2-negative high-risk early breast cancer: efficacy in nodal subgroups.

This study analyzed efficacy of abemaciclib plus endocrine therapy in monarchE for specific nodal subgroups of HR-positive, HER2-negative high-risk early breast cancer. In cohort 1 (91% of patients), the authors reported long-term outcomes across N1 high-risk (1–3 positive nodes with grade 3 and/or tumor size ≥5 cm), N2 (4–9 positive axillary lymph nodes), and N3 (≥10 positive axillary lymph nodes) subgroups with median follow-up of 76.8 months. The subgroup results provide clinically actionable evidence on whether the recurrence/mortality benefit of abemaciclib+ET extends across increasing nodal burden.

Cortes J, Johnston SRD, Martin M et al. · ESMO open · (2026) · View on PubMed ↗ · Free PDF ↗

Treatment of Multiple Myeloma: ASCO Living Guideline, Version 2026.1.3.

This ASCO Living Guideline update studied evidence and clinical recommendations for treatment of multiple myeloma across patient populations addressed in the ASCO guideline framework. The key finding is that the guideline is continuously updated via a systematic, scheduled literature review process to reflect rapidly evolving multiple myeloma evidence while emphasizing clinician judgment and accounting for individual patient variation. Its significance is that it provides an up-to-date, methodologically standardized decision-support tool for multiple myeloma therapy selection in routine oncology practice.

Banerjee R, Messersmith H, Ebraheem M et al. · Journal of clinical oncology : official journal of the American Society of Clinical Oncology · (2026) · View on PubMed ↗

Giredestrant plus Everolimus in Advanced Breast Cancer.

This phase 3, open-label randomized trial studied giredestrant (oral ER degrader) plus everolimus (oral mTOR inhibitor) in patients with ER-positive, HER2-negative locally advanced or metastatic breast cancer who progressed after CDK4/6 inhibitor plus endocrine therapy. The key finding was that targeting the ER pathway with giredestrant while inhibiting PI3K/AKT/mTOR signaling with everolimus improved outcomes versus the control regimen (details truncated in the abstract). Clinically, the study supports a post-CDK4/6 progression strategy combining ER-pathway blockade with mTOR inhibition to overcome endocrine-therapy resistance.

Mayer EL, Tolaney SM, Martín M et al. · The New England journal of medicine · (2026) · View on PubMed ↗

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Cancer microenvironment, stromal and metastasis biology

When Neutrophils Do Not Die: Senescence as a New Axis of Tumor Immunosuppression.

This Cancer Discovery commentary highlights findings from single-cell RNA sequencing of neutrophils in colorectal cancer liver metastases to define a senescence-driven immunosuppression axis. The key finding is that a glucose-deprived metastatic microenvironment induces BHLHE40 upregulation, generating a senescent tumor-associated neutrophil (TAN1) population that promotes angiogenesis and excludes CD8+ T cells. The significance is identifying BHLHE40-driven neutrophil senescence as a potential therapeutic target to reverse tumor immune evasion.

Droin L, Garner H · Cancer discovery · (2026) · View on PubMed ↗

Osteoclasts intercept meningeal lymphatic paths for dural metastasis.

The study investigated how meningeal lymphatic dysfunction and osteoclast activity influence dural metastasis in a mouse model of tumor progression. It found that osteoclasts intercept meningeal lymphatic paths, coinciding with impaired meningeal lymphatic drainage and characteristic cranial erosion patterns that distinguish dural metastasis from other metastatic routes. These findings identify meningeal lymphatic dysfunction as a mechanistic driver of dural metastasis and suggest new therapeutic targets in the osteoclast–lymphatic axis for advanced cancers such as breast and lung cancer.

Zeng R, Zhao J, Peng H et al. · Nature · (2026) · 1 citations · View on PubMed ↗

Prefibrotic bone marrow microenvironment is a hallmark of clonal hematopoiesis.

This work used single-cell transcriptomic profiling of freshly isolated human bone marrow samples, combined with histology and spatial transcriptomics, to define how clonal hematopoiesis of indeterminate potential (CHIP) remodels the bone marrow microenvironment. CHIP was associated with fibro-inflammatory remodeling, including expansion of fibroblasts into cancer-associated fibroblast-like states and increased collagen/extracellular matrix remodeling programs in mesenchymal and vascular compartments. These results mechanistically link CHIP to a pro-tumorigenic stromal niche, informing risk biology and potential microenvironment-targeted interventions.

Aguilar-Navarro AG, Edun G, Gower M et al. · Nature immunology · (2026) · 1 citations · View on PubMed ↗ · Free PDF ↗

Exercise Modulates Microbial Metabolites and Induces Stromal Remodeling in Pancreatic Cancer.

This study analyzed human pancreatic ductal adenocarcinoma (PDAC) tumors from the PancFit trial and used a murine PDAC model to test how exercise alters the tumor microenvironment and microbial metabolites. The key finding was that exercise reduced α-smooth muscle actin (αSMA)-expressing stromal cells and that these stromal changes were influenced by the microbiome, including reduced αSMA+ cells and Il6-expressing inflammatory cancer-associated fibroblasts (details truncated). The significance is that it links exercise to microbiome-mediated stromal remodeling, supporting mechanistic biomarkers for exercise-based adjunct therapy in PDAC.

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

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Cancer genomics, epigenetics and regulatory architecture

Extrachromosomal DNA as a platform for epigenetic reprogramming in cancer.

This review studied extrachromosomal DNA (ecDNA) in cancer as a regulatory platform for epigenetic reprogramming beyond its role in oncogene amplification. It found that ecDNA can reshape chromatin accessibility, enhancer activity, 3D genome organization, nuclear architecture, and transcriptional output, enabling transcriptional plasticity and rapid adaptation to selective pressures. The work is significant for cancer biology because it highlights ecDNA-driven regulatory mechanisms that may be targetable to limit tumor aggressiveness.

Liu BX, Zhou L, Lai S et al. · Molecular cancer · (2026) · View on PubMed ↗ · Free PDF ↗

Population-scale immune multiome atlas reveals regulatory disease mechanisms.

This Nature study constructed a population-scale immune multiome atlas by simultaneously profiling chromatin accessibility and gene expression across immune cells and integrating single-cell QTL mapping to connect regulatory variants to disease mechanisms. The key finding was that paired snATAC-seq and gene expression measurements across many individuals reveal regulatory architectures that mechanistically link non-coding variants to gene regulation and disease. This is scientifically significant because it provides an empirical framework for interpreting regulatory genetic variation in immune-mediated disease.

Kanai M, Delorey TM, Honkanen J et al. · Nature · (2026) · View on PubMed ↗

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Infectious disease: antiviral and vaccine biology

Mitochondrial proteome of the apicomplexan Babesia divergens.

This study characterized the nuclear-encoded mitochondrial proteome of the tick-transmitted apicomplexan parasite Babesia divergens by enriching mitochondria and performing protein mass spectrometry with protein correlation profiling. The authors generated BdMitoCarta, a high-confidence inventory of 525 mitochondrial proteins, and showed broad conservation of the B. divergens mitoproteome across Apicomplexa. This resource is scientifically significant because it expands targets and pathways relevant to mitochondrial biology and potential drug development for babesiosis, including context for atovaquone’s mitochondrial DNA targets.

Betsinger CN, Calvo SE, Mian SY et al. · Current biology : CB · (2026) · View on PubMed ↗

Acanthamoeba ATP synthase structure reveals the TCA cycle is tethered to OXPHOS.

Using cryo-electron microscopy of unenriched mitochondrial lysate combined with mass spectrometry proteomics, this work resolved structures of endogenous mitochondrial ATP synthase (complex V), Hsp60, and respiratory complex III from the protozoan pathogen Acanthamoeba castellanii. The study revealed that Acanthamoeba ATP synthase can be captured in an IF1-inhibited state and that Acanthamoeba-specific subunits/extensions stabilize the ATP synthase molecular machine, linking the TCA cycle to oxidative phosphorylation (OXPHOS). These structural insights are significant for understanding how eukaryotic energy metabolism is evolutionarily rewired in protists and may inform broader principles of mitochondrial bioenergetics.

Fry MY, Luce BE, Stefely JA et al. · Cell · (2026) · View on PubMed ↗

World Gastroenterology Organisation Practice Guidelines.

These World Gastroenterology Organisation practice guidelines reviewed and updated hepatitis B treatment pathways, focusing on global elimination targets, prevention of new infections, and screening/linkage to care in resource-limited settings. The key finding was that guideline priorities emphasize preventing mother-to-child transmission and improving antiviral prophylaxis strategies, building on WHO updates from 2015 and 2024. This is clinically significant because it standardizes hepatitis B care to accelerate elimination efforts worldwide.

Lee AU, Brand M, Cabrera MC et al. · Journal of clinical gastroenterology · (2026) · View on PubMed ↗

Host cell traversal by Plasmodium parasites drives sterilizing T cell-mediated immunity following immunization.

This study used rodent vaccination models to determine how Plasmodium sporozoite traversal through multiple host cells before hepatocyte infection shapes sterilizing T cell immunity. Active sporozoite cell traversal was required for sterilizing immunity regardless of how much intrahepatic parasite development occurred in the immunizing parasites. The findings identify host-cell traversal as a critical immunogenic determinant for malaria vaccine design aimed at achieving sterile protection.

Rodrigues A, Mendes AM, Gonçalves R et al. · Nature microbiology · (2026) · 1 citations · View on PubMed ↗ · Free PDF ↗

Innate immune sensing of Plasmodium sporozoite cell traversal drives protective T cell responses.

This study isolated GFP+ Plasmodium berghei and Plasmodium falciparum sporozoites and assessed innate immune activation by exposing them to mouse bone marrow-derived macrophages and human peripheral blood mononuclear cells, using bulk and single-cell RNA sequencing. Sporozoite traversal induced a distinctive innate activation program resembling cell-wounding responses, and traversal-deficient sporozoites failed to trigger the same protective T cell–supporting innate signaling. Scientifically, it connects sporozoite cell traversal to innate sensing pathways that shape protective T cell responses, guiding rational attenuation strategies for malaria vaccines.

Pohl KG, Gao X, McGowan J et al. · Nature microbiology · (2026) · 1 citations · View on PubMed ↗

A small molecule inhibits Ebola virus entry through glycoprotein stabilization.

This study used DNA-encoded chemical library screening against Ebola virus glycoprotein (EBOV GP) to identify and optimize a small-molecule entry inhibitor, MWAC-3634. MWAC-3634 bound EBOV GP with high affinity (Kd ~40.7 nM), neutralized infection with sub-nanomolar potency (IC50 ~0.65 nM), and structural cryo-EM at 2.54 Å showed it occupies a hydrophobic cavity at the GP subunit interface. These results support MWAC-3634 as a potent, structurally defined candidate for inhibiting EBOV entry and advancing antiviral development.

Bu F, Ye G, Sharma KL et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

8 weeks versus 12 weeks of sofosbuvir-velpatasvir for treatment-naive, non-cirrhotic, chronic hepatitis C (RESOLVE): a multicentre, open-label, non-inferiority, randomised controlled trial in India.

This multicentre, open-label, non-inferiority randomized controlled trial (RESOLVE) compared 8 weeks versus 12 weeks of sofosbuvir 400 mg plus velpatasvir 100 mg in treatment-naive, non-cirrhotic adults with chronic hepatitis C virus (HCV) mono-infection in India. It tested whether the shorter regimen is non-inferior for achieving virologic clearance (cure) compared with the standard 12-week course. The significance is practical because it evaluates a shorter, potentially more accessible treatment duration for non-cirrhotic HCV patients.

Goel A, Rungta S, Kumar V et al. · Lancet (London, England) · (2026) · View on PubMed ↗

Amikacin Liposome Inhalation Suspension in Newly Diagnosed Mycobacterium avium Complex Lung Disease: A Phase 3b, Double-blind, Randomized Clinical Trial (ENCORE).

This phase 3b, double-blind, randomized clinical trial studied amikacin liposome inhalation suspension (ALIS; 590 mg) added to guideline-based multidrug therapy (azithromycin and ethambutol) in adults newly diagnosed with Mycobacterium avium complex lung disease (MACLD) who had not initiated antibiotics. The key finding was that ALIS plus MDT was evaluated for superiority in efficacy and safety compared with placebo plus MDT in a 1:1 randomized design (primary results are not shown in the truncated abstract). Clinically, it tests whether inhaled ALIS can improve outcomes when used upfront rather than only for refractory MACLD.

Daley CL, Morimoto K, Thomson R et al. · American journal of respiratory and critical care medicine · (2026) · View on PubMed ↗ · Free PDF ↗

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Infectious disease: bacterial persistence and host niches

Hyperosmotic niche adaptation and tissue polyamines underlie MRSA persistence in the kidney.

The study investigated how methicillin-resistant Staphylococcus aureus (MRSA) persists in the kidney by using an intravenous USA300 MRSA mouse infection model with multiplexed imaging, dual-species transcriptomics, host and bacterial genetics, and cell-based assays. It identified the renal inner medulla as a reservoir where MRSA survives immune surveillance in a hyperosmotic niche by co-opting host tissue polyamines and delaying neutrophil recruitment. This mechanistic insight highlights hyperosmotic adaptation and polyamine dependence as potential therapeutic targets to eradicate renal MRSA persistence.

Kanazawa N, Martens CP, Makino S et al. · Science translational medicine · (2026) · View on PubMed ↗

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Immunology and immune cell regulation (non-cancer)

A TBK1/ULK1 signalling axis couples lysosomal stress to TFEB activation.

This mechanistic study identified a nutrient-independent lysosomal signaling pathway in which the TBK1/ULK1 axis couples lysosomal stress to activation of the transcription factor TFEB. It found that TBK1 or ULK1 is recruited to lysosomes via v-ATPase-driven signaling, thereby promoting TFEB activation and coordinating catabolic/lysosomal adaptation programs. The significance is that it clarifies how lysosomal stress is transduced to TFEB, offering potential targets for diseases involving lysosomal dysfunction and TFEB-driven transcriptional programs.

Esposito A, Bayramoglu I, Varriale C et al. · Nature · (2026) · View on PubMed ↗

Type 2 immune history trains lung macrophages for viral disease tolerance.

This study examined how type 2 immune history trains lung macrophages for viral disease tolerance using mouse models of prior type 2 inflammation induced by Nippostrongylus brasiliensis followed by heterologous lethal H1N1 influenza challenge. The key finding was that nerve- and airway-associated macrophages (NAMs) expand after type 2 inflammation and acquire epigenetically imprinted “trained” properties that improve tolerance to subsequent viral disease. This is significant because it links immune training to macrophage subsets and suggests tolerance-focused strategies to mitigate severe respiratory viral immunopathology.

Damani-Yokota P, Yordanov Y, Bernier ED et al. · Nature · (2026) · View on PubMed ↗ · Free PDF ↗

Salicylic acid engages central metabolic regulators SnRK1 and TOR to govern immunity by differential phosphorylation of NPR1.

This study investigated how the plant immune regulator NPR1 integrates salicylic acid (SA) signals with nutrient-sensing kinases to control immunity through differential phosphorylation. The authors found that in the absence of pathogen challenge, TOR phosphorylates NPR1 at Ser-55/59 to inhibit it, whereas during defense responses SA lowers sugar phosphate levels and enhances SNF1-related protein kinase 1 (SnRK1) activity to promote NPR1 activation via phosphorylation changes. This mechanistic framework links SA-mediated defense to metabolic state through TOR/SnRK1-dependent NPR1 post-translational control, advancing understanding of how plants coordinate immunity and metabolism.

Chen Y, Withers J, Sun Y et al. · Cell · (2026) · View on PubMed ↗ · Free PDF ↗

Aire is a cell-intrinsic regulator of natural IgM-secreting cells.

This study examined whether the autoimmune regulator Aire directly regulates natural IgM-secreting cells in the spleen and bone marrow. The authors found that Aire is expressed in Aire+IgM+ antibody-secreting cells with natural IgM-secreting cell features, arising primarily from B-1a and marginal zone B cells, and that innate signals can drive plasmablast differentiation in vitro while synergistic B cell survival and growth factor signaling support their growth. These findings establish Aire as a cell-intrinsic regulator of natural IgM-secreting cell development and maintenance, extending Aire’s role beyond thymic T cell tolerance.

Sayed A, Yamano T, Steinert M et al. · Immunity · (2026) · View on PubMed ↗ · Free PDF ↗

Cranial bone marrow-derived monocytes promote neuroinflammation in chronic traumatic brain injury.

The study examined whether cranial bone marrow (CBM)-derived monocytes drive chronic neuroinflammation after chronic traumatic brain injury (cTBI) by combining clinical specimens, cell-tracing, multiomics profiling, transgenic animal models, adoptive cell transfer, and a proof-of-concept randomized clinical trial. cTBI induced persistent aberrant myelopoiesis, and CBM-derived immune cells promoted sustained neuroinflammatory pathology. These findings identify CBM/monocyte biology as a mechanistic contributor to long-term cTBI decline and suggest new targets for preventing chronic inflammation in older patients.

Lu Z, Wang C, Gong P et al. · Science translational medicine · (2026) · View on PubMed ↗

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Neuroinflammation, neurodegeneration and brain biomarkers

Neuroinflammation and Autophagy in Neurodegeneration: Cellular Mechanisms and Therapeutic Strategies.

This review studied how neuroinflammation and dysregulated autophagy contribute to neurodegenerative diseases (including Huntington’s disease, Parkinson’s disease, Alzheimer’s disease, and ALS) and evaluated emerging therapeutic strategies targeting these pathways. It found that impaired macroautophagy/mitophagy and persistent inflammatory signaling act together to drive toxic protein aggregation and progressive neuronal loss. The synthesis is clinically significant because it supports combined anti-inflammatory and autophagy-modulating therapeutic approaches as rational strategies for multiple neurodegenerative disorders.

Verma A, Kushwaha SKS, Kushwaha N et al. · CNS & neurological disorders drug targets · (2026) · View on PubMed ↗

Prion-like transmission of human tau strains in the mouse brain.

The study tested whether human tau strains can be transmitted in a prion-like manner by injecting tau filaments from brains of individuals with Alzheimer’s disease or corticobasal degeneration into wild-type mice. It found that injected human tau filaments seed amyloid filament assembly of mouse tau while retaining structural identity consistent with the originating human strain. This supports the prion hypothesis for tau neurodegeneration and provides an experimental framework for strain-specific disease propagation.

Lövestam S, Shimozawa A, Tarutani A et al. · Nature · (2026) · 1 citations · View on PubMed ↗ · Free PDF ↗

Single-cell profiling and genetic regulation of alternative polyadenylation in the human brain.

The study generated a single-cell atlas of alternative polyadenylation (APA) in the aged human brain by profiling ~2 million cells from 379 postmortem brains, including individuals with and without Alzheimer’s disease (AD). It found that APA changes provide an independent mechanistic layer for gene regulation in AD and that genes with APA alterations are distinct from those showing expression changes. This enables cell type–resolved mapping of APA regulation and improves understanding of how APA contributes to genetic disease risk in the human brain.

Nan J, Boix CA, Shi S et al. · Nature genetics · (2026) · View on PubMed ↗ · Free PDF ↗

Written in development and lost in ageing: the grammar of cellular identity.

This theoretical/mechanistic study proposes that ageing in mammals reflects progressive decanalization of cellular identity driven by erosion of a regulatory “grammar” established during development. It argues that development writes global chromatin programs that constrain identity across timescales, while ageing reflects imperfect maintenance of these constraints, producing predictable identity drift. The framework provides a testable epigenetic/chromatin basis for how cellular identity becomes less stable with age.

Yücel AD, Molière A, Gladyshev VN · Nature · (2026) · View on PubMed ↗

Brain network localization of gray matter alterations and executive dysfunction in pediatric ADHD.

This study examined pediatric ADHD by mapping meta-analytic gray matter volume (GMV) and executive dysfunction findings onto large-scale brain networks using coordinate-informed functional connectivity network mapping (FCNM). It assessed whether spatially distributed regional abnormalities converge within brain networks in developing brains and evaluated reproducibility and cross-disorder specificity. The significance lies in identifying network-level substrates of ADHD that may better explain executive dysfunction than isolated regional findings.

Zeng Y, Cheng J, Xia M et al. · Journal of child psychology and psychiatry, and allied disciplines · (2026) · View on PubMed ↗

Circadian control of dopaminergic signaling to the mushroom body regulates sleep through rhythmic Pka-C1 transcription in Drosophila.

This study examined how circadian control of dopaminergic signaling to the Drosophila mushroom body regulates sleep via rhythmic Pka-C1 transcription in Kenyon cells. Using an in vivo luciferase reporter plus in silico analysis, CRISPR mutagenesis, and chromatin immunoprecipitation, the authors found that the γ lobe is the primary site of rhythmic Pka-C1 expression and that rhythmic Pka-C1 transcription drives daytime wakefulness. These results link circadian pacemaker output to dopamine pathway activity through Pka-C1 transcriptional control, identifying a mechanistic node for sleep regulation in vivo.

Lago Solis B, Koch R, Nagoshi E · Current biology : CB · (2026) · View on PubMed ↗ · Free PDF ↗

A TMEM119-tankyrase axis restrains microglial phagocytosis to maintain memory and enables pharmacological forgetting.

This study investigated how the microglia-specific protein TMEM119 regulates microglial phagocytosis to maintain memory in adult mice. The authors found that TMEM119 acts as a constitutive intracellular brake by sequestering tankyrase, preventing axin degradation and thereby limiting actin-nucleating free APC protein to reduce phagocytosis, and that TMEM119 ablation increases surveillance/phagocytic activity and enables pharmacological forgetting. The work identifies a TMEM119–tankyrase–axin/actin axis as a targetable regulator of microglial synapse elimination with potential implications for memory persistence and therapeutic “forgetting.”

Sun S, Wang C, Bian Y et al. · Neuron · (2026) · View on PubMed ↗

Purinergic receptor activation rectifies autism-associated endothelial dysfunction.

This study examined whether purinergic receptor signaling can correct endothelial dysfunction caused by the 16p11.2 deletion in mouse models of autism. In 14-day-old and adult male 16p11.2-deficient mice, endothelial cells showed bioenergetic failure with reduced intracellular ATP, and intra- or extracellular ATP rescued endothelial function in vitro via P2Y2 receptor activation; P2Y2 activation also restored cerebrovascular reactivity in 16p11.2-deficient arterioles ex vivo. The results support a causal role for endothelial ATP/purinergic signaling in 16p11.2-related neurovascular abnormalities and suggest P2Y2-targeted strategies for ASD-associated vascular dysfunction.

Ouellette J, Warsi S, Romero P et al. · Neuron · (2026) · View on PubMed ↗

Disentangling Age-Related and Disease-Specific Effects on Upper Cervical Cord Area in Patients With Multiple Sclerosis.

This cross-sectional, multicenter MRI study examined age-related versus disease-specific effects on mean upper cervical cord area (MUCCA) in people with multiple sclerosis (MS) and healthy controls (HCs) aged 18–70 years across three Italian sites. The key finding was that MS is associated with a disease-specific reduction in MUCCA beyond what is expected from aging, with modulation by sex and age at disease onset (as described in the abstract). Scientifically, it clarifies how cervical cord atrophy relates to MS biology versus normal aging, improving interpretation of MRI biomarkers of disability progression.

Jain K, Storelli L, Valsasina P et al. · Neurology · (2026) · 1 citations · View on PubMed ↗

Speech clocks decode dementia phenotypes, social exposome, and biological aging.

This study developed and validated a large-scale, cross-national “speech clock” using acoustic and linguistic features from 2928 individuals across five Latin American countries, spanning healthy controls, mild cognitive impairment, Alzheimer’s disease, and non-language/language-dominant frontotemporal dementia. The key finding was that speech age gaps (SAGs), derived from supervised models estimating chronological age, differentiated dementia phenotypes and related to social exposome and biological aging measures (truncated in the abstract). Scientifically and clinically, it offers a scalable, noninvasive digital biomarker approach for characterizing dementia subtypes and aging-related risk.

Hernandez H, Pedraza LK, Santamaria-Garcia H et al. · Science advances · (2026) · View on PubMed ↗ · Free PDF ↗

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Developmental biology and brain development atlases

Pediatric Human Olfactory Epithelium Mirrors Adult Structure and Function in a Human Olfactory Organoid Model.

This study investigated developmental differences in human olfactory epithelium (OE) structure, gene expression, and function using pediatric and adult specimens and a human olfactory organoid model. The key finding is that pediatric human OE mirrors adult structure and function within the organoid system, suggesting relative maturation of key OE features across childhood (full molecular details truncated). Scientifically, this supports organoid models for studying age-related olfactory dysfunction and for identifying developmental determinants of olfactory receptor and epithelial function.

Bach R, Chauhan A, Xiang M et al. · International forum of allergy & rhinology · (2026) · View on PubMed ↗ · Free PDF ↗

γδ T cell receptor dependencies define a unique immunosurveillance modality.

The study mapped spatiotemporal clonal architecture in the newborn mouse forebrain by combining lentiviral barcoding across major forebrain subdivisions with spatial transcriptomics. It found distinct clonal lineage relationships and previously unrecognized differences in the generation of ventral versus dorsal medium spiny neurons across regions including cortex, hippocampus, striatum, thalamus, and olfactory bulb. This creates a developmental atlas linking progenitor clones to anatomical cell types, enabling mechanistic hypotheses for how forebrain diversity emerges.

Veland N, Garcia-Cassani B, Zarco-Cuadrillero Á et al. · Nature · (2026) · View on PubMed ↗ · Free PDF ↗

Autism-associated SCN2A deficiency disrupts cortico-striatal circuitry in human brain assembloids.

This study tested how autism-associated heterozygous SCN2A protein-truncating variants affect cortico-striatal circuitry using human brain assembloids. In genotype-defined assembloids, SCN2A deficiency impaired long-range cortical axonal projections, reduced striatal spine density, and attenuated excitatory cortico-striatal synaptic transmission. These findings provide a human-model mechanism for SCN2A-driven ASD by pinpointing both projection deficits and intrinsic striatal dysfunction as contributors to disrupted cortico-striatal connectivity.

Chen X, Zhang J, Wu J et al. · Neuron · (2026) · View on PubMed ↗

NAT10 governs development through the Xrp1-mediated stress response rather than its RNA acetylation activity.

This Drosophila study examined how NAT10 regulates development through the Xrp1-mediated stress response rather than through its known RNA acetylation activity (ac4C). The key finding was that NAT10 knockdown caused eye-to-antenna transformation, JNK activation, and apoptosis, impaired rRNA processing and ribosomal assembly via reduced rRNA ac4C, and activated the integrated stress response in which Xrp1 was a key mediator. The significance is that it redefines NAT10’s in vivo functional mechanism, linking NAT10 loss to stress-response control of protein synthesis and development.

Wang L, Xue Z, Gao S et al. · Science advances · (2026) · View on PubMed ↗ · Free PDF ↗

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Genetics and genetic epidemiology (non-cancer)

Human genetics implicates a BACH2-NRF2 axis in fetal haemoglobin activation.

The study used large multi-ancestry genome-wide association analyses of fetal hemoglobin (HbF) levels in 28,279 individuals to identify genetic regulators of HbF activation, followed by functional validation of candidate genes. It found that the high-HbF causal variant rs1010474-C reduces BACH2 expression and elevates HbF, and that direct perturbation or inhibition of BACH2 increases HbF. These results implicate a BACH2–NRF2 axis as a therapeutic target for activating HbF in hemoglobinopathies.

Guo CJ, Arora UP, Cheng X et al. · Nature · (2026) · View on PubMed ↗ · Free PDF ↗

PABPN1 pathogenic expansion in the UK Biobank: reframing genetic prevalence of oculopharyngeal muscular dystrophy.

This genetic epidemiology study investigated pathogenic expansion of PABPN1 in the UK Biobank to refine prevalence estimates for oculopharyngeal muscular dystrophy (OPMD) caused by a GCN trinucleotide repeat expansion. Using UK Biobank data, it focused on how different repeat lengths (including the commonly discussed pathogenic 12–18 alanine–encoding range and the GCN11 allele) relate to dosage effects, incomplete dominance, and reduced penetrance. Scientifically, reframing genetic prevalence in a large cohort helps improve risk estimates and interpretation of genotype–phenotype relationships for PABPN1 expansion carriers.

Villella C, Gagliardi D, Sebastiani E et al. · Journal of neurology, neurosurgery, and psychiatry · (2026) · View on PubMed ↗

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Metabolism, obesity and incretin therapeutics

A mitochondrial carrier turns on the heat.

This Science commentary/article describes how an orphan mitochondrial carrier integrates circadian, dietary, and environmental signals to regulate brown fat metabolism. The key finding is that mitochondrial carrier activity provides a molecular node connecting “when to burn” (circadian cues) with “what to burn” (dietary inputs) and “how to adapt” (temperature). This is significant because it identifies a mechanistic link between mitochondrial transport and thermometabolic regulation that could be leveraged for metabolic disease interventions.

van der Laan M · Science (New York, N.Y.) · (2026) · View on PubMed ↗

Mitochondrial carrier SLC25A34 links clock, diet, and temperature control of adipocyte lipid cycling.

This study investigated how circadian rhythms, diet, and temperature signals converge on the orphan mitochondrial transporter SLC25A34 to control adipocyte lipid cycling. It found that the adipocyte clock suppresses Slc25a34 via REV-ERB transcriptional repressors during the sleep phase, while lipid-rich diet and cold/active-phase cues relieve repression and promote Slc25a34 transcription through peroxisome proliferator-activated receptors (PPARs). The work is significant because it identifies SLC25A34 as a molecular integrator of clock, diet, and temperature that regulates mitochondrial lipid flux in adipocytes.

Karavaeva I, Basse AL, Trammell SAJ et al. · Science (New York, N.Y.) · (2026) · View on PubMed ↗

Survodutide Once Weekly in Adults with Obesity and Type 2 Diabetes.

This multinational, double-blind phase 3 trial studied once-weekly survodutide (a glucagon receptor–GLP-1 receptor dual agonist) in adults with type 2 diabetes and obesity (BMI ≥27). Survodutide produced clinically meaningful improvements in weight and metabolic outcomes compared with control arms (details truncated in the provided abstract). These findings support survodutide as a potential next-generation incretin-based therapy for managing both obesity and type 2 diabetes in the same patient population.

Wharton S, le Roux CW, Startseva E et al. · The New England journal of medicine · (2026) · View on PubMed ↗

Effects of a Low-Carbohydrate Diet Combined With Exercise on HbA1c in Adults With Type 2 Diabetes: A Bayesian Multilevel Network and Dose-Response Meta-Analysis.

This Bayesian multilevel network meta-analysis and dose-response meta-analysis compared low-carbohydrate diets (carbohydrate-restricted diets, CRDs) combined with exercise versus other regimens in adults with type 2 diabetes using randomized controlled trial data. The study synthesized arm-level changes in HbA1c and used network meta-analysis methods (including CINeMA) to estimate incremental benefits and effect modifiers across comparisons. Clinically, the results aim to clarify which CRD+exercise strategies produce the largest HbA1c reductions and how dose and patient factors influence response.

Wang X, Jiao M, Ma W · Diabetes, obesity & metabolism · (2026) · View on PubMed ↗

Cardiovascular safety of orforglipron versus insulin glargine in adults with type 2 diabetes at increased cardiovascular risk (ACHIEVE-4): a phase 3, event-driven, randomised, open-label, non-inferiority, active comparator trial.

This phase 3, event-driven, randomized, open-label, non-inferiority trial (ACHIEVE-4) compared cardiovascular outcomes of orforglipron, an oral non-peptide GLP-1 receptor agonist, versus insulin glargine in adults with type 2 diabetes at increased cardiovascular risk. It was designed to determine whether orforglipron is non-inferior to insulin glargine for major adverse cardiovascular events. The clinical significance is that it directly informs cardiovascular safety for a new class of non-peptide GLP-1 therapy in high-risk diabetes populations.

Klein KR, Wysham C, Tuttle KR et al. · Lancet (London, England) · (2026) · View on PubMed ↗

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Cardiovascular, renal and cardiometabolic risk

Effects of high-dose supplemental oxygen therapy on pulmonary haemodynamics at 3250 m in high-altitude residents at risk for pulmonary hypertension.

This open-label, non-randomised sequential trial studied the haemodynamic effects of high-dose supplemental oxygen therapy in Kyrgyz high-altitude residents (>2500 m) at risk for pulmonary hypertension, using echocardiography under ambient air and after >15 minutes of oxygen. High-dose oxygen reduced systolic pulmonary artery pressure (sPAP) and helped distinguish the contribution of hypoxic vasoconstriction versus fixed vascular remodelling to chronically elevated sPAP in this population. These findings support using oxygen responsiveness on echocardiography to refine risk stratification and mechanistic understanding of high-altitude pulmonary hypertension (HAPH).

Vella A, Müller J, Omuralieva A et al. · BMJ open respiratory research · (2026) · View on PubMed ↗

Survival outcomes after liver transplantation in acute-on-chronic liver failure: A prospective study.

This prospective multicenter study evaluated 1-year survival after liver transplantation (LT) in adults with decompensated cirrhosis with acute-on-chronic liver failure grades 1–3 (ACLF-2/ACLF-3), and compared outcomes with patients declined for LT. Patients with ACLF-2 or ACLF-3 who were declined for LT had very high 1-year mortality (73% and 88%, respectively), while the study assessed post-LT survival to clarify the survival benefit of LT across ACLF severity. The results are clinically important for transplant decision-making and prognostication in advanced cirrhosis with multiple organ failures.

Gustot T, Bernal W, Fernández J et al. · Journal of hepatology · (2026) · View on PubMed ↗

Drug coated balloon vs. drug eluting stent in calcified de novo coronary lesions: Long term outcomes from the SPARTAN registry.

This retrospective SPARTAN registry analysis compared long-term outcomes of drug-coated balloon (DCB) versus drug-eluting stent (DES) strategies for operator-reported angiographically calcified de novo coronary lesions treated with percutaneous coronary intervention (PCI). The study found differential long-term clinical outcomes between DCB and DES approaches in calcified de novo lesions, addressing a key evidence gap for stent-less therapy in this high-risk lesion subset. These data can inform interventional strategy selection for calcified coronary disease where lesion preparation, stent expansion, and restenosis risk are major concerns.

Natarajan R, Corballis N, Merinopoulos I et al. · The American journal of cardiology · (2026) · View on PubMed ↗

Hypertension fuels osteoarthritis through neuroendocrine signaling.

This study examined how hypertension accelerates osteoarthritis (OA) through neuroendocrine signaling in joints predisposed by mechanical injury or aging, using nationwide cohort analyses and hypertensive mouse models. It found that OA-primed chondrocytes up-regulate the arginine vasopressin receptor 1A (AVPR1A), making them responsive to circulating AVP, and that AVP–AVPR1A signaling promotes cartilage catabolism while suppressing anabolic regulators. These findings are clinically significant because they identify a hypertension-linked, targetable AVP/AVPR1A pathway that may help explain and potentially mitigate OA progression in hypertensive patients.

Kim SJ, Kim HE, Chung KH et al. · Science (New York, N.Y.) · (2026) · View on PubMed ↗

Predicted 10-year cardiometabolic risk among hospital staff: a cross-sectional study.

This cross-sectional study used a localized digital risk assessment platform with machine learning–based modeling to estimate predicted 10-year cardiometabolic risk among hospital staff in Taiwan, particularly nurses and shift-working healthcare workers. The key finding was identification of high-risk occupational subgroups for chronic diseases such as hypertension and type 2 diabetes, enabling precision health targeting (full quantitative results truncated). Scientifically, it demonstrates an occupational-health application of ML risk stratification to guide prevention strategies in healthcare workers exposed to irregular schedules and stress.

Wu CY, Wu YW, Wu HY et al. · Frontiers in public health · (2026) · View on PubMed ↗

Beyond the Threshold: Continuous Creatinine Change and Outcomes After Endovascular Thrombectomy for Acute Ischemic Stroke.

This secondary analysis of the CAN-REST registry evaluated whether continuous creatinine change within 48 hours after endovascular thrombectomy (EVT) predicts outcomes in 6638 adults with acute ischemic stroke, beyond dichotomous contrast-associated acute kidney injury (CA-AKI) thresholds. The key finding was that subthreshold early creatinine changes carry graded prognostic information for post-EVT outcomes, not captured by binary CA-AKI definitions. Clinically, this supports using continuous kidney-function trajectories to better risk-stratify patients after EVT and potentially refine monitoring and interventions.

Schwarz G, Cascio Rizzo A, Ambler G et al. · Stroke · (2026) · View on PubMed ↗

Pharmacological treatment strategies to prevent heart failure across the cardiovascular-kidney-metabolic spectrum: an EJHF Expert Consensus Statement.

This European Journal of Heart Failure (EJHF) expert consensus statement synthesized evidence for pharmacological strategies to prevent heart failure across the cardiovascular–kidney–metabolic (CKM) spectrum, focusing on comorbid obesity, type 2 diabetes, chronic kidney disease, hypertension, and atherosclerotic cardiovascular disease. The key finding is a structured set of recommended foundational therapies (including renin–angiotensin system approaches, with additional classes discussed but truncated in the abstract) tailored to CKM phenotypes, especially heart failure with preserved ejection fraction (HFpEF). The clinical significance is harmonized guidance for preventing HF in high-risk multimorbid patients rather than treating single conditions in isolation.

Inciardi RM, Abdin A, Abdelhamid M et al. · European journal of heart failure · (2026) · View on PubMed ↗

Efficacy and Safety of Oral Non-Statin Lipid-Lowering Therapies in Dyslipidaemia: A Systematic Review and Network Meta-Analysis.

This systematic review and network meta-analysis evaluated oral non-statin lipid-lowering therapies in adults with dyslipidaemia who were statin-intolerant or not achieving LDL-C targets. It found comparative efficacy and safety differences across non-statin options for percent/absolute LDL-C reduction and related lipid outcomes, clarifying which agents perform best for LDL-C lowering when statins are inadequate. The findings are scientifically and clinically significant because they guide evidence-based selection of oral non-statin regimens to reduce atherosclerotic cardiovascular disease risk.

Hodrob T, Saad RJ, Hamdy A et al. · Endocrinology, diabetes & metabolism · (2026) · View on PubMed ↗ · Free PDF ↗

Strategic Application of Post-exercise Cold-Water Immersion to Enhance Performance Recovery and Adaptation: An Umbrella Review of 15 Published Systematic Reviews with Meta-analysis.

This umbrella review studied post-exercise cold-water immersion (CWI) interventions and their effects on exercise performance recovery and adaptation by synthesizing 15 systematic reviews with meta-analyses. The key finding was that the evidence base varies in methodological quality and certainty, affecting how confidently CWI can be recommended for specific recovery/adaptation outcomes. This is significant for sports medicine because it provides an evidence-quality–aware framework for using CWI in athletic training and recovery decisions.

Berjisian E, Miraftabi H, Ihsan M et al. · Sports medicine - open · (2026) · View on PubMed ↗ · Free PDF ↗

Intramuscular Fat as a Biomarker of Muscle Health: Strengths, Limitations and Open Challenges.

This narrative review synthesized evidence on intramuscular fat (IMF, or myosteatosis) as a biomarker of skeletal muscle health across conditions including metabolic disease, osteoarthritis, cardiovascular disease, and cancer. It highlights that while excess IMF correlates with poorer strength/power and adverse outcomes, increased IMF is not always pathological, leaving key uncertainties about interpretation and standardization. Scientifically, the review frames IMF’s strengths and limitations and identifies open challenges for using IMF as a reliable biomarker beyond muscle mass or cross-sectional area.

Spence C, Belzunce MA, Di Laura A et al. · Journal of cachexia, sarcopenia and muscle · (2026) · View on PubMed ↗ · Free PDF ↗

Pharmacological interventions for acute major depression and bipolar depression with mixed features: A systematic review and dose-related network meta-analysis across different age groups.

This systematic review and dose-related network meta-analysis synthesized randomized controlled trials in adults with acute major depression or bipolar depression with mixed features, stratifying analyses across different age groups. It compares pharmacological interventions by depressive symptom change, response, and acceptability while modeling dose effects. The results are scientifically significant because they provide quantitative, dose-informed comparative efficacy and tolerability to guide treatment selection for mixed-feature depression across ages.

Fornaro M, Di Lorenzo C, Nunez N et al. · Journal of affective disorders · (2026) · View on PubMed ↗

Prognostic role of the Child-Turcotte-Pugh classification and ALBI grade in patients without cirrhosis and hepatocellular carcinoma.

This cohort study assessed whether the Child-Turcotte-Pugh (CTP) classification and albumin-bilirubin (ALBI) grade predict prognosis in patients without cirrhosis and without hepatocellular carcinoma (HCC). It found prognostic value of CTP and/or ALBI in non-cirrhotic, non-HCC populations (including unresectable HCC cohorts and patients treated with atezolizumab/bevacizumab or durvalumab/tremelimumab in external databases). The clinical significance is that these widely used liver-function risk tools may help stratify outcomes even outside classic cirrhosis/HCC settings.

Balcar L, Brunetti L, Pomej K et al. · JHEP reports : innovation in hepatology · (2026) · View on PubMed ↗ · Free PDF ↗

Global, regional, and national burden of exposure to chewing tobacco, 1990-2023: a systematic analysis of the Global Burden of Disease Study 2023.

This Global Burden of Disease Study 2023 analysis estimated global, regional, and national prevalence of chewing tobacco exposure and the attributable health burden from 1990–2023 in people aged 15 years and older across 204 countries and territories. It quantifies how chewing tobacco use and its health impacts have changed over time, distinct from other smokeless tobacco products. The significance is policy-relevant because it provides updated, trackable burden estimates to support targeted tobacco control interventions for chewing tobacco.

The Lancet. Global health · (2027) · View on PubMed ↗ · Free PDF ↗

Sex differences in the efficacy, acceptability, and tolerability of antipsychotics in people with acute schizophrenia: individual participant data pairwise, dose-response, and network meta-analyses.

This individual participant data meta-analysis performed pairwise, dose-response, and network meta-analyses of antipsychotics in adults with acute schizophrenia to evaluate sex differences in efficacy, acceptability, and tolerability. It uses trial data from Vivli and YODA platforms (fixed-dose trials as main analyses) to compare outcomes between females and males across antipsychotic options. The clinical significance is that it can refine personalized prescribing by clarifying whether treatment benefits and side-effect profiles differ by sex.

Furukawa Y, Siafis S, Schneider-Thoma J et al. · The lancet. Psychiatry · (2026) · View on PubMed ↗ · Free PDF ↗

Identification of shared and divergent molecular pathways linking ambient air pollutants to mortality and major chronic diseases through proteomic profiling.

This study used proteomic profiling to identify shared versus pollutant- and outcome-specific molecular pathways linking ambient air pollutants to mortality and major chronic diseases. Leveraging UK Biobank proteomics from 48,645 participants, the authors characterized proteomic signatures associated with overall and individual pollutants (PM2.5, PM10, NO2, and NOx) and then tested potential mediating proteins underlying associations with mortality and chronic disease outcomes. The work helps map candidate biological mechanisms that may explain how air pollution contributes to multiple diseases and identifies proteins that could mediate these effects.

Jiang Y, Zhou S, Wu Q et al. · Redox biology · (2026) · View on PubMed ↗ · Free PDF ↗

A high intensity vs. casual speed walking intervention to reverse frailty among older adults: a cluster randomized controlled trial.

The study compared high-intensity walking (HIW) versus casual-speed walking (CSW) in a cluster randomized controlled trial to reverse frailty among older adults aged 60 years and older. HIW was tested for superiority in improving frailty outcomes relative to CSW in prefrail and frail participants recruited from 14 retirement communities. If effective, this would provide an actionable, scalable exercise prescription to reduce frailty and disability in aging populations.

Danilovich M, Rubin DS, Conroy DE et al. · PloS one · (2026) · View on PubMed ↗ · Free PDF ↗

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Autoimmunity, inflammatory disease and clinical management

Decision-making in paediatric palliative sedation: A vignette survey across five European countries.

This vignette survey studied how physicians across five European countries make decisions about initiating and managing paediatric palliative sedation therapy (PST) in two end-of-life scenarios. The key finding was that physician approaches varied in consultation processes and clinical procedures for PST initiation, reflecting the lack of comprehensive international/national guidelines. This is significant for guiding future guideline development and standardizing decision-making in paediatric palliative care.

Ferri Perez A, Robijn L, Beernaert K et al. · European journal of pediatrics · (2026) · View on PubMed ↗

Pheochromocytoma Across the Perioperative Course: Current Concepts and Clinical Management.

This review article synthesized current concepts and perioperative management strategies for patients with pheochromocytoma across the surgical course. It emphasizes that diagnosis requires biochemical confirmation of catecholamine excess followed by imaging localization, and that perioperative care should involve a multidisciplinary team with careful antihypertensive management to prevent target-organ complications. The clinical significance is improved recognition and safer perioperative planning to reduce morbidity from myocarditis/cardiomyopathy, cerebrovascular events, and diabetes mellitus.

Mirrakhimov AE, Bashall N · Anesthesiology research and practice · (2026) · View on PubMed ↗

Sugar-rich foods exacerbate antibiotic-induced microbiome disruption.

This clinical study tested whether diet composition affects gut microbiome disruption during extreme antibiotic perturbation by analyzing 9,419 meals from 173 hospitalized patients undergoing haematopoietic cell transplantation with longitudinal microbiome sampling. The key finding was that intake of sweets and sugars during antibiotic exposure predicted exacerbated dysbiosis, including reduced alpha-diversity and other adverse microbiome dynamics. The significance is that it identifies a modifiable dietary factor that could worsen microbiome recovery during antibiotic treatment, informing supportive care strategies in vulnerable patients.

Dai A, Ballweg A, Jogia W et al. · Nature · (2026) · 1 citations · View on PubMed ↗ · Free PDF ↗

A two-hit mechanism triggers autoimmune hair loss.

The study examined the initiation of autoimmune hair loss in a mouse model by testing how transient regulatory T (Treg) cell depletion during the hair cycle affects CD8+ T-cell responses and hair follicle stem cell (HFSC) survival. It found that Treg depletion specifically during the anagen phase triggers CD8+ T-cell-mediated destruction of immune-privileged HFSCs, causing autoimmune alopecia, and that susceptibility depends on sympathetic nerve activity. This reveals a two-hit mechanism—immune dysregulation plus physiological neural activation—that could inform timing- and pathway-specific interventions for tissue-targeted autoimmunity.

Cui J, Wu P, Chang Y et al. · Nature · (2026) · View on PubMed ↗

Immune Checkpoint Inhibitor Therapy Triggers Autoimmune Cerebellar Ataxia with Anti-P/Q-type VGCC Antibody and Anti-mGluR5 Antibodies: A Case Report.

This case report studied a 61-year-old man with small cell lung cancer who developed autoimmune cerebellar ataxia after durvalumab (an anti–PD-L1 immune checkpoint inhibitor) therapy. The patient had anti–P/Q-type voltage-gated calcium channel (VGCC) antibodies and anti–mGluR5 antibodies, and he improved after early immunotherapy and discontinuation of ICI therapy. The report is significant because it implicates anti-VGCC antibodies (and possibly anti-mGluR5) in ICI-triggered autoimmune cerebellar ataxia, supporting antibody-guided clinical evaluation and management.

Nakamura S, Yamada K, Yaguchi H et al. · Internal medicine (Tokyo, Japan) · (2026) · View on PubMed ↗ · Free PDF ↗

Comparative effectiveness and safety of upadacitinib versus vedolizumab in anti-TNF-exposed patients with ulcerative colitis.

This multicenter retrospective cohort study compared real-world effectiveness and safety of upadacitinib versus vedolizumab in anti-TNF-exposed adults with ulcerative colitis (UC) who had a partial adapted Mayo score ≥2. Outcomes were assessed at weeks 16 and 26 with endoscopy at week 26, and the primary endpoint was steroid-free symptomatic remission (SFSR) at week 16 (rectal bleeding subscore = 0, with additional criteria truncated). Clinically, the results aim to guide treatment selection in anti-TNF-exposed UC patients by comparing symptom and endoscopic outcomes across two different mechanisms.

Wan J, Zhang H, Yuan X et al. · Inflammatory bowel diseases · (2026) · View on PubMed ↗

Restoring epithelial health in epithelial-driven disease through an early treat-to-target approach: improving patient care towards clinical remission.

This invited Epithelial Science Expert Group review assessed airway epithelial health and strategies to restore epithelial barrier, immune activity, and mucociliary dynamics in upper and lower inflammatory airway diseases. It highlights an early treat-to-target approach as a way to restore epithelial health and improve the likelihood of achieving clinical remission. The synthesis is clinically significant because it reframes epithelial dysfunction as a modifiable driver of airway inflammation and supports earlier, targeted management to improve outcomes.

Dorscheid D, Aegerter H, Caminati M et al. · The Journal of allergy and clinical immunology · (2026) · View on PubMed ↗

Low back pain flares: Reflections on how physical activity, sleep, and stress shape individual experiences.

This qualitative study used semi-structured face-to-face interviews and inductive reflexive thematic analysis in 29 adults with low back pain to explore how individuals perceive the roles of physical activity, sleep, and stress in “flares.” It identified how these factors are experienced as shaping flare onset, intensity, and emotional impact at the individual level. The significance is that patient-centered understanding of flare drivers can inform more tailored self-management and behavioral interventions for fluctuating low back pain.

Dorgelo P, Besomi M, Collyer M et al. · The journal of pain · (2026) · View on PubMed ↗ · Free PDF ↗

Single-Cell Mapping of the Gut Epithelium Reveals Paneth Cell Dysfunction and Lysozyme Deficiency in Peanut Allergy.

This study used single-cell RNA sequencing (scRNA-seq) to map the small intestinal epithelium in naïve peanut allergy-susceptible CC027 mice and identify epithelial dysfunction mechanisms. It reports Paneth cell dysfunction and lysozyme deficiency as key features associated with peanut allergy susceptibility. The scientific significance is that it pinpoints specific epithelial cell defects (Paneth/lysozyme axis) that could be targeted to prevent or treat peanut allergy.

Clough KM, Gomez-Martinez I, Cannon G et al. · Cellular and molecular gastroenterology and hepatology · (2026) · View on PubMed ↗ · Free PDF ↗

Real-world effectiveness and safety of risankizumab induction and maintenance therapy in pediatric patients with Crohn’s disease: a multicenter retrospective analysis.

The study evaluated real-world effectiveness, durability, safety, and dosing of risankizumab in pediatric Crohn’s disease by analyzing a global multicenter retrospective cohort of patients under 18 years initiating risankizumab monotherapy (2022–2025). Risankizumab induction and maintenance were assessed using corticosteroid-free clinical remission (wPCDAI-based), clinical response, CRP remission, intestinal ultrasound remission, and remission at Weeks 30 and 54. These data address the evidence gap for pediatric use of risankizumab and inform clinicians about expected outcomes and safety in routine practice.

Spencer EA, Buck Q, Collen LV et al. · Journal of Crohn’s & colitis · (2026) · View on PubMed ↗

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Generated automatically on October 02, 2026 from PubMed’s trending articles. Summaries are AI-generated; always consult the original publication for clinical or research decisions.