PubMed Trending Research Digest — July 09, 2026

Automated digest · 95 articles · 15 research areas · July 09, 2026

Overview

Across this week’s papers, a dominant theme is precision targeting—either by exploiting specific biological dependencies or by stratifying patients using increasingly granular molecular and clinical data. In oncology, multiple studies converge on vulnerabilities that are not captured by single biomarkers alone: metastatic breast cancer cells show cystine addiction; gastric and pancreatic cancers reveal metabolism–epigenetic linkages (ALDH6A1–MMA–KDM5C–H3K4me2; HDAC5–FOXA1 acetylation driving HIF1α programs); and tumor-derived apoptotic extracellular vesicles can rewire mitochondrial metabolism to influence hepatocellular carcinoma progression. Meanwhile, immune-focused work highlights how microenvironmental context governs response—such as immune-excluded brain metastases in NSCLC and lymphatic remodeling driven by Jagged1+ Tregs—supporting combination or sequencing strategies (e.g., radiotherapy plus checkpoint blockade, anti–PD-1/anti–CTLA-4 to reshape brain-metastasis immunity).

A second major thread is “systems biology” approaches that connect molecular mechanisms to outcomes. Several studies use multi-omics and computational frameworks—single-cell atlases of myeloma TME ecotypes, chromatin accessibility subgrouping in AML, and multi-omics risk scores in heart failure—to move beyond one-dimensional prognostication. In parallel, diet–microbiome and metabolic interventions are increasingly mechanistic: time-restricted eating shifts liver fat and fecal microbiota; obesity-associated anti-tumor immunity depends more on diet–gut axis than generic metabolic dysfunction; and probiotic metabolite profiles can drive cross-feeding that shapes colonization.

Finally, the digest underscores broad translational momentum beyond cancer. Neurodegeneration papers (C9ORF72, TDP-43/ANXA11, microglial TDP-43, and VPS13C structure) emphasize subcellular mechanisms—ion-channel dysregulation, protein aggregation interfaces, interferon–oligodendrocyte dysfunction, and lipid-transfer conformational control—while cardiovascular and infectious disease studies refine risk prediction and surveillance (cognitive impairment–AF links; stroke risk indices; adult SARI pathogen profiling; and malaria resistance marker mapping). Together, these findings reflect a field-wide shift toward mechanism-informed, data-rich interventions.

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Cancer metabolism & metabolic vulnerabilities

Reprogramming of valine metabolism mediated by abnormally low ALDH6A1 expression promotes invasive metastasis of gastric cancer.

This study used a CRISPR-Cas9 metabolic knockout screen integrated with patient transcriptomes to identify ALDH6A1 as a mitochondrial enzyme that suppresses invasion in gastric cancer, and then investigated downstream mechanisms. It showed that abnormally low ALDH6A1 reprograms valine metabolism by blocking terminal valine catabolism, causing methylmalonic acid (MMA) accumulation that inhibits the histone demethylase KDM5C and increases H3K4me2 at invasion gene promoters including ANGPT2 and MMP7. These findings link a specific metabolic-epigenetic axis (ALDH6A1–MMA–KDM5C–H3K4me2) to metastatic progression, suggesting potential therapeutic targets.

Wang J, Han L, Li G et al. · Science advances · (2026) · View on PubMed ↗

Tumor-derived apoptotic extracellular vesicles impede hepatocarcinoma progression by disrupting mitochondrial metabolism.

This study investigated whether tumor-derived apoptotic extracellular vesicles (Apo-EVs) alter hepatocellular carcinoma (HCC) progression by disrupting mitochondrial metabolism using in vitro and in vivo models. Apo-EVs impeded HCC progression by affecting tumor cell proliferation/apoptosis and by carrying functional cargo that modulated ATP synthesis and metabolic regulation. These mechanistic insights suggest Apo-EVs could be explored as therapeutic or biomarker-relevant mediators targeting mitochondrial metabolic vulnerabilities in HCC.

Chen Y, Wang X, Yuan T et al. · Journal of translational medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Bispecific 10E8.4/iMab broadly neutralizing antibody in people with or without HIV-1: a partially randomized phase 1 trial.

The study evaluated the safety, pharmacokinetics, antiviral activity, and immunologic effects of the bispecific antibody 10E8.4/iMab in a partially randomized phase 1 trial in people with or without HIV-1. 10E8.4/iMab, which targets the HIV-1 envelope membrane-proximal external region (10E8.4 arm) and human CD4 (iMab arm), was administered IV or SC and assessed for early tolerability (2-week primary outcome) along with CD4+ and CD8+ T-cell dynamics and long-term safety. This first-in-human dataset informs clinical development of a dual-target bnAb strategy for HIV prevention and treatment.

Theodore DA, Mayer BT, Rolle CP et al. · Nature medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Substrate recognition and transport mechanism of the human proton-coupled amino-acid transporter 1 (SLC36A1).

The study determined the substrate recognition and transport mechanism of the human proton-coupled amino-acid transporter 1, SLC36A1 (hPAT1), using cryo-electron microscopy structures. It reported cryo-EM structures of hPAT1 in apo form and bound to three chemically distinct substrates—D-serine, nipecotic acid, and the CNS-active drug D-cycloserine—at ~3.4–3.5 Å resolution. These structural insights clarify how hPAT1 couples H+ transport to amino-acid analog uptake and mTORC1/lysosomal amino-acid export regulation, informing rational targeting of this transporter.

Yin J, Zhang S, Liu C et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Loss of the USP22 deubiquitylase confers resistance to chemotherapy in small cell lung cancer.

This study used in vivo CRISPR deletion screening in patient-derived xenograft (PDX) models of small cell lung cancer (SCLC) to identify genetic drivers of chemotherapy resistance to cisplatin–etoposide. Loss of the SAGA complex deubiquitylase USP22 conferred cisplatin–etoposide resistance in two chemosensitive PDX models, and restoring USP22 expression reversed resistance in a PDX model with a homozygous truncating USP22 mutation. These results implicate USP22 as a mechanistic determinant of SCLC chemoresistance and a potential therapeutic target to prevent relapse.

Best S, Hippe DS, Grunblatt E et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

ACSL3 inhibits ferroptosis in gastric cancer through the activation of unfolded protein response following endoplasmic reticulum stress.

This study investigated the role of ACSL3 (long-chain acyl-CoA synthetase 3) in gastric cancer (GC) using in vivo and in vitro experiments to determine how it affects ferroptosis and tumor progression. ACSL3 inhibited ferroptosis and promoted GC progression by activating endoplasmic reticulum (ER) stress–triggered unfolded protein response (UPR) via YY1 nuclear translocation, with YY1 directly binding the USP37 promoter to enhance USP37 transcription. These mechanistic links position the ACSL3–YY1–USP37–UPR axis as a regulator of ferroptosis susceptibility and a potential target pathway in GC.

Wang H, Jiao J, Yang W et al. · Cell death & disease · (2026) · View on PubMed ↗ · Free PDF ↗

Targeting Cystine Addiction Suppresses Breast Cancer Lung Metastasis.

This study used in vivo and ex vivo MYC-driven breast tumor models to define metabolic vulnerabilities of lung-metastasizing cells, applying stable isotope-resolved metabolomics, mass spectrometry imaging, and single-cell RNA sequencing. The authors report that targeting cystine addiction suppresses MYC-driven breast cancer lung metastasis. These findings identify cystine metabolism as a tractable therapeutic vulnerability for metastatic breast cancer and support metabolism-guided anti-metastatic drug development.

Tarragó-Celada J, Mahmood AS, Panina Y et al. · Cancer research · (2026) · View on PubMed ↗

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Tumor microenvironment, immune modulation & immunotherapy

Metabolically and epigenetically reprogrammed splenic TRNP1hiCD8+ T cells exacerbate liver fibrosis.

The study investigated whether splenic TRNP1hiCD8+ T cells in humans and mouse models of metabolic dysfunction-associated steatotic liver disease (MASLD)/MASH drive liver fibrosis, focusing on metabolic and epigenetic reprogramming and the mechanism of pro-fibrotic signaling. TRNP1hiCD8+ T cells were expanded in MASLD/MASH and promoted fibrosis via secretion of INSR-α, with demethylated DNA and altered histone marks (including increased H3K27ac and reduced H3K27me3) and enhancer–promoter chromatin topology changes supporting the pro-fibrotic program. This links a specific immune-cell subset and epigenetic remodeling to fibrogenesis in MASLD/MASH, highlighting INSR-α–mediated pathways as potential therapeutic targets.

Zhang L, Wang Y, Wei K et al. · Nature genetics · (2026) · View on PubMed ↗

SMOC2 mediates GLI1+ mesenchymal cell-driven fibrostenosis and predicts postoperative recurrence in Crohn’s disease.

The study assessed whether SMOC2 expressed by GLI1+ mesenchymal cells drives fibrostenosis in Crohn’s disease and whether it predicts postoperative recurrence, using single-cell RNA sequencing of human and mouse intestinal tissue plus clinical tissue analyses. GLI1+ mesenchymal cells mediated fibrostenotic progression in Crohn’s disease models, and SMOC2 was implicated as a key mediator with postoperative recurrence prediction value. This identifies a GLI1+ mesenchymal–SMOC2 axis as a potential biomarker and therapeutic target for preventing Crohn’s fibrostenosis and recurrence.

Wang D, Zhao X, Yang Q et al. · Gut · (2026) · View on PubMed ↗

Macrophage-Induced Senescent Cancer-Associated Fibroblasts Promote SASP-Mediated Chemoresistance in Colorectal Cancer.

This study used a machine learning-based Cellular Senescence Prediction Model (CSPM) trained on single-cell RNA sequencing to identify senescent cancer-associated fibroblasts (sCAFs) in colorectal cancer (CRC) and then tested their role in chemoresistance. It found that higher sCAF abundance correlated with impaired chemotherapy responsiveness and poor prognosis, and that macrophage-induced senescent CAFs promote SASP-mediated chemoresistance in preclinical CRC models including subcutaneous tumors and patient-derived organoids (PDOs). These findings suggest that targeting senescence/SASP programs in CAFs could improve chemotherapy efficacy in CRC.

Yang S, Chen Y, Liu S et al. · Cancer research · (2026) · View on PubMed ↗

Fibroblasts: a diverse population of cells balancing homeostasis, wound healing, regeneration, inflammation, fibrosis, and cancer across organs.

This review examined the roles of fibroblasts and fibroblast-like cells across organs in development, homeostasis, wound healing, regeneration, inflammation, fibrosis, and cancer. It highlights that fibroblasts act as ECM-producing “sentinels” regulating epithelial, endothelial, and immune cell function and recruitment, while also contributing to maladaptive fibrosis and tumor progression. Understanding this balance is clinically important because targeting fibroblast states may improve outcomes in fibrotic disease and cancer without disrupting essential homeostatic tissue maintenance.

Yang X, Steffani M, Nadella S et al. · JCI insight · (2026) · View on PubMed ↗ · Free PDF ↗

Primary sclerosing cholangitis displays distinct colonic mucosa topography yet a shared mast cell state with ulcerative colitis.

This study compared colonic mucosal biology in patients with primary sclerosing cholangitis–ulcerative colitis (PSC-UC) versus ulcerative colitis (UC) using single-cell mRNA and antigen receptor sequencing, 16S rRNA gene profiling, and spatial transcriptomics across four colon regions during endoscopic remission or relapse. PSC-UC showed distinct colonic mucosa topography from UC while sharing a mast-cell state with UC. These findings suggest that PSC-UC has UC-like mast-cell–driven immune programming but region-specific tissue organization that may help explain differences in flare patterns and colorectal cancer risk.

Tearle JL, Sviriaeva E, Zhang F et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Anti-PD-1 plus anti-CTLA-4 blockade overcomes immune exclusion in NSCLC brain metastases by enhancing CD8+ T cell responses and promoting tertiary lymphoid structure formation.

This study evaluated immune resistance in non-small cell lung cancer (NSCLC) brain metastases by integrating clinical outcome analyses, paired human tissue profiling, and syngeneic mouse models, focusing on responses to nivolumab (anti–PD-1) plus ipilimumab (anti–CTLA-4). Combination therapy improved intracranial disease control and was associated with an immune-excluded phenotype characterized by fewer CD8+ cytotoxic T lymphocytes and fewer tertiary lymphoid structures than primary tumors, which the syngeneic model recapitulated. Clinically, these data support anti–PD-1/anti–CTLA-4 strategies to overcome brain-metastasis immune exclusion by boosting CD8+ T-cell responses and promoting tertiary lymphoid structure formation.

Hosoya K, Ozasa H, Tsuji T et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Discovery of a non-canonical TREM2-S100A9 axis that drives pro-tumorigenic macrophage polarization and sensitizes ovarian clear cell carcinoma to IL-17 blockade.

This study examined how ovarian clear cell carcinoma (OCCC) shapes the tumor microenvironment by characterizing tumor-associated macrophage (TAM) polarization, focusing on a non-canonical TREM2–S100A9 axis and its impact on IL-17 blockade sensitivity. TREM2 was highly expressed on OCCC-related TAMs and promoted pro-tumorigenic M2 polarization, with mechanistic work indicating TREM2 bypassed classic adaptor signaling and directly interacted with downstream components to drive the pathway. The findings identify a TREM2–S100A9 macrophage program that could both explain immunosuppression in OCCC and sensitize tumors to IL-17–targeted therapy.

Zhang ST, Zhang SM, Jiang F et al. · Cell death discovery · (2026) · View on PubMed ↗ · Free PDF ↗

Chinese Expert Consensus on Radiotherapy Combined with Immunotherapy for Unresectable Lung Cancer (2026 Edition).

This Chinese expert consensus reviewed evidence and provided recommendations on combining radiotherapy with immunotherapy for unresectable lung cancer, synthesizing mechanistic rationale and clinical trial data. The consensus emphasizes the synergistic effects of radiotherapy-induced immune modulation with immune checkpoint blockade and outlines practical considerations for patient selection and treatment sequencing. Clinically, it aims to standardize care pathways for unresectable lung cancer where radiotherapy–immunotherapy combinations are increasingly used.

Wang L, Liu Y, Zhao W et al. · Cancer letters · (2026) · View on PubMed ↗

SERD Wars: Clinical Integration of Emerging Endocrine-Directed and Precision Therapies in Breast Cancer.

This review article synthesized how emerging endocrine-directed and precision therapies are being integrated into clinical decision-making for breast cancer, particularly endocrine-resistant metastatic disease. It highlighted that acquired ESR1 mutations drive ligand-independent estrogen receptor activation and reduce sensitivity to standard antiestrogens, motivating next-generation ER-directed therapies. Scientifically and clinically, it frames how to sequence and combine precision endocrine strategies to improve outcomes in HR+/HER2- metastatic breast cancer.

Lloyd MR, Shatsky RA, Love N et al. · JCO oncology practice · (2026) · View on PubMed ↗

Jagged1+ Tregs mediate lymphatic remodeling in tumor-draining lymph nodes.

This study investigated how Jagged1-expressing regulatory T cells (Jag1+ Tregs) shape tumor-draining lymph node (tdLN) remodeling in the B16-F10 melanoma mouse model, using conditional Jag1 deletion in Tregs (Foxp3ΔJag1) and transcriptomic profiling. Jag1 expression increased in late-stage tdLN Tregs, and deleting Jag1 in Tregs attenuated tdLN expansion with stromal-related transcriptional changes linked to lymphatic endothelial cell (LEC) biology. The results implicate Jagged1 signaling from Tregs as a driver of lymphatic remodeling during tumor progression, suggesting a potential immuno-stromal target to limit metastatic spread.

Xu JZ, Tsai PH, PokWai Lui P et al. · Cell reports · (2026) · View on PubMed ↗ · Free PDF ↗

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T-cell biology, regulatory T cells & immune checkpoints

Clinical rationale for thymic restoration in adult immunosenescence.

This review examined the scientific rationale for thymic restoration as a strategy to counter adult immunosenescence, focusing on age-related thymic involution and its downstream effects on T-cell immunity. It highlights that reduced FOXN1-driven thymopoiesis leads to diminished naïve T-cell output, a contracted TCR repertoire, and impaired central tolerance, contributing to worse infection/cancer/autoimmunity risk and poorer vaccine responses (including to SARS-CoV-2). The synthesis supports ongoing development of thymic restoration interventions as a way to rejuvenate immune function in older adults.

Sewell PE, Jensen C · Immunity & ageing : I & A · (2026) · View on PubMed ↗ · Free PDF ↗

Transcription factor BHLHE40 expression in group 3 innate lymphoid cells and RORγt⁺ antigen-presenting cells coordinates intestinal immunity.

This mechanistic immunology study used conditional deletion models to define how the transcription factor BHLHE40 regulates group 3 innate lymphoid cells (ILC3s) and RORγt+ antigen-presenting cells (APCs) in intestinal immunity. BHLHE40 coordinated mucosal immune programs by driving cytokine effector transcription in ILC3s and by being required in RORγt+ APCs, with TL1A-induced Bhlhe40 expression amplifying effector programs via epigenetic modulation of chromatin accessibility. These findings identify BHLHE40 as a central transcriptional node linking ILC3 and APC function, offering a potential target for modulating intestinal immune balance.

Yang W, Pires S, Cardakli E et al. · Immunity · (2026) · View on PubMed ↗

Both soluble and cell surface CD137 expressed by Foxp3+ CD4 T cells restrain autoimmune diabetes.

This study examined how CD137 expressed by Foxp3+ CD4 regulatory T cells (Tregs) restrains autoimmune diabetes using the NOD mouse model of type 1 diabetes (T1D). Foxp3+ Treg-specific deletion of CD137 reduced soluble CD137 and accelerated T1D, driven by increased clonal expansion and effector differentiation of T cells in pancreatic islets, and CD137 deficiency impaired Treg suppressive differentiation. The findings establish both soluble and cell-surface CD137 as functional brakes on autoimmune diabetes and suggest CD137 pathways as therapeutic targets.

Nabi R, Lin CW, Wang Y et al. · The Journal of experimental medicine · (2026) · View on PubMed ↗ · Free PDF ↗

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Epigenetics, chromatin regulation & transcriptional control

Chromatin landscape and epigenetic heterogeneity of acute myeloid leukaemia.

The study profiled acute myeloid leukemia (AML) chromatin accessibility using ATAC-seq in the eCHROMA cohort of 1,563 newly diagnosed patients to define epigenetic subgroups and relate them to multi-omics features. AML could be classified into 16 subgroups based on chromatin accessibility profiles, and integrative analyses linked chromatin states with genetic and transcriptomic variation. This supports epigenetic heterogeneity as a major axis of AML stratification, with potential implications for prognosis and therapy selection beyond DNA mutations alone.

Ochi Y, Liew-Littorin M, Nannya Y et al. · Nature · (2026) · View on PubMed ↗

Epigenetic biomarkers and the progression of Barrett’s oesophagus to oesophageal adenocarcinoma: a systematic review protocol.

This protocol outlines a systematic review to identify epigenetic biomarkers associated with progression of Barrett’s oesophagus (BO) to oesophageal adenocarcinoma (OAC). The review will synthesize evidence from studies using epigenetic assays (e.g., DNA methylation and related biomarker approaches) to predict which BO patients will progress, in the context of current dysplasia-guided endoscopic surveillance. Establishing validated epigenetic predictors could reduce unnecessary surveillance biopsies and improve risk stratification for BO patients.

Johnston DN, Coleman HG, McKnight AJ et al. · Systematic reviews · (2026) · View on PubMed ↗ · Free PDF ↗

PP2A phosphatase regulates Hippo signalling in dual manner.

The study investigated how the serine/threonine phosphatase PP2A regulates Hippo signaling in Drosophila cell culture and wing discs, focusing on the PP2A holoenzyme containing the Wrd regulatory subunit (PP2AWrd). PP2AWrd counteracted Crumbs-mediated Hippo pathway activation by dephosphorylating and stabilizing the Expanded (Ex) FERM-domain protein. This reveals a dual regulatory mechanism for PP2A in Hippo signaling and clarifies how polarity cues are integrated to control tissue growth.

Sekar A, Rizzo A, Sins E et al. · The EMBO journal · (2026) · View on PubMed ↗ · Free PDF ↗

ChAHP silences SINE retrotransposons by inhibiting TFIIIB recruitment.

The study investigated how the ChAHP complex represses transcription of SINE retrotransposons, focusing on SINE B2 elements in mouse embryonic stem cells. It found that ChAHP is a key repressor by inhibiting TFIIIB recruitment to SINE B2 promoters, whereas DNA methylation and heterochromatin play only a minor role in this context. These findings clarify a specific POL III transcription control mechanism for SINE silencing and suggest new targets for limiting transposon-driven genome instability.

Schnabl-Baumgartner J, Mohn F, Schwaiger M et al. · Molecular cell · (2026) · 1 citations · View on PubMed ↗ · Free PDF ↗

Remodeling activity of ChAHP restricts transcription factor access to chromatin.

The study examined how the ChAHP complex remodels chromatin to restrict transcription factor access, using mouse embryonic stem cells and focusing on the ChAHP components ADNP, CHD4, and HP1. It found that CHD4 remodeling activity is essential for antagonizing CTCF binding and silencing transposon transcription, while HP1 proteins are dispensable. This mechanistic insight links a defined chromatin remodeling function to transcription factor exclusion and transposon repression.

Ahel J, Mohn F, Schwaiger M et al. · Molecular cell · (2026) · 1 citations · View on PubMed ↗ · Free PDF ↗

HDAC5 depletion promotes hyper-acetylation of FOXA1 and potentiates HIF1α transcriptional activation in pancreatic cancer.

The study investigated in pancreatic ductal adenocarcinoma models how depletion of histone deacetylase 5 (HDAC5) affects FOXA1 acetylation and downstream transcriptional programs. It found that HDAC5 deacetylates FOXA1 at lysine 270 (K270), and that HDAC5 loss causes FOXA1 K270 hyper-acetylation that reprograms FOXA1 to HIF1α-target gene transcription start sites, potentiating HIF1α transcriptional activation. This identifies an HDAC5–FOXA1 acetylation switch that promotes hypoxia signaling in PDAC and suggests a potential epigenetic vulnerability.

Qin G, Yu H, Zhao Y et al. · Molecular cell · (2026) · View on PubMed ↗

Convergent mechanisms in Wnt and Hedgehog signaling.

This review summarizes convergent mechanisms shared by the Wnt and Hedgehog (Hh) signaling pathways, focusing on how intracellular signal transmission is regulated. It highlights evidence that tethered pseudosubstrate inhibition of kinases is a core shared mechanism in both pathways, alongside other parallels such as phosphorylation-dependent control of transcriptional effectors. The convergence on common regulatory logic suggests that Wnt and Hh can produce distinct outputs while using overlapping molecular control strategies, with implications for pathway-targeted therapeutics.

Myers BR, Zalatan JG, Virshup DM · Science signaling · (2026) · View on PubMed ↗

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Genomics, biomarkers & multi-omics risk stratification

Aneuploidy selects for the acquisition of driver genes in breast cancer.

The study developed and applied CRISPR-KOALA, a CRISPR knockout/activation linked high-throughput bidirectional screening assay, to determine how aneuploidy selects for driver gene acquisition in immunocompetent mouse models of basal-like breast cancer (BLBC). Using CRISPR-KOALA to screen mouse orthologs of 3,752 genes located within the ten most frequent human chromosome-arm-level alterations in BLBC, the authors identified gene drivers whose gain/loss effects are favored by aneuploidy. This advances causal mapping of aneuploidy-driven tumorigenesis and provides a scalable approach to pinpoint actionable driver genes in copy-number–driven cancers.

Al-Zahrani KN, Langille ER, Nurtanto J et al. · Nature · (2026) · View on PubMed ↗

ApoE lipoproteins in the central nervous system under homeostasis and role in Alzheimer’s disease and related disorders.

This review summarized the role of apolipoprotein E (ApoE) lipoproteins in the CNS under homeostasis and their involvement in Alzheimer’s disease and related disorders. It emphasizes that ApoE lipoproteins—primarily secreted by astrocytes (with microglial ApoE under certain conditions)—carry distinct lipid/protein cargo that influences brain lipid homeostasis and disease processes. Understanding ApoE lipoprotein biology could inform therapeutic strategies targeting ApoE-mediated pathways in Alzheimer’s disease.

Strickland MR, Holtzman DM · Molecular neurodegeneration · (2026) · View on PubMed ↗ · Free PDF ↗

Proteomic markers enhance mortality prediction in heart failure.

This study evaluated whether molecular risk stratification using a cardiovascular polygenic risk score (PRS) from DNA sequence polymorphisms, a methylation risk score (MRS) from epigenome-wide associations, and a 23-protein proteomic score (ProteomicDeat) improves mortality prediction in 2432 patients with heart failure from the G-CHF registry. The proteomic score provided incremental prognostic information beyond established clinical predictors, enhancing risk stratification for mortality. These findings support adding multi-omics (especially proteomics) to clinical models to better capture heart-failure progression biology and improve prognostic accuracy.

Meyre PB, Li Y, da Rocha GL et al. · European heart journal · (2026) · View on PubMed ↗

Oncogenic PIK3CA mutation enhances tumor immunogenicity through the IRF1-NLRC5-MHC-I axis in urothelial carcinoma.

This retrospective study analyzed 67 patients with metastatic urothelial carcinoma treated with immune checkpoint inhibitors using targeted next-generation sequencing with a 440-gene panel to identify genomic biomarkers of immunogenicity and treatment outcomes. Oncogenic PIK3CA mutations were associated with increased tumor immunogenicity through an IRF1–NLRC5–MHC-I axis, linking PIK3CA status to potential ICI responsiveness. The results suggest PIK3CA-driven pathway activity could help refine biomarker selection for immunotherapy in metastatic urothelial carcinoma.

Su YL, Huang SY, Kuo CW et al. · Journal for immunotherapy of cancer · (2026) · View on PubMed ↗ · Free PDF ↗

Transcriptomics of type 1 diabetes progression: a validation study in newly diagnosed patients.

The study validated transcriptomic biomarkers of type 1 diabetes progression in newly diagnosed patients using an independent follow-up INNODIA cohort and combined it with the original cohort for increased power. It assessed whether early gene expression changes after diagnosis predict later C-peptide decline, focusing on insulin secretion trajectory variability. This supports transcriptome-based risk stratification for disease progression and could help tailor monitoring and future interventions in newly diagnosed type 1 diabetes.

Suomi T, Starskaia I, Rasool O et al. · EBioMedicine · (2026) · View on PubMed ↗ · Free PDF ↗

Single Cell Analysis of the Tumor Microenvironment Landscape Across the Disease Spectrum of Multiple Myeloma.

This study used integrated paired single-cell RNA sequencing plus T-cell and B-cell receptor sequencing to map the tumor microenvironment (TME) across the multiple myeloma disease spectrum in bone marrow samples from 235 patients. The authors identified dynamic shifts in immune-cell abundance and functional states and, using non-negative factorization of cell-subset composition, defined five reproducible TME “ecotypes” with coordinated cellular architectures. This single-cell atlas provides a framework for understanding immune dysregulation and therapeutic resistance and for stratifying patients by TME state.

Dang M, Moreno Rueda LY, Acevedo Calado MJ et al. · Blood · (2026) · View on PubMed ↗

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Targeted therapies & drug development (small molecules/ADCs/CAR-T/biologics)

Microglial TDP-43 mediates myelin refinement and represses Tyrobp cryptic exon inclusion in mice.

The study examined how microglial TDP-43 loss affects early postnatal mouse brain development, using MRI plus confocal and electron microscopy, and spatial transcriptomics to assess oligodendrocyte-related pathways. Mice lacking microglial TDP-43 showed structural brain changes, myelin refinement defects, and an interferon-responsive transcriptional program linked to oligodendrocyte dysfunction, with early depletion also producing motor deficits. These findings identify microglial TDP-43 as a regulator of myelin maturation and suggest that interferon/oligodendrocyte dysregulation may contribute to neurodegeneration-relevant phenotypes in TDP-43 proteinopathies.

Compagnion AC, Ivanov A, Rana A et al. · Nature neuroscience · (2026) · View on PubMed ↗

Chemically synthesized, non-capped and non-polyadenylated peptide-coding RNA efficiently induces antigen-specific CD8+ T cells.

The study examined whether short, chemically synthesized, non-capped and non-polyadenylated peptide-coding RNA oligonucleotides can be translated to stimulate antigen-specific CD8+ T cells in vitro and in vivo. The authors found that a ChemRNA design with a 5’-OH-AUG-coding sequence-3’-OH structure efficiently induces antigen-specific CD8+ T-cell responses despite lacking typical mRNA features such as the 5’ cap and 3’ poly(A) tail. This challenges canonical mRNA design rules and supports a simplified RNA vaccine modality for eliciting CD8+ T-cell immunity.

Frei J, Eisel D, Jarzebska NT et al. · Nature biomedical engineering · (2026) · View on PubMed ↗ · Free PDF ↗

Mavacamten shows broad benefit in human and mouse models of MYBPC3-related hypertrophic cardiomyopathy.

The study tested whether mavacamten benefits hypertrophic cardiomyopathy (HCM) driven by MYBPC3 variants by combining mechanistic mouse knock-in models (including cMyBP-C p.R502W) with human and mouse experimental systems. Mavacamten showed broad benefit across models, and in the p.R502W knock-in mice the variant produced pathogenic remodeling with preserved cMyBP-C localization, linked to reduced cMyBP-C–myosin affinity, increased Ca2+ sensitivity, and a favored ON myosin state. These results support mavacamten as a potentially broadly effective therapy for MYBPC3-related HCM, including mechanisms distinct from truncation variants.

Sen-Martín L, Fernández-Trasancos Á, López-Unzu MÁ et al. · Nature cardiovascular research · (2026) · View on PubMed ↗

Mantle cell lymphoma artificial intelligence prognostic index using hematoxylin and eosin histology.

The study developed and validated MAIPI (MCL Artificial Intelligence Prognostic Index), a deep learning prognostic model trained on hematoxylin and eosin (H&E) images of diagnostic biopsies from mantle cell lymphoma (MCL) patients. MAIPI predicted clinical outcomes in an independent cohort treated with immunochemotherapy with and without ibrutinib, demonstrating prognostic performance without requiring specialized molecular assays. This provides a practical, pathology-only risk stratification tool that could help guide treatment selection in MCL.

Lippl J, Reinke S, Koch K et al. · Leukemia · (2026) · View on PubMed ↗ · Free PDF ↗

Functional and omics-based rationale for the induction of BRCAness by androgen receptor pathway inhibitors to sensitize prostate cancer to PARP inhibition, regardless of HRR status.

The study assessed whether androgen receptor pathway inhibitors (ARPIs) induce “BRCAness” to sensitize prostate cancer to PARP inhibition regardless of homologous recombination repair (HRR) status. Using prostate cancer cell lines, metastatic patient-derived organoids (mPDOs), and LN-metastatic tissue slice cultures, the authors tested olaparib and talazoparib with ARPIs (abiraterone, enzalutamide, apalutamide) and used HRDetect plus multi-omics analyses to define response mechanisms in HRR-negative settings. This provides a functional and omics-based rationale for combining ARPIs with PARP inhibitors beyond HRR biomarkers in metastatic castration-resistant prostate cancer.

Elsesy ME, Moustafa A, Oh-Hohenhorst SJ et al. · British journal of cancer · (2026) · View on PubMed ↗ · Free PDF ↗

Ifebemtinib plus garsorasib as first-line treatment for KRASG12C-mutated non-small-cell lung cancer in China: a multicentre, single-arm expansion cohort from a phase 1b/2 trial.

This multicenter phase 1b/2 single-arm expansion cohort evaluated first-line ifebemtinib (a selective oral FAK inhibitor) plus garsorasib (a KRASG12C inhibitor) in patients with KRASG12C-mutated non-small-cell lung cancer in China. The combination demonstrated clinically meaningful safety and anti-tumor activity in this KRASG12C population, consistent with preclinical synergy between FAK inhibition and KRASG12C blockade. The study supports further development of dual targeting strategies for KRASG12C NSCLC by combining pathway inhibition with KRAS-specific therapy.

Song Z, Li X, Lin R et al. · The Lancet. Respiratory medicine · (2026) · View on PubMed ↗

A ligandable PNT domain establishes ERG as a directly targetable oncogenic driver in prostate cancer.

The study investigated whether ERG, driven by the TMPRSS2:ERG gene fusion in metastatic prostate cancer, contains a druggable pocket and remains therapeutically targetable. Using inducible shRNA in TMPRSS2:ERG-positive VCaP cells, it showed ERG dependency for growth and identified a ligandable pocket within ERG’s N-terminal Pointed (PNT) domain. This establishes ERG as a directly targetable oncogenic driver and provides a structural rationale for developing PNT-domain ERG inhibitors.

Wang X, Liu W, Yang J et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗ · Free PDF ↗

Structural insights into the nairovirus nucleoprotein endonuclease activity.

This study investigated the nucleoprotein (NP) of the representative nairovirus Tacheng tick virus 1 (TcTV1) to determine whether, beyond genome encapsidation, NP has additional roles during viral replication. TcTV1 NP binds nucleic acids in a sequence-independent manner and forms tetramer-based ribonucleoprotein complexes, accompanied by a conformational rearrangement that enables endonuclease activity. These structural insights into the NP endonuclease mechanism identify a potential antiviral target in nairovirus replication where no effective therapies currently exist.

Li Z, Du S, Gao F et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗ · Free PDF ↗

Concurrent administration of BCMA and GPRC5D chimeric antigen receptor (CAR) T cells in advanced multiple myeloma.

This phase I dose-escalation trial assessed safety of concurrent infusion of BCMA-directed and GPRC5D-directed chimeric antigen receptor (CAR) T cells in heavily pre-treated relapsed/refractory multiple myeloma. Patients received either MCARH125 (BCMA CAR T) alone or in combination with MCARH109 (GPRC5D CAR T), with the primary objective being safety of concurrent administration. The trial addresses antigen heterogeneity (variable BCMA and GPRC5D expression) by testing a dual-target strategy that could reduce immune escape in advanced myeloma.

Mailankody S, Mitra S, Herrera K et al. · Blood · (2026) · View on PubMed ↗

G protein-coupled receptor SmGPCR9 interacts with neuropeptides and controls spermatogenesis in Schistosoma mansoni.

This study characterized the orphan Class A (rhodopsin-like) G protein-coupled receptor SmGPCR9 (Smp_244240) in the parasite Schistosoma mansoni to determine how it interacts with neuropeptides and regulates male reproduction. The authors report that SmGPCR9 binds neuropeptides and controls spermatogenesis, linking GPCR–neuropeptide signaling to male fertility in schistosomes. These findings identify a parasite-specific signaling node that could be exploited for interventions against schistosomiasis by targeting reproductive biology.

Geetha S, Haeberlein S, Hahnel S et al. · PLoS pathogens · (2026) · View on PubMed ↗ · Free PDF ↗

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Clinical trials & comparative effectiveness (oncology/other)

Nutrition Therapy in Critically Ill Adults.

This article reviewed evidence on nutrition therapy in critically ill adults, focusing on early enteral versus parenteral nutrition and dosing strategies during the acute phase of critical illness. It concluded that early enteral nutrition supports gut integrity and microbiome health, that short-term parenteral nutrition is a safe alternative when enteral feeding is not possible, and that early full-dose energy delivery offers no benefit over restrictive dosing and may increase gastrointestinal and metabolic complications—especially in patients with circulatory shock or at risk for refeeding syndrome. Clinically, it supports restrictive energy delivery and individualized route/dosing decisions to reduce complications while maintaining nutritional adequacy.

Patel JJ, McClave SA · The New England journal of medicine · (2026) · View on PubMed ↗

Ensartinib in Resected ALK-Positive Non-Small-Cell Lung Cancer.

This phase 3, double-blind randomized trial studied ensartinib (225 mg once daily) versus placebo in patients with completely resected ALK-positive stage IB–IIIB non-small-cell lung cancer (NSCLC) after adjuvant chemotherapy, with disease-free survival as the primary endpoint in stage II–IIIB disease. The abstract indicates the trial was designed to determine whether ensartinib improves disease-free survival compared with placebo over 24 months. If positive, ensartinib would establish a second-generation ALK inhibitor as an effective adjuvant therapy to reduce recurrence risk in resected ALK-positive NSCLC.

Yue D, Huang M, Song P et al. · The New England journal of medicine · (2026) · View on PubMed ↗

Setmelanotide for the Treatment of Acquired Hypothalamic Obesity.

This phase 3 trial evaluated setmelanotide, a melanocortin-4 receptor agonist (1.5–3.0 mg subcutaneously once daily), versus placebo in participants aged ≥4 years with acquired hypothalamic obesity. The study tested whether setmelanotide produces clinically meaningful weight reduction over 52 weeks after dose escalation. Positive results would support setmelanotide as a targeted pharmacologic option for acquired hypothalamic obesity, a condition with limited effective treatments.

Miller JL, van Santen HM, Phillips SA et al. · The New England journal of medicine · (2026) · View on PubMed ↗

Lung Transplant for Refractory Lung-Limited Stage IV Non-Small Cell Lung Cancer.

This prospective, single-center registry study analyzed outcomes of lung transplant in 98 adults with medically refractory, lung-limited stage IV NSCLC and compared survival with medical management alone among 404 adults. The abstract indicates the study was designed to characterize post-transplant outcomes and quantify survival benefit relative to non-surgical management in this historically excluded population. If improved survival is demonstrated, lung transplant could become a reconsidered option for carefully selected patients with lung-limited stage IV NSCLC.

Bharat A, Kurihara C, Chung LI et al. · JAMA · (2026) · View on PubMed ↗

Global cancer statistics 2024: GLOBOCAN estimates of incidence and mortality worldwide for 34 cancers in 186 countries.

This article reports updated global cancer incidence and mortality estimates for 2024 using GLOBOCAN data across 186 countries for 34 cancers, with projections to 2050 based on demographic trends and the Human Development Index. It estimates 20.6 million new cancer cases and 9.8 million cancer deaths worldwide in 2024 (excluding nonmelanoma skin cancer: 19.5 million and 9.7 million, respectively). These statistics are significant for global health planning by quantifying current cancer burden and forecasting future needs for prevention, diagnosis, and treatment.

Sung H, Filho AM, Laversanne M et al. · CA: a cancer journal for clinicians · (2026) · View on PubMed ↗

Deprescribing in Patients With Cardiovascular Disease Experiencing Polypharmacy: A Scientific Statement From the American Heart Association.

This American Heart Association scientific statement reviewed evidence and gaps regarding deprescribing strategies for patients with cardiovascular disease experiencing polypharmacy across the age spectrum. The key finding is that, despite widespread polypharmacy and known harms, there is limited actionable guidance on when and how to initiate deprescribing in cardiovascular populations. Scientifically and clinically, it supports development of standardized, patient-centered deprescribing approaches to reduce inappropriate medication use and adverse outcomes.

DiDomenico RJ, Marrs JC, Bress AP et al. · Circulation · (2026) · View on PubMed ↗

Oncologic outcome and safety profile of first-line enfortumab vedotin plus pembrolizumab vs. conventional chemotherapy in advanced urothelial cancer.

This multicenter database study compared first-line enfortumab vedotin plus pembrolizumab (EVP) versus conventional chemotherapy in 642 patients with locally advanced or metastatic urothelial cancer (la/mUC). The key finding is the characterization of short-term oncologic outcomes and safety (including RECIST v1.1 response and progression-free survival) for EVP relative to comparator regimens in real-world practice. Clinically, these data inform treatment selection and risk–benefit discussions for patients receiving EVP as first-line therapy.

Miyake M, Nishimura N, Oda Y et al. · Exploration of targeted anti-tumor therapy · (2026) · View on PubMed ↗ · Free PDF ↗

M1C IS NECESSARY FOR DARAXONRASIB RESISTANCE OF NSCLC KRAS(G12C) MUTANT CELLS.

This preprint investigated mechanisms of acquired resistance to the KRAS(G12C) inhibitor daraxonrasib (RMC-6236) in NSCLC cell models (H358, H2122, and patient-derived MGH1112 KRAS(G12C)) with acquired daraxonrasib resistance. The key finding is that the oncogenic protein M1C is induced as a protective response and is necessary for daraxonrasib resistance, with effects linked to signaling pathways including SHP2 and STAT1/3 and NF-κB activation. Scientifically, identifying M1C as a resistance dependency suggests a potential target to overcome or prevent daraxonrasib resistance in KRAS(G12C) mutant NSCLC.

Takamori S, Haratake N, Nonaka K et al. · bioRxiv : the preprint server for biology · (2026) · View on PubMed ↗ · Free PDF ↗

Autoimmune Disease Risk With GLP-1RA, DPP-4i, and SGLT2i Treatment in Patients With Diabetes.

This randomized controlled trial tested whether a ketogenic diet improves metabolic dysfunction and psychiatric symptoms in people with schizophrenia-spectrum or bipolar-1 disorders, comparing ketogenic diet (KETO, n=28) versus diet-as-usual (DAU, n=30) for 1 month. The key finding is that metabolic improvements induced by the ketogenic diet correlate with symptom improvement in psychosis. Clinically, this supports ketogenic diet–mediated metabolic changes as a potential adjunct pathway for improving psychotic symptoms in these populations.

Mahajan A, Bates DW, Doria A et al. · ACR open rheumatology · (2026) · View on PubMed ↗ · Free PDF ↗

Metabolic Improvements with a Ketogenic Diet Correlate with Symptom Improvement in Psychosis: A Randomized Controlled Trial.

This study used emulated target trials with TriNetX electronic health record data (2016–2023) to compare autoimmune disease risk among adults with type 2 diabetes initiating DPP-4 inhibitors (DPP-4i), GLP-1 receptor agonists (GLP-1RA), or SGLT2 inhibitors (SGLT2i) and without prior autoimmune disease. The key finding is the comparative immunologic safety assessment of these diabetes drug classes with propensity score matching to balance baseline characteristics. Clinically, the results help guide safer selection of glucose-lowering therapy for patients concerned about autoimmune adverse outcomes.

Abram SV, Kyner JM, Vu A et al. · Schizophrenia bulletin · (2026) · View on PubMed ↗

Global Prevalence of Obsessive-Compulsive and Related Disorders: A Systematic Review and Modeling Study.

This systematic review and Bayesian modeling study estimated the global prevalence of obsessive-compulsive disorder (OCD) and related disorders (hoarding disorder, excoriation disorder, body dysmorphic disorder, and trichotillomania) using population-representative studies with DSM or ICD-10 diagnoses. The key finding is a synthesized, globally modeled prevalence distribution across OCD and the obsessive-compulsive and related disorders. Scientifically and clinically, these estimates address major epidemiologic gaps and can inform public health planning and resource allocation for mental health services worldwide.

Jeong YD, Son Y, Jeon S et al. · The American journal of psychiatry · (2026) · View on PubMed ↗

Comparison of epcoritamab, lenalidomide, and rituximab versus usual care in relapsed/refractory follicular lymphoma.

This adjusted comparative analysis evaluated the effectiveness of epcoritamab plus lenalidomide and rituximab (epcoritamab+R2) versus usual care in adults with relapsed/refractory follicular lymphoma (R/R FL). The study was motivated by the lack of head-to-head comparisons between epcoritamab+R2 and chemoimmunotherapy (CIT), building on prior pivotal data showing epcoritamab+R2 superiority over R2 alone. If epcoritamab+R2 demonstrates improved outcomes versus CIT, it would support a treatment shift toward CD3×CD20 bispecific antibody–based regimens in later-line R/R FL.

Falchi L, Hutchings M, Tybor D et al. · Oncoimmunology · (2026) · View on PubMed ↗ · Free PDF ↗

Impact of Invasive Intracranial Pressure Monitoring on Outcomes in Older Adults with Severe Traumatic Brain Injury: A Systematic Review and Meta-Analysis.

This systematic review and meta-analysis evaluated whether invasive intracranial pressure monitoring (ICPM) improves outcomes in older adults with severe traumatic brain injury (TBI). It included studies enrolling patients >55 years with severe TBI defined by Glasgow Coma Scale (GCS) ≤8, comparing management with versus without ICPM, and pooled results using a random-effects approach. Clarifying benefit or lack of benefit in older patients could refine guideline recommendations that currently rely on mixed-age evidence.

Cueva-Cañola LE, Natera-Rodriguez DE, Ramírez-Navarro DI et al. · Neurocritical care · (2026) · View on PubMed ↗

Longitudinal multiomics profiling of extracorporeal cross-circulation with pig liver xenografts in human decedents.

The study investigated host–xenograft interactions in extracorporeal liver cross-circulation (ELC) using gene-edited porcine liver xenografts in human brain-dead decedents via longitudinal multiomics (proteomics, lipidomics, metabolomics) plus spatial transcriptomics and histology. The porcine grafts maintained parenchymal structure with immune cell infiltration and IgM deposition on endothelial cells, while multiomics profiling was used to characterize evolving blood and tissue responses over time. These findings provide mechanistic insight into immune and molecular barriers that may limit ELC and guide optimization of xenograft-based bridge therapies for liver failure.

Guo Q, Wang C, Mauduit V et al. · Nature medicine · (2026) · View on PubMed ↗

Advances in heterogeneity and classification of osteoarthritis.

This article is a narrative review summarizing how osteoarthritis (OA) heterogeneity arises from genetic and pathophysiological differences across joints, patients, and disease stages, and how this heterogeneity affects clinical manifestations, treatment response, and prognosis. It highlights that current disease-modifying OA drug approaches and treatment technologies have not yet reliably slowed progression, partly due to mismatches between therapeutic mechanisms and OA patient subtypes. The review synthesizes emerging classification strategies and mechanistic pathways to support more precise OA stratification for future interventions.

Huang T, Shu J, Wu Z et al. · Bone research · (2026) · View on PubMed ↗ · Free PDF ↗

Aging and cancer: current understandings and future perspectives.

This review summarizes current evidence connecting aging to cancer and outlines future research directions. It organizes shared mechanisms into four pathway categories—nutrient sensing/energy metabolism, stress response/genome maintenance, inflammatory/microenvironmental signaling, and sirtuin-mediated epigenetic/transcriptional modulation—emphasizing overlapping and distinct roles across aging and tumorigenesis. The synthesis supports a mechanistic framework for developing age-informed cancer prevention and therapies.

Li Q, Chan YT, Wu J et al. · Signal transduction and targeted therapy · (2026) · View on PubMed ↗ · Free PDF ↗

Association of Vitamin B6 and Homocysteine-ACTH Coupling With Depressive and Anxiety Symptoms in Burning Mouth Syndrome: An Exploratory Case-Control Study.

This exploratory case-control study compared plasma vitamin B6, homocysteine, and adrenocorticotropic hormone (ACTH) concentrations between patients with burning mouth syndrome (BMS) and controls and examined their interrelationships with depressive and anxiety symptoms. The study was motivated by the idea that B6, homocysteine (one-carbon metabolism), and ACTH (neuroendocrine stress signaling) form biologically connected pathways relevant to BMS and nociplastic pain mechanisms. Clinically, identifying these coupling patterns could help define biological subtypes of BMS linked to psychological distress and stress-related neuroendocrine dysfunction.

Lebel A, Guillouet C, Porporatti A et al. · Journal of oral rehabilitation · (2026) · View on PubMed ↗ · Free PDF ↗

Dupilumab treatment improves linear growth and bone biomarkers in children with atopic dermatitis: Post hoc analysis of a phase 3 randomized, placebo-controlled clinical trial and an open-label extension study.

This post hoc analysis of a phase 3 randomized, placebo-controlled trial plus an open-label extension evaluated children aged 6–11 years with atopic dermatitis treated with dupilumab versus placebo, focusing on linear growth outcomes and bone mineralization biomarker alkaline phosphatase (BALP). Dupilumab treatment improved height gain and favorably affected BALP levels over time compared with placebo, indicating improved growth-related and mineralization biology. These data support dupilumab’s potential to mitigate growth and bone health concerns in pediatric severe atopic dermatitis.

Irvine AD, Paller AS, Siegfried EC et al. · Journal of the American Academy of Dermatology · (2026) · View on PubMed ↗

Standard-dose unfractionated heparin versus low-dose unfractionated heparin and low-molecular-weight heparin in extracorporeal life support (RATE): an open-label, randomised, non-inferiority trial.

This open-label, randomized, non-inferiority trial (RATE) compared standard-dose unfractionated heparin (UFH) versus low-dose UFH and versus low-molecular-weight heparin (LMWH) in patients receiving extracorporeal life support (ECMO). The study tested whether lower-intensity anticoagulation is non-inferior to standard UFH for thrombotic outcomes while potentially reducing bleeding risk. If non-inferiority was supported, it would directly inform safer anticoagulation targets for ECMO patients.

Minnen OV, Lansink-Hartgring AO, van Amstel RBE et al. · Lancet (London, England) · (2026) · View on PubMed ↗

Real-world evidence of sacituzumab govitecan in metastatic triple-negative breast cancer: an updated multicenter analysis.

The study analyzed real-world effectiveness and safety of the Trop-2-directed antibody-drug conjugate sacituzumab govitecan (SG) in metastatic triple-negative breast cancer across 17 Italian oncology centers. In 256 women with mTNBC treated with SG (217 retrospective and 39 prospective), the authors report updated multicenter outcomes intended to reflect heterogeneous routine clinical practice. This provides practical evidence to complement trial data and inform clinicians about expected benefits and risks of SG in broader patient populations.

Caputo R, Buono G, Martinelli C et al. · ESMO open · (2026) · View on PubMed ↗ · Free PDF ↗

Tagraxofusp, Azacitidine, and Venetoclax in Blastic Plasmacytoid Dendritic Cell Neoplasm.

This phase 2 clinical trial evaluated the combination of tagraxofusp (TAG; CD123-directed toxin), azacitidine (AZA), and venetoclax (VEN; BCL2 inhibitor) in patients with blastic plasmacytoid dendritic cell neoplasm (BPDCN). In previously untreated or relapsed/refractory BPDCN, patients received 28-day cycles with AZA (days 1–7), VEN (days 1–21), and TAG (days 4–6), building on prior evidence of BPDCN dependence on BCL2 and TAG resistance reversal by AZA. The study tests whether dual epigenetic/BCL2 targeting plus CD123-directed cytotoxicity improves outcomes in an orphan, aggressive malignancy.

Lane AA, Luskin MR, Keating JH et al. · Blood · (2026) · View on PubMed ↗

The Missense Mutant ClC-5 (E211A), associated with Proton/Chloride Uncoupling Exacerbates Renal Pathology Compared to the ClC-5 null Mutant.

This study compared renal phenotypes in mice carrying the ClC-5 uncoupling missense mutation E211A (abolishing proton transport while preserving chloride conductance) versus ClC-5 null mice, in the context of dent disease type 1 caused by CLCN5 mutations. The authors report that the ClC-5 E211A uncoupling mutation exacerbates renal pathology compared with the ClC-5 null mutant. Clinically, this indicates that uncoupling mutations can be more damaging than complete loss of function, refining genotype–phenotype expectations and guiding mutation-specific therapeutic approaches.

Bostanci A, Lyu P, Jiang C et al. · Kidney360 · (2026) · View on PubMed ↗ · Free PDF ↗

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Neurodegeneration & proteinopathies

Targeting of CH25H to boost p62-dependent autophagic degradation of α-synuclein in cell and mouse models of Parkinson’s disease.

This study identified cholesterol 25-hydroxylase (CH25H) as a regulator of p62-dependent autophagic degradation of α-synuclein using bulk RNA sequencing of substantia nigra from the MPTP mouse model and reanalysis of patient iPSC-derived astrocyte datasets, followed by validation in mouse tissue. It found elevated CH25H expression in PD-associated astrocytes and demonstrated that targeting CH25H boosts p62-dependent autophagic clearance of α-synuclein in cell and mouse models of Parkinson’s disease (PD). The work supports CH25H as a potential therapeutic target to enhance α-synuclein turnover and slow PD pathology.

Zhang X, Han R, Zhang W et al. · Science translational medicine · (2026) · View on PubMed ↗

Annexin A11 and TDP-43: core players in neurodegeneration.

The article reviewed evidence that Annexin A11 (ANXA11) and TDP-43 are core pathological players in neurodegeneration, particularly in frontotemporal lobar degeneration with TDP-43 pathology (FTLD-TDP) type C. It highlights that ANXA11 co-aggregates with TDP-43 in all FTLD-TDP type C cases and that cryo-EM revealed heteromeric ANXA11–TDP-43 filaments, supporting a direct protein–protein pathological interaction. This strengthens ANXA11–TDP-43 complex formation as a mechanistic target for understanding and potentially intervening in TDP-43 proteinopathies.

Smith CL, Robinson JL, Lee EB · Acta neuropathologica · (2026) · View on PubMed ↗ · Free PDF ↗

Cryo-EM structure of soluble VPS13C suggests its regulation by a conformational switch and by calmodulin.

The study used cryo-electron microscopy to determine the near-atomic structure of soluble VPS13C, a bridge-like lipid transfer protein implicated in Parkinson’s disease, to understand how its conformation regulates lipid transfer. It identified a lipid-transfer nonpermissive conformation in which the C-terminal VAB adaptor module blocks the egress of the lipid-transfer bridge, and it suggested regulation by a conformational switch and calmodulin. This structural mechanism advances how VPS13C is controlled to coordinate organelle lipid redistribution and may inform therapeutic approaches for VPS13C-related disease.

Li D, Wang X, Hao H et al. · Molecular cell · (2026) · View on PubMed ↗ · Free PDF ↗

Cell competition overcomes host tissue resistance to unleash tumor growth in a Drosophila brain cancer model.

This study used a Drosophila brain cancer model driven by cancer stem cells that originate during development and grow in a cortex glia network to examine tumor–microenvironment interactions over time. The authors found a biphasic interplay in which early-stage glial infiltration and later-stage morphological, molecular, and functional changes in cortex glia accompany tumor progression. The work highlights how “cell competition” can overcome host tissue resistance to unleash tumor growth, informing strategies to disrupt tumor–glia dynamics.

Gualtieri M, Jabre S, Mornico D et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗ · Free PDF ↗

Striatal neuron dysfunction in C9ORF72-FTD/ALS is driven by AIS and potassium channel dysregulation.

This study modeled C9ORF72-FTD/ALS by generating inhibitory striatal medium spiny neurons (MSNs) from human induced pluripotent stem cells carrying the C9ORF72 repeat expansion and comparing them with isogenic-corrected and control neurons, alongside patient-derived motor neurons. Using whole-cell electrophysiology, pharmacological perturbations, and high-resolution imaging, the authors identify that C9ORF72 MSNs develop intrinsic dysfunction driven by AIS (axon initial segment) and potassium channel dysregulation. These mechanistic insights connect a specific neuronal subdomain and ion-channel pathology to C9ORF72 neurodegeneration, informing targeted therapeutic strategies.

Pasniceanu IS, Atwal MS, Santos Souza CD et al. · Cell reports · (2026) · View on PubMed ↗ · Free PDF ↗

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Neuroscience circuits & brain function

Parallel anterior cingulate cortex pathways underlie dissociable social and attentional outputs.

This neuroscience study mapped two glutamatergic subpopulations in the anterior cingulate cortex (ACC) that project to the zona incerta (ZI) or the limbic sector of the thalamic reticular nucleus (lTRN) and assessed their effects on social and attentional behaviors. It found that the ACC→ZI and ACC→lTRN pathways differentially control social interaction versus attentional allocation, with deficits in both behaviors when both were disrupted. The results clarify circuit-level mechanisms that may underlie overlapping social and attentional impairments seen in disorders such as autism spectrum disorder (ASD).

Wang F, Chen M, Lyu M et al. · Science advances · (2026) · View on PubMed ↗

α2-Adrenergic receptor modulates 5-HT2A-mediated behavioral effects of MDMA and psilocybin in mice.

The study examined whether the α2-adrenergic receptor modulates behavioral effects of the serotonergic psychedelics MDMA and psilocybin in mice, with attention to 5-HT2A-mediated head-twitch responses (HTRs). The authors found that MDMA (but not psilocybin) robustly increased 5-HT and norepinephrine (NE) in the medial prefrontal cortex, and that blocking extracellular NE release unmasked MDMA’s 5-HT2A-linked behavioral effects. This suggests that α2-adrenergic/NE signaling can gate psychedelic-like behaviors induced by MDMA, informing mechanistic models of entactogen polypharmacology.

Rosado AF, Yu AL, Yang JH et al. · Molecular psychiatry · (2026) · View on PubMed ↗ · Free PDF ↗

Astrocytic ankyrin-2 enables memory persistence in the mouse hippocampus.

This study investigated how astrocytes regulate long-term memory persistence in adult mice by testing the requirement of astrocytic ankyrin-2 (Ank2) using astrocyte-specific Ank2 deletion and assessing synaptic plasticity and astrocyte–engram neuron connectivity. Astrocytic Ank2 was required for memory persistence, with Ank2 loss impairing remote memory and disrupting maintenance of long-term potentiation while reducing astrocyte contacts with engram neurons. Scientifically, the work links BDNF-driven astrocyte morphogenesis and truncated tropomyosin receptor kinase (Trk) signaling to Ank2-dependent support of persistent memory.

Kim H, Lim J, Kim J et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

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Neurodevelopmental genetics & developmental biology

An intrinsic cytoskeletal oscillator establishes neuronal polarity.

The study investigated how neuronal polarity is established, using live imaging and genetic loss-of-function in vivo, along with optogenetic control and local cytoskeletal perturbations in cultured neurons. It found that growth cones alone do not direct polarization, and instead the soma initiates an oscillatory program characterized by periodic actin branching that primes axon selection. These results reveal an intrinsic cytoskeletal oscillator mechanism for axon–dendrite asymmetry, offering a new targetable framework for understanding developmental neuronal wiring.

Lin TC, Coles CH, Alfadil E et al. · Nature · (2026) · View on PubMed ↗

Characterization of the genotypic and phenotypic spectrum of TCF7L2-related neurodevelopmental disorder (TRND).

This study characterized an international cohort of 76 pediatric patients with TCF7L2-related neurodevelopmental disorder (TRND) caused by mono-allelic predicted loss-of-function (pLOF) variants in the Wnt/β-catenin pathway transcription factor TCF7L2. The key finding is the detailed phenotypic spectrum derived from multi-source case ascertainment (GeneMatcher, DECIPHER, and literature/repository data) for patients with pLOF TCF7L2 variants and neurodevelopmental features. Clinically, defining TRND improves diagnosis, counseling, and genotype–phenotype understanding for children with TCF7L2 pLOF variants.

Nijim S, Kim M, Denish M et al. · Genetics in medicine : official journal of the American College of Medical Genetics · (2026) · View on PubMed ↗ · Free PDF ↗

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Vision & ocular biology

A peripheral subpopulation of retinal pigment epithelium resists oxidative damage through SERPINE3-mediated Caspase-1 inhibition.

This study examined regional heterogeneity of retinal pigment epithelium (RPE) degeneration in human and macaque samples and used SERPINE3-GFP knock-in mice to identify a peripheral RPE subpopulation. The peripheral RPE cells resist oxidative damage through SERPINE3-mediated caspase-1 inhibition, distinguishing them from more vulnerable RPE regions. The work provides a mechanistic basis for why certain RPE regions degenerate in macular atrophy and suggests SERPINE3/caspase-1 as a potential therapeutic axis to preserve vision.

Li H, Johnson-Stephenson T, Kunze VP et al. · The Journal of clinical investigation · (2026) · View on PubMed ↗ · Free PDF ↗

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Cardiovascular risk, stroke & heart failure prognostication

Loss of Pericytic Integrin-β1 Exacerbates Blood-Brain Barrier Damage and Hemorrhagic Brain Injury.

This preclinical study tested whether pericyte-specific loss of integrin-β1 (Itgb1) worsens blood-brain barrier (BBB) injury and hemorrhagic brain injury in mice by crossing Atp13a5-CreER with Itgb1 floxed alleles and inducing intracerebral hemorrhage. The key finding is that pericytic integrin-β1 knockout exacerbates BBB damage and hemorrhagic injury compared with controls. Scientifically, it implicates pericyte ECM–integrin signaling as a mechanistic driver of BBB integrity during stroke-related hemorrhage.

Culha-Taskin I, Nasrollahi A, Yao Y · Stroke · (2026) · View on PubMed ↗

MAD-MT Score: A Tool to Optimize Patient Selection for Mechanical Thrombectomy in Distal Vessel Occlusions.

This retrospective international registry study developed the MAD-MT score to optimize patient selection for mechanical thrombectomy in acute distal and medium vessel occlusion stroke. The key finding is that integrating clinical need with procedural risk in a multivariable model can stratify which patients are more suitable for EVT versus medical management. Clinically, MAD-MT aims to reduce inappropriate EVT and improve outcomes by better targeting thrombectomy to patients most likely to benefit.

Chen H, Lakhani DA, Salim HA et al. · Stroke · (2026) · View on PubMed ↗

Association of C-reactive protein-triglyceride glucose index and its modified indices with stroke risk in individuals at cardiovascular-kidney-metabolic syndrome stages 0-3: a population-based cohort study.

This population-based cohort study assessed whether the C-reactive protein–triglyceride–glucose index (CTI) and seven adiposity-modified CTI variants predict stroke risk in adults at Cardiovascular-Kidney-Metabolic (CKM) syndrome stages 0–3. Using 3,348 participants from the China Health and Retirement Longitudinal Study (CHARLS), it evaluated baseline, cumulative, and longitudinal changes in these indices and their association with incident stroke. If the modified CTI indices improve risk prediction, they could refine stroke stratification by integrating inflammation and insulin resistance with adiposity measures.

Yang D, Deng Y, Su Z et al. · Cardiovascular diabetology · (2026) · View on PubMed ↗ · Free PDF ↗

Cognitive Impairment and Incident Atrial Fibrillation in Individuals without Stroke: Evidence from Two Prospective Cohort Studies and Mendelian Randomization Analysis.

This study tested whether cognitive impairment predicts incident atrial fibrillation (AF) independent of stroke using two prospective cohorts (Kailuan and UK Biobank) and complemented the analysis with Mendelian randomization. Across 18,392 Kailuan participants (MMSE) and 377,248 UK Biobank participants (domain-specific cognitive tests), cognitive impairment was associated with higher risk of developing AF even among participants free of stroke and AF at baseline, supporting a brain–heart axis. The results strengthen the case for cognitive screening as a risk stratification tool for AF and provide evidence consistent with a potential causal relationship.

Wu Z, Huang Z, Peng Y et al. · European journal of preventive cardiology · (2026) · View on PubMed ↗

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Endocrinology, obesity & metabolic disease interventions

Comparative effects of drugs for adults with overweight or obesity: systematic review and network meta-analysis.

The study systematically reviewed and performed network meta-analysis of randomized controlled trials comparing drugs for adults with overweight or obesity, evaluating 24 outcomes using frequentist random-effects and Bayesian dose-response models with GRADE and Cochrane RoB 2. It synthesized comparative benefits and harms across available pharmacotherapies to support evidence-based decision making for policymakers, payers, clinicians, and patients. This provides an up-to-date comparative effectiveness framework to guide drug selection for obesity management.

Nong K, Shi Q, Xie X et al. · BMJ (Clinical research ed.) · (2026) · View on PubMed ↗

Pharmacological Interventions for Weight Reduction in Patients With Schizophrenia Treated With Antipsychotics: A Systematic Review and Network Meta-Analysis.

This systematic review and network meta-analysis evaluated pharmacological interventions for weight reduction in patients with schizophrenia spectrum disorders treated with antipsychotics. It synthesized evidence from multiple databases to compare how different drug strategies affect body weight changes in antipsychotic-treated populations. The findings aim to provide comparative guidance for managing antipsychotic-induced weight gain and reducing cardiometabolic risk.

Stogios N, Agarwal SM, Maksyutynska K et al. · JAMA psychiatry · (2026) · View on PubMed ↗

Role of GLP-1 receptor agonists in the prevention and treatment of obesity-related cancer.

This review evaluated evidence on how GLP-1 receptor agonists (GLP-1 RAs) might prevent and treat obesity-related cancers. It synthesizes data suggesting anticancer effects through modulation of insulin signaling, inflammation, and cellular proliferation, with reported protective associations across multiple cancer types (e.g., prostate, breast, pancreatic, gynecological, glioma, and oral squamous cell cancer). If supported by stronger prospective trials, GLP-1 RAs could become dual-purpose therapies addressing both obesity/metabolic risk and cancer risk.

Muscogiuri G, Del Vecchio G, Colangeli L et al. · Internal and emergency medicine · (2026) · View on PubMed ↗ · Free PDF ↗

High-impact physical activity participation and 12-month risk of joint replacement: a longitudinal mediation analysis of 17 661 patients with knee or hip osteoarthritis.

This longitudinal mediation analysis used data from the GLA:D registry (17,661 patients with knee or hip OA) to test whether high-impact physical activity predicts 12-month risk of total hip replacement (THR) or total knee replacement (TKR) and to identify mediators. High-impact physical activity participation was assessed via the UCLA Activity Scale and categorized into high-, high-intensity, moderate-intensity, and low-intensity groups, with outcomes measured as self-reported THR/TKR at 12 months. The study’s significance lies in clarifying whether and how higher-impact activity influences joint replacement risk in OA, informing guideline recommendations about activity type and intensity.

Liew BXW, Grønne DT, Roos EM et al. · British journal of sports medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Time-restricted eating, liver health, and fecal microbiota in adults with overweight or obesity: a randomized controlled trial.

This multicenter randomized controlled trial tested whether an 8-hour time-restricted eating (TRE) regimen combined with usual care (Mediterranean diet-based education) versus usual care alone improves hepatic fat fraction and liver health markers and alters fecal microbiota in adults with overweight or obesity. TRE groups showed changes in liver fat and liver-related measures assessed by MRI and elastography-based parameters, alongside microbiota shifts measured by 16S rRNA gene sequencing. The findings suggest that circadian-aligned dietary restriction may benefit liver health and gut microbial ecology in metabolic-risk populations.

Dote-Montero M, Clavero-Jimeno A, Cortés-Martín A et al. · JHEP reports : innovation in hepatology · (2026) · View on PubMed ↗ · Free PDF ↗

Temporal changes in cortisol secretion and their association with long-term outcomes in benign adrenal incidentalomas: a retrospective cohort study.

This retrospective cohort study in adults with benign adrenal incidentalomas assessed longitudinal changes in cortisol secretion using repeated 1-mg overnight dexamethasone suppression test (1-mg DST) results and cumulative cortisol exposure. Temporal patterns of cortisol secretion and cumulative exposure were associated with long-term cardiometabolic outcomes and mortality, indicating that a single DST may not fully capture risk. Scientifically and clinically, it supports monitoring cortisol dynamics over time in MACS to better predict adverse outcomes.

Suntornlohanakul O, Reimondo G, Ghislieri M et al. · The lancet. Diabetes & endocrinology · (2026) · View on PubMed ↗ · Free PDF ↗

Insulin resistance and type 2 diabetes as allostatic responses to chronic nutrient excess.

The study examined insulin resistance, impaired glucose-stimulated insulin secretion, modest hyperglycemia, and glucosuria as functional “allostatic” responses to chronic nutrient excess in obesity-related prediabetes and early type 2 diabetes. The authors propose that these metabolic changes can be beneficial adaptations rather than purely pathological defects, potentially explaining why glucose-lowering drugs (e.g., sulfonylureas, thiazolidinediones, and insulin) do not consistently improve long-term outcomes. This reframes type 2 diabetes pathophysiology and could shift therapeutic strategies toward preserving or modulating adaptive responses instead of focusing only on glycemia.

Prentki M, Nolan CJ, James DE et al. · Cell metabolism · (2026) · View on PubMed ↗

GLP-1 and MASH: When weight loss isn’t the whole story.

This article reviewed evidence on metabolic dysfunction-associated steatohepatitis (MASH) and highlighted a new study showing that GLP-1 receptor signaling on intrahepatic sinusoidal endothelial cells mediates semaglutide’s weight loss-independent hepatoprotective effects. The key finding emphasized that the therapeutic benefit is not solely explained by weight loss, but by direct GLP-1 receptor actions within the diseased liver microenvironment. Clinically, this supports refining GLP-1-based therapy mechanisms and may guide patient selection or combination strategies targeting hepatic endothelial pathways.

Long MT, Krarup N, Knop FK · Cell metabolism · (2026) · View on PubMed ↗

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Infectious disease epidemiology & surveillance

Meningococcal B Vaccine to Prevent Neisseria gonorrhoeae Infection.

The study conducted a multicenter, double-blind, randomized, placebo-controlled trial in men who have sex with men (MSM) to test whether two doses of the four-component meningococcal serogroup B vaccine (4CMenB) reduce Neisseria gonorrhoeae infection risk. Participants with recent N. gonorrhoeae infection or infectious syphilis who were HIV-negative on HIV pre-exposure prophylaxis or living with HIV were randomized to 4CMenB versus placebo and followed with STI screening. If effective, this would support repurposing 4CMenB as a preventive vaccine strategy for gonorrhea in high-risk populations.

Seib KL, Donovan B, Jin F et al. · The New England journal of medicine · (2026) · View on PubMed ↗

Viral Pathogen-Specific Severe Acute Respiratory Infections in Hospitalised Adults in Europe: Epidemiological Findings from the id.DRIVE Study 2024-2025.

This epidemiological study used the multicountry id.DRIVE surveillance dataset to characterize viral pathogen-specific severe acute respiratory infections (SARI) in hospitalized adults across Europe. Adults (≥18 years) hospitalized in Spain, Italy, and Germany during 2024–2025 were tested using reverse transcription–based viral diagnostics, and the study described clinical characteristics and outcomes by pathogen. These findings help fill gaps in adult, patient-level respiratory virus surveillance beyond influenza and COVID-19 and can guide hospital preparedness and targeted prevention.

Newell K, Vroom N, Marques C et al. · Infectious diseases and therapy · (2026) · View on PubMed ↗ · Free PDF ↗

Mapping the prevalence of molecular markers of Plasmodium falciparum artemisinin partial resistance in Africa: a systematic review and spatiotemporal modelling study.

This systematic review and spatiotemporal modeling study mapped the prevalence of Plasmodium falciparum kelch13 (k13) mutations associated with artemisinin partial resistance across Africa and also modeled mdr1 and crt mutations as markers of reduced susceptibility to ACT partner drugs. The analysis inferred high-resolution geographic and temporal trends in ART-R marker prevalence, helping distinguish local emergence from geographic expansion. These results provide actionable surveillance targets to guide malaria control policy and anticipate threats to artemisinin-based combination therapies.

Young NW, Meier-Scherling CPG, Cuomo-Dannenburg G et al. · The Lancet. Infectious diseases · (2026) · View on PubMed ↗ · Free PDF ↗

Epidemiological characteristics of amebiasis in Japan from 2001 to 2022.

This study analyzed government surveillance data on amebiasis in Japan from 2001–2022 to characterize epidemiological trends, including during the COVID-19 pandemic, by place of infection. Using piecewise mixed-effect regression with knots at 2018 and 2020 and Poisson regression for year-to-year changes, the authors quantified shifts in case trends over time. These findings clarify how public health disruptions and changing transmission conditions may have altered amebiasis epidemiology in Japan.

Iida K, Mori H, Remez D et al. · PloS one · (2026) · View on PubMed ↗ · Free PDF ↗

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Microbiome & diet–microbiome interactions

Diet-microbiome synergy underlies obesity-associated immunotherapy efficacy.

The study tested how diet–microbiome interactions shape obesity-associated anti-tumor immunity and immune checkpoint inhibitor (ICI) efficacy across 12 mouse diet models spanning obesity biology. Obesity-associated ICI responses were poorly correlated with metabolic dysfunction and instead depended on the diet–gut axis, with obesogenic diets producing gut-microbiota and immune features associated with ICI sensitivity. This provides a mechanistic framework for why BMI can predict ICI benefit and suggests that diet–microbiome modulation could improve immunotherapy responses.

Desharnais L, Swaby A, Messaoudene M et al. · Nature · (2026) · View on PubMed ↗

Dopamine-driven mitochondrial reverse electron transport in immune cells mediates gut-brain ROS signaling during sleep deprivation.

This study investigated how sleep deprivation triggers gut-brain reactive oxygen species (ROS) signaling by examining dopamine (DA) and mitochondrial reverse electron transport (RET) in immune cells in Drosophila. It found that both mechanical and thermogenetic sleep deprivation (and associated stress) increase DA biosynthesis, leading to initial ROS accumulation in gut subregions (including the proventriculus) and PV-resident hemocytes via DA-driven activation of mitochondrial RET. The results define a DA–mitochondrial RET mechanism in immune cells as a signaling pathway linking sleep loss to systemic oxidative stress.

Zhang Y, Lee JH, Yu Z et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗

A metabolite-dependent mechanism by which Bifidobacterium animalis subsp. lactis promotes Bacteroides colonization.

This study examined how the metabolite profile of the probiotic Bifidobacterium animalis subsp. lactis affects colonization by the gut anaerobe Bacteroides spp. in co-culture experiments using omics and metabolomics approaches. B. animalis subsp. lactis promoted Bacteroides growth under anaerobic conditions, and metabolomic analysis identified >150 unique metabolites in B. animalis subsp. lactis supernatants that were absent from other Bifidobacterium strains. These findings support a mechanism of metabolite-dependent cross-feeding that could be leveraged to improve early human gut colonization and microbiome-targeted therapies.

Shahin K, Wang L, He Z et al. · Gut microbes · (2026) · View on PubMed ↗ · Free PDF ↗

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Generated automatically on July 09, 2026 from PubMed’s trending articles. Summaries are AI-generated; always consult the original publication for clinical or research decisions.