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PubMed Trending Research Digest — August 09, 2026

A curated digest of 98 trending PubMed articles, automatically categorised and summarised across 15 research areas.

PubMed Trending Research Digest — August 09, 2026

Automated digest · 98 articles · 15 research areas · August 09, 2026

Overview

Across this week’s set of papers, a dominant theme is mechanistic biology linking metabolism to immune function and disease progression. Multiple studies connect nutrient/metabolite pathways to mitochondrial endpoints (including gut microbial metabolites affecting mitochondrial function), to tumor immune evasion (e.g., tryptophan metabolism/AhR signaling, glycolysis-driven metastasis, and glyco-immune surveillance via glycocalyx remodeling), and to therapy resistance (such as immunotherapy resistance mediated by metabolic and microenvironmental constraints). Together, these works reinforce a “metabolism–immunity” axis as a tractable target for both biomarker development and combination strategies.

A second major thread is translational and clinical decision support—spanning long-term effectiveness/safety data (e.g., lanadelumab and deucravacitinib), risk stratification tools (CRP in psoriatic arthritis; lipid–inflammation indices and TyG-VLR for cardiometabolic risk; genomic staging validation in myeloma), and evidence synthesis for practice (guidelines for schizophrenia in LMICs; updated AMR guidance; network meta-analyses for osteoporosis prevention/treatment). Several studies also emphasize the need for better biomarkers to monitor treatment response or guide selection, including limitations of candidate biomarkers (e.g., plasma p-tau217 for donanemab TRAC) and the promise of multi-omics/immune-state profiling for immunotherapy outcomes.

Finally, the digest highlights expanding frontiers in immune modulation and neurobiology. Reviews and mechanistic studies cover immune checkpoint regulation (CTLA-4 in Sjögren’s; IL-6 trans-signaling in neurodegeneration), engineered immune cell approaches (adoptive T-cell “living drugs” and CAR T safety considerations), and neuroinflammatory/neuromodulatory strategies (vagus nerve–microbiome links, stress-linked chromatin priming in dopamine circuits, and neuromodulation for post-stroke recovery). Collectively, the field is moving toward more precise, mechanism-informed interventions—often integrating systems-level data (omics, spatial profiling, and longitudinal cohorts) to anticipate heterogeneity and improve outcomes.


Gut microbiome metabolites & mitochondrial function

A three-metabolite microbiota-associated signature for early risk stratification of gestational diabetes mellitus.

This multicenter nested case-control and prospective study developed an early gestational diabetes mellitus (GDM) risk stratification signature using gut microbiota-associated metabolites in 2,693 pregnant women. Integration of untargeted metabolomics with metagenomics identified a three-metabolite signature that was consistently dysregulated in GDM and enabled earlier prediction than standard oral glucose tolerance testing at 24–28 weeks. Scientifically and clinically, it supports a noninvasive, early-pregnancy biomarker approach for identifying women at high risk for GDM and potentially improving downstream cardiometabolic prevention.

Ma S, Zhang C, Yao Y et al. · Cardiovascular diabetology · (2026) · View on PubMed ↗ · Free PDF ↗

Vagus nerve-driven microbiota homeostasis: a promising integrative add-on therapy for neurodevelopmental disorders.

This article reviewed evidence on how vagus nerve signaling can regulate gut microbiota homeostasis and thereby influence neurodevelopmental disorder (NDD) biology via the microbiota-gut-brain axis (MGBA). It highlights that early-life dysbiosis and MGBA-mediated immune, metabolic, and neural communication pathways can shape neurodevelopmental trajectories, motivating vagus nerve-based microbiota modulation as an add-on therapy concept. Clinically, this integrative framework supports developing vagus nerve–microbiome interventions to improve outcomes in NDDs by correcting peripheral drivers of brain development.

Azabou E, Frouin PY, Bellaïche M et al. · Frontiers in neuroscience · (2026) · View on PubMed ↗ · Free PDF ↗

Microbiome as a prediction of immunotherapy response in lung cancer.

This narrative review studied whether the gut and oral microbiome can predict response to immune checkpoint inhibitors (ICIs) in lung cancer. It reports that microbiome composition and related immune effects can correlate with efficacy, primary/acquired resistance, and immune-related adverse events (irAEs), supporting microbiome profiling as a noninvasive biomarker for ICI response and toxicity. Scientifically, it frames microbiome–systemic immunity interactions as actionable targets to improve patient selection and management for lung cancer immunotherapy.

Rojas L, Zuluaga J, Cardona AF · Frontiers in immunology · (2026) · View on PubMed ↗ · Free PDF ↗

Mechanistic pathways linking gut microbial metabolites, microbial structural products, and host-microbe co-metabolites to mitochondrial function.

This systematic review synthesized evidence (searched PubMed, Scopus, and Web of Science through March 2026) linking gut-derived microbial metabolites across ten metabolite classes to direct mitochondrial endpoints in host cells. It found that gut microbial metabolites exert diverse effects on mitochondrial function, including bioenergetic enhancement and direct mitochondrial toxicity, organized into four metabolite–mitochondrial outcome groupings after excluding contextual evidence from certainty assessments. These findings support a mechanistic framework for how specific gut metabolite classes may causally modulate mitochondrial biology and thereby influence host metabolic and disease phenotypes.

Frye RE, Rossignol DA · Gut microbes · (2026) · View on PubMed ↗ · Free PDF ↗


Bone health & osteoporosis (including CKD/GIOP)

Vitamin B12 alleviates spliceosomopathy via phospholipid remodeling.

This work studied Verheij syndrome caused by PUF60 mutations by using a Caenorhabditis elegans model, human cell lines, and patient-derived samples to test whether vitamin B12 can correct splicing defects. It showed that PUF60 (RNP-6) deficiency disrupts splicing of genes involved in one-carbon metabolism and phospholipid remodeling, impairing SAM/SAH cycling and phosphatidylcholine synthesis, which triggers integrated stress response and compromises mTORC1 signaling. The significance is that vitamin B12 alleviates spliceosomopathy through metabolic/phospholipid remodeling, suggesting a potential targeted therapeutic strategy for PUF60-related disease.

Kölschbach J, Dafsari HS, Baum E et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Prognostic Value of Psoas Muscle Index Improvement in Patients Undergoing Transjugular Intrahepatic Portosystemic Shunt.

This multicenter retrospective study evaluated whether early improvement in psoas muscle index (PMI) after transjugular intrahepatic portosystemic shunt (TIPS) predicts outcomes in patients with cirrhosis and sarcopenia. In 390 patients, PMI was measured by CT before TIPS and about 1 month afterward, and sarcopenia reversal was defined by sex-specific PMI cutoffs (>6.36 cm2/m2 for men and >3.92 cm2/m2 for women), with associations tested against overall survival and hepatic decompensation outcomes. Clinically, early PMI improvement after TIPS may serve as a prognostic marker to stratify risk and guide supportive management in sarcopenic cirrhosis.

Wang H, Zhang X, Zhu X et al. · Journal of vascular and interventional radiology : JVIR · (2026) · View on PubMed ↗

CKD-associated osteoporosis in patients with CKD G4-5D: a pragmatic treatment approach.

This paper discusses a pragmatic treatment approach to CKD-associated osteoporosis in patients with advanced chronic kidney disease stages G4–G5D, in the context of the 2023 KDIGO terminology and guidance. It emphasizes that fracture risk is several-fold higher in CKD G4–G5D than in age- and sex-matched kidney-healthy populations and that management should overlap with postmenopausal osteoporosis workups while being individualized to CKD-specific factors. Scientifically and clinically, the framework aims to guide safer selection of bone fragility therapies in CKD where evidence and diagnostic/therapeutic considerations differ from standard osteoporosis.

Evenepoel P, Jørgensen HS · Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · (2026) · View on PubMed ↗

Effectiveness of Anti-Osteoporotic Medications in the Management of Glucocorticoid-Induced Osteoporosis: A Systematic Review and Network Meta-Analysis on Behalf of the ECTS Clinical Action Group.

This systematic review and network meta-analysis compared anti-osteoporotic medications (AOM) for prevention and treatment of glucocorticoid-induced osteoporosis (GIOP) in adults receiving oral glucocorticoids. Using randomized and comparative observational evidence identified through searches up to December 2025, it evaluated effects on lumbar-spine, femoral-neck, and total-hip areal bone mineral density (aBMD) changes. The results aim to rank therapies by comparative efficacy to inform clinical selection of AOM for GIOP risk reduction.

Yavropoulou MP, Ter Wee MM, Naciu AM et al. · European journal of endocrinology · (2026) · View on PubMed ↗

Impact of GLP-1 Receptor Agonists on Bone Metabolism.

This mini-review evaluated published evidence on how glucagon-like peptide-1 receptor agonists (GLP-1RAs)—used in type 2 diabetes mellitus (T2DM) and obesity—affect bone metabolism and skeletal outcomes in people with T2DM and obesity. It highlights a clinical tension in which GLP-1RAs may improve skeletal health via better metabolic control while substantial weight loss could increase bone loss and fracture risk. The review is clinically significant because it frames bone health monitoring and risk–benefit considerations for GLP-RA therapy in T2DM/obesity populations.

Vadini V, Duan D, Moseley KF · The Journal of clinical endocrinology and metabolism · (2026) · View on PubMed ↗


Hereditary angioedema & biologic prophylaxis

Sustained Effectiveness of Lanadelumab in Preventing Hereditary Angioedema Attacks: The ENABLE Study.

This Phase 4 prospective ENABLE study followed patients with hereditary angioedema (HAE) aged ≥12 years who initiated lanadelumab 300 mg every 2 weeks per labeling across Europe and the Middle East for up to 36 months (NCT04130191). The study assessed long-term effectiveness for preventing HAE attacks as the primary objective and tracked safety and patient-reported health-related quality of life over extended exposure. These real-world long-term data are important for confirming sustained prophylactic benefit and tolerability of lanadelumab in routine clinical practice.

Zanichelli A, Wuillemin WA, Magerl M et al. · Clinical and translational allergy · (2026) · View on PubMed ↗ · Free PDF ↗


Autoimmunity prediction & screening (T1D/CD/AITD)

Long-Term Follow-Up Incidence of Type 1 Diabetes and Associated Autoimmune Diseases in First-Degree Relatives.

Using the DiaUnion 1.0 study within the DanDiabKids biobank, this work followed 1427 Danish first-degree relatives (siblings) of children newly diagnosed with type 1 diabetes (T1D) to characterize one-time autoantibodies and genetic risk and to measure long-term progression to T1D, celiac disease (CD), or autoimmune thyroid disease (AITD). Autoantibodies were measured for T1D (GADA, IAA, IA2A, ZnT8A), CD (tTGA), and AITD (TPOA) using ADAP technology with radiobinding confirmation, alongside genotyping to define risk profiles. The findings are scientifically and clinically significant because they refine prediction of autoimmune disease development in genetically at-risk relatives, informing screening and prevention strategies.

Christensen JH, Petersen GL, Kaur S et al. · Diabetes, obesity & metabolism · (2026) · View on PubMed ↗ · Free PDF ↗


Acute myeloid leukemia (AML) treatment intensification

MBNL1 hijacks a structured single-stranded distal DNA element to sustain FLT3 expression in KMT2A-rearranged leukemias.

This work studied the mechanism sustaining FLT3 expression in KMT2A-rearranged leukemias by identifying the RNA-binding protein MBNL1 as a regulator. Using DepMap dataset exploration and combinatorial CRISPR screens, the authors showed that MBNL1 promotes leukemia survival by sustaining FLT3 expression in a KMT2A-r context and that MBNL1 binds a structured single-stranded DNA element containing five consecutive guanines within the FLT3 enhancer via its zinc finger domains. Targeting the MBNL1–FLT3 enhancer interaction could provide a therapeutic vulnerability for KMT2A-r acute leukemias with FLT3 dependence.

Che M, Fields S, Yi S et al. · Science advances · (2026) · View on PubMed ↗ · Free PDF ↗

Expression of RUNX1::RUNX1T1 deregulates the proteome, induces C/EBPβ suppression, and blocks myeloid differentiation.

This study examined how expression of the AML fusion oncoprotein RUNX1::RUNX1T1 (RUNX1::ETO) affects the human hematopoietic stem/progenitor cell (HSPC) proteome. Mass spectrometry showed RUNX1::RUNX1T1 expression altered 257 proteins and was associated with downregulation of C/EBPβ (CEBPB), consistent with lower CEBPB expression in t(8;21) AML despite generally high CEBPB mRNA in AML. These proteomic and transcriptional links help explain how RUNX1::RUNX1T1 blocks myeloid differentiation and suggest C/EBPβ pathway suppression as a mechanistic vulnerability in t(8;21) AML.

Azevedo A, Leckenby A, Nicholson R et al. · Blood neoplasia · (2026) · View on PubMed ↗ · Free PDF ↗

DECIDER-2: Prospective randomized multicenter phase III trial of decitabine and venetoclax administered in combination with all-trans retinoic acid or placebo in patients with acute myeloid leukemia who are ineligible for induction chemotherapy.

DECIDER-2 was a prospective randomized multicenter Phase III trial in older, medically ineligible acute myeloid leukemia (AML) patients testing decitabine plus venetoclax (DAC+VEN) combined with all-trans retinoic acid (ATRA) versus DAC+VEN with placebo. The trial was designed to determine whether ATRA add-on improves outcomes based on prior in vitro priming of AML cells by DAC, building on earlier DECIDER Phase II results. This is clinically significant because it evaluates a potential regimen intensification strategy for induction-ineligible AML patients who have limited therapeutic options.

Grishina O, Schmoor C, Sellner C et al. · BMC cancer · (2026) · View on PubMed ↗ · Free PDF ↗


Health economics & hospital burden (birth defects, etc.)

Inpatient Hospitalization Charges for Children With Birth Defects in Texas, 2021-2023.

This retrospective Texas population study analyzed pediatric inpatient discharges (ages 0–17) from 2021–2023 using the Texas Hospital Inpatient Discharge Public Use Data File to quantify hospitalization charges associated with birth defects. Birth-defect hospitalizations were identified by ICD-10 codes Q00–Q99 in any of 26 diagnosis fields, and median inflation-adjusted charges were compared between hospitalizations with and without birth defects. The results are significant for health-economic planning by providing Texas-specific estimates of the financial burden of birth defects in children.

Betancourt D, Shumate C, Gandhi H et al. · Birth defects research · (2026) · View on PubMed ↗ · Free PDF ↗


Psoriasis & psoriatic arthritis outcomes/biomarkers

The World Psychiatric Association (WPA) Guideline on Schizophrenia Spectrum Disorders Management for Low- and Middle-Income Countries.

This work developed a World Psychiatric Association (WPA) guideline for schizophrenia spectrum disorder management specifically for low- and middle-income countries (LMICs) using a systematic review and three Delphi rounds with LMIC experts. The guideline prioritizes early intervention, continuity of care, and integration of psychosocial interventions with pharmacological treatment tailored to resource-limited settings. Clinically, it provides an evidence-based framework to improve SSD outcomes where mental health services and specialist capacity are constrained.

Castaldelli-Maia JM, Ng RMK, Javed A et al. · The International journal of social psychiatry · (2026) · View on PubMed ↗ · Free PDF ↗

CRP at diagnosis in psoriatic arthritis: what it means and associations with long-term outcomes.

This real-world cohort study evaluated 609 patients with psoriatic arthritis (PsA) to determine how C-reactive protein (CRP) levels at diagnosis (>0.5 mg/dL vs ≤0.5 mg/dL) relate to clinical features and long-term outcomes. Elevated CRP at diagnosis was analyzed for prognostic associations using multivariable logistic regression models built from univariate predictors. If confirmed, baseline CRP could serve as a practical risk stratifier to guide intensity of follow-up and management in PsA.

Dimopoulou AE, Papagoras C, Kyriazi N et al. · Rheumatology (Oxford, England) · (2026) · View on PubMed ↗ · Free PDF ↗

Deucravacitinib 5-Year Safety and Efficacy Results in Plaque Psoriasis: A Phase 3 Open-Label Extension of Randomized Clinical Trials.

This Phase 3 open-label extension reported 5-year safety and efficacy outcomes for deucravacitinib, an oral selective TYK2 inhibitor, in adults with moderate-to-severe plaque psoriasis enrolled from the randomized PSO-1 and PSO-2 trials. Patients were randomized to placebo, deucravacitinib 6 mg once daily, or apremilast 30 mg twice daily in the parent trials, and those enrolled at 52 weeks entered the long-term extension receiving open-label deucravacitinib. These long-term data are clinically significant for establishing durability of response and long-term tolerability of deucravacitinib in plaque psoriasis.

Armstrong AW, Lebwohl M, Warren RB et al. · American journal of clinical dermatology · (2026) · View on PubMed ↗ · Free PDF ↗


Glioma biology & mechanotransduction

Neuroligin-3-CSPG4 interaction maintains oligodendrocyte precursor cell progenitor state and promotes glioma proliferation through mechanotransduction.

This study investigated how neuroligin-3 (NLGN3) signaling regulates oligodendrocyte precursor cell (OPC) state and glioma growth, focusing on the NLGN3–CSPG4 pathway in glioma and normal glial counterparts. It found that shed NLGN3 binds CSPG4 (NG2) on glioma and OPCs, promotes CSPG4 shedding via ADAM10, and alters membrane tension to activate mechanotransduction primarily through PIEZO1, thereby promoting glioma proliferation. The mechanistic insight is significant because it links a neuron-derived adhesion cue (NLGN3) to a defined mechanotransduction axis (ADAM10/CSPG4/PIEZO1) that could be targeted to limit glioma progression.

Kim YS, Gillespie SM, Geraghty AC et al. · Nature neuroscience · (2026) · View on PubMed ↗ · Free PDF ↗


Critical illness & ICU-acquired muscle dysfunction

Rethinking Muscle Wasting in Critical Illness: A Systematic Review and Meta-Analysis of Myofiber Size and Protein Turnover.

This systematic review and meta-analysis synthesized skeletal muscle biopsy findings in adults with critical illness to quantify myofiber cross-sectional area and protein turnover variables. Across included studies, it pooled evidence on the biological basis of muscle wasting by comparing myofiber size and protein turnover measures between critical illness and control conditions. These findings help refine mechanistic targets and outcome biomarkers for preventing or treating ICU-acquired skeletal muscle dysfunction.

González-Seguel F, Robinson CM, Caceres-Parra C et al. · Critical care medicine · (2026) · View on PubMed ↗ · Free PDF ↗


Psychiatric care guidelines & mental health interventions

Therapeutic approaches for difficult-to-treat rheumatoid arthritis: a systematic literature review of current evidence.

This systematic literature review evaluated therapeutic approaches for difficult-to-treat rheumatoid arthritis (D2T RA) across defined clinical scenarios, including patients with active disease and limited options, those with ≥2 prior biologic/targeted synthetic DMARD failures, and those with poor quality of life despite low objective disease activity. It summarized evidence on efficacy and safety of pharmacologic and non-pharmacologic interventions based on a structured set of research questions aligned with prior EULAR considerations. Clinically, the review consolidates current evidence to inform treatment selection and guideline updates for patients with refractory or atypical D2T RA presentations.

Shams G, Dorgó AM, Ripepi C et al. · RMD open · (2026) · View on PubMed ↗

Effectiveness of acupuncture and related therapies for post-stroke insomnia: A systematic review and Bayesian network analysis.

This systematic review and Bayesian network analysis evaluated acupuncture and related therapies for post-stroke insomnia using randomized controlled trials identified from eight databases. It synthesized evidence with network meta-analysis (R and Stata) and assessed bias using a Cochrane-recommended risk-of-bias tool to compare effects across different acupuncture interventions. The findings are significant for determining relative effectiveness and safety of acupuncture-based options for improving insomnia outcomes after stroke.

Tang J, Tan H, Xiao L et al. · Medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Adolescent multi-omics and Mendelian randomization reveal transdiagnostic molecular mechanisms in psychiatric disorders.

This study used adolescent blood-derived multi-omics and Mendelian randomization to identify transdiagnostic molecular mechanisms across multiple psychiatric disorders. Using genome-wide analyses of single nucleotide polymorphisms linked to DNA methylation and gene expression in 1,274 healthy adolescents from the IMAGEN cohort (with replication), it then applied Mendelian randomization across six neuropsychiatric disorders to infer causal relationships. The approach is significant because it connects genetic regulation of epigenetic/transcriptional traits to shared mechanisms that may guide diagnosis and treatment across psychiatric conditions.

Qian L, Shi R, Yu X et al. · Nature. Mental health · (2026) · View on PubMed ↗ · Free PDF ↗


Inflammatory bowel disease (UC) immunomodulation & imaging

Association of oral vancomycin prophylaxis with Clostridium difficile infection in hematopoietic stem cell transplant recipients: A systematic review and meta-analysis.

This systematic review and meta-analysis evaluated whether oral vancomycin prophylaxis (OVP) prevents Clostridium difficile infection (CDI) in hematopoietic stem cell transplant (HSCT) recipients. Across included post-HSCT studies, OVP was assessed for its association with CDI risk using odds ratios and Review Manager 5.4. If supported by the pooled results, OVP could inform CDI-prevention strategies in HSCT patients who have high baseline CDI incidence.

Amir M, Kamal K, Jahangir MA et al. · Medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Clinical appraisal of handheld intestinal ultrasound in inflammatory bowel disease: Where are we now?

This article reviewed the clinical use of handheld intestinal ultrasound (HHIUS) for inflammatory bowel disease (IBD) in comparison with conventional, cart-based gastroenterologist-performed intestinal ultrasound (IUS). It reports that early HHIUS studies show reproducibility and diagnostic performance comparable to conventional IUS for selected tasks, especially bowel wall thickness assessment, but adoption is constrained by practical workflow and device limitations. Clinically, HHIUS could expand noninvasive, bedside monitoring of IBD if issues around cost, portability, and standardized use are addressed.

Miyatani Y, Hudson A, Kellar A et al. · Inflammatory bowel diseases · (2026) · View on PubMed ↗

Rhoifolin Alleviates Ulcerative Colitis by Targeting NMNAT1 and Activating SIRT1-FOXO1 Signaling to Enhance ILC3s Effector Function.

This preclinical study tested Rhoifolin in mouse models of ulcerative colitis (DSS- and TNBS-induced) and investigated how it modulates innate lymphoid cell type 3 (ILC3) effector function. Rhoifolin dose-dependently alleviated colitis by selectively enhancing ILC3 effector activity, increasing IL-22 production and strengthening epithelial barrier integrity without broadly altering ILC3 proliferation, apoptosis, homing, differentiation, or key ILC3 subset distributions. These results support Rhoifolin as a candidate therapy that boosts mucosal immune homeostasis while preserving barrier function in UC.

Yang H, Zhang Y, Feng S et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗ · Free PDF ↗

Senkyunolide I Inhibits mtDNA-cGAS-STING Signaling in Macrophages via Targeting VDAC1 Oligomerization to Attenuate Ulcerative Colitis.

This preclinical study examined senkyunolide I (SEI) in experimental ulcerative colitis models and macrophages to determine whether it suppresses mtDNA-driven cGAS-STING signaling. Using proteomics and AI modeling plus mechanistic validation in intestinal tissues and cultured macrophages, the authors found SEI inhibited the cGAS-STING pathway by targeting VDAC1 oligomerization. These findings suggest SEI may attenuate UC inflammation by blocking mitochondrial DNA sensing and downstream interferon signaling.

Ye Z, Huang Y, Han B et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗ · Free PDF ↗


Cancer metabolism & immune evasion (metabolic reprogramming)

Comparative Treatment Outcomes Across Actionable Genomic Alterations in NSCLC: A Large Multicenter Real-World Study.

This retrospective multicenter real-world study evaluated treatment outcomes in 810 Japanese patients with advanced or recurrent non-small-cell lung cancer (NSCLC) harboring actionable genomic alterations treated with molecular targeted therapy from 2017–2023. Patients were grouped by actionable alteration type—EGFR mutations versus ALK/ROS1/RET fusions versus other alterations (including MET exon 14 skipping, BRAF V600E, and KRAS G12C)—and efficacy and safety were compared across these genomic groups. The study provides comparative effectiveness and tolerability data that can guide expectations and decision-making when selecting targeted therapies based on specific actionable driver alterations.

Kato Y, Nishijima N, Takahashi S et al. · JTO clinical and research reports · (2026) · View on PubMed ↗ · Free PDF ↗

NPTXR as a novel therapeutic target: efficacy of antibody-drug conjugates in preclinical tumor models.

This preclinical cancer study evaluated NPTXR (neuronal pentraxin receptor) as a therapeutic target by generating antibody-drug conjugates (ADCs) using the fully humanized monoclonal antibody YB-800 (YB-800ADCs) in tumor models. NPTXR expression in cancer tissues supported ADC targeting, and the YB-800ADCs demonstrated anti-tumor efficacy in preclinical settings. The work positions NPTXR-directed ADCs as a candidate targeted therapy strategy for cancers with elevated NPTXR expression.

Lyndin M, Janicot M, Müller J et al. · Cancer cell international · (2026) · View on PubMed ↗ · Free PDF ↗

The mitochondria enzyme OGDH defends against disulfidptosis by licensing METTL3-regulated NRF2 translation.

This Nature Cell Biology study examined how the mitochondrial enzyme OGDH protects cells from disulfidptosis by regulating METTL3-dependent NRF2 translation. It showed that OGDH supports succinyl-CoA production for METTL3 succinylation, enabling succinylated METTL3 to recognize m6A on NRF2 mRNA and thereby license NRF2 translation, which increases TrxR1 expression and promotes resistance to disulfidptosis. These mechanistic insights link mitochondrial metabolism (OGDH) to an m6A/METTL3/NRF2 translational program that helps tumor cells survive glucose-starved stress, suggesting potential targets to counter disulfidptosis resistance.

Chen XY, Xu KJ, Zhou JX et al. · Nature cell biology · (2026) · View on PubMed ↗

Metabolic reprogramming drives pancreatic β cell neogenesis from α cells.

This study investigated whether PRC2 inhibitors can reprogram human or experimental pancreatic islet α cells into β cell–enriched states, focusing on the AR–ETV1 complex and metabolic pathways. The authors found that PRC2 inhibition induces β cell-enriched gene expression in α cells, with AR inhibition suppressing glycogen synthesis and enhancing the pentose phosphate pathway. The work is significant because it identifies a mechanistically defined, epigenetic/metabolic route to β cell neogenesis that could be leveraged for diabetes cell-therapy strategies.

Zhang Y, Lu G, Xie W et al. · Nature chemical biology · (2026) · View on PubMed ↗ · Free PDF ↗

Reversible epiblast regionalization determines differentiation potential of human pluripotent stem cells.

This study examined how reversible epiblast regionalization affects differentiation potential of human pluripotent stem cells (hPSCs), linking chromatin state to developmental competence. It found that erosion of bivalent chromatin marks at developmental gene loci (independent of DNA methylation) drives acquisition of a posterior epiblast-like state and premature developmental gene expression, reducing default neural differentiation capacity and brain organoid formation. The significance is that it supports a chromatin-based explanation for hPSC differentiation bias and motivates chemical chromatin restoration approaches to improve regenerative and disease-modeling outcomes.

Sutcliffe MA, Wong E, Wingett SW et al. · Nature biotechnology · (2026) · 1 citations · View on PubMed ↗ · Free PDF ↗

Charting intratumor heterogeneity from bench to bedside.

This Review synthesized evidence on how intratumor heterogeneity is measured and interpreted across the cancer care continuum, from multiregion tissue and multiomic profiling to functional studies and longitudinal plasma sampling. It concludes that tumor ecosystems evolve dynamically through genetic and non-genetic mechanisms in both cancer cells and the microenvironment, and that this should inform evolution-aware diagnostics and therapies. The significance is a conceptual and practical framework for translating heterogeneity insights into treatment strategies that anticipate evolutionary trajectories.

Wan JCM, McGranahan N, Swanton C · Nature cancer · (2026) · View on PubMed ↗

The Plasmodium heme detoxification protein functions in mitochondrial protein synthesis.

This study investigated the Plasmodium heme detoxification protein (HDP) using genetic manipulation, microscopy, bioenergetics, and proteomics to clarify its role in hemozoin formation and mitochondrial function. It found that HDP localizes to mitochondria rather than the digestive vacuole, that HDP inactivation does not affect heme biomineralization, but that it causes mitochondrial depolarization and hypersensitivity to the antimalarial proguanil. The significance is that it refines a validated malaria drug target mechanism by linking HDP to mitochondrial protein synthesis/fitness rather than directly to hemozoin crystallization.

Sarrazin L, Rosenthal MR, Kloehn J et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Heat stress promotes pre-tRNA capping to modulate cap-dependent translation in Saccharomyces cerevisiae.

This study examined how heat stress in Saccharomyces cerevisiae promotes pre-tRNA capping to modulate cap-dependent translation. It mapped pre-tRNA capping across nearly all pre-tRNAs, determined transcription start sites for tRNA genes, and found that capping efficiency is influenced by the base pairing of the pre-tRNA 5′ end. The significance is that it reveals a heat-responsive RNA processing mechanism that can regulate translation by controlling pre-tRNA stability and cap-dependent protein synthesis.

Kikuchi I, Ohira T, Nakatsuka T et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Circulating B cell and T cell activation states predict clinical outcomes in melanoma and reveal dynamic immune reinvigoration with checkpoint inhibitor immunotherapy.

This study profiled circulating B cell and T cell activation states in treatment-naïve melanoma patients and healthy individuals using high-dimensional mass cytometry, and then analyzed longitudinal samples from patients treated with immune checkpoint inhibitor (CPI) immunotherapy. It found that specific B cell and T cell activation states measured before and during treatment predicted clinical outcomes and revealed dynamic immune reinvigoration associated with CPI therapy. These immune-state biomarkers could help forecast response and immune-related adverse events (irAEs), enabling better patient selection and monitoring for checkpoint inhibitor treatment.

Booth L, Adams R, Clifford A et al. · Journal for immunotherapy of cancer · (2026) · View on PubMed ↗ · Free PDF ↗

PARP7-mediated mono-ADP-ribosylation stabilizes MYH9 to ensure actin cap integrity and chromosome segregation in mouse oocytes.

This mouse oocyte study investigated whether PARP7, a mono-ADP-ribosyltransferase, regulates meiotic actin cap integrity and chromosome segregation by stabilizing the actin-associated motor protein MYH9. Using PARP7 knockdown and pharmacological inhibition, along with metabolomic profiling of NAD+ dynamics and multi-omics target mapping, it showed that PARP7-mediated mono-ADP-ribosylation stabilizes MYH9 to preserve actin cap structure and ensure accurate chromosome segregation during meiosis. Scientifically, it identifies a PARP7–MYH9 post-translational control axis as a key regulator of oocyte meiotic fidelity, with implications for understanding fertility and gamete quality.

Cao G, Liu S, Liu Y et al. · Journal of advanced research · (2026) · View on PubMed ↗ · Free PDF ↗

A thermoregulatory module for timekeeping in Arabidopsis.

This study investigated how the circadian clock component PRR9 (PSEUDO-RESPONSE REGULATOR 9) enables temperature adaptation in Arabidopsis, focusing on temperature entrainment and temperature compensation. It found that high temperature increases PRR9 protein accumulation and triggers liquid-liquid phase separation, which inhibits CCA1 transcription and promotes recruitment of the m6A-removal factor ALKBH9B to accelerate CCA1 mRNA degradation, with SETD7 implicated in the thermal response network. Scientifically, it proposes a PRR9-centered mechanism linking phase separation, m6A dynamics, and transcriptional control to maintain robust circadian temperature compensation.

He Y, Wang X, Su C et al. · Developmental cell · (2026) · View on PubMed ↗

TGF-β1 drives neutrophil extracellular traps formation to promote CD8+ T cell exhaustion via the ERK-c-Fos-JunB axis, mediating gastric cancer immunotherapy resistance.

The study examined how TGF-β1 influences neutrophil extracellular traps (NETs) and CD8+ T cell exhaustion in advanced gastric cancer patients treated with anti-PD-1, using single-cell RNA sequencing plus flow cytometry, multiplex immunofluorescence, and in vitro co-culture. It found that TGF-β1 drives NET formation to promote CD8+ T cell exhaustion through an ERK–c-Fos–JunB signaling axis, contributing to resistance to anti-PD-1 immunotherapy. These findings identify the TGF-β1–NET–ERK/c-Fos/JunB pathway as a mechanistic target to overcome PD-1 blockade resistance in gastric cancer.

Qu Z, Wang Z, Hu Y et al. · Journal for immunotherapy of cancer · (2026) · View on PubMed ↗

β-glucan elicits APOE-dependent peripheral trained immunity to suppress hepatocellular carcinoma.

The study investigated whether whole β-glucan particle–induced trained immunity in an APOE-dependent manner can suppress hepatocellular carcinoma (HCC) using orthotopic mouse models. It reported that β-glucan elicits peripheral trained immunity in an APOE-dependent way that enhances antitumor immune activity against HCC. This supports APOE as a key host factor for β-glucan–based immunomodulation and provides a rationale for leveraging trained immunity to improve HCC outcomes.

Jiang N, Wu T, Yang R et al. · Journal for immunotherapy of cancer · (2026) · View on PubMed ↗

Tumor-derived CDHR2-enriched extracellular vesicles engage ANPEP on liver sinusoidal endothelial cells to facilitate transendothelial migration in PDAC.

The study analyzed patient-derived extracellular vesicles (EVs) and liver metastasis mechanisms in pancreatic ductal adenocarcinoma (PDAC), identifying the EV-enriched membrane protein CDHR2 and its interaction with ANPEP on liver sinusoidal endothelial cells. It found that CDHR2-enriched tumor EVs engage ANPEP to facilitate transendothelial migration, promoting hepatic colonization, and that CDHR2 knockdown in PDAC cells reduces proliferation, migration, and invasion. This mechanistic EV–receptor pathway (CDHR2→ANPEP) highlights a potential therapeutic target to prevent or limit liver metastasis in PDAC.

Wang R, Wang Y, Xiao S et al. · Cancer letters · (2026) · View on PubMed ↗

Clamp conformational flexibility and dynamics in archaeal and eukaryotic RNA polymerases revealed by cryo-EM.

The study used cryo-EM to characterize clamp conformational flexibility and dynamics in archaeal and eukaryotic RNA polymerases, comparing them to bacterial RNAP behavior across evolutionary lineages. It found that archaeal-eukaryotic RNAPs exhibit distinct clamp dynamics and require a more extensive set of general transcription factors (GTFs) than bacterial RNAP, reflecting different initiation requirements for promoter DNA binding, duplex unwinding, and template positioning. These structural insights clarify how RNAP clamp motion and factor dependence evolved to control transcription initiation across domains of life.

Fordjour GNR, Palao L, Murakami K et al. · The Journal of biological chemistry · (2026) · View on PubMed ↗

The microenvironment dictates glyco-immune surveillance via HSF1-mediated metabolism.

This study investigated how the tumor microenvironment regulates glyco-immune surveillance through HSF1-mediated metabolism using normal epithelial cells cultured under conditions mimicking healthy versus cancerous tissue properties. The authors found that microenvironmental hyperglycemia alters the epithelial glycocalyx composition and thickness in part via mechanosensitive pathways linked to HSF1-dependent metabolic programs. These findings suggest that targeting HSF1-driven metabolic control of glycocalyx remodeling could modulate immune recognition in hyperglycemic tumor contexts.

Tharp KM, Park S, Timblin GA et al. · Science advances · (2026) · View on PubMed ↗ · Free PDF ↗

APOE+ macrophages and POSTN+CAFs form immune-exclusion niche driving immunotherapy resistance in clear-cell renal carcinoma.

This study examined how stromal-immune niches drive immune-exclusion and immunotherapy resistance in clear-cell renal cell carcinoma (ccRCC) by focusing on APOE+ macrophages and POSTN+ cancer-associated fibroblasts (CAFs). Using spatial transcriptomics and single-cell profiling, the authors defined a peritumoral niche where POSTN+CAFs interlaced with APOE+ tumor-associated macrophages excluded CD8+ T cells from tumor cores and was enriched in poor-prognosis, immune-checkpoint blockade (ICB)-refractory patients. The results implicate this ECM-remodeling, immunosuppressive ligand–receptor, metabolically reprogrammed niche as a mechanistic driver of ICB resistance and a potential target for combination therapies.

Ge Q, Ge S, Wang Z et al. · Science advances · (2026) · View on PubMed ↗ · Free PDF ↗

Transposable elements and homotypic niches drive immune dynamics and resistance in melanoma epigenetic-based immunotherapy.

This study investigated how transposable elements and epigenetic “homotypic niches” shape immune dynamics and resistance in melanoma under epigenetic-based immunotherapy pressure. Using longitudinal patient biopsies from the phase 1b NIBIT-M4 trial (DNA methyltransferase 1 inhibitor plus anti-CTLA-4) with single-cell multiome and spatial transcriptomics, the authors identified multiple malignant meta-programs, including a rare Wnt/β-catenin state and a dedifferentiated neural crest-like state enriched in nonresponders. The findings link specific epigenetically driven programs and transposable-element-associated niche dynamics to therapeutic resistance, suggesting biomarkers and targets for improving response to epi-immunotherapy.

Ciervo E, Ceccarelli F, Di Giacomo AM et al. · Science advances · (2026) · View on PubMed ↗

Monounsaturated fatty acid biosynthesis is critical for streptococcal envelope homeostasis and stress tolerance.

This study investigated how monounsaturated fatty acid (MUFA) biosynthesis supports streptococcal envelope homeostasis and stress tolerance in Streptococcus species. It focuses on the de novo MUFA synthesis route within the fab pathway versus host fatty acid uptake via the fak pathway, examining how de novo MUFA production affects physiology and virulence-associated traits (details truncated). The work supports MUFA biosynthesis as a potential antimicrobial target by linking lipid metabolism to bacterial survival under stress and to pathogenic fitness.

Baker JL, Tang J, Guo M et al. · Journal of bacteriology · (2026) · View on PubMed ↗ · Free PDF ↗

circZNF148 Drives Glucose Metabolism Reprogramming to Enhance Metastasis and Immune Evasion via HK1 Stabilization in Triple-Negative Breast Cancer.

This study used circRNA sequencing in glucose-metabolism-stressed triple-negative breast cancer (TNBC) cells and lung metastasis models to identify circZNF148 as a driver of metastasis and immune evasion. Mechanistically, circZNF148 promoted glycolysis by scaffolding the interaction between hexokinase 1 (HK1) and the deubiquitinase adaptor ADRM1, stabilizing HK1 and thereby enhancing tumor metabolic reprogramming. Targeting the circZNF148–HK1 axis could represent a strategy to limit TNBC progression and immune escape.

Jin Y, Zhao W, Wang L et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗ · Free PDF ↗

Plasma P-tau217 for detecting amyloid clearance after donanemab in Alzheimer’s disease.

This phase 3 TRAILBLAZER-ALZ 2 trial analysis evaluated whether plasma phosphorylated tau at threonine 217 (plasma p-tau217) can detect treatment-related amyloid clearance (TRAC) after donanemab in early symptomatic Alzheimer’s disease. Plasma p-tau217 showed suboptimal diagnostic performance for identifying post-treatment TRAC by amyloid PET, based on receiver operating characteristic (ROC) analysis (with TRAC defined as <24.1 centiloids). Scientifically, the findings suggest p-tau217 may be insufficient as a standalone biomarker for monitoring donanemab-induced amyloid clearance, informing how clinicians and trials should track response.

Collins EC, Lu M, Beck R et al. · Alzheimer’s & dementia : the journal of the Alzheimer’s Association · (2026) · View on PubMed ↗ · Free PDF ↗

HPV-driven metabolic reprogramming promotes T cell exhaustion: targeting immunometabolic barriers with natural products.

This review studied how high-risk human papillomavirus (HR-HPV) oncoproteins E6/E7 drive immunometabolic changes in the cervical cancer tumor microenvironment that promote CD8+ T cell exhaustion (TEX). It reports that HPV-driven nutrient availability shifts, lactate accumulation, and lipid peroxidation create metabolic barriers that impair anti-tumor T cell function and can undermine immune checkpoint blockade (ICB). The synthesis supports targeting immunometabolic constraints—potentially with natural products—as a strategy to restore T cell activity in HPV-associated cancers.

Wei L, Menghui H, Dandan Z et al. · Frontiers in immunology · (2026) · View on PubMed ↗ · Free PDF ↗

Real-world treatment patterns in stage III and IV melanoma patients: insights from a global multi-center chart review study.

This multi-center retrospective chart review studied real-world treatment patterns and therapy exposure in stage III and IV melanoma patients, focusing on those treated with anti–PD-1 immune checkpoint inhibitors. Across 22 centers in Australia, France, Germany, South Korea, the UK, and the US (2018–2021 for the aggregate cohort), it estimated the proportion of stage III/IV patients exposed to different therapies and described patterns among anti–PD-1-treated patients in adjuvant versus advanced settings. The results are significant for understanding how immunotherapy is used outside clinical trials and for identifying gaps or variability that could inform future treatment optimization.

Kim M, Gaughan EM, Azpeitia A et al. · Frontiers in immunology · (2026) · View on PubMed ↗ · Free PDF ↗

SLC7A5 promotes colorectal cancer liver metastasis by reprogramming tryptophan metabolism through the Kyn/XANA‒AhR axis and reshaping the immune microenvironment.

This study investigated how the tryptophan transporter SLC7A5 promotes colorectal cancer liver metastasis (CRLM) by reprogramming tryptophan metabolism through the Kyn/XANA–AhR axis and altering the immune microenvironment. Integrating public datasets and clinical specimens, it validated SLC7A5’s role in proliferation and metastasis using in vitro assays and in vivo models, and used targeted metabolomics and isotope tracing to define kynurenine pathway changes linked to AhR signaling (as truncated in the abstract). The mechanistic link between SLC7A5–tryptophan metabolism–AhR signaling and immune remodeling is clinically significant because it suggests metabolic-immune pathway targeting as a strategy to limit CRLM.

Luo Y, Li L, Li S et al. · Clinical and translational medicine · (2026) · View on PubMed ↗ · Free PDF ↗


Neuroimmunology & neuroinfectious cell therapies

This study engineered full-length human TDP-43 with an N-terminal nuclear export signal (NES) while preserving the native 3’ UTR autoregulatory module to test how persistent cytoplasmic export bias affects TDP-43 homeostasis in HEK293T and differentiated SH-SY5Y cells. NES-driven cytoplasmic bias promoted detergent-insoluble (insoluble) TDP-43 accumulation and linked it to nuclear splicing defects and nuclear dysfunction. The results mechanistically connect chronic TDP-43 export bias to insoluble aggregation and nuclear pathology, informing therapeutic strategies aimed at restoring nuclear function and TDP-43 localization.

Toyama G, Koide S, Yamagishi T et al. · Neurobiology of disease · (2026) · View on PubMed ↗

Targeting the IL-17C-M2 macrophage axis ameliorates fibrosis in endometriosis through MAPK/ERK signaling.

This study investigated endometriosis mechanisms by testing whether targeting the IL-17C–M2 macrophage axis reduces fibrosis via MAPK/ERK signaling in human endometriotic lesions and in an endometriosis mouse model. Using spatial transcriptomics and cellular interaction analyses, it found that IL-17C promotes M2 macrophage polarization and extracellular matrix pro-fibrotic programs, and that IL-17C neutralization with the MOR106 antibody ameliorated ectopic lesion growth and fibrosis through MAPK/ERK signaling. These findings identify the IL-17C–M2 macrophage–MAPK/ERK pathway as a potential therapeutic target to treat fibrotic progression in endometriosis.

Li J, Yao B, Chu L et al. · Journal of translational medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Effectiveness of anti-CD19 CAR T-cell therapy for high-grade B-cell lymphoma in Japan: a single-institution analysis.

This single-institution retrospective analysis studied efficacy of anti-CD19 CAR T-cell therapy in Japanese patients with relapsed/refractory high-grade B-cell lymphoma (HGBCL), including axicabtagene ciloleucel and lisocabtagene maraleucel. Among 15 treated patients (10 axicabtagene ciloleucel, 5 lisocabtagene maraleucel), the study evaluated clinical outcomes such as response and survival following CAR T-cell infusion. The significance lies in providing Japan-specific real-world effectiveness data for HGBCL, a subgroup with comparatively limited published evidence.

Ochi T, Makita S, Hiratsuka A et al. · International journal of clinical oncology · (2026) · View on PubMed ↗

Interleukin-6 trans-signalling as a selectively targetable driver of neurodegeneration.

This review examined how interleukin-6 (IL-6) trans-signalling—driven by soluble IL-6 receptor acting on gp130-expressing cells—contributes to neurodegeneration across disorders including amyotrophic lateral sclerosis, Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, and multiple sclerosis. It highlights mechanistic links between IL-6 trans-signalling and dysregulated immune, glial, neuronal, and vascular function, contrasting it with classical membrane IL-6R signalling that is often associated with homeostatic/reparative effects. Targeting IL-6 trans-signalling is proposed as a selectively actionable strategy to modulate chronic neuroinflammation and potentially slow or prevent neurodegenerative progression.

Risby-Jones G, Lee JD, Fung JN · Trends in neurosciences · (2026) · View on PubMed ↗ · Free PDF ↗

SOHO State of the Art Updates and Next Questions | Best of Stem Cell Transplant: Recent Advances in Allogeneic Hematopoietic Cell Transplantation.

This article reviewed recent practice-changing evidence in allogeneic hematopoietic cell transplantation, focusing on donor selection, graft-versus-host disease (GVHD) prevention, and post-transplant relapse management in patients undergoing transplant. It emphasizes the near-universal adoption of post-transplant cyclophosphamide (PTCy) as GVHD prophylaxis, which reduces the historical primacy of human leukocyte antigen (HLA) matching and supports comparable outcomes with mismatched unrelated donors and haploidentical donors. Clinically, these advances broaden feasible donor options and refine GVHD and relapse strategies to improve transplant outcomes.

Gilligan M, Gomez-Arteaga A · Clinical lymphoma, myeloma & leukemia · (2026) · View on PubMed ↗

Subtypes of neurons in the cerebellar cortex.

This perspective article synthesized evidence that cerebellar cortex neurons are more diverse than previously thought, emphasizing findings enabled by single-nucleus RNA sequencing (snRNA-seq). It reports that snRNA-seq shows each major cerebellar neuron class contains multiple transcriptionally distinct subtypes, and it discusses how mapping and functional characterization of this diversity reshape models of cerebellar computation. The significance is conceptual and methodological: transcriptomic subtype resolution is reframing how cerebellar circuit function is understood.

Regehr WG, Macosko EZ, Hull CA · Neuron · (2026) · View on PubMed ↗

Early-life stress alters H3K4me1 in VTA to prime stress sensitivity.

This mouse study examined how early-life stress produces long-lasting stress sensitivity by altering chromatin in the ventral tegmental area (VTA) dopamine system. Using bottom-up mass spectrometry, viral-mediated epigenome editing, RNA sequencing, patch-clamp electrophysiology, and behavioral assays, it found that early-life stress enriches H3K4me1-associated open chromatin and primed/active enhancers and increases the H3K4 monomethylase SETD7, with epigenome editing experiments mimicking stress-like priming. The results identify an H3K4me1–SETD7 chromatin mechanism that primes VTA neurons for heightened later stress responses, suggesting potential targets for preventing stress-related vulnerability.

Kim HJJ, Geiger LT, Balouek JA et al. · Neuron · (2026) · View on PubMed ↗

Chronic xenogeneic GVHD after CAR T cell therapy limits long-term safety assessment of CAR effects using NSG mouse model.

The study evaluated long-term safety limitations of xenogeneic CAR T cell therapy using an NSG mouse model of chronic xenogeneic graft-versus-host disease (xenoGVHD), focusing on how donor T cell memory phenotype affects outcomes. It found that generating CAR T cells from memory-phenotype human T cells markedly altered the xenoGVHD outcome after tumor clearance compared with prior observations using naïve T cells, thereby changing the long-term xenoGVHD profile. This is significant for preclinical CAR T cell safety assessment because it shows that donor T cell phenotype can confound or reshape long-term xenogeneic toxicity readouts.

Firoz WA, Sheng MK, Ruivo P et al. · Blood advances · (2026) · View on PubMed ↗ · Free PDF ↗

Contemporary Management of Relapsed or Refractory Chronic Lymphocytic Leukemia.

This article reviewed contemporary management strategies for relapsed or refractory chronic lymphocytic leukemia (CLL)/small lymphocytic lymphoma (SLL) in the era of targeted agents. It emphasized that treatment selection at first relapse should incorporate clinical factors (status, progression kinetics, Richter transformation assessment) and genomic re-evaluation, particularly acquired resistance mutations and TP53 aberrations, while noting multiple effective options after frontline covalent BTK inhibitors and venetoclax-based fixed-duration or MRD-guided regimens. Clinically, it provides a framework to personalize subsequent therapy and anticipate resistance mechanisms in RR CLL/SLL.

Castonguay M, Seymour JF · Journal of clinical oncology : official journal of the American Society of Clinical Oncology · (2026) · View on PubMed ↗

Acute Attack Treatment Escalation and Subsequent Relapse Risk in Pediatric Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease.

The study assessed whether escalation of acute therapy at the first attack in pediatric myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) affects relapse risk, comparing steroid-only treatment versus steroid-plus escalation (IVIG and/or plasma exchange after high-dose IV methylprednisolone). Using a retrospective single-center cohort (2015–2024) with Kaplan–Meier and adjusted Cox regression, it evaluated early (≤1 year) and overall relapses. The results are clinically important because they inform whether treatment escalation strategy at the first attack changes the subsequent disease course in pediatric MOGAD.

Bartolomeo S, Nistri R, Kim NN et al. · Neurology · (2026) · View on PubMed ↗ · Free PDF ↗

Capsid stabilization reprograms the nuclear fate of the HIV genome.

This study examined how capsid stabilization by lenacapavir (LEN) alters the nuclear fate of the HIV genome in macrophages. Using ultrastructural and localization analyses, the authors showed that LEN-treated HIV-1 maintains conical capsids within CPSF6-enriched HIV-1-induced membraneless organelles (HIV-1-MLOs) that are rerouted to chromatin-associated PML nuclear bodies (PML-NBs) for molecular exchange without condensate fusion with nuclear speckles. By redirecting HIV trafficking and nuclear processing, capsid stabilization provides a mechanistic basis for LEN’s antiretroviral activity in macrophage reservoirs.

Mourer T, Harastani M, Cuche C et al. · Science advances · (2026) · View on PubMed ↗ · Free PDF ↗

A genotype-first approach reveals the molecular basis of pyrin inflammasome activation.

This study used a genotype-first approach to define molecular mechanisms of pyrin inflammasome activation in pyrin-associated autoinflammatory diseases (PAADs) caused by MEFV (pyrin) variants. Using a cell-based pyroptosis assay, the authors stratified 265 MEFV missense variants and identified previously uncharacterized pathogenic variants, then characterized how the pyrin B30.2 domain interacts with CDC42 to regulate pyrin intracellular trafficking and activation. This provides a functional framework for interpreting MEFV variants of uncertain significance and for mechanistically linking CDC42-dependent trafficking to inflammasome activation.

Iwata N, Kuchitsu Y, Hijikata A et al. · Science immunology · (2026) · 3 citations · View on PubMed ↗

An N-terminal CDC42 T43I variant reveals the mechanism of pyrin inflammasome activation.

This study investigated how an N-terminal CDC42 variant (p.T43I) causes autoinflammation by altering pyrin inflammasome activation. In patients and mechanistic experiments, the authors demonstrated that the region around CDC42 residue T43 interacts with the carboxyl-terminal B30.2 domain of pyrin to regulate pyrin localization and activation, and that the p.T43I substitution strengthens the CDC42–pyrin interaction via additional van der Waals contacts. These results clarify a CDC42–pyrin molecular mechanism underlying severe autoinflammatory disease and support variant-specific diagnostic and therapeutic considerations.

Aoki M, Iannuzzo A, Mertz P et al. · Science immunology · (2026) · 3 citations · View on PubMed ↗

T cell-intrinsic AIM2 exacerbates lung inflammation in OVA-LPS- and HDM-induced asthma models.

This study assessed whether the DNA sensor AIM2 contributes to lung inflammation in asthma models and compared its relevance to NLRP3. Using analyses of human datasets and mouse models of allergic asthma induced by ovalbumin (OVA)-LPS or house dust mite (HDM), the authors found increased AIM2 expression in severe asthma and in neutrophilic asthma phenotypes and then tested AIM2’s functional role in these models. If AIM2 is causal, targeting AIM2 could represent a strategy to reduce neutrophil-associated airway inflammation and disease severity in specific asthma endotypes.

Chou WC, Hsu M, Wrobel JA et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗

Overcoming immunogenic gaps in malaria subunit vaccines by broadening CSP regions targeted.

This experimental study used B cell receptor (BCR) knock-in mice to test whether broadening the Plasmodium falciparum circumsporozoite protein (PfCSP) regions targeted can overcome immunogenic gaps in malaria subunit vaccines, including R21/Matrix M and RTS,S/AS01. It found that R21-included PfCSP epitopes elicited robust B cell responses to the immunodominant major repeats but not to other protective epitopes such as the minor repeat and junction, and it defined a minimal peptide that can elicit minor-repeat-specific B cell responses and generate highly protective antibodies (abstract truncated). These findings are significant for next-generation malaria vaccine design aimed at improving breadth and durability of protective immunity beyond the major repeat region.

Koo JH, Tripathi P, Flores-Garcia Y et al. · The Journal of experimental medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Mechanisms of antibody-mediated enhancement of immune responses.

This article examined mechanisms by which preexisting antibodies modulate immune recall responses, particularly germinal center (GC) and plasmablast (PB) compartments. It reports that antibody “memory” and antibody-mediated effects can enhance GC/PB development and alter the affinity threshold for B cell recruitment into immune responses, based on mechanistic experiments (details truncated). Understanding these processes is important for designing vaccines and antibody-based therapies that optimize memory B cell responses and affinity maturation.

Cipolla M, MacLean AJ, Hernandez B et al. · The Journal of experimental medicine · (2026) · View on PubMed ↗

Adoptive T-cell therapies in neuroinfectious and neuroinflammatory diseases.

This article is a narrative review describing adoptive T-cell therapies as emerging “living drugs” for neuroinfectious and neuroinflammatory diseases. It highlights that engineered or transferred T cells can expand, adapt, and persist in vivo, potentially addressing treatment-refractory immune dysfunction across neurological autoimmune disorders and infections. Scientifically, it frames how these therapies may overcome limitations of conventional immunomodulators and supports continued clinical trial development in neurology.

Lambert N, Cortese I · Brain : a journal of neurology · (2026) · View on PubMed ↗

Hormone replacement therapy and its association with LATE-NC in older adults.

This study examined whether long-ago hormone replacement therapy (HRT) is associated with limbic-predominant age-related transactive response DNA-binding protein 43 (TDP-43) encephalopathy neuropathological change (LATE-NC) in older adults using the Religious Orders Study and Memory and Aging Project (n=2056; ≥65 years; males n=640, females n=1416). The key finding was not available in the provided abstract text because the results were truncated. If the original association is replicated, it would support a role for sex-hormone exposure in modulating neurodegenerative neuropathology risk beyond Alzheimer’s disease.

Kim YM, Colcord K, Sajjadi SA et al. · Alzheimer’s & dementia : the journal of the Alzheimer’s Association · (2026) · View on PubMed ↗ · Free PDF ↗

Validation of the new IMS/IMWG consensus genomic staging (CGS) of high-risk multiple myeloma (HRMM) in a contemporary cohort of 1209 patients.

This retrospective validation study assessed the International Myeloma Society (IMS)/International Myeloma Working Group (IMWG) consensus genomic staging (CGS) criteria for high-risk multiple myeloma (HRMM) in a contemporary single-center cohort of 1209 newly diagnosed patients with complete CGS data (except TP53 mutations). The key finding was that 25.2% of patients met HRMM criteria under the new CGS, but the prognostic performance results were truncated in the abstract. Clinically, validating CGS in real-world contemporary treatment settings supports more consistent risk stratification and treatment planning for HRMM.

Kastritis E, Filippatos C, Gavriatopoulou M et al. · HemaSphere · (2026) · 2 citations · View on PubMed ↗ · Free PDF ↗

This multi-cohort ECHO Consortium study (4159 mother-child pairs from 15 cohorts; births 2006–2020) tested whether urinary exposure to organophosphate ester flame retardants and plasticizers (OPEs) during pregnancy is associated with autism-related outcomes in children. The key finding was not available in the provided abstract text because the results were truncated. Scientifically and clinically, identifying specific OPE biomarkers linked to autism-related outcomes could inform exposure reduction policies and risk assessment during pregnancy.

Ames JL, Ferrara A, Feng J et al. · Environmental health perspectives · (2026) · View on PubMed ↗

This study assessed health-related quality of life (HRQoL) in patients with relapsed/refractory multiple myeloma treated with linvoseltamab in the LINKER-MM1 trial (n=117; median follow-up 21.3 months). The key finding was not fully provided in the truncated abstract text, but HRQoL was measured longitudinally using EORTC QLQ-C30, the QLQ-MY20 module, and EQ-5D-3L at baseline and scheduled follow-ups. Clinically, demonstrating meaningful HRQoL changes alongside efficacy and safety would support patient-centered benefit of linvoseltamab in R/RMM.

Hoffman JE, Bumma N, Richter J et al. · Blood neoplasia · (2026) · View on PubMed ↗ · Free PDF ↗

The role and function of CTLA-4 in Sjögren’s syndrome.

This review studied the immunoregulatory role of the immune checkpoint receptor CTLA-4 in Sjögren’s syndrome (SS), including how it interacts with other inhibitory pathways such as PD-1, TIGIT, and TIM-3. It concludes that CTLA-4 participates in a multi-layered immunosuppressive network that shapes genetic susceptibility, T cell subsets, and inflammatory cytokine levels in SS. Understanding CTLA-4’s network effects is significant for rationally evaluating CTLA-4–targeted therapies and for predicting immune modulation in SS.

Wen J, Zhang L, Xie L et al. · Frontiers in immunology · (2026) · View on PubMed ↗ · Free PDF ↗

SSRI/SNRI and long COVID in children and adolescents with neuropsychiatric conditions: a cohort study from the RECOVER Initiative.

This cohort study investigated whether SSRI/SNRI exposure is associated with long COVID outcomes in children and adolescents with pre-existing neuropsychiatric conditions using the RECOVER Initiative data. Among 110,955 pediatric patients across 37 US health systems, it found associations between SSRI/SNRI use and long COVID-related outcomes (post-infectious symptom risk), consistent with potential effects on immune and autonomic pathways. These findings are clinically relevant because they may inform risk stratification and medication considerations for pediatric neuropsychiatric patients after COVID-19.

Zhou T, Zhang B, Lu Y et al. · Nature. Mental health · (2026) · View on PubMed ↗ · Free PDF ↗


Perioperative care & emergency diagnostics

Infectious Diseases Society of America 2026 Guidance on the Treatment of Antimicrobial-Resistant Gram-Negative Infections.

This IDSA 2026 guidance article reviewed and updated treatment recommendations for antimicrobial-resistant Gram-negative infections, focusing on ESBL-producing Enterobacterales (ESBL-E), AmpC-producing Enterobacterales (AmpC-E), carbapenem-resistant Enterobacterales (CRE), difficult-to-treat resistant Pseudomonas aeruginosa (DTR P. aeruginosa), carbapenem-resistant Acinetobacter baumannii (CRAB), and Stenotrophomonas maltophilia. The key output is an evidence-informed, updated set of regimen suggestions replacing prior IDSA AMR treatment guidance for these resistance phenotypes. Clinically, it standardizes management choices to improve outcomes and antimicrobial stewardship in patients with serious AMR Gram-negative infections.

Tamma PD, Bonomo RA, Heil EL et al. · Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · (2026) · View on PubMed ↗

Machine Learning Characterization of Readmissions After Chronic Subdural Hematoma Hospitalizations.

The study used a retrospective cohort from the Nationwide Readmissions Database (2016–2022) to characterize 90-day readmissions after chronic/subacute subdural hematoma (cSDH/sSDH) hospitalizations and to identify patient phenotypes with distinct readmission risk profiles using machine learning-driven clustering. It aimed to quantify the incidence and diversity of readmission events beyond surgical recurrence and to determine their outcomes. This is significant for improving risk stratification and trial design by capturing heterogeneous, clinically meaningful readmission patterns after cSDH/sSDH.

Chen H, Colasurdo M, McIntyre MK et al. · Neurology · (2026) · View on PubMed ↗

Pain response after palliative-intent radiotherapy for pancreatic cancer: a systematic review.

This systematic review evaluated pain response after palliative-intent radiotherapy for pancreatic cancer (PC)-related pain across published studies from 1971–2024. It identified 11 eligible studies and summarizes the most commonly used palliative radiotherapy schedules (with details truncated in the abstract). The findings are intended to inform evidence-based expectations for symptom relief and to guide selection of palliative RT regimens for patients with PC pain.

Makita K, Hiroshima Y, Takehana K et al. · International journal of clinical oncology · (2026) · View on PubMed ↗

Diagnostic role of N-terminal pro-B-type natriuretic peptide (NT-proBNP) in pediatric syncope in the emergency department: a prospective study.

This prospective emergency department study assessed the diagnostic efficacy of serum N-terminal pro-B-type natriuretic peptide (NT-proBNP) in children with syncope to distinguish cardiac from non-cardiac causes. It measured NT-proBNP alongside conventional cardiac biomarkers, telecardiography, and 12-lead electrocardiography, with echocardiography for all participants and additional TILT testing and 24-hour Holter monitoring in a subset. If validated, NT-proBNP could improve rapid risk stratification of pediatric syncope in the ED by identifying children more likely to have cardiac syncope.

Dedeoglu S, Turan C, Dogan E et al. · European journal of pediatrics · (2026) · View on PubMed ↗

Effect of Pre-operative Intravenous Crystalloid Bolus on Post-Induction Blood Pressure - a randomized blinded intervention trial.

This randomized, single-blind, blinded-intervention trial tested whether a pre-operative intravenous crystalloid bolus reduces post-induction hypotension in high-risk adult patients undergoing major non-cardiac surgery under general anesthesia. The study specifically targeted post-induction blood pressure outcomes after induction, comparing patients receiving a crystalloid bolus versus control. If effective, this would provide a simple perioperative fluid strategy to mitigate a modifiable risk factor for adverse outcomes.

Eichinger M, Reiterer C, Eichlseder M et al. · Anesthesiology · (2026) · View on PubMed ↗ · Free PDF ↗

Stillbirths at 22- and 28-weeks’ gestation or longer for the states in India: findings from the Global Burden of Disease Study 2023.

This analysis used Global Burden of Disease Study 2023 estimates to quantify stillbirth rates (SBR) at WHO ICD-11 definition gestational age cut-offs (≥22 weeks) and compared them with the traditional late-gestation cut-off (≥28 weeks) for states in India. The key finding was not fully provided in the truncated abstract text, but the study’s stated purpose highlights substantial underestimation when using only ≥28 weeks and emphasizes large state-level heterogeneity. Public-health significance lies in improving stillbirth surveillance and enabling state-specific policy targeting by using the ≥22-week definition.

The Lancet regional health. Southeast Asia · (2026) · View on PubMed ↗ · Free PDF ↗

Bilateral transcutaneous auricular nerve stimulation promotes motor function recovery after stroke: A randomized controlled trial.

This randomized controlled trial evaluated whether bilateral transcutaneous auricular nerve stimulation (BtaNS) improves motor function recovery after stroke compared with conventional unilateral left-sided transcutaneous auricular nerve stimulation (LtaNS), focusing on comprehensive post-stroke limb rehabilitation. The key finding was not included in the provided abstract text because the results were truncated. If BtaNS is superior and safe, it would provide a noninvasive neuromodulation option to broaden rehabilitation strategies beyond upper-limb-focused protocols.

Wang J, Liu Q, Zhou Y et al. · Therapeutic advances in neurological disorders · (2026) · View on PubMed ↗ · Free PDF ↗


Cardiometabolic risk prediction & kidney outcomes

Baseline, repeated-measure burden, and two-time-point patterns of the triglyceride-glucose index-visceral lipid ratio (TyG-VLR) and incident cardiovascular disease in cardiovascular-kidney-metabolic (CKM) syndrome stages 0-3: a longitudinal China Health and Retirement Longitudinal Study (CHARLS) analysis.

This longitudinal CHARLS analysis studied whether triglyceride-glucose index–visceral lipid ratio (TyG-VLR) at baseline, its repeated-measure “burden,” and two-time-point TyG-VLR patterns predicted incident cardiovascular disease (CVD) across cardiovascular-kidney-metabolic (CKM) syndrome stages 0–3 in a Chinese population. Higher TyG-VLR burden and adverse two-time-point TyG-VLR trajectories were associated with greater risk of developing CVD and CVD subtypes during follow-up. These findings support TyG-VLR as an accessible, longitudinal cardiometabolic risk marker for earlier identification of people at risk before overt CVD in CKM stages 0–3.

Lu AM, Han HJ, Xu Q et al. · Cardiovascular diabetology · (2026) · View on PubMed ↗

Temporal comparison of clinical practice and outcomes in heart failure: the JROADHF and JROADHF-NEXT studies.

This study compared real-world heart failure (HF) management and outcomes across two Japanese registries, JROADHF (2013) and JROADHF-NEXT (2019–2021), using propensity score matching to assess temporal changes. After matching, it evaluated how shifts in guideline-recommended HF therapies and care processes were associated with differences in patient outcomes between eras. The findings help quantify whether improvements in HF practice over time translated into better outcomes, informing future quality-improvement efforts.

Tohyama T, Ikeda M, Watanabe T et al. · European heart journal · (2026) · View on PubMed ↗

Bruton’s tyrosine kinase inhibitors and cardiovascular risk: a meta-analysis.

This meta-analysis systematically reviewed Phase 3 randomized controlled trials of Bruton’s tyrosine kinase inhibitors (BTK inhibitors)—ibrutinib, acalabrutinib, and zanubrutinib—to estimate the risk of incident non-fatal ischemic major adverse cardiovascular events (MACE) associated with BTK-I exposure. Across included RCTs, BTK-I treatment was assessed for its association with ischemic MACE risk while accounting for the known cardiovascular effects of BTK inhibitors such as bleeding risk, hypertension, and atrial fibrillation. The results provide evidence to better balance efficacy and cardiovascular safety when prescribing BTK inhibitors.

Alexandre J, Font J, Haddad S et al. · European heart journal · (2026) · View on PubMed ↗

Artificial intelligence in drug discovery - what it is, where we stand and the path forward.

This Perspective reviewed how artificial intelligence (AI) methods are being used in drug discovery and assessed progress toward clinically safer, more efficacious medicines delivered faster. It concludes that, despite many AI approaches and benchmarks, evidence for clinically relevant impact remains limited, potentially due to insufficient focus on clinical translation during model development. The article’s significance is to set a roadmap for improving translational rigor of AI in drug discovery rather than relying on performance metrics alone.

Bender A, Thomas MC, Scannell JW et al. · Nature reviews. Drug discovery · (2026) · View on PubMed ↗

Large-scale whole-genome sequencing reveals the landscape and health implications of de novo mutations.

This large cohort study used whole-genome sequencing of 24,030 individuals from 7,851 parent–offspring families to map de novo single-nucleotide variants (dnSNVs) and assess how parental aging and ART relate to mutation burden and offspring health. It identified 390,924 dnSNVs and showed distinct paternal versus maternal mutational patterns, with maternal DNM accumulation accelerating at advanced ages and increased paternal dnSNVs partially explaining the association between advanced parental age and shorter gestational length. The significance is that it provides a high-resolution genomic and epidemiologic framework for understanding how reproductive factors shape de novo mutation landscapes with downstream pregnancy outcomes.

Qin N, Dai J, Jiang Y et al. · Nature medicine · (2026) · View on PubMed ↗ · Free PDF ↗

The dynamic spectrum of steatotic liver disease: the global perspective.

This global perspective reviewed steatotic liver disease (SLD) as a spectrum that includes metabolic dysfunction-associated SLD, metabolic and alcohol-related liver disease, and alcohol-related liver disease, emphasizing overlap rather than strict categories. It highlights that cardiometabolic risk factors (obesity, type 2 diabetes, hypertension, dyslipidemia) are common across subtypes and interact synergistically with alcohol to accelerate fibrosis progression, while both alcohol exposure and metabolic risks change over time. The significance is that it supports dynamic risk assessment and management approaches to better predict fibrosis progression and liver mortality.

Younossi ZM, Zelber-Sagi S, Kalligeros M et al. · Nature reviews. Gastroenterology & hepatology · (2026) · View on PubMed ↗

Effect of semaglutide on kidney outcomes in the SELECT, FLOW, and SOUL trials: a prespecified pooled analysis.

This prespecified pooled analysis assessed the kidney effects of the GLP-1 receptor agonist semaglutide in participants with chronic kidney disease (FLOW) or atherosclerotic cardiovascular disease (SELECT and SOUL) using participant-level data from randomized placebo-controlled trials. Across these diverse populations, semaglutide reduced clinically important kidney outcomes compared with placebo, with effects evaluated across prespecified analyses and dosing regimens (subcutaneous 1.0 mg in FLOW, 2.4 mg in SELECT, and oral 14 mg in SOUL). The findings support semaglutide as an evidence-based therapy to improve renal outcomes in type 2 diabetes with CKD and related high-risk groups.

Mann JFE, Badve SV, Baeres FMM et al. · The lancet. Diabetes & endocrinology · (2026) · View on PubMed ↗

Plasma proteomics linking primary and secondary diseases: Insights into molecular mediation from UK Biobank data.

The study used plasma proteomics from 53,030 UK Biobank participants to identify circulating protein mediators linking three primary cardiometabolic diseases (diabetes, hypertension, dyslipidemia) to 18 secondary outcomes, integrating mediation analysis, Mendelian randomization, and machine learning. It reported 998 significant mediation pathways (per the abstract) and used causal inference and predictive modeling to prioritize proteins that may mediate disease progression. This provides a data-driven map of potentially actionable molecular mediators connecting cardiometabolic risk to downstream complications.

Qian H, Wu C, Li B et al. · Med (New York, N.Y.) · (2026) · View on PubMed ↗

TRIM29-dependent AKR1B10 degradation ameliorates MASH.

This study investigated the role of aldo-keto reductase family 1 member B10 (AKR1B10) in metabolic dysfunction-associated steatohepatitis (MASH) and how it is regulated by the E3 ubiquitin ligase TRIM29. The authors found AKR1B10 elevated in patient tissues and serum correlating with disease severity, and that Akr1b10 genetic ablation in mice attenuated high-fat/high-cholesterol diet-induced steatosis, inflammation, and fibrosis, while TRIM29-dependent AKR1B10 degradation ameliorated MASH. These data support TRIM29–AKR1B10 axis modulation as a potential therapeutic strategy for MASH.

Ma Z, Li J, Li X et al. · Science advances · (2026) · View on PubMed ↗ · Free PDF ↗

Evaluation of the frequency, risk factors, and outcomes of splanchnic vein thrombosis in myeloproliferative neoplasms: a retrospective cohort study.

This multicenter retrospective cohort study analyzed 289 adults with splanchnic vein thrombosis (SVT) associated with myeloproliferative neoplasms (MPNs) to define frequency, risk factors, treatment patterns, and survival outcomes. It reports a median age of 49 years with 74% of patients under 60, and it aims to characterize prognostic factors and anticoagulation strategies, though the key results are truncated in the abstract. Clinically, identifying SVT risk profiles and outcome drivers in MPN patients can support more tailored anticoagulation and management decisions.

Demirci U, Baysal M, Aksoy E et al. · Journal of thrombosis and thrombolysis · (2026) · View on PubMed ↗

Four healthy lifestyle behaviours and adult-onset AD risk: A prospective Study from UK Biobank.

This prospective UK Biobank analysis investigated whether adherence to four healthy lifestyle behaviors—never smoking, no/moderate alcohol, optimal sleep duration, and regular physical activity—is associated with adult-onset atopic dermatitis (AD) incidence. It used Cox proportional hazards models to estimate associations with incident adult-onset AD (full results truncated). If lifestyle-linked risk reductions are confirmed, the findings could support prevention strategies for adult-onset AD in the general population.

Xu B, Zhou S, Gao Y et al. · Journal of the European Academy of Dermatology and Venereology : JEADV · (2026) · View on PubMed ↗ · Free PDF ↗

BEACON-HCC: Best evidence and north american consensus on treatment allocation for hepatocellular carcinoma.

This paper describes BEACON-HCC, a North American consensus framework for hepatocellular carcinoma (HCC) treatment allocation developed using a modified Delphi process with 20 multidisciplinary experts. It integrates current evidence and expert voting into a structured system and includes a pilot evaluation using 29 real-world patient cases (details truncated). The significance is that BEACON-HCC aims to improve contemporary, evidence-informed treatment selection in HCC as therapeutic options evolve.

Singal AG, Agopian VG, Dawson LA et al. · Hepatology (Baltimore, Md.) · (2026) · View on PubMed ↗

Association of non-conventional lipid-inflammatory parameters with incident hypertension risk: a prospective cohort study.

This prospective cohort study assessed 6,891 participants from the China Health and Retirement Longitudinal Study (2011–2020) to evaluate whether non-conventional lipid-inflammatory parameters predict incident hypertension. Using multivariable Cox proportional hazards regression, it tested independent associations of baseline and cumulative lipid-inflammatory metrics and inflammatory composites with future hypertension risk. The findings could support improved cardiovascular risk prediction by combining lipid indices with inflammatory biomarkers beyond standard lipid measures.

Zhao M, Wang M, Li Z et al. · Journal of global health · (2026) · View on PubMed ↗ · Free PDF ↗

Growth Hormone and Cancer Risk: A Two-Sample Bidirectional Mendelian Randomization Study with Mediation Testing.

This two-sample bidirectional Mendelian randomization study assessed whether genetically predicted growth hormone (GH) levels causally influence cancer risk across 16 cancer types using published GWAS genetic instruments. The key finding was not fully available in the provided abstract text (results were truncated), though the analysis used inverse-variance weighted MR with MR-Egger, MR-PRESSO, and pleiotropy testing plus mediation testing via specific metabolites. If confirmed, these results would clarify whether GH therapy-related cancer risk is causal and could inform safer endocrine treatment strategies.

Yan ZM, Zou YZ, Chen YG et al. · Endocrine, metabolic & immune disorders drug targets · (2026) · View on PubMed ↗

Anifrolumab versus Belimumab for Cardiovascular Disease Risk in Systemic Lupus Erythematosus.

Using an emulated target trial with TriNetX electronic health record data (67 organizations, 2020–2025), this study compared cardiovascular disease (CVD) risk after initiation of anifrolumab (type I interferon receptor antagonist) versus belimumab in adults with systemic lupus erythematosus (SLE). The key finding was not included in the provided abstract text because the results section was truncated. Clinically, establishing whether IFN-I blockade (anifrolumab) versus B-cell inhibition (belimumab) differentially affects CVD risk would directly guide treatment selection and patient counseling in SLE.

Mahajan A, Whittelsey M, Vleugels RA et al. · Arthritis & rheumatology (Hoboken, N.J.) · (2026) · View on PubMed ↗

CDK5RAP3-Mediated Mitochondrial RQC Alleviates Pathological Cardiac Hypertrophy.

This mechanistic study investigated how CDK5RAP3-mediated mitochondrial ribosome quality control (RQC) affects pathological cardiac hypertrophy in cardiomyocytes. Using translating ribosome affinity purification coupled with mass spectrometry to profile ribosome-interacting proteins, along with cardiomyocyte-specific gene knockout or AAV-mediated overexpression, and hypertrophy models including transverse aortic constriction (in vivo) and phenylephrine stimulation (in vitro), the key finding was that CDK5RAP3-mediated mitochondrial RQC alleviates pathological cardiac hypertrophy (details truncated in the abstract). Scientifically, it identifies CDK5RAP3/RQC as a potential therapeutic axis for translation/mitochondrial stress pathways driving hypertrophic remodeling.

Peng Y, Cai W, Du T et al. · Circulation research · (2026) · View on PubMed ↗

This epidemiologic study quantified global amputation-related disability from 1990 to 2021 and projected future burden to 2050 by amputation subtype and geography. Using Global Burden of Disease (GBD) 2021 data for prevalence and years lived with disability (YLDs) across seven subtypes and Bayesian age-period-cohort (BAPC) modeling for projections, it characterized geographic variation and demographic patterns. These findings are important for health-system planning and for targeting rehabilitation and prevention resources to where disability burden is expected to grow.

Cuan X, Zhang J, Lu Z et al. · Journal of cachexia, sarcopenia and muscle · (2026) · View on PubMed ↗ · Free PDF ↗



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