One post tagged with "Reproductive biology & infertility"

Automated digest · 98 articles · 15 research areas · April 23, 2026

Overview​

Across this week’s set, a dominant thread is the coupling of metabolism to cell fate—spanning mitochondrial lipid/redox control, lactate-driven epigenetic regulation, and ferroptosis sensitivity. Work on aging in C. elegans links declining phosphatidylcholine (PC) synthesis to mitochondrial aging as a malleable trigger, while related studies emphasize redox timing (circadian redox oscillations) and ER glutathione export (SLC33A1) as mechanistic control points. In parallel, multiple cancer papers converge on metabolic “switches” that determine whether tumors undergo regulated death: PRMT5 inhibition sensitizes B-cell lymphomas to ferroptosis via an AKT–MYC–ATF5–SLC7A11 axis; FAAH promotes ferroptosis resistance in lung adenocarcinoma through STAT3 palmitoylation; and broader reviews synthesize how programmed cell death programs shape immune microenvironments and therapy response.

A second major theme is immunotherapy optimization through microenvironment engineering and immune targeting. Several studies focus on how to overcome immunosuppression in solid tumors: intracellular IL-23R supports AML mitotic viability via non-canonical spindle interactions; NKG2A-defined dysfunctional NK cells in ovarian cancer can be targeted to improve NK–CD8+ coordination; and cycling Tregs emerge as orchestrators of immune escape during DCIS-to-invasive progression. Complementing these, microbiome-directed approaches (including F. prausnitzii enzyme-specific effects on PD-L1 trafficking and evidence that fecal bile acid normalization after FMT may mediate recurrent C. difficile improvements) reinforce the idea that immune outcomes can be tuned by metabolic ecology. Clinical translation is reflected in multiple guideline/consensus and comparative-effectiveness efforts (e.g., MELAS/SLE consensus, cardiogenic shock recommendations, and comparative stent/ICI reaction risk syntheses), underscoring a push toward standardized decision-making.

Finally, the digest highlights a growing emphasis on biomarkers and mechanistic mapping—especially for neurodegeneration and aging risk. Sleep variability and plasma klotho are explored as early indicators of Alzheimer’s pathology and cognitive decline, while imaging/analysis advances (brain-age gap via MRI with causal inference; BRIDGE for voxel-to-cell ground truth mapping) aim to connect signals to underlying biology. Developmental and systems-level resources (human peri-gastrulation embryo models, fetal olfactory atlases, and whole-organism spatial transcriptomics) further show how new experimental platforms are accelerating mechanistic discovery. Together, these studies suggest the field is increasingly moving from descriptive associations toward controllable biological levers—metabolic, immune, and temporal—to improve outcomes across aging, infection, and cancer.

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Mitochondrial biology & aging​

Aging-associated decline of phosphatidylcholine synthesis is a malleable trigger of natural mitochondrial aging.​

The study investigated how aging-associated changes in phosphatidylcholine (PC) synthesis affect mitochondrial aging in wild-type Caenorhabditis elegans and in long-lived clk-1(qm30) and isp-1(qm150) mitochondrial mutants, using proteomics, lipidomics, genetics, functional assays, and follow-up transcriptomics/metabolomics in humans. It found that a decline in PC synthesis is a malleable trigger of natural mitochondrial aging, linking lipid metabolic remodeling to mitochondrial functional deterioration despite persistent mitochondrial inefficiency. These findings suggest that targeting PC biosynthesis/lipid metabolic pathways could be a strategy to modulate mitochondrial aging and improve metabolic resilience during late life.

Poliezhaieva T, Li Y, Chaudhari PS et al. · Nature communications · (2026) · View on PubMed ↗

SLC33A1 exports oxidized glutathione to maintain endoplasmic reticulum redox homeostasis.​

This study investigated how the endoplasmic reticulum (ER) maintains redox balance, focusing on glutathione transport in mammalian cells. Using rapid ER immunopurification for proteome/metabolome profiling combined with CRISPR screening, it identified SLC33A1 as the major ER exporter of oxidized glutathione (GSSG), where loss of SLC33A1 disrupts ER redox homeostasis. The significance is that SLC33A1-mediated GSSG export is a key mechanistic control point for ER function and secretory/membrane protein maturation.

Liu S, Gad M, Li C et al. · Nature cell biology · (2026) · View on PubMed ↗

Redox rhythms promote fitness by modulating ageing-dependent reprogramming.​

This study examined how age-related disruption of redox oscillations affects organismal fitness and aging-dependent transcriptional reprogramming in male aged mice. It found that disrupted redox rhythms are common diurnal alterations during aging and that time-restricted antioxidant/pro-oxidant interventions restore redox rhythms, improving glucose metabolism, motor performance, and aging-related phenotypes in liver and skeletal muscle. The significance is that targeting circadian redox timing may be a strategy to mitigate aspects of metabolic and functional decline with age.

Wang X, Cui SS, Li XK et al. · Nature metabolism · (2026) · View on PubMed ↗

Single-mRNA imaging and modeling reveal coupled translation initiation and elongation rates.​

This eLife study used SunTag live-cell single-mRNA imaging together with a TASEP-based hidden Markov model to quantify translation initiation and elongation rates across mRNAs with diverse coding sequences. It found strong coupling between initiation and elongation such that ribosome density remained consistently low (≤12% occupancy), and this homeostatic coupling persisted during pharmacological inhibition of the elongation factor eIF5A. These mechanistic insights improve quantitative models of protein synthesis and may guide strategies to modulate translation in disease.

Lamberti I, Chao JA, Gobet C et al. · eLife · (2026) · View on PubMed ↗

Uncovering shared and tissue-specific molecular adaptations to intermittent fasting in liver, brain, and muscle.​

This study used comprehensive proteomics and transcriptomics to characterize shared and tissue-specific molecular adaptations to intermittent fasting in male C57BL/6 mice across liver, skeletal muscle, and cerebral cortex. After 16-hour daily fasting for 4 months (IF16), intermittent fasting improved metabolic markers (lower blood glucose, HbA1c, and cholesterol; higher ketone bodies) and produced organ-specific proteomic/transcriptomic responses. These findings clarify how intermittent fasting remodels metabolism differently by tissue, informing translational biomarker and mechanism studies for metabolic flexibility.

Fan Y, De Silva S, Tabassum NI et al. · eLife · (2026) · View on PubMed ↗

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Cardiometabolic health (diet, drugs, biomarkers)​

Evidence-Based Recommendations on the Use of Inclisiran in Patients With Chronic Kidney Disease.​

This evidence-based recommendations manuscript studied the clinical use of inclisiran in patients with chronic kidney disease (CKD), synthesizing available clinical trial evidence and expert specialist opinion to create a practical suitability stratification tool. It concluded that inclisiran—an siRNA targeting hepatic PCSK9 synthesis—can be used to address CKD-associated dyslipidemia and ASCVD risk, particularly where statin intolerance or polypharmacy limits options. Scientifically and clinically, the recommendations support a structured approach to deploying long-acting PCSK9-targeting therapy to improve LDL-C management in CKD.

Sharma S, Kalra S, Sahay M et al. · Nephrology (Carlton, Vic.) · (2026) · View on PubMed ↗

The Effect of Empagliflozin on Renal Outcomes in Patients With Established Cardiovascular Disease: Systematic Review and Meta-Analysis of Randomised Placebo-Controlled Trials.​

This systematic review and meta-analysis studied the effect of empagliflozin (an SGLT2 inhibitor) on renal outcomes in patients with established cardiovascular disease by pooling randomized placebo-controlled trials. It found that empagliflozin improves renal outcomes compared with placebo, with attention to effect size and potential heterogeneity across cardiovascular populations. The results are clinically important because they strengthen evidence for using empagliflozin to protect kidney function in high-risk patients with coexisting CVD.

Bahardoust M, Rad FN, Mousavi S et al. · Endocrinology, diabetes & metabolism · (2026) · View on PubMed ↗

Associations of plant-based diets with all-cause and cause-specific mortality and life expectancy among participants with cardiometabolic disorders from UK, US, and China.​

This study examined associations between plant-based diet patterns and all-cause and cause-specific mortality and life expectancy among 78,151 participants with cardiometabolic disorders (obesity, diabetes, or CVD) across UK Biobank, NHANES, and CLHLS. It found that plant-based diet indices were associated with differences in mortality risk and estimated life expectancy in these high-risk populations. The findings are significant because they inform dietary counseling and public health strategies aimed at improving longevity in people with cardiometabolic disease.

Tan B, Li Z, Chen P et al. · European journal of preventive cardiology · (2026) · View on PubMed ↗

Fructose: metabolic signal and modern hazard.​

This review studied the metabolic signaling roles of fructose versus glucose in modern diets and their links to metabolic disease and other outcomes. It reports that fructose acts as a signal of metabolic plenty, promoting triglyceride synthesis and fat accumulation under chronic overnutrition, thereby driving features of metabolic syndrome and being increasingly implicated in cancer and dementia. The significance is that it frames fructose as a distinct metabolic hazard beyond simple caloric excess, informing risk assessment and potential dietary interventions.

Johnson RJ, Lanaspa MA, Tolan DR et al. · Nature metabolism · (2026) · View on PubMed ↗

Oral microbiome signatures predict biological age and host health.​

This study evaluated whether oral microbiome composition can serve as a quantitative biomarker of biological age and health by analyzing oral microbiome data from two NHANES cohorts (N=4,675) and validating in an external cohort (N=1,293) using machine learning. It identified 64 age-dependent bacterial genera, trained a model to predict chronological age, and defined an Oral Microbiome Aging Acceleration (OMAA) score that independently associated with all-cause mortality and frailty. These results support oral microbiome signatures as non-invasive predictors of healthspan-related outcomes.

Zhao JJ, Hu M, Li S et al. · Nature communications · (2026) · View on PubMed ↗

Dual Roles of Adipose Tissue in Skeletal Muscle Regeneration: Pro-Regenerative Versus Maladaptive.​

This review synthesized evidence on how adipose tissue can either promote or impair skeletal muscle regeneration depending on context, focusing on the regenerative microenvironment. The key finding was that appropriately regulated adipose presence supports metabolic support and paracrine signaling during repair, whereas excessive or dysregulated ectopic fat accumulation drives maladaptive regeneration and persistent functional impairment. Scientifically and clinically, it frames adipose modulation as a potential therapeutic target to improve outcomes in muscle repair and sarcopenia-related conditions.

Lu C, Lu F, Cai J · Journal of cachexia, sarcopenia and muscle · (2026) · View on PubMed ↗

Sarcopenic Obesity in Children: An Emerging Complication Evidenced by Clinical Data and a Juvenile Mouse Model.​

This study investigated sarcopenic obesity in children by combining clinical assessments in 1447 children (DXA body composition; grip strength in a separate cohort of 349) with a juvenile mouse model of high-fat diet (HFD)-induced obesity. The key finding was that childhood obesity was associated with impaired musculoskeletal health consistent with sarcopenic obesity, and mechanistic analyses in juvenile versus adult-onset HFD models implicated underlying molecular pathways affecting muscle development. The work highlights sarcopenic obesity as an emerging pediatric complication and provides a translational preclinical framework for mechanism-driven interventions.

Wang S, Zhang W, Qin Z et al. · Journal of cachexia, sarcopenia and muscle · (2026) · View on PubMed ↗

Long-term effects of plant vs. animal protein supplementation on body composition, muscle strength, physical performance, and cardiometabolic risk factors in adults:a systematic review and meta-analysis of randomized controlled trials.​

This systematic review and meta-analysis studied long-term (≥6 months) supplementation with plant-based protein (PBP) versus animal-based protein (ABP) in adults, focusing on body composition, muscle strength, physical performance, and cardiometabolic risk factors using randomized controlled trials. The key finding is the pooled comparative effect of PBP vs ABP on these outcomes over extended durations (with effect sizes and confidence intervals extracted from included trials). Clinically, it informs dietary protein-source decisions for adults aiming to improve musculoskeletal and cardiometabolic health over the long term.

Yimam MA, Roberts J, O'Callaghan A et al. · Frontiers in nutrition · (2026) · View on PubMed ↗

Latest advances and controversies of exercise therapy in the management of type 2 diabetes.​

This mini-review studied exercise therapy for type 2 diabetes, synthesizing recent evidence on exercise modalities, dosing, and the gap between ideal efficacy and real-world effectiveness. It reports that high-intensity interval training (HIIT) is time-efficient and is associated with superior reductions in glycated hemoglobin (HbA1c), while concurrent training (aerobic plus resistance) provides the broadest metabolic benefits. Clinically, it supports tailoring exercise prescriptions toward HIIT or combined aerobic-resistance programs to maximize glycemic and overall health outcomes in type 2 diabetes.

Hao J, Zhang H · Frontiers in endocrinology · (2026) · View on PubMed ↗

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GLP-1/obesity & adverse effects​

Effects of GLP-1 Receptor Agonists on Muscle Mass, Strength, and Quality in MASLD: A Systematic Review.​

This systematic review studied how GLP-1 receptor agonists (GLP-1RAs) affect muscle mass, strength, and muscle quality in adults with metabolic dysfunction-associated steatotic liver disease (MASLD) by including interventional and observational studies up to December 2, 2025. It assessed muscle outcomes using imaging and body-composition techniques such as computed tomography or MRI, dual-energy X-ray absorptiometry, and bioelectrical impedance analysis. The review is clinically relevant because it clarifies whether GLP-1RA–driven weight loss in MASLD compromises or preserves skeletal muscle health, which is crucial for patient function and frailty risk.

Iorra F, Jayakar T, Yee M et al. · Liver international : official journal of the International Association for the Study of the Liver · (2026) · View on PubMed ↗

GLP-1 therapies and hair loss: A systematic review of current evidence and implications for counseling.​

This systematic review studied GLP-1 receptor agonist–specific associations with hair loss by screening 133 studies and including 24 primary articles that reported alopecia outcomes related to GLP-1 RA use. It found that semaglutide and tirzepatide showed the highest incidence rates and strongest pharmacovigilance signals for hair loss, with characterization of alopecia subtypes and discussion of potential mechanisms. The evidence is important for clinicians to counsel patients starting GLP-1 therapies about the risk of alopecia and to monitor/manage this adverse effect.

Gupta AK, Teasell EM, Economopoulos V et al. · Science progress · (2026) · View on PubMed ↗

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Microbiome & gut–immune/metabolic axes​

Lactate metabolism-driven lactylation: paradoxical modulation of intestinal inflammation and malignancy.​

This review studied lactate metabolism-driven lactylation as a mechanism that can paradoxically modulate both intestinal inflammation and malignancy. It summarized how lactate-dependent lactylation (an epigenetic modification) links metabolic state to immune and cancer-related pathways, framing lactate metabolism/lactylation as potential therapeutic targets. The scientific significance is that it provides a mechanistic rationale for developing interventions that manipulate lactate signaling to treat gut inflammatory disease and intestinal cancers.

Liu J, Liu Y, Zhang H et al. · Journal of translational medicine · (2026) · View on PubMed ↗

Faecalibacterium prausnitzii enzyme reprograms PD-L1 trafficking and sensitizes colorectal cancer to immunotherapy in mice.​

This study examined how the gut bacterium Faecalibacterium prausnitzii and its enzyme phosphoribosyl pyrophosphate synthetase (fpPRPS) affect PD-L1 trafficking and immunotherapy response in colorectal cancer (CRC) using CRC patient cohort analyses, in vitro assays, and azoxymethane/dextran sulfate sodium (AOM/DSS) and Apcmin/+ mouse CRC models. F. prausnitzii extracts (via fpPRPS) inhibited tumor development and sensitized CRC to immunotherapy by reprogramming PD-L1 trafficking. These findings suggest a microbiome-derived, enzyme-specific mechanism that could be leveraged to improve CRC immunotherapy efficacy.

Ji S, Liu Y, Xu Y et al. · Nature microbiology · (2026) · View on PubMed ↗

Re-establishing bile acid composition after treatment of recurrent Clostridioides difficile infection with fecal microbiota transplantation compared with oral vancomycin or a 12-strain bacterial mixture.​

In a subgroup of a randomized controlled trial in patients with recurrent Clostridioides difficile infection, fecal bile acid composition was longitudinally assessed after fecal microbiota transplantation (FMT) versus an oral vancomycin control or a 12-strain bacterial mixture, using fecal bile acid profiling and 16S rDNA sequencing. FMT more effectively re-established a bile acid composition closer to a “normal” profile than vancomycin or the 12-strain mixture, supporting bile acid normalization as a treatment-relevant mechanism. This controlled evidence strengthens the scientific rationale for targeting bile acid ecology to improve outcomes in recurrent C. difficile infection.

Rode AA, Duboc H, Lamazière A et al. · Gut microbes · (2026) · View on PubMed ↗

Intestinal dysbiosis exacerbates skin inflammation via microbial metabolite-driven Th2 cell differentiation.​

In mice and in human atopic dermatitis (AD) patients, the study tested how intestinal dysbiosis drives skin inflammation through microbial metabolite-driven Th2 differentiation, using Toll-like receptor 4 (TLR4) epithelial deficiency as a mechanistic perturbation. TLR4 deficiency reshaped the microbiome by reducing Akkermansia muciniphila and enriching CutC-expressing bacteria, increasing choline-to-trimethylamine conversion and circulating TMAO, which promoted Th2 differentiation and worsened AD-like inflammation. The finding that plasma TMAO levels were elevated in AD patients and correlated with severity links a specific gut microbial metabolic axis to human disease activity.

Yu L, Peng S, Chen X et al. · Immunity · (2026) · View on PubMed ↗

A bidirectional brain-fat body axis for pathogen avoidance.​

In Drosophila melanogaster, this study identified a bidirectional fat body–brain communication pathway that mediates pathogen avoidance, using immune receptor and antimicrobial peptide requirements in both tissues. Pathogen sensing in octopaminergic neurons activated fat body calcium signaling via an octopamine receptor, triggering fat body dopamine release that acted through Dop1R1 in the brain to suppress pathogen intake. The work clarifies how peripheral immune detection is translated into coordinated behavioral avoidance through defined neuromodulators.

Wang Y, De Backer JF, Muria A et al. · Neuron · (2026) · View on PubMed ↗

Improving immunotherapy in solid tumors using FMT.​

This article reviewed clinical evidence that fecal microbiota transplantation (FMT) is used to improve first-line immune checkpoint inhibitor efficacy in patients with solid tumors, focusing on renal cell carcinoma, cutaneous melanoma, and non-small cell lung cancer. The key finding is that FMT benefits appear driven by functional microbiome remodeling, depletion of deleterious taxa, and systemic immunometabolic modulation that enhances anti-tumor immune responses. This supports microbiome-directed therapeutic strategies—specifically FMT—to augment immunotherapy outcomes in multiple solid-tumor settings.

Davar D, Zarour HM, Trinchieri G · Cell · (2026) · View on PubMed ↗

Mitochondrial translation elongation controls OXPHOS biogenesis by coordinating synthesis and folding of mitochondrially encoded proteins.​

This study investigated how mitochondrial translation elongation regulates oxidative phosphorylation (OXPHOS) biogenesis in the fungus Neurospora crassa, centering on the mitochondrial ribosomal RNA (rRNA) methyltransferase 1 (MRM1) gene. The key finding is that MRM1 promotes OXPHOS biogenesis by repressing mitochondrial translation elongation through RNA–ribosome interactions mediated by its N-terminal intrinsically disordered region, independently of its catalytic activity. Scientifically, it identifies a non-enzymatic, interaction-based control point linking mitochondrial translation dynamics to mtDNA-encoded respiratory protein production.

Xie L, Ren S, Zhang L et al. · Molecular cell · (2026) · View on PubMed ↗

Effect of Probiotics on the Clinical Outcome and Inflammatory Response in Gastric Cancer Surgery: A Double Blinded Randomized Control Trial.​

This double-blind randomized placebo-controlled trial studied whether probiotics improve postoperative outcomes and inflammatory/immune responses in gastric cancer patients undergoing open gastrectomy. The key finding is that probiotic administration (10 days, per the abstract) was evaluated for effects on length of hospital stay, nutritional status, and postoperative inflammatory and immune markers compared with placebo. Clinically, the trial tests whether gut microbiota modulation can reduce postoperative complications and immune dysfunction in gastric cancer surgery patients.

Pal D, Anandhi A, Keerthi AR et al. · Journal of gastrointestinal cancer · (2026) · View on PubMed ↗

Pharmacological interventions targeting the gut-brain axis in neurological disorders: mechanisms and translational applications.​

This article reviewed pharmacological interventions that target the gut–brain axis in neurological disorders, focusing on mechanistic pathways linking microbiota changes to brain outcomes. The key finding was that gut microbiota–gut–brain communication can modulate neuroinflammation, neurotransmission, and blood–brain barrier integrity through neural, immune, endocrine, and metabolic routes, supporting translational therapeutic concepts. Scientifically, it consolidates evidence for gut–brain axis modulation as a strategy for neurological and psychiatric disease treatment development.

Li X, Zhou W, Yang S et al. · Frontiers in neuroscience · (2026) · View on PubMed ↗

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Cancer cell death & tumor vulnerabilities​

PRMT5 inhibition sensitizes B-cell lymphoma cells to ferroptosis.​

This study examined whether inhibiting PRMT5 affects ferroptosis sensitivity in B-cell lymphoma cell models, including diffuse large B-cell lymphoma (DLBCL) and mantle cell lymphoma (MCL). It found that PRMT5 inhibition sensitizes these lymphoma cells to ferroptosis by upregulating SLC7A11 (cystine import for glutathione biosynthesis) through an AKT–MYC–ATF5 signaling axis. The clinical significance is that targeting PRMT5 may be a therapeutic strategy to trigger ferroptotic cell death in PRMT5-overexpressing B-cell lymphomas.

Liu Y, Chen R, Gao X et al. · Leukemia · (2026) · View on PubMed ↗

Programmed cell death in lung cancer: mechanisms, immune responses, and therapeutics.​

This review studied programmed cell death (PCD) pathways in lung cancer, covering apoptosis, pyroptosis, ferroptosis, and necroptosis and their interactions with immune responses and therapies. It concludes that PCD mechanisms shape tumor immune microenvironments and influence resistance or responsiveness to treatments such as immune checkpoint blockade and cytotoxic chemotherapy. The significance is that understanding these PCD pathways can guide development of combination or next-generation therapeutics that overcome immune evasion in lung cancer.

Liu Y, Chen Q, Xu J et al. · Apoptosis : an international journal on programmed cell death · (2026) · View on PubMed ↗

FAAH initiates a positive feedback loop to promote lung adenocarcinoma progression through inhibition of ferroptosis.​

This study investigated fatty acid amide hydrolase (FAAH) as a regulator of ferroptosis in lung adenocarcinoma (LUAD) by analyzing LUAD patient data and manipulating FAAH in LUAD cells. FAAH was upregulated in LUAD and promoted a positive feedback loop that inhibited ferroptosis by enhancing STAT3 palmitoylation through conversion of N-palmitoylethanolamine to palmitic acid. Targeting FAAH may therefore restore ferroptotic cell death and provide a therapeutic strategy for LUAD.

He X, Tang C, Jiang T et al. · Cell death and differentiation · (2026) · View on PubMed ↗

Cell death in cancer.​

This review examined how cancer cells evade cell death and how restoring cell death requires understanding multiple cell-death programs beyond apoptosis, including necroptosis, pyroptosis, ferroptosis, and other emerging pathways. It finds that while apoptosis remains the dominant program induced by radiation and many chemotherapies, non-apoptotic death programs can drive inflammation and modulate tumor–stroma–immune interactions that influence immunotherapy outcomes. The significance is that targeting specific cell-death pathways could improve therapeutic efficacy and reshape immune responses in cancer treatment.

Conrad M, Strasser A, Jost PJ et al. · Cell · (2026) · View on PubMed ↗

Rational Design of Schiff Base Copper Chelators as Potent Necroptosis Inducers for Anticancer Therapy.​

The study designed and tested novel Schiff base copper chelators to induce necroptosis for anticancer therapy, evaluating their activity in cancer models relevant to “copper addiction.” The key finding was that rational structural modifications of Schiff base ligands produced potent, copper-specific chelators that trigger necroptosis more effectively than less optimized chelation approaches. This supports a drug-design strategy that exploits tumor copper dependence to drive programmed necrotic cell death as a potential anticancer mechanism.

Yu LB, Guan QX, Huang ST et al. · Journal of medicinal chemistry · (2026) · View on PubMed ↗

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Cancer immunotherapy & tumor microenvironment​

NKG2A inhibition promotes NK cell-CD8+ T cell interactions to improve anticancer immunity in ovarian carcinoma.​

This study characterized NK-cell heterogeneity and its impact on NK–CD8+ T cell interactions in ovarian carcinoma, focusing on NKG2A expression, using transcriptomic and spatial profiling of patient samples plus functional experiments in syngeneic mouse models. High-grade serous ovarian carcinoma (HGSOC) contained dysfunctional NK cells expressing the co-inhibitory receptor NKG2A, and inhibiting NKG2A improved anticancer immunity by promoting reciprocal activation between NK cells and CD8+ T cells. Clinically, NKG2A blockade could enhance coordinated NK–T cell responses in HGSOC.

Lanickova T, Angelidou A, Hensler M et al. · Nature communications · (2026) · View on PubMed ↗

Identification of cycling regulatory T cell precursors as conductors of immune escape during breast carcinoma progression.​

The study used transcriptomic mapping of immune landscapes across normal breast, ductal carcinoma in situ (DCIS), and invasive breast cancer (IBC) cohorts, and then tested mechanisms in a rat breast cancer model to define cycling regulatory T cell (cycTreg) roles during DCIS-to-IBC progression. Cycling regulatory T cells were identified as an orchestrator of immunosuppression in IBC, with cycTreg frequency predicting cytotoxic CD8+ T-cell features, TCR diversity, disease-specific survival in IBC, and recurrence in DCIS. These findings suggest cycTreg precursors drive immune escape and could serve as prognostic biomarkers and therapeutic targets to improve outcomes in breast cancer progression.

Bui TM, Jimenez ER, Li Z et al. · Cancer cell · (2026) · View on PubMed ↗

Unlocking the potential of T cell engagers in solid tumors.​

This article reviewed the development and clinical design principles of T cell engagers (TCEs) for solid tumors, focusing on challenges such as tumor target heterogeneity, immunosuppressive microenvironments, and on-target toxicity. It concludes that improved target selection, creative protein engineering, and thoughtful clinical trial design are central to overcoming these barriers for next-generation solid-tumor TCEs. The work is significant because it frames how to translate TCE success from hematologic malignancies into safer, more effective solid-tumor immunotherapies.

Wingrove E, Bailis JM, Farago AF et al. · Cancer cell · (2026) · View on PubMed ↗

Mapping intratumor heterogeneity across layers for advancing immunotherapy.​

The study reviewed and conceptually integrated approaches to map intratumor heterogeneity (ITH) across multiple layers—genetic, epigenetic, transcriptional, proteomic, and immunopeptidomic—linking these layers to immune recognition. It highlights that variation in antigen processing and peptide abundance across tumor clones and cell states creates spatially and temporally distinct immunological niches that shape immunotherapy responses. This is significant because it motivates immunotherapy development strategies that target not just mutations but also dynamic antigen presentation and immunopeptidome heterogeneity.

Marine JC, Bartok O, Sagie S et al. · Cell · (2026) · View on PubMed ↗

Combinatorial delivery of low-dose radiotherapy and immunotherapy to patients with immune-excluded tumors enhances CD8+ T cell functionality.​

In a multi-cohort phase I clinical trial (RACIN), 25 patients with multimetastatic immune-excluded solid tumors received low-dose radiotherapy (LDRT) combined with immune-based regimens including nivolumab plus ipilimumab and additional agents (aspirin or celecoxib) plus low-dose cyclophosphamide. The combinatorial LDRT plus immunotherapy approach enhanced CD8+ T cell functionality in these immune-excluded tumors. This provides clinical rationale for using LDRT to convert “cold” tumors into more immunologically responsive settings for checkpoint blockade.

Ochoa-de-Olza M, Rayroux N, Imbimbo M et al. · Clinical cancer research : an official journal of the American Association for Cancer Research · (2026) · View on PubMed ↗

Viral vector-free generation of orthogonal IL-2-responsive CAR T cells through gene editing of IL-2 and its receptor.​

This study investigated viral vector-free generation of orthogonal IL-2-responsive CAR T cells by gene editing IL-2 and its receptor, producing orthogonal IL-2Rβ (oIL-2Rβ) mutations in T cells via prime editing. The key finding is that prime editing achieved ~72% average efficiency, produced functional oIL-2Rβ that enriched with oIL-2, and improved CAR T-cell engraftment, efficacy, and toxicity in vivo comparably to conventional cotransduction approaches. Scientifically, it demonstrates a safer manufacturing route for orthoCAR T cells and shows that IL-2 pathway orthogonalization can be engineered to enhance therapeutic performance.

Zhang Q, Wu Y, Yang J et al. · Blood immunology & cellular therapy · (2025) · View on PubMed ↗

One-step knock-in CAR constructs in human NK cells enable scalable, TGFβ1-resistant immunotherapy for solid tumors.​

Researchers engineered primary human NK cells using a one-step electroporation delivery of Cas9 ribonucleoprotein plus a dsDNA donor to knock out TGFBR2 and knock in a mesothelin CAR, and compared performance against a two-step AAV approach with dexamethasone (Dex) used during manufacturing. The key finding is that this scalable one-step knock-in strategy yields TGFβ1-resistant CAR-NK cells with enhanced anti-solid-tumor activity despite TGFβ-mediated immunosuppression in the tumor microenvironment. Clinically, this supports a practical manufacturing route for CAR-NK therapies targeting mesothelin-positive solid tumors while overcoming a major resistance mechanism driven by TGFβ signaling.

Yee SM, Jeong JH, Kim D et al. · Theranostics · (2026) · View on PubMed ↗

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Cancer genomics/epigenetics & DNA damage​

Tools and tactics for studying alternative splicing.​

This review studied how alternative splicing is mapped and functionally tested across model systems, emphasizing recent advances in long-read sequencing, CRISPR-based splicing assays, population genetics, and deep learning approaches. It reports that long-read sequencing now enables isoform-resolved profiling at bulk, single-cell, and spatial levels, while CRISPR perturbations can directly test the functional impact of specific splicing isoforms. These developments are significant because they accelerate mechanistic discovery of splicing dysregulation in diseases such as rare genetic disorders and cancer and improve the ability to interpret splicing “language” from sequence.

Sousa-Luís R, Carmo-Fonseca M · Nature reviews. Genetics · (2026) · View on PubMed ↗

MRE11 proximal polyadenylation site-mediated looping impacts transcription and genomic stability.​

Researchers studied how the proximal polyadenylation site (pPAS) of the DNA damage response gene MRE11 regulates transcription and genome stability by enabling PAS-promoter looping and RNA polymerase recycling. Deleting the MRE11 pPAS disrupted looping, reduced MRE11 transcription and MRN complex (MRE11-RAD50-NBS1) levels, and caused ectopic DNA replication with reduced viability under overgrowth conditions, phenocopying hypomorphic MRE11 mutations. This mechanistic link between alternative polyadenylation control and DDR function identifies a new regulatory layer for maintaining genomic stability.

Huang K, Brault ME, Cong K et al. · Molecular cell · (2026) · View on PubMed ↗

A recipe for chaos: Extrachromosomal DNA and the hallmarks of cancer.​

This article reviewed evidence that extrachromosomal DNA (ecDNA) contributes to rapid genome change and therapy resistance in aggressive cancers by enabling oncogenic elements to evolve outside Mendelian inheritance. It proposes integrating ecDNA biology into the hallmarks of cancer framework to identify ecDNA-specific vulnerabilities distinct from conventional mutation-targeting approaches. The significance is that ecDNA may represent a mechanistic driver of genomic chaos and a new therapeutic entry point for resistant cancers.

Wong IT, Bailey C, Wu S et al. · Cell · (2026) · View on PubMed ↗

Targeting genomic instability in cancer.​

This review summarized how genomic instability both fuels cancer evolution and creates therapeutic vulnerabilities, and it traced how targeting it has evolved from chemotherapy and external beam radiation to PARP inhibitors in homologous recombination repair-deficient tumors and other DNA damage response targets. It also highlights newer tumor-targeted DNA-damaging modalities, including antibody-drug conjugates (ADCs) and radiopharmaceuticals, as emerging strategies. The clinical significance is that exploiting genomic instability can improve treatment selectivity and effectiveness, particularly in DNA repair–defective or instability-high tumors.

Yap TA, Manning HC, Sapra P et al. · Cell · (2026) · View on PubMed ↗

Decoding RNA splicing pathology: Alternative splicing in amyotrophic lateral sclerosis and its therapeutic potential.​

This article reviewed RNA splicing pathology in amyotrophic lateral sclerosis (ALS), emphasizing therapeutic implications of dysregulated alternative splicing controlled by genes such as TARDBP, FUS/EWSR1/TAF15 (FET family), SOD1, and C9orf72. The key finding is that mutations or mislocalization of these RNA-processing proteins produce nuclear loss-of-function and cytoplasmic gain-of-function toxicity, promoting splicing defects and downstream neurodegeneration. The scientific significance is that splicing-regulatory pathways and specific ALS genes represent rational targets for developing mechanism-based therapies.

Priya R, Tanti GK, Jain BP · Biochemical and biophysical research communications · (2026) · View on PubMed ↗

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Cancer signaling & metastasis mechanisms​

Integrative single-cell analysis reveals endothelial diversity in the vasa vasorum of human atherosclerosis.​

This study used integrative single-cell RNA sequencing to characterize endothelial diversity in the vasa vasorum associated with human atherosclerosis. By integrating five scRNA-seq datasets (17,367 vascular endothelial cells) and validating morphology histologically, it identified SULF1+ arterial endothelial cells as a major EndMT-associated subcluster and capillary-like endothelial cells as key mediators of angiogenesis, with a trajectory model describing tip-to-stalk transitions. The significance is that it provides a cell-type-resolved map of endothelial programs in atherosclerotic microvessels, highlighting targets linked to EndMT and angiogenesis.

Wu Y, Xue Z, Sun T et al. · Communications biology · (2026) · View on PubMed ↗

ELMO2 is a therapeutic vulnerability in mesenchymal-like and drug-resistant non-small cell lung cancer.​

This study tested whether ELMO2 is a therapeutic vulnerability in mesenchymal-like and drug-resistant non-small cell lung cancer (NSCLC) by suppressing ELMO2 and assessing autophagy/cell death pathways, including FAK activity, in relevant NSCLC models. ELMO2 suppression induced excessive autophagy and cell death through FAK inhibition, and ELMO3 acted as a compensatory paralog creating a synthetic lethal interaction with ELMO2 loss. Because ZEB1 repressed ELMO3 transcription in mesenchymal-like cells, ZEB1-high states may be particularly sensitive to ELMO2-targeted blockade.

Li M, Xue Y, Chang Y et al. · Nature communications · (2026) · View on PubMed ↗

Aberrant laminin signaling drives melanocyte dedifferentiation and unveils a tractable therapeutic target in vitiligo.​

This study investigated how aberrant laminin signaling drives melanocyte dedifferentiation in vitiligo by comparing healthy skin and vitiligo tissue microenvironments and analyzing basement-membrane niche changes. In vitiligo, reduced laminin-211 and increased laminin-332 shifted melanocyte interactions toward integrin α3β1–laminin-332, accompanied by Rho–F-actin remodeling and coordinated pathway changes consistent with a dedifferentiation-like, potentially reversible state. The work identifies tractable targets within laminin–integrin signaling that may be exploited to treat or reverse vitiligo progression.

Yang F, Yang L, Lai S et al. · Nature communications · (2026) · View on PubMed ↗

Cancer cachexia: A tumor-driven disorder of whole-body homeostasis.​

The article synthesized evidence on cancer cachexia as a tumor-driven systemic disorder affecting whole-body homeostasis, emphasizing mechanisms spanning immune, metabolic, endocrine, and neural networks. It highlights that cachexia—marked by skeletal muscle atrophy and adipose tissue loss—reduces function and quality of life, impairs treatment tolerance, and worsens survival across multiple cancers. Clinically, this underscores the need for mechanistically informed therapies to prevent or reverse cachexia and improve cancer treatment outcomes.

Zhang Y, Nipp RD, Janowitz T et al. · Cancer cell · (2026) · View on PubMed ↗

Hallmarks of liver cancer: Therapeutic implications.​

This review analyzed how the cancer hallmarks framework applies to primary liver cancer, particularly hepatocellular carcinoma (HCC) and intrahepatic cholangiocarcinoma (iCCA), and discussed therapeutic implications. It reports that HCC commonly exhibits hallmarks such as sustaining proliferative signaling, accessing vasculature, and avoiding immune detection, with improved outcomes in advanced disease driven by immunotherapies, while iCCA shows distinct hallmark patterns including proliferative signaling and other pathway features. The significance is that mapping liver cancer biology to hallmarks can guide rational selection and combination of targeted and immunotherapeutic strategies.

Llovet JM, Pinyol R, Affo S et al. · Cell · (2026) · View on PubMed ↗

Spatial Mapping of the Precancer-to-Cancer Transition in Breast and Prostate.​

This work studied the precancer-to-cancer transition in breast and prostate hormone-driven adenocarcinomas using lightsheet microscopy on intact tumors and a multimodal serial-section workflow combining volumetric reconstruction with spatial transcriptomics across 51 cases. The key finding is that transitional junctions between precancerous and invasive regions show distinct gene-expression programs, including breast associations with loss of MGP and PLAT and prostate associations with GDF15, ALDH1A3, ANPEP, and FA (as reported in the abstract). Clinically, mapping these spatial molecular shifts can reveal actionable drivers of invasion and improve understanding of how local tissue architecture and gene regulation jointly enable malignancy progression.

Storrs E, Mo CK, Chou WH et al. · Cancer discovery · (2026) · View on PubMed ↗

UFMylation Suppresses Hepatocellular Carcinoma Metastasis by Inhibiting β-catenin-Driven Hybrid EMT and NK Cell Evasion.​

This study analyzed human hepatocellular carcinoma (HCC) specimens and mechanistically tested how ubiquitin-fold modifier 1 (UFM1) conjugation (UFMylation) affects metastasis and immune evasion, identifying Emerin (EMD) as a UFMylation substrate. The key finding is that reduced UFMylation destabilizes EMD via proteasomal degradation, leading to nuclear β-catenin accumulation, hybrid epithelial–mesenchymal transition (EMT), enhanced tumor migration, and NK cell evasion. Clinically, UFMylation status may serve as a prognostic marker and a potential therapeutic lever to suppress HCC metastasis and improve anti-tumor immunity.

Xu M, Gao X, Zhao J et al. · Cancer research · (2026) · View on PubMed ↗

Targeting Tumour Microtubes to Disrupt Glioma Networks.​

This study investigated glioma stem cells (GSCs) and their tumor microtubes (TMs) that enable glioma network communication, using coordinated proteomics and functional screening in glioma models. It identified the inner mitochondrial component FASTKD2 as essential for TM-local protein synthesis, and showed that targeting FASTKD2 reduces tumor stemness and growth by disrupting coordinated mitochondrial support of TM-mediated signaling. Scientifically and therapeutically, FASTKD2 emerges as a mechanistic vulnerability to break glioma networks and potentially overcome therapy resistance driven by TM connectivity.

Rich J, Huang T, Zhang P et al. · Research square · (2026) · View on PubMed ↗

Single-Cell Transcriptomics Reveals Riluzole as an Osteoarthritis Candidate Drug via OB-NE Signaling Modulation and CTSS/NOS1 Inhibition.​

This study used single-cell RNA sequencing of human femoral head tissue to identify osteoarthritis (OA) drug candidates, applying integrated bioinformatics (differential expression, enrichment, and cell–cell communication analysis), network-proximity drug repositioning, and Mendelian randomization (MR) to test causal links between drug targets and OA; it then evaluated effects in a triclocarban (TCC)-induced zebrafish OA model. The key finding is that riluzole emerges as an OA candidate drug via modulation of OB–NE (osteoblast–immune cell) signaling and inhibition of CTSS and NOS1. The significance is a target- and pathway-informed repositioning of riluzole for OA with mechanistic support from human single-cell data and in vivo disease modeling.

Liu K, Li JL, Chen Y et al. · Drug design, development and therapy · (2026) · View on PubMed ↗

WNT5a-Mediated Aberrant Actin Filament Dynamics Drive Cardiac Pathogenic Phenotypes in LMNA-Related Emery-Dreifuss Muscular Dystrophy.​

This Circulation study investigated LMNA-related Emery-Dreifuss muscular dystrophy (EDMD) by recruiting five patients with LMNA sequence variations, generating patient-specific induced pluripotent stem cells (iPSCs), and examining how WNT5a-mediated actin filament dynamics drive cardiac pathogenic phenotypes. The key finding is that WNT5a signaling aberrantly alters actin filament dynamics, contributing to disease-relevant cardiac abnormalities in LMNA-EDMD. Scientifically and clinically, it links a specific signaling–cytoskeleton mechanism to LMNA cardiomyopathy and suggests WNT5a/actin pathway modulation as a potential therapeutic direction.

Fan H, Wang X, Liu X et al. · Circulation · (2026) · View on PubMed ↗

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Neurodegeneration & brain biomarkers​

Dysfunction of the episodic memory network in the Alzheimer's disease cascade.​

This study examined episodic memory (EM) network dysfunction across Alzheimer’s disease (AD) progression by analyzing longitudinal functional MRI data from the DZNE DELCODE study (>1,000 measurements) and relating EM activation/deactivation to disease progression model scores. With increasing AD biomarker and neurodegeneration progression, voxel-wise analyses showed widespread loss of EM deactivation and activation, with nonlinear trajectories for deactivation loss. These findings link EM network breakdown to the AD cascade and may help refine biomarkers for tracking disease progression.

Lattmann R, Vockert N, Bernal J et al. · Nature communications · (2026) · View on PubMed ↗

Night-to-night rapid eye movement sleep variability: A relevant marker of early amyloid-β deposition.​

This study examined cognitively unimpaired older adults with cerebral amyloid deposition to determine whether night-to-night rapid eye movement (REM) sleep variability predicts early amyloid-β (Aβ) deposition, using objective multi-night sleep monitoring with the Somno-Art wearable device and Florbetapir PET. The key finding is that Aβ-positive individuals show altered sleep patterns, with REM sleep variability associated with regional amyloid deposition and related cognitive/psychoaffective outcomes (as summarized in the abstract). Scientifically and clinically, it suggests a noninvasive sleep biomarker that may help detect early AD pathology before clinical symptoms.

Montagne B, Boulin M, Hamel A et al. · Alzheimer's & dementia : the journal of the Alzheimer's Association · (2026) · View on PubMed ↗

Elevated plasma klotho levels attenuate Alzheimer's disease pathologies and cognitive decline in APOE ε4 carriers.​

This study investigated whether elevated plasma klotho levels attenuate Alzheimer’s disease (AD) pathologies and cognitive decline in older adults stratified by apolipoprotein E (APOE) ε4 carrier status, analyzing 354 participants. The key finding is that higher plasma klotho is associated with lower AD-related biomarkers on imaging and/or plasma measures and with reduced cognitive decline, with APOE ε4-dependent relationships supported by stratified interaction and mediation analyses. The significance is that plasma klotho could be a modifiable or prognostic biomarker linked to AD risk specifically in APOE ε4 carriers.

Yang J, Wang J, Chai W et al. · Alzheimer's & dementia : the journal of the Alzheimer's Association · (2026) · View on PubMed ↗

Brain age gap as biomarker linking cardiovascular diseases genetic susceptibility and causality.​

This study used UK Biobank T1-weighted MRI to build a 3D vision transformer (3D-ViT) model that predicts brain age and computes brain age gap (BAG), then tested causal relationships between BAG and cardiovascular disease (CVD) using bidirectional Mendelian randomization. The key finding was evidence of brain–heart interactions, with acute myocardial infarction (AMI) and chronic ischemic heart disease (CIH) associated with decelerated brain aging in the causal framework. This is significant because BAG may serve as an imaging-derived biomarker linking genetic susceptibility and causality to systemic aging risk in CVD.

Lyu S, Zhang R, Peng K et al. · iScience · (2026) · View on PubMed ↗

Voxel-accurate MRI-microscopy Correlation Enables AI-powered Prediction of Brain Disease States.​

This study investigated how to map MRI signals to cellular-level biological ground truth by developing BRIDGE, a platform integrating in vivo MRI with in vivo two-photon microscopy and ex vivo super-resolution microscopy. The key finding is that BRIDGE enables voxel-accurate, longitudinal co-registration so that MRI signal origins can be linked to cellular/anatomical features, enabling AI training on these ground-truth mappings. This is significant because it can improve AI-powered prediction of brain disease states by grounding imaging biomarkers in biological mechanisms.

Schroers J, Yang Y, Reyhan E et al. · Theranostics · (2026) · View on PubMed ↗

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Neuroimmunology & neuroinflammation therapeutics​

Cancer neuroscience: The past, the present, and the road ahead.​

This perspective reviewed how cancer neuroscience—bidirectional neuro–cancer interactions—affects cancer initiation, growth, metastasis, and treatment resistance, and how cancer can reprogram neural circuits to produce neuropsychiatric symptoms. It emphasizes that understanding mechanisms such as neuron-to-cancer synapses and neuro–immuno-oncological paracrine interactions could enable “neuroscience-instructed” cancer therapies. The scientific significance is a roadmap for integrating neural biology with oncology to improve disease control and patient quality of life.

Winkler F, Heuer S, Althammer F et al. · Cell · (2026) · View on PubMed ↗

CAR Treg therapies for neurodegenerative diseases.​

This article reviews how chimeric antigen receptor regulatory T cells (CAR Tregs) are being explored for neurodegenerative diseases, focusing on Treg biology and their potential to recognize immune triggers from misfolded/aggregated self-proteins in the CNS. It highlights the concept that CAR Tregs could be engineered to suppress chronic immune responses driven by protein aggregates that contribute to neural injury. If translated successfully, CAR Treg targeting of aggregation-associated antigens could provide a cell-specific immunotherapy strategy to slow or prevent neuroinflammation-driven progression in neurodegenerative disorders.

Stein DN, Gendelman HE · iScience · (2026) · View on PubMed ↗

Meningeal macrophages regulate fibroblasts to influence meningeal lymphatic function following traumatic brain injury.​

This study examined how meningeal macrophages regulate fibroblasts to influence meningeal lymphatic function after traumatic brain injury (TBI), using single-cell RNA sequencing, confocal microscopy, and flow cytometry. It identified a distinct meningeal fibroblast population that secretes VEGF-C and showed that manipulating macrophage–fibroblast signaling (including via clodronate liposomes and PDGF-C interventions) alters meningeal lymphatic function following TBI. Clinically, it suggests a macrophage-driven VEGF-C fibroblast axis as a potential therapeutic target to restore lymphatic clearance and immune trafficking after TBI.

Guo X, Zhu Y, Gao S et al. · Theranostics · (2026) · View on PubMed ↗

Nuclear export modulates TDP-43 phase transitions and cytoplasmic aggregation.​

This study investigated how nuclear export regulates TAR DNA-binding protein 43 (TDP-43) phase transitions and cytoplasmic aggregation using chemical and genome-wide genetic screening in cells expressing an RNA-binding–defective TDP-43 mutant that models an ALS-associated variant. The key finding is that multiple cellular processes—including RNA splicing, protein translation, proteostasis imbalance, and nuclear export—modulate the liquid-to-solid phase transition and aggregation behavior of TDP-43. The significance is identifying nuclear export as a controllable regulator of TDP-43 pathology, offering potential targets for therapeutic intervention in ALS and related neurodegenerative diseases.

Chin N, Zhang Q, Zou J et al. · bioRxiv : the preprint server for biology · (2026) · View on PubMed ↗

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Fibrosis & inflammatory lung disease​

Hdac11 promotes idiopathic pulmonary fibrosis through macrophage M2-type polarization and myofibroblast accumulation by inhibiting Parkin-dependent mitophagy.​

This study assessed the role of histone deacetylase 11 (Hdac11) in idiopathic pulmonary fibrosis (IPF) by analyzing Hdac11 expression in IPF lungs and using genetic ablation and adoptive transfer of Hdac11-deficient macrophages. Hdac11 upregulation in alveolar macrophages promoted M2 macrophage polarization and macrophage-to-myofibroblast transition-like reprogramming, leading to increased myofibroblast accumulation and profibrotic gene expression, whereas Hdac11 deficiency markedly attenuated fibrosis. Mechanistically, the study implicated impaired Parkin-dependent mitophagy as a driver of the anti-fibrotic effect, positioning Hdac11 as a potential therapeutic target in IPF.

Nie Y, Xu L, Liu Y et al. · Nature communications · (2026) · View on PubMed ↗

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Hematologic malignancies & infections (HSCT/AML/lymphoma)​

Clinical and Microbiological Insights Into Invasive Fusariosis Following Allogeneic Hematopoietic Stem Cell Transplantation: A 15-Year Single-Center Analysis.​

This 15-year single-center retrospective analysis studied invasive fusariosis cases among 2,359 allogeneic hematopoietic stem cell transplant (HSCT) recipients for hematological malignancies (2010–2024), using multigene sequencing for Fusarium species identification and antifungal susceptibility testing. Seventeen proven invasive fusariosis cases (7.2/1000) were identified, with patients more often having prior HSCT and with high mortality despite prophylaxis and treatment. Clinically, the work highlights the need for heightened surveillance and optimized antifungal management strategies for Fusarium infection in post-allogeneic HSCT patients, especially those with prior transplant exposure.

Yamamoto J, Ogura S, Takagi S et al. · Transplant infectious disease : an official journal of the Transplantation Society · (2026) · View on PubMed ↗

The diagnostic and prognostic utility of blood metagenomic next-generation sequencing for invasive pulmonary aspergillosis.​

This retrospective study enrolled 95 patients with Aspergillus detected by blood fungal metagenomic next-generation sequencing (mNGS) and used modified EORTC/MSGERC criteria to distinguish invasive pulmonary aspergillosis (n=60) from colonization (n=35). It assessed diagnostic and prognostic utility of blood mNGS fungal load (reads per million) alongside serological biomarkers galactomannan (GM) and 1,3-β-D-glucan (BDG). If validated, combining blood mNGS fungal load with GM/BDG could improve clinical discrimination and risk stratification for IPA versus colonization.

Chen Y, Tang X, Lu S et al. · Microbiology spectrum · (2026) · View on PubMed ↗

Profiling medical mycologists: Results from a global survey of the ESCMID Fungal Infection Study Group (EFISG).​

This cross-sectional global survey characterized the medical mycology workforce using the ESCMID Fungal Infection Study Group (EFISG) as a representative international network. The study aimed to map training, roles, and research/education patterns among medical mycologists worldwide. Such workforce profiling can guide coordinated efforts to address invasive fungal infection burden, diagnostic gaps, and antifungal resistance.

Salmanton-García J, Lagrou K, Lanternier F et al. · Medical mycology · (2026) · View on PubMed ↗

Total marrow irradiation-based conditioning for allogeneic hematopoietic stem cell transplantation in patients with hematologic malignancies: A multicenter real-world study.​

This multicenter real-world study evaluated total marrow irradiation (TMI)-based conditioning for allogeneic hematopoietic stem cell transplantation (allo-HSCT) in patients with hematologic malignancies across four Chinese centers (2017–2024). The key finding was that TMI-based conditioning was feasible and associated with measurable overall survival and disease control outcomes, with safety assessed via nonrelapse mortality and graft-versus-host disease-related endpoints. Clinically, the large cohort strengthens evidence for TMI as a conditioning option in allo-HSCT outside tightly controlled trials.

Zhang Y, Zhang R, Cao X et al. · Cell transplantation · (2026) · View on PubMed ↗

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Reproductive biology & infertility​

Biallelic mutations in ANAPC13 cause female infertility characterized by oocyte maturation arrest both in humans and mice.​

Researchers investigated biallelic ANAPC13 mutations in human patients with infertility and in mouse models to determine whether ANAPC13 loss causes oocyte maturation arrest, focusing on the anaphase-promoting complex/cyclosome (APC/C) pathway. ANAPC13 mutations produced oocyte maturation arrest in both humans and mice, phenocopying defects seen with other APC/C subunits. This establishes ANAPC13 as a causal gene for a specific ART-refractory infertility mechanism and informs genetic diagnosis and mechanistic understanding of meiotic progression failure.

Wang Y, Ding Z, Liu X et al. · American journal of obstetrics and gynecology · (2026) · View on PubMed ↗

Oxytocin signaling in adipocytes is required for normal milk fat production.​

This study examined the role of oxytocin signaling in adipocytes for milk fat production by using dams lacking oxytocin receptors specifically in adipose tissue (OxtrΔAd) and identifying the relevant oxytocin source. Adipocyte OXTR loss reduced milk triglycerides and impaired pup weight gain, and the effect was mediated by oxytocinergic sympathetic neurons; dietary fat supplementation rescued the triglyceride deficit. These results define a neuroendocrine (oxytocin–adipocyte) control of lactation that could inform interventions for impaired milk production.

Li E, Yuan Y, Sun H et al. · Cell metabolism · (2026) · View on PubMed ↗

Development of a DUX4-targeting antibody oligonucleotide conjugate as a therapy for FSHD.​

This preclinical/therapeutic development study created Delpacibart braxlosiran (del-brax/AOC 1020), an antibody–oligonucleotide conjugate designed to treat facioscapulohumeral muscular dystrophy (FSHD) by targeting DUX4 expression in skeletal muscle. The key finding was that the TfR1-targeted delivery of DUX4 mRNA–targeting siRNA (siDUX4.6) reduced DUX4 mRNA levels and demonstrated therapeutic activity consistent with effective muscle delivery. This is significant because it advances a targeted RNA-silencing strategy for FSHD by coupling gene-specific knockdown to receptor-mediated delivery.

Malecova B, Sala D, Melikian GM et al. · Nucleic acids research · (2026) · View on PubMed ↗

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Developmental biology & regenerative models​

A transgene-free, human peri-gastrulation embryo model presents trilaminar embryonic disc-, amnion- and yolk sac-like structures.​

This study developed a transgene-free human peri-gastrulation embryo model (peri-gastrulation trilaminar embryonic disc, PTED) derived from primed human pluripotent stem cells. It found that PTED embryoids form trilaminar embryonic disc-like, amnion-like, and yolk sac-like structures and show primitive hematopoiesis, with lineage tracing supporting mesodermal organization between dorsal amnion and ventral definitive yolk sac. The scientific significance is that PTED provides a tractable in vitro system to study early human embryogenesis and lineage specification during peri-gastrulation.

Sun S, Zheng Y, Kim YS et al. · Nature cell biology · (2026) · View on PubMed ↗

A single-cell and spatial atlas of early human olfactory development.​

This study mapped early human olfactory development in male and female fetuses (7–12 post-conception weeks) using integrated single-nucleus RNA sequencing (snRNA-seq) and multiplexed error-robust fluorescence in situ hybridization (MERFISH) to resolve cell types and spatial gene-expression dynamics in the fetal nasal region. The atlas identified 32 distinct cell types and provided spatial-temporal markers across the olfactory epithelium and adjacent tissues. This resource improves mechanistic understanding of human olfactory lineage development and supports future studies of developmental disorders affecting smell.

Mbouamboua Y, Lebrigand K, Nampoothiri S et al. · Nature communications · (2026) · View on PubMed ↗

Molecular architecture of the ciliary base in mammalian multiciliated cells.​

This preprint studied the molecular architecture of the ciliary base in mammalian multiciliated cells from the mammalian trachea using cryo-focused ion beam (cryo-FIB) milling and cryo-electron tomography (cryo-ET), complemented by in situ cross-linking mass spectrometry (XL/MS) and ultrastructure expansion microscopy (U-ExM). The authors report in situ 3D structural and molecular insights into the transition zone and basal body/ciliary environment that had been poorly defined. Scientifically, the work provides a mechanistic framework for how ciliary base components organize to support motile cilia function and may inform future studies of ciliopathies.

McCafferty CL, Brunet M, van den Hoek H et al. · bioRxiv : the preprint server for biology · (2026) · View on PubMed ↗

Whole-organism spatial transcriptomics at single-cell resolution in C. elegans.​

This preprint developed or applied whole-organism spatial transcriptomics at single-cell resolution in Caenorhabditis elegans to map gene expression across intact worms while addressing limitations in spatial resolution and multiplexing. The key finding is that the approach enables profiling multiple gene expression patterns in the native anatomical context of whole animals at single-cell scale. The scientific significance is enabling circuit- and behavior-linked molecular mapping in a genetically tractable organism, accelerating discovery of spatially organized gene regulation.

Aguirre Aguilera JD, Wan X, Tischbirek CH et al. · bioRxiv : the preprint server for biology · (2026) · View on PubMed ↗

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Clinical guidelines, comparative effectiveness & trial evidence​

Diagnostic Criteria and Management of MELAS and Stroke-Like Episodes: Consensus-Based Statements.​

This consensus article studied diagnostic criteria and management strategies for mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS) and mitochondrial stroke-like episodes (SLE) across pediatric and adult populations using an international Delphi process coordinated by ERN EURO-NMD and the US Mitochondrial Medicine Society. It produced standardized, consensus-based recommendations for defining, diagnosing, and treating MELAS/SLE to reduce variability in clinical practice. The guideline is significant because it provides a unified framework for earlier recognition and more consistent management of these rare mitochondrial disorders.

Mancuso M, Bellusci M, Carelli V et al. · European journal of neurology · (2026) · View on PubMed ↗

Romosozumab Versus Teriparatide for the Treatment of Postmenopausal Osteoporosis: An Overview of Systematic Reviews With Direct and Indirect Meta-Analyses.​

This overview of systematic reviews studied the comparative efficacy and safety of romosozumab versus teriparatide for postmenopausal osteoporosis by summarizing 13 eligible systematic reviews with meta-analyses identified through searches up to November 2023. It reported that romosozumab did not show a significant difference in falls risk at 12–24 months while synthesizing broader comparative outcomes on fracture risk and safety. The overview is significant for informing treatment selection between anabolic osteoporosis therapies in postmenopausal women.

Bandeira TFGS, Aguiar PM, Vianna CMM et al. · International journal of rheumatic diseases · (2026) · View on PubMed ↗

Boron neutron capture therapy (BNCT) for experimental bladder cancer: systemic or intravesical approach.​

This experimental study evaluated boron neutron capture therapy (BNCT) for bladder cancer in Wistar rats, comparing systemic versus intravesical delivery of borophenilalanine and benchmarking against conventional radiotherapy (cRT). It used carcinogen-induced bladder cancer models and assessed tumor staging/burden as well as proliferative and apoptotic indexes after BNCT delivered at the MARK TRIGA-II reactor versus cRT. The significance is that it tests whether route of boron delivery (systemic vs intravesical) changes antitumor and pro-inflammatory outcomes relative to standard radiotherapy in bladder cancer.

Teke K, Özer C, Yaprak Bayrak B et al. · British journal of cancer · (2026) · View on PubMed ↗

UK BioCoin: swift trait-specific summary statistics regression for UK Biobank.​

This study developed UK BioCoin (UKC), a computational method for generating trait-specific summary statistics regression for UK Biobank without requiring individual-level data access. Using UK Biobank data (505 traits, ~10 million SNPs), UKC produced summary statistics that closely matched individual-level covariate-adjusted results while achieving ~80× greater computational efficiency. The method enables more flexible, user-specified covariate adjustments for genetic association analyses using only summary statistics.

He J, Qi G, Ying J et al. · Nature communications · (2026) · View on PubMed ↗

Efgartigimod in Sjögren's disease: a phase 2, randomised, placebo-controlled, parallel-group, double-blinded, proof-of-concept study (RHO).​

In adults with Sjögren’s disease, this phase 2 multicentre randomized, double-blind, placebo-controlled proof-of-concept study (RHO) evaluated intravenous efgartigimod 10 mg/kg once weekly for 24 weeks versus placebo, with efficacy assessed using the CRESS responder composite at week 24. Efgartigimod increased the proportion of CRESS responders and improved multiple secondary domains of systemic disease activity, patient-reported symptoms, tear/salivary gland function, and serology compared with placebo. These findings provide early clinical proof-of-concept for FcRn inhibition as a therapeutic strategy in Sjögren’s disease.

Peene I, Verstappen GM, Arends S et al. · Annals of the rheumatic diseases · (2026) · View on PubMed ↗

Thiamine deficiency in cancer patients at initial admission to a palliative care unit: a single-centre cross-sectional study.​

This single-centre cross-sectional study of end-of-life cancer patients at initial admission to a palliative care unit measured whole-blood thiamine concentrations using high-performance liquid chromatography to determine the prevalence of thiamine deficiency and associated factors. Thiamine deficiency was common on admission, and the study identified clinical factors linked to lower thiamine status. The results highlight the need for routine screening and potential thiamine repletion strategies in palliative oncology populations.

Sato R, Ishida M, Uchida N et al. · BMJ supportive & palliative care · (2026) · View on PubMed ↗

Gastrointestinal Disorders in Scleroderma.​

This review synthesized evidence on gastrointestinal disorders across the spectrum of scleroderma/systemic sclerosis, emphasizing how vasculopathy, immune-mediated inflammation, and neuropathy drive GI involvement from esophagus to bowel. It summarizes the high prevalence of esophageal disease (including dysphagia and GERD) and other segment-specific complications such as gastroparesis and gastric antral vascular ectasia (GAVE). Clinically, the article provides an integrated framework to guide recognition, risk stratification, and management of GI manifestations in systemic sclerosis.

Quigley EMM, McMahan ZH, Kulkarni S et al. · Gastroenterology · (2026) · View on PubMed ↗

Lumen-apposing metal stents vs. self-expandable metal stents for endoscopic ultrasound-guided choledocoduodenostomy: a network meta-analysis of randomized controlled trials.​

Using a network meta-analysis of randomized controlled trials, investigators compared lumen-apposing metal stents (LAMS)—specifically cautery-enhanced LAMS (CE-LAMS)—versus self-expandable metal stents (SEMS) for endoscopic ultrasound-guided choledocoduodenostomy (EUS-CDS), with ERCP as a common comparator in malignant distal biliary obstruction. The analysis evaluated relative outcomes for stent patency and safety between CE-LAMS-based and conventional SEMS-based strategies. These comparative effectiveness results help clinicians choose the optimal EUS-CDS stent strategy to balance patency and adverse events in malignant distal biliary obstruction.

Spadaccini M, Chen YI, van Wanrooij RLJ et al. · Endoscopy · (2026) · View on PubMed ↗

Accelerating discovery of cancer causes for prevention in the era of rising early-onset cancers.​

This perspective addressed the rising incidence of early-onset cancers and the need to accelerate discovery of causes for prevention by integrating epidemiologic and mechanistic research. It argues that birth-cohort effects and global epidemiologic shifts require new frameworks that connect tissue-level biology with cause discovery and translation into prevention/interception strategies. The significance is that improved cause-discovery pipelines could enable earlier interventions and reduce the burden of cancers in younger populations.

Shi M, Patti GJ, Gunter MJ et al. · Cell · (2026) · View on PubMed ↗

Orthokeratology for stable mild-to-moderate keratoconus: a pilot study on safety and corneal remodeling via quantitative OCT analysis.​

This pilot prospective cohort study evaluated overnight orthokeratology (Ortho-K) using Euclid Emerald lenses in 14–21-year-old patients with stable mild-to-moderate keratoconus (Amsler–Krumeich grades I–II), assessing corneal remodeling with quantitative optical coherence tomography (OCT) over 18 months. The key finding is that Ortho-K was assessed for safety and for measurable epithelial and Bowman's layer structural changes alongside visual and refractive outcomes (UCVA/BCVA, refraction, axial length, and corneal topography). Scientifically, it provides early evidence that quantitative OCT can track corneal remodeling effects of Ortho-K in keratoconus.

Zhang C, Hu Z, Li W et al. · International ophthalmology · (2026) · View on PubMed ↗

Infusion-Related Reactions from Immune Checkpoint Inhibitors in Solid Tumors: A Proportional and Network Meta-Analysis.​

This proportional and network meta-analysis studied infusion-related reactions (IRRs) across immune checkpoint inhibitor (ICI) therapies in solid tumors by pooling phase 3 randomized controlled trials comparing CTLA-4, PD-1, PD-L1, and LAG-3 inhibitors (including dual ICI regimens) versus placebo/observation. The key finding is that IRR incidence varies by ICI type and regimen, and the analysis estimates odds ratios using random-effects network meta-analysis and additional proportional meta-analysis (as described in the abstract). Clinically, it provides comparative risk estimates to inform selection and monitoring strategies for IRRs during ICI treatment.

Fujiwara Y, Takahashi T, Tsuchiya K et al. · Targeted oncology · (2026) · View on PubMed ↗

A model-based prion vaccine protects a transgenic mouse line carrying a Gerstmann-Sträussler-Scheinker disease mutation.​

The study developed and tested a model-based prion vaccine designed to mimic predicted surface immunogenic features of the infectious prion conformer (PrPSc) in a transgenic mouse line carrying a Gerstmann-Sträussler-Scheinker (GSS) disease mutation. The vaccine protected the transgenic mice against prion disease, outperforming prior immunization strategies that primarily targeted the normal cellular prion protein (PrPC). This supports a structure-informed vaccination strategy for prion diseases where direct targeting of heterogeneous PrPSc has been difficult.

Fang A, Tang X, Fleming M et al. · Acta neuropathologica · (2026) · View on PubMed ↗

Romosozumab versus teriparatide for risk of dementia in individuals with osteoporosis: a target trial emulation study.​

This target-trial emulation study analyzed longitudinal Japanese claims data from 69,543 individuals with osteoporosis to compare romosozumab initiation versus teriparatide initiation for incident dementia risk. Romosozumab initiation was associated with a lower risk of dementia compared with teriparatide initiation. If confirmed prospectively, these findings could inform bone–brain risk management when selecting osteoporosis therapies.

Hatano M, Okada A, Sasabuchi Y et al. · Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · (2026) · View on PubMed ↗

The ecological dynamics of skin microbiota in skin health and diseases.​

This 2026 review synthesized evidence on how skin microbiota composition and function relate to skin health and diseases, focusing on host–microbe interactions relevant to conditions such as atopic dermatitis, psoriasis, and acne. It highlights that dysbiosis and specific taxa (e.g., Staphylococcus aureus and Cutibacterium acnes) can either promote or protect against disease through immune and barrier-related mechanisms. The review frames skin microbiome profiling as a potential avenue for improved diagnostics and microbiome-targeted therapies.

Pu P, Wang Y, Liu X et al. · Clinical microbiology reviews · (2026) · View on PubMed ↗

Exposure to air pollution and risk of gastrointestinal diseases: a systematic review and meta-analysis of epidemiological evidence.​

This systematic review and meta-analysis evaluated epidemiologic studies linking air pollution exposure to gastrointestinal diseases, including both long- and short-term exposures to PM2.5, PM10, and gaseous pollutants (NO2, SO2, CO, O3). Across 70 included studies, the authors synthesized pollutant-specific associations with GI outcomes using random-effects models per pollutant increment. The findings support an evidence-based link between air pollution and GI disease risk, informing public health and risk-reduction priorities.

Hao M, Zhang J, Yang Z et al. · Epidemiologic reviews · (2026) · View on PubMed ↗

Transcatheter Intra-Arterial Delivery of a Platelet-Derived Extracellular Vesicle-Enriched Preparation for Attenuating Skeletal Muscle Ischaemia-Reperfusion Injury in a Rodent Forelimb Model.​

This rodent forelimb ischemia–reperfusion injury (IRI) study tested transcatheter intra-arterial delivery of a platelet-derived extracellular vesicle (EV)-enriched preparation to attenuate skeletal muscle IRI. The approach was designed to exploit platelet EV anti-inflammatory and antioxidant properties to reduce sterile reperfusion injury. These preclinical data support EV-based vascular delivery as a potential therapeutic strategy for limb reperfusion syndromes.

Selim OA, Sarcon A, Behfar A et al. · Journal of extracellular vesicles · (2026) · View on PubMed ↗

Safety and Efficacy of Direct Oral Anticoagulants Versus Vitamin K Antagonists for Cerebrovascular Ischemic Outcomes in Non-Valvular Atrial Fibrillation: A Systematic Review and Meta-Analysis.​

This systematic review and meta-analysis compared direct oral anticoagulants (DOACs) versus vitamin K antagonists (VKAs) for cerebrovascular ischemic outcomes in non-valvular atrial fibrillation. Using PRISMA 2020-guided searches of PubMed, ClinicalTrials.gov, and the Cochrane Library, it synthesized randomized trial evidence on ischemic stroke/TIA and related safety outcomes. The results aim to inform anticoagulant selection for stroke prevention in non-valvular AF.

Nasir A, Anwar N, Kamran AB et al. · Clinical cardiology · (2026) · View on PubMed ↗

Oropharyngeal cancer mortality in the United States, 1999-2023: a surveillance analysis using CDC WONDER.​

This surveillance analysis used CDC WONDER data to examine oropharyngeal cancer (OPC) mortality trends and demographic/geographic disparities in the United States from 1999 to 2023. The key finding was that age-adjusted OPC mortality rates increased over time (from 1999 to 2023) with patterns suggesting evolving disparities across the period. Public-health significance lies in identifying changing mortality burden and subgroup differences to guide prevention, screening, and resource allocation.

Deng W, Cao L, Li Z · Frontiers in oncology · (2026) · View on PubMed ↗

Comparative effectiveness of non-pharmacological traditional Chinese medicine therapies for chronic fatigue syndrome: a systematic review and network meta-analysis.​

This systematic review and network meta-analysis compared non-pharmacological Traditional Chinese Medicine (TCM) therapies for chronic fatigue syndrome (CFS) using a broad database search completed January 1, 2026. The key finding was an evidence-based ranking of comparative effectiveness across different non-pharmacological TCM interventions, with study quality and confidence assessed using risk-of-bias tools and CINeMA. Clinically, it helps clinicians and researchers identify which TCM modalities may offer the best symptom benefit for CFS while highlighting gaps for future trials.

Zhang Y, Zhou Y, Xu H et al. · Frontiers in medicine · (2026) · View on PubMed ↗

Experts' recommendations for the management of adult patients with cardiogenic shock.​

This work studied expert consensus recommendations for managing adult cardiogenic shock (CS), using the GRADE framework developed by French Intensive Care Society (SRLF) and French Society of Cardiology (SFC) with input from SFAR and the French Society of Thoracic Surgery. The key finding is a structured, updated guideline set addressing CS management across etiologies in adults, reflecting evidence appraisal and recommendation grading. Clinically, it aims to standardize care and improve outcomes in a high-mortality condition where prior European recommendations were more than a decade old.

Aissaoui N, Delmas C, Merdji H et al. · Annals of intensive care · (2026) · View on PubMed ↗

Clinical and endocrine effects of pharmacological therapy in endometriosis: a systematic review and meta-analysis.​

This systematic review and meta-analysis evaluated clinical and endocrine effects of pharmacological therapies for endometriosis in women, including combined oral contraceptives (COCs), progestins, GnRH analogues, levonorgestrel-releasing intrauterine system (LNG-IUS), and relugolix, across 149 clinical trials. The key finding is that these hormonal and non-hormonal treatments show benefits of varying magnitude on clinical/endocrine outcomes, with evidence quality assessed using Jadad and GRADE and effect sizes extracted when available. Scientifically and clinically, it consolidates comparative evidence to guide selection of endometriosis therapies based on the strength of outcomes and reliability of the data.

Sun R, Xu H, Ma R et al. · Frontiers in endocrinology · (2026) · View on PubMed ↗

Redefining standards: a comprehensive systematic review of practice changing advances in GU oncology from ASCO and ESMO 2025.​

This comprehensive systematic review studied practice-changing advances in genitourinary (GU) oncology from ASCO and ESMO 2025, synthesizing pivotal phase II/III randomized controlled trials across bladder, kidney, prostate, penile, and testicular cancers. The key finding is that 2025 trial results are reshaping therapeutic standards through novel mechanisms and more refined personalization strategies. Clinically, it provides an evidence-focused map of how 2025 data should influence current GU cancer treatment paradigms.

Ismaili N · Frontiers in endocrinology · (2026) · View on PubMed ↗

Translational Models for Glioblastoma: Revolutionizing Drug Development and Personalized Medicine through Clinical Insights.​

This article reviewed translational experimental models for glioblastoma (GBM) drug development, focusing on how current preclinical platforms (cell lines, 2D cultures, and animal models) fail to capture GBM tumor microenvironment, blood–brain barrier function, and interpatient heterogeneity. It highlights that late-stage clinical trial failures reflect limited predictive value of conventional models and argues for advanced translational systems to better mirror these determinants of therapeutic resistance. The significance is improved model-to-clinic translation for personalized GBM therapies and more reliable selection of candidate drugs before late-stage testing.

Lee G, Kim YJ, Ham SJ et al. · Theranostics · (2026) · View on PubMed ↗

Exploring medication adherence and illness perception in patients with neuroimmune diseases: a cross-sectional study.​

This cross-sectional study examined medication adherence and illness perception in patients with neuroimmune diseases—myasthenia gravis (MG), multiple sclerosis (MS), and neuromyelitis optica spectrum disorder (NMOSD)—enrolling individuals from the outpatient neurology clinic at West China Hospital, Sichuan University (March–August 2025) with ≥6 months of treatment. The key finding is the identification of factors associated with adherence and the relationship between adherence and illness perception using the Eight-Item Morisky Medication Adherence Scale (MMAS-8). Clinically, the results aim to inform interventions to improve long-term adherence and prognosis in chronic neuroimmune conditions.

Fu R, Wang X, Shi Z et al. · Frontiers in immunology · (2026) · View on PubMed ↗

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Generated automatically on April 23, 2026 from PubMed's trending articles. Summaries are AI-generated; always consult the original publication for clinical or research decisions.