Early detection of cancer remains challenging due to the extremely low concentration of biomarkers present during initial disease stages. Dysregulation of key signaling pathways, including cyclin-dependent kinase (CDK) networks, drives uncontrolled cell proliferation and tumor progression, underscoring the need for highly sensitive, label-free biosensing technologies. Conventional analytical methods such as ELISA and PCR offer reliable detection but require complex sample preparation, fluorescent labeling, and long processing times, limiting their suitability for rapid diagnostics. This work introduces a novel label-free Biological Micro-Opto-Electro-Mechanical System (BioMEMS) platform based on an unbalanced Michelson interferometer with DBR mirrors to interrogate the minute spectral shifts induced by biomolecular interactions. A microcantilever is suspended above a silicon-on-insulator (SOI) waveguide, where the specific binding of biomarkers generates compressive surface stress, causing a downward deflection that reduces the cantilever-to-waveguide gap. This displacement modulates the effective refractive index of the sensing arm through enhanced evanescent-field coupling. The resulting phase variation is further detected through the high-sensitivity Michelson interferometric architecture, enabling ultrasensitive spectral interrogation. Numerical simulations using COMSOL Multiphysics demonstrate a narrow full width at half maximum (FWHM) of 27.6 nm, a quality factor (Q) of 53.34, and an overall sensitivity of 75.74 µm/(N/m). These results highlight the potential of the proposed platform for early cancer detection and precise monitoring of dysregulated signaling pathways.

Accurate intraoperative tumour localisation remains challenging in minimally invasive colorectal surgery because tactile palpation is lost and conventional markers can migrate or provide imprecise localisation. Building on a preceding tri-frequency study that identified 13.56 MHz as the preferred RFID band for the intended application, this work develops a shaft-compatible NFC antenna-reader platform and evaluates its electromagnetic behaviour from bench-top reference media to five-layer tissue-equivalent phantoms.

A Ø3 × 25 mm Fair-Rite Material 67 ferrite-rod antenna was designed from material and geometric parameters using finite-rod demagnetisation, inductance, resonance, and field calculations, followed by FEM cross-validation and experimental characterisation. The primary dataset comprised 480 detection distance measurements (2 media × 4 tag angles × 30 repetitions × 2 encapsulation variants). Phantom testing added 1440 measurements at 22 °C and 600 measurements at 37 °C across three fabrication batches, with the 37 °C non-coaxial subset limited to one batch.

The fabricated antenna measured 16.9 µH versus a 17.4 µH analytical estimate (-2.9%), with loaded Q = 23. The coaxial detection range was 16.45 ± 0.29 mm in air and 16.26 ± 0.21 mm in saline; angle was the dominant determinant of range (partial η² = 0.989). In the multi-layer phantom, detection was 100% at 0 and 10 mm perirectal fat thickness under coaxial alignment at 22 °C, whereas performance declined markedly with angular misalignment and no detections occurred at fat thicknesses ≥ 20 mm. Across detectable phantom configurations, FEM showed r² = 0.994, RMSE = 0.81 mm, and mean bias +0.70 mm. Bare and resin-overcoated tags showed no statistically detectable range difference. Multi-tag discrimination reached 100% for up to three tags separated by ≥20 mm under coaxial alignment, but deteriorated with angular misalignment.

The study demonstrates a physics-informed route from antenna miniaturisation to measured system performance, and defines the present operating envelope under controlled bench and tissue-equivalent phantom conditions. The electromagnetic measurements apply to the antenna-electronics subassembly; integrated-shaft, multi-prototype, multi-operator, ex vivo, and in vivo validation remain necessary before clinical performance can be determined.

Postprocedural defect management following gastric endoscopic submucosal dissection (ESD) remains controversial. Asian practice has traditionally favored meticulous prophylactic hemostasis without routine closure, supported by routine post-ESD hospitalization, whereas Western centers increasingly use endoscopic suturing, closure, and shielding to prevent delayed bleeding, perforation, and hospitalization. This review evaluates contemporary evidence on defect closure and shielding, emphasizing risk stratification and evolving practice patterns.

Durable mechanical closure may reduce delayed bleeding in selected high-risk patients, particularly those receiving antithrombotic therapy or with elevated BEST-J scores. Emerging techniques, including the reopenable clip-over-the-line method (ROLM), endoscopic hand suturing (EHS), endoscopic suturing platforms, and dedicated closure devices, demonstrate high technical success and favorable safety. Evidence quality remains limited, comprising retrospective studies, propensity-matched cohorts, and a single underpowered randomized controlled trial, with substantial heterogeneity in closure technique, patient populations, lesion characteristics, and baseline bleeding risk. Meticulous vessel identification, coagulation, and selective clipping still achieve favorable outcomes in expert centers without routine closure. Shielding with polyglycolic acid (PGA) sheets, fibrin glue, and polymer-based barriers offers an intermediate option when durable closure is impractical.

Current evidence does not support universal closure of all gastric ESD defects. Management should instead be selective, risk-stratified, and technique-conscious integrating bleeding risk, lesion characteristics, procedural setting, and local closure expertise. Low-risk defects may be safely managed with meticulous hemostasis alone, whereas durable closure appears most beneficial in carefully selected high-risk patients. Prospective comparative studies are needed to define which methods provide clinically meaningful, scalable benefit.

Acute lymphoblastic leukemia (ALL) is the most common childhood cancer, with survivors frequently experiencing long-term neurocognitive morbidities. Here, we utilize the TOTXVI clinical trial data to elucidate the mechanisms underlying treatment-related neurocognitive side effects in pediatric ALL patients by incorporating brain connectivity network data. To enable such analysis, we propose a high-dimensional mediation analysis method with a novel network mediation structural shrinkage (NMSS) prior, which is particularly suited for analyzing high-dimensional brain structural connectivity network data that serve as mediators. Our method is capable of addressing the structural dependencies of brain connectivity networks including sparsity, effective degrees of nodes, and modularity, yielding accurate estimates of the high-dimensional coefficients and mediation effects. We demonstrate the effectiveness and superiority of the proposed NMSS method through simulation studies and apply it to the TOTXVI data, revealing significant mediation effects of brain connectivity on visual processing speed directed by IT intensity. The findings shed light on the potential of targeted interventions to mitigate neurocognitive deficits in pediatric ALL survivors.

Intracranial tuberculomas are rare manifestations of extrapulmonary tuberculosis that can closely mimic malignant posterior fossa tumors in children, particularly in tuberculosis-endemic regions. The radiological and clinical overlap with aggressive neoplasms such as atypical teratoid/rhabdoid tumor (AT/RT) poses a significant diagnostic challenge. A 5-year-old immunocompetent boy presented with progressive headache and irritability. Magnetic resonance imaging (MRI) of the brain revealed a large (45 × 38 mm) lesion in the cerebellar vermis and left hemisphere with mass effect on the fourth ventricle and brainstem, causing obstructive hydrocephalus. A ventriculoperitoneal (VPMP) shunt was placed for hydrocephalus management. Subsequently, left suboccipital craniectomy with tumor decompression was performed. Intraoperative crush biopsy was initially reported as atypical rhabdoid tumor. However, final histopathological examination revealed extensive granulomatous inflammation with epithelioid cell granuloma, Langhans-type giant cells, and macrophages. Immunohistochemistry showed CD68 positivity (confirming macrophagic nature), EMA negativity (ruling out meningothelial tumor), and vimentin positivity in fibrotic tissue. Acid-fast bacilli (AFB) staining was positive. The final impression was chronic granulomatous pathology consistent with tuberculosis. This case underscores the importance of maintaining a high index of suspicion for CNS tuberculoma in the differential diagnosis of posterior fossa space-occupying lesions in children, particularly in endemic regions. Intraoperative crush biopsy may be misleading, and definitive histopathological examination with special stains is essential to avoid misdiagnosis and inappropriate treatment. Early confirmation of tuberculosis can dramatically alter management from aggressive oncological therapy to curative antitubercular treatment.

Hepatocellular carcinoma (HCC) immune escape is co-driven by tumor malignant proliferation and an immunosuppressive tumor microenvironment, characterized by frequently impaired natural killer (NK) cell function. Previous research indicated that HCC cell-secreted extracellular vesicles (EVs) deliver miR-17-5p, inhibiting the RUNX1 pathway and downregulating the activating receptor NKG2D in NK cells, which ultimately results in NK cell dysfunction. Although chimeric antigen receptor (CAR)-T therapy has achieved remarkable efficacy in hematological malignancies, it encounters significant challenges in treating solid tumors, including HCC. Recent studies have confirmed that CAR-T cell-derived EVs (CAR-T EVs) retain CAR targeting specificity and carry cytotoxic effectors such as granzyme B and perforin, demonstrating independent antitumor potential.

This study aimed to develop engineered CAR-T EVs loaded with a miR-17-5p inhibitor (EV-miR inhibitor) and evaluate their combined therapeutic efficacy against HCC through direct tumor cytotoxicity and restoration of NK cell function.

This study constructed NKG2D-targeted third-generation CAR-T cells, isolated CAR-T EVs via ultracentrifugation, characterized EV properties using multiple assays, and generated engineered CAR-T EVs loaded with a miR-17-5p inhibitor (EV-miR inhibitor). The therapeutic effects of this system against HCC were verified both in vitro and in a zebrafish HCC xenograft model.

CAR-T EVs exhibited characteristic cup-shaped morphology and robust expression of canonical EV markers together with the engineered NKG2D extracellular domain. Results indicated that CAR-T EVs entered HCC cells and exhibited concentration-dependent cytotoxicity against HCC cells without affecting the viability of normal hepatocytes. The loading of the miR-17-5p inhibitor was efficient, and the procedure did not alter the morphology, particle size, or marker expression of CAR-T EVs. EV-miR inhibitor effectively restored NKG2D and RUNX1 expression in miR-17-5p-overexpressing NK cells, significantly enhancing NK cell cytotoxicity against HCC and promoting IFN-γ secretion in vitro. In vivo experiments further confirmed that EV-miR inhibitor treatment markedly enhanced the antitumor activity of NK cells, leading to significant tumor growth inhibition in zebrafish xenografts.

In conclusion, this study demonstrates that NKG2D-targeted CAR-T EVs exert combined anti-HCC activities through direct tumor cytotoxicity and restoration of NK cell function, providing a novel immunotherapeutic strategy for HCC.

Malignant melanoma is a highly aggressive skin cancer. Dacarbazine (DTIC) chemotherapy, while historically used, is limited by poor solubility, short half-life, and systemic toxicity. Fe₃O₄ nanoparticles have been explored as drug delivery vectors with potential for photothermal conversion and Fenton-like catalytic activity. Cell membrane-camouflaged platforms may offer improved tumor targeting.

A biomimetic nanoplatform (Fe₃O₄PD@CCM) was engineered by encapsulating an Fe₃O₄ core within a DTIC-loaded PLGA-PEG2000 matrix, followed by functionalization with B16F10 cancer cell membranes. Physicochemical properties were characterized by dynamic light scattering (DLS), scanning electron microscopy (SEM), and liquid chromatography-mass spectrometry (LC-MS). Antitumor effects were assessed in B16F10 melanoma cells and in a subcutaneous syngeneic mouse model (n=4 per group).

Fe₃O₄PD@CCM Nanoparticles (NPs) exhibited a hydrodynamic diameter of ~25-30 nm, sustained DTIC release, and retention of membrane proteins. In vitro, the Fe₃O₄PD@CCM + NIR (Near-infrared irradiation) group showed reduced cell viability, increased apoptosis, G2/M phase arrest, and elevated intracellular reactive oxygen species (ROS) levels compared to controls. In vivo, Cy5-labeled Fe₃O₄PD@CCM NPs showed preferential fluorescence accumulation in tumors relative to non-coated NPs, with whole-body fluorescence diminishing within 24 h. In a 12-day efficacy study, Fe₃O₄PD@CCM + NIR treatment was associated with reduced tumor growth compared to control groups. Acute biosafety assessment at 24 h post-injection of a single high dose (200 mg/kg) revealed no overt abnormalities in the evaluated hematological, biochemical, or histopathological parameters.

Fe₃O₄PD@CCM NPs combined with NIR suppressed B16F10 cell activity in vitro and subcutaneous tumor growth in a preliminary mouse model. These findings represent a proof-of-concept demonstration. Further studies-including detailed mechanistic validation, long-term toxicity assessment, and evaluation in more clinically relevant models-are required to assess the translational potential of this platform.

Serum-capped silver nanoparticles (AgNPs), synthesized using naturally occurring serum proteins and reducing agents, represent a green nanotechnology platform with potential for safer and more selective therapy. This study compared the safety and anticancer efficacy of serum-capped AgNPs with polyvinyl alcohol (PVA)-capped AgNPs.

Serum-capped AgNPs (~18 nm, zeta potential -8.9 mV) were synthesized from human serum and administered intravenously in mice (0.1 mL/dose). PVA-capped AgNPs of equivalent silver concentration served as controls. Effects were assessed in a mouse hepatoma model, WRL-68, and Hep-G2, two different liver-derived cell lines using histopathology, biochemical analysis, MTT assay, estimation of proliferative potential by cell cluster formation assay, scratch assay, and hexosamine assays.

Serum-capped AgNPs showed a wider safety margin and lower toxicity in mice and normal WRL-68 cells compared with PVA-capped AgNPs, while exhibiting stronger cytotoxicity against hepatoma and Hep-G2 cancer cells. Treated mice showed improved survival, and favorable histopathological and biochemical profiles indicated reduced systemic toxicity. In the hepatoma model, serum-capped AgNPs, cisplatin, and their combination demonstrated significant anticancer effects, with combination therapy showing the strongest response.

Serum-capped AgNPs provide a safer and more selective nanotherapeutic approach by enhancing compatibility with normal host cells while retaining potent anticancer activity. Serum-derived capping improves biological precision and reduces systemic toxicity compared with conventional AgNP formulations. These findings support further investigation of serum-capped AgNPs as potential broad-spectrum anticancer (and antimicrobial) agents and for future personalized nanomedicine applications.

Laterally spreading tumors (LST) are flat colorectal neoplasms with an accelerated risk of malignant transformation and interval colorectal cancer. Despite their clinical importance, the molecular and microbial mechanisms underlying LST's aggressive biology remain poorly understood. Thus, we aimed to characterize the transcriptomic and microbial landscape of LST in comparison with paired protruding lesions and the adjacent normal colonic tissue.

Formalin-fixed, paraffin-embedded tissues from 36 samples were obtained from 15 adults and analyzed using RNA sequencing and 16S rRNA gene amplicon sequencing. Patterns of the differential gene expression were assessed using Gene Set Enrichment Analysis and Ingenuity Pathway Analysis. Microbial community composition and its predicted functional capacity were evaluated with analysis of compositions of microbiomes with bias correction in QIIME 2 and Phylogenetic Investigation of Communities by Reconstruction of Unobserved States 2, respectively.

Compared with paired protruding lesions and normal tissue, LST exhibited a distinct protumorigenic transcriptomic profile marked by the activation of MYC, E2F, mTOR, DNA damage, and senescence-associated secretory phenotype pathways, as well as robust proinflammatory signaling driven by TNF, NF-κB, IL-1, and IL-17. LST tissue also demonstrated a permissive environment for genomic instability. Microbiome analysis revealed enrichment of Fusobacterium and depletion of beneficial taxa, including Lactococcus, accompanied by predicted suppression of carbohydrate fermentation and short-chain fatty acid production, as well as altered sulfur metabolism. Fusobacterium abundance correlated with increased TNF expression, supporting a microbiota-driven inflammatory niche in LST.

LST are characterized by a unique inflammatory/metabolic/senescence axis that distinguishes them from other paired colorectal tissue samples. This procarcinogenic signature is driven by a Fusobacterium-enriched and carbohydrate-fermentation-depleted microbial ecosystem. These findings highlight the gut microbial ecosystem as a critical cofactor in LST pathogenesis and further support that combined host/microbiota-targeted strategies may improve colorectal cancer prevention in this population. Given the exploratory nature and limited cohort size, these findings require validation in larger prospective cohorts with metagenomic and metabolomic integration.

Chimeric antigen receptor (CAR) T cells are capable to eliminate cancer cells in the treatment of hematologic malignancies, yet the efficacy is frequently inconsistent and limited by cancer cell resistance and antigen-loss resulting in early tumor relapses. While CAR T cells are deemed to be the primary effectors in controlling the tumor, maturing evidence indicates that therapeutic outcomes are shaped by a broader immune cell network involving both the endogenous adaptive and innate immunity. In this review, we reframe CAR T cell therapy as the induction of a multi-system immune response rather than a uni-directional cytotoxic cell-autonomous intervention. We discuss the respective contributions of CAR T cells, innate immune cells, and host adaptive immunity in controlling tumor progression and outline strategies to recruit innate immunity using TRUCKs, armored CAR T cells, as well as immunological adjuvants to surmount current limitations. Finally, we address the risks associated with excessive innate immune activation and propose that a calibrated, broad immune cell activation should be viewed as design principle for next-generation CAR T cell therapies.