Introduction: Sonodynamic therapy (SDT) is a promising approach that combines low-intensity ultrasound (LIUS) with a sensitizing agent to induce therapeutic effects. Curcumin-coated silver nanoparticles (Cur@AgNPs) have shown potential as a sensitizer, demonstrating adverse effects on cancer cell survival. This study examined the apoptotic effects of US waves in the presence of Cur@AgNPs on MCF7 breast cancer cells. Methods and Materials: MCF7 cells were cultured and divided into different treatment groups. Cur@AgNPs were synthesized and characterized using various techniques, confirming their size to be approximately 29.3 ± 5.6 nm. The IC50 of Cur@AgNPs in MCF7 cells was determined to be 48.23 µg/ml through the MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay. LIUS radiation was applied to the cells in different modes, both with and without Cur@AgNPs. Cell viability was evaluated using the MTT assay and reactive oxygen species (ROS) production was measured. Colony formation assay and real-time PCR were conducted to evaluate cell death and changes in gene expression of Bcl-2-associated X protein (Bax), B-cell lymphoma-2 (Bcl-2), and Caspase-3, respectively. Results: The findings confirmed the successful synthesis of Cur@AgNPs with a uniform size of approximately 29.3 ± 5.6 nm. In the continuous wave (CW) and pulse wave (PW) modes, 50% and 25%, cell viability was measured at 65.01% ± 1.35%, 73.75% ± 1.80%, and 80.76% ± 1.57%, respectively. Cell viability in CW with Cur@AgNPs was 16.9% ± 4%. The plating efficiency (PE) of the combined treatment group was 13.66 ± 1.24, compared to 39.33 ± 1.24 for the US.CW group and 68.66 ± 2.62 for the Cur@AgNPs group. Also, the expression of proapoptotic genes, such as Bax and Caspase-3, increased, while the expression of the antiapoptotic gene Bcl-2 decreased in MCF7 cells treated with the SDT. Flow cytometry analysis revealed increased rates of early apoptosis (21.22% ± 3.82%) and late apoptosis (36.59% ± 4.5%) in the US.CW + Cur@AgNPs. Conclusion: This study provides novel insights into the induction of apoptosis in MCF7 breast cancer cells through SDT in the presence of Cur@AgNPs as a sonosensitizer. These findings support the potential of SDT as an effective therapeutic approach for breast cancer treatment using nonionizing and noninvasive methods.

Orbital venous lymphatic malformations or lymphangiomas are choristomas of the orbit. Common in the pediatric population, the lesion is notorious for spreading into various anatomical spaces due to its infiltrative nature. Additionally, the vascular nature poses challenges to complete removal. Hemorrhages are not uncommon in the lesion, which may result in permanently compromised ocular function. Medical management involves injecting sclerosant into the cystic areas of the lesion, resulting in shrinkage and collapse, followed by total excision, which is the most suitable treatment option. The authors present a series of cases in which lymphangiomas have been completely excised using this minimal manipulative approach.

Current primary tumor treatments include curative resection, chemotherapy, and radiotherapy. However, these conventional methods lack precise drug delivery. Hydrogels, adaptable to the biological characteristics of different tumors, offer potential as drug delivery systems and represent a significant area of research in tumor treatment. In this study, we aimed to conduct a bibliometric analysis to reveal the current progress and future prospects of hydrogels for drug delivery in cancer.

Publications concerning hydrogels in tumor drug delivery were retrieved from the Web of Science Core Collection (WoSCC) database. Data regarding countries/regions, institutions, journals, authors, and document types were collected. Bibliometric analysis and network visualization were performed using CiteSpace, HisCite, VOSviewer, Alluvial Generator, and R software.

China, the United States, and India were the leading contributing countries. Of the 98 relevant categories, 94 experienced citation bursts between 2000 and 2024. The research team led by Professor Pourmadadi Mehrab demonstrated substantial influence in this field. The International Journal of Biological Macromolecules was the most prolific journal. The top three emergent categories originated in 2020 or later, are "Chemistry, Applied", "Engineering, Environmental", and "Biochemistry & Molecular Biology". "Designing hydrogels for controlled drug delivery" was the most highly cited article. Recent emergent keywords included immunotherapy, immunogenic cell death, carboxymethyl cellulose, and antibacterial. Key concept alluvial flow visualization revealed six terms: peritoneal carcinomatosis, iron oxide nanoparticles, drug delivery, release kinetics, carbon dots, and pathway. Nano-composite hydrogels, immunotherapy, quercetin, pancreatic cancer, and oral cancer exhibited recent activity within the cited article timeline, suggesting these areas as potential future research hotspots.

This bibliometric analysis identifies future research directions within the developing field of hydrogels for drug delivery in cancer. This study provides recommendations and directions for the development of hydrogels as tumor drug delivery systems.

Oncolytic viruses (OVs) offer a promising antitumor strategy by selectively lysing tumor cells and simultaneously activating innate and adaptive immune responses. Recent studies have shed light on the immunostimulatory mechanisms of OVs, particularly oncolytic adenovirus (OAds), which are emerging as leading candidates due to their favorable safety profile, genomic stability, and efficient transduction capacity. Despite the significant progress made by immune checkpoint inhibitors (ICIs) in antitumor therapy, treatment resistance continues to be a major barrier to their clinical effectiveness. OVs and ICIs work synergistically: OVs reprogram the immunosuppressive tumor microenvironment (TME) through immune cell recruitment and pro-inflammatory cytokine production, potentially overcoming ICI resistance. In turn, ICIs enhance T cell function by blocking inhibitory signaling pathways. This review highlights recent preclinical and clinical advancements in the therapeutic potential of combining OAds with ICIs, while also addressing critical translational challenges. We propose a strategic framework for optimizing the development and clinical trial design of these combination therapies to advance precision immunotherapy.

Hepatocellular carcinoma (HCC) is a classic inflammation related cancer with most cases arising from chronic liver disease (CLD). This study investigates immune dysregulation that occurs during the progression of CLD to HCC by delineating changes in immune cell composition and distribution within the liver microenvironment.

Mice were injected with Diethylnitrosamine (DEN) at 4 weeks of age, followed by continuous tri-weekly injections of carbon tetrachloride (CCl₄) for 6 and 21 weeks to induce liver fibrosis and HCC. Naïve and Phosphate-buffered saline (PBS) corn oil treated mice were used as controls. Immune cell profiling was performed using multiplex immunofluorescence and flow cytometry analyses.

The spatial analysis of immune cell populations in HCC reveals stable leukocytes overall, with notable increases in myeloid cells, particularly infiltrating macrophages (Inf mph). Indeed, Inf mph show a progressive enrichment from control to tumor, reaching a 5-fold and 10-fold increase in the invasive margin (IM) and surrounding non-tumor tissue (NTT) regions, respectively. T lymphocytes, especially CD4+ T cells but not CD8+ T cells, significantly expand, with CD4+ cells increasing up to 10-fold in the IM and NTT regions of HCC livers. Regulatory T cells (Tregs) population exhibits an extraordinary 125-fold and 80-fold surge in the IM and NTT regions, respectively.

The DEN-CCl₄ induced HCC mouse model replicates key immunosuppressive features of human HCC, notably increased Tregs and macrophages, which provides a robust platform for testing immunotherapies. The prominence of immune cells in the IM region underscores its importance as a critical interface modulating tumor-immune interactions, while the elevated immune presence in the NTT region reflects broader immune dysregulation associated with advanced CLD, and potentially facilitating tumor progression.

The proteasome (prosome, macropain) is a key cellular organelle responsible primarily for protein homeostasis, by degrading damaged or misfolded proteins. Proteasome-processed protein fragments can then be further trimmed and funneled to the major histocompatibility complex class I (MHC-I) antigen presentation pathway for cell surface display and immune recognition. Various types of proteasomes can be found in mammalian cells with different expression patterns and cleavage abilities. As such, the immunoproteasome (ImP) preferentially cleaves proteins to yield MHC-I-compatible fragments. It is constitutively expressed by some immune cells and can be induced by pro-inflammatory signals. Interestingly, it was also found to be expressed in multiple types of cancers and proteasome activity can be modulated by some cancer therapies. A better understanding of its impact on cancer progression, prognosis and treatment response is therefore needed to guide treatment decisions. In this review, we focus on the multiple roles of the ImP in cancer, including its interplay with the immune system, as well as its impact on patient outcomes.

Cancer nanomedicine holds transformative potential, but its clinical translation remains hindered by the lack of preclinical models that accurately mimic human tumor complexity. Conventional approaches often overlook the dynamic tumor microenvironment (TME) and interpatient variability, leading to unreliable predictions of nanodrug behavior. Here, we present tumor organoids as a transformative solution. These three-dimensional cultures retain the original tumor's architecture, molecular profiles, and TME interactions. Through concrete examples spanning pancreatic, breast, and glioblastoma cancers, we showcase how organoids reliably evaluate nanodrug delivery efficiency, therapeutic effects, and safety profiles. In addition, the establishment of large-scale organoid biobanks further facilitates rapid drug screening and tailored treatment strategies, significantly improving preclinical success rates. Therefore, the organoid-driven paradigm not only overcomes long-standing challenges in tumor modeling but also paves a faster, more reliable path toward clinically effective nanotherapies.

Conventional diagnostic tools, including ultrasound, fine-needle aspiration cytology, and intraoperative frozen section pathology, may fail to reliably distinguish between benign and malignant FNs, leading to unnecessary or inadequate surgical interventions. We aimed to develop and validate a deep learning (DL) system for the preoperative diagnosis of follicular-patterned thyroid neoplasms (FNs) using routine ultrasound images, with the goal of improving diagnostic accuracy and reducing unnecessary procedures.

In this multicenter, retrospective study, we included 3817 patients (2877 [75.4%] female) with a definitive diagnosis of FNs from 11 centers across China. All patients underwent preoperative ultrasound examinations. The dataset comprised 9393 ultrasound images, including thyroid follicular adenoma (n = 1787, 4317 images), follicular carcinoma (n = 446, 1593 images), and follicular variant of papillary thyroid carcinoma (n = 1584, 3483 images) collected between 2012 and 2025. A state-of-the-art OverLoCK (Overview-first-Look-Closely-next ConvNet with Context-Mixing Dynamic Kernels) model was developed on a dataset comprising 2728 patients (6625 images) and validated on an internal cohort (n = 683, 1905 images) and an external cohort (n = 406, 863 images). Model performance was evaluated using the area under the curve (AUC), accuracy, sensitivity, specificity, positive predictive value (PPV), negative predictive value (NPV), and F1 score. Model calibration was evaluated using calibration curves, while clinical usefulness was assessed through decision curve analysis (DCA).

The OverLoCK model exhibited excellent performance in both the internal and external validation sets. In the internal validation cohort, the OverLoCK model achieved an AUC of 0.937 (95% confidence interval [CI]: 0.919-0.954), with accuracy of 90.9% (95% CI: 87.7-92.0), sensitivity of 93.9% (95% CI: 91.5-95.6), specificity of 84.8% (95% CI: 82.6-86.0), PPV of 92.7% (95% CI: 90.7-93.8), NPV of 87.2% (95% CI: 86.0-91.0), and F1 score of 0.911% (95% CI: 0.887-0.932). In the external validation cohort, the model yielded an AUC of 0.853 (95% CI: 0.832-0.876), accuracy of 82.8% (95% CI: 81.7-84.4), sensitivity of 84.5% (95% CI: 82.5-86.2), specificity of 81.1% (95% CI: 79.2-84.5), PPV of 80.4% (95% CI: 79.0-84.0), NPV of 85.1% (95% CI: 83.2-87.7), and F1 score of 0.839 (95% CI: 0.802-0.877). The DL model demonstrates good agreement between the predicted and actual probabilities of malignancy. DCA confirmed that the model was clinically useful.

Our study demonstrates that a DL-based system can provide a noninvasive, accurate, and reliable tool for the preoperative diagnosis of FNs. By improving diagnostic precision, this approach has the potential to optimize clinical decision-making and reduce the burden of overtreatment in patients with FNs. Further prospective studies are warranted to validate these findings in real-world clinical settings.

This work was supported by the National Key Research and Development Program of China (2023YFF1204600), the National Natural Science Foundation of China (82227802 and 82302190), the Clinical Frontier Technology Program of the First Affiliated Hospital of Jinan University (No. JNU1AF-CFTP-2022-a01201), the Science and Technology Projects in Guangzhou (202201020022, 2023A03J1036, 2023A03J1038, 2025A04J7006), the Outstanding Young Talents of Guangdong Special Support Program (Health Commission of Guangdong Province) (0720240213), and the Science and Technology Youth Talent Nurturing Program of Jinan University (21623209).

VEXAS (vacuoles, E1 enzyme, X-linked, auto-inflammatory, somatic) is a recently discovered syndrome of autoinflammatory origin affecting mainly older patients with a clinical picture encompassing a variety of hematological and rheumatological conditions. We aimed to gather current knowledge on patient-reported outcomes (PRO) and morbidity burden of VEXAS patients.

A scoping review conducted via PubMed (last updated September 2024) identified studies involving VEXAS patients, excluding studies primarily addressing hematologic adverse events or laboratory parameters, with no lower date restriction. A double-review process was applied from screening to data charting. Outcomes included the prevalence of manifestations of VEXAS-related morbidity burden and their aggregated rates, adhering to the PRISMA-ScR guidelines.

Out of 357 records, 31 studies met the inclusion criteria, analyzing 1437 patients. The median study sample size was 40 patients (IQR 16-59). Most studies (96·8%) were non-interventional and mostly conducted in France (38·7%) and the USA (32·3%). The median age at symptom onset was 67 years (IQR 66-68·6). Myelodysplastic syndrome was the most common concomitant disease, present in 93·6% of studies. No studies documenting PROs were identified. Skin and pulmonary involvement were the most frequently reported manifestations, appearing in 100% and 96·8% of studies, respectively. Moreover, skin lesions had the highest median prevalence (83·6%, IQR 76-90), followed by fever (81·2%, IQR 67·5-89) and general constitutional symptoms (76%, IQR 54·8-85·3). All symptoms identified in this review were clinician-reported.

Our findings may provide preliminary insights into future PRO assessment strategies for VEXAS syndrome. We also advocate for international concerted efforts for a rapid uptake of PRO evidence-based data that can help inform the development of patient-centric therapies for this rare disease.

This work was supported by AIRC5×1000 call "Metastatic disease: the key unmet need in oncology" to MYNERVA project, #21267 Myeloid Neoplasms Research Venture AIRC. Detailed description is available at http://www.progettoagimm.it.

Colorectal cancer (CRC) is a highly lethal gastrointestinal malignancy with substantial global health implications. Although mitochondrial metabolism genes play a crucial role in CRC development, their prognostic significance remains unclear.

This study systematically analyzed the expression and prognostic value of mitochondrial metabolism-related genes in CRC patients, establishing a risk model using data from TCGA and GEO databases. We also investigated the tumor microenvironment (TME), immune cell infiltration, tumor mutation burden, microsatellite instability (MSI), and drug sensitivity. Core mitochondrial metabolism-related gene, TMEM86B was identified and its functions validated through cell-based assays and in vivo mouse models.

Fifteen mitochondrial metabolism-related genes were identified, including HSD3B7, ORC1, GPSM2, NDUFA4L2, CHDH, LARS2, TMEM86B, FABP4, TNFAIP8L3, HMGCL, GDE1, ACOX1, ARV1, HDC, and GSR. The nomogram, which incorporates independent prognostic genes TMEM86B, TNFAIP8L3, HDC, and key clinical features pTNM stage (pathological Tumor-Node-Metastasis), age, was created to predict patient outcomes. Notable differences in immune cell infiltration were observed between risk groups. The risk score was associated with TME genes and immune checkpoints, indicating an immunosuppressive environment in high-risk groups. Furthermore, TIDE analysis revealed that integrating the risk score with immune score, stromal score, or microsatellite status improved the prediction of immunotherapy response across different CRC patient subgroups. Core mitochondrial metabolism-related gene, TMEM86B promotes colorectal cancer progression by enhancing cell proliferation, migration, and invasion, and its downregulation significantly inhibits tumor growth both in vitro and in vivo.

Our findings indicate that the risk model associated with mitochondrial metabolism may serve as a dependable prognostic indicator, facilitating tailored therapeutic strategies for CRC patients. TMEM86B promotes colorectal cancer progression, and its downregulation inhibits tumor growth in vitro and in vivo.