Giant mediastinal teratomas in the pediatric population are uncommon entities that may grow insidiously and cause significant compression of intrathoracic structures. We report the case of a 10-year-old girl with a two-year history of progressive exertional dyspnea, chest pain, orthopnea, and increasing thoracic enlargement. Chest radiography demonstrated marked mediastinal widening, and contrast-enhanced chest CT revealed a predominantly cystic mediastinal mass measuring approximately 15 × 14 cm, with mediastinal shift and ipsilateral lung collapse. Routine laboratory tests were within normal limits, and surgical resection confirmed a mature mediastinal teratoma. The patient had an uneventful postoperative course, and follow-up CT showed complete pulmonary re-expansion with no residual lesion. This case highlights the clinical and imaging features that should raise suspicion for a giant mediastinal teratoma in children and underscores the importance of reporting these cases given the limited pediatric literature available.

Multiple myeloma (MM) is a malignant hematologic neoplasm that primarily affects the bone marrow and can invade other organs, leading to diverse clinical manifestations. Presentation with gastrointestinal bleeding as the initial symptom is exceptionally rare. We report a case of MM in a 46-year-old man who presented with gastrointestinal bleeding and severe anemia. Routine endoscopic evaluation was inconclusive, but further hematologic and imaging investigations confirmed multiple myeloma. The patient was successfully treated with bortezomib-based chemotherapy and supportive care. This case emphasizes the importance of considering plasma cell dyscrasias in patients with unexplained GI bleeding and anemia, particularly when conventional gastrointestinal causes are excluded.

Vascular malignancy may rarely present as soft tissue swelling related to a spontaneous pseudoaneurysm. Our case report highlights the importance of prompt clinical examination, imaging, and surgical exploration for diagnosing vascular sarcoma presenting as a spontaneous pseudoaneurysm in a healthy patient.

Renal cell carcinoma (RCC) is a common urinary malignancy with high postoperative recurrence, and current therapies are limited by toxicity or insufficient efficacy. Efficient sonodynamic therapy (SDT) strategies capable of generating reactive oxygen species (ROS) are urgently needed. This study aimed to develop a high-performance MOF-based heterojunction sonosensitizer to enhance ROS generation and achieve effective anti-tumor activity.

We synthesized HKUST-1@TiO₂ heterojunctions and characterized their morphology, electronic structure, and ROS generation capacity. In vitro, OSRC-2 cells were treated with HKUST-1@TiO₂ ± ultrasound; cell viability, proliferation, apoptosis, and intracellular ROS were assessed. In vivo, nude mice bearing OSRC-2 xenografts received HKUST-1@TiO₂ ± ultrasound; tumor growth, histopathology, and biosafety markers were analyzed.

HKUST-1@TiO₂ exhibited efficient heterojunction formation, which enhanced charge separation and ROS production under ultrasound. In vitro, the combination treatment significantly reduced cell viability, decreased Ki67-positive area, and increased the number of TUNEL-positive cells. Intracellular ROS staining confirmed effective ROS accumulation in tumor cells. In vivo, tumor volume and weight were significantly reduced, with no detectable organ toxicity.

HKUST-1@TiO₂ heterojunctions effectively augment SDT through enhanced intracellular ROS generation, inducing tumor cell apoptosis and inhibiting proliferation. This study addresses the unmet need for efficient and safe SDT for RCC and provides a promising strategy with translational potential.

Osteosarcoma (OS) is the most prevalent primary malignant bone tumor in children and adolescents, characterized by aggressive local invasion, early distant metastasis (predominantly lung metastasis), and poor prognosis. Conventional clinical regimens, mainly neoadjuvant chemotherapy combined with surgical resection, are limited by severe systemic toxicity, multidrug resistance, low tumor targeting, and unsatisfactory outcomes for metastatic OS, with the 5-year survival rate of metastatic patients remaining below 30%. Nanodrug delivery systems (NDDS) have emerged as a transformative strategy to address these bottlenecks by enabling targeted drug/gene delivery, controlled release, enhanced tumor accumulation, and reduced off-target effects. This review systematically summarizes the pathological characteristics and therapeutic dilemmas of OS, highlights recent advances in diverse NDDS including lipid nanoparticles, polymeric nanoparticles, carbon-based nanomaterials, extracellular vesicles, gold nanoparticles, and hydrogels for OS therapy, with a special focus on strategies to counteract lung metastasis. We further discuss the clinical translation challenges of NDDS in OS, especially pediatric-specific concerns, and propose future directions such as stimuli-responsive nanocarriers, biomimetic nanoparticles, combination therapy, and inhalable nanomedicines for pulmonary metastatic lesions. Overall, NDDS hold great promise to revolutionize OS treatment by improving therapeutic efficacy and safety, particularly in overcoming lung metastasis and chemoresistance.

Nanozymes, a class of nanomaterials capable of mimicking the functions of natural enzymes, have garnered significant attention in biomedical fields because of their stable catalytic activity, high efficiency, low cost, and tunable enzyme-like properties. In recent years, advances in nanotechnology have led to the development of numerous nanozymes with redoxase-like activities, which have been widely applied in biosensing and disease treatment, demonstrating considerable potential. In this review, we first summarize the redoxase-like activity of nanozymes. From the perspective of redox regulation, we discuss the catalytic mechanisms of nanozymes in biosensing applications, elaborate on the molecular mechanisms involved in tumor therapy, including the induction of apoptosis and ferroptosis, and examine their catalytic pathways in antibacterial and anti-inflammatory treatments. Finally, we also discuss the current limitations and future challenges of nanozymes in biomedical applications, aiming to provide insights for the rational design and clinical translation of next-generation nanozyme-based platforms.

In recent years, significant progress has been made in lung cancer treatment paradigms with the continuous unraveling of the tumor microenvironment and the ongoing advancement of immunotherapy. As an emerging immunotherapy modality, Immune Cell Engagers (ICEs) aim to effectively mobilize the body's antitumor immune response by targeting tumors and activating immune effector cells such as T cells, NK cells, and myeloid cells. Recent studies have indicated that T-cell engagers (TCEs), exemplified by bispecific T-cell engagers (BiTEs), can enhance T-cell immunological activity within the lung cancer microenvironment and demonstrate significant antitumor effects in both in vitro and in vivo experiments. However, the highly heterogeneous nature of the lung cancer microenvironment and its complex immunosuppressive networks limit the therapeutic efficacy of ICEs. Meanwhile, key challenges remain in improving target cell specificity, lowering toxicity to non-target cells, and optimizing pharmacokinetics. This review systematically summarizes the mechanisms of action and recent advances of ICEs in lung cancer immunotherapy, explores innovative development directions for next-generation ICEs, and highlights their significant potential in driving paradigm shifts in lung cancer immunotherapy.

Triple-negative breast cancer (TNBC) is an aggressive subtype with high malignancy and poor prognosis. Immunotherapy is a promising treatment for TNBC patient. Although T cell-mediated tumor killing related genes (TTKRGs) play critical roles in antitumor immunity, their prognostic value and potential function in TNBC is still unclear.

Transcriptomic data from TCGA-BRCA and TTKRGs were curated to determine the prognostic genes in TNBC and a prognostic model was further established. GSE135565 dataset was used to validate the prognostic model. Furthermore, the differences between risk groups were compared through ESTIMATE, clinical correlation, drug sensitivity, immune checkpoint, tumor microenvironment. GSEA and GeneMANIA analysis were performed to explore the potential mechanism.

Intersection of 1,933 differentially expressed genes (DEGs) and 1,109 TTKRGs yielded 88 candidate genes, and PODN, SEMA7A, GPR34, and COCH were identified as prognostic genes for TNBC. A prognostic model was further successfully established and validated. The model exhibited good predictive performance in both training and validating sets with AUC values all above 0.6. Our studies confirmed the pathological stages were associated with risk scores and there were significant differences in the drug sensitivity, immune checkpoint expression, and tumor microenvironment among different risk groups. The two groups were enriched in pathways of cell cycle and immune regulation and the four prognostic genes were associated with transcription factors such as SP1, MYC, and CTCF.

We constructed a robust prognostic model based on four T cell-mediated tumor killing (TTK)-related genes. Beyond predicting survival, this signature effectively decodes the immunosuppressive tumor microenvironment (TME) in TNBC, characterized by stromal activation, M2 macrophage polarization, and T cell exhaustion. These findings highlight novel immune evasion mechanisms and provide a theoretical foundation for targeting next-generation immune checkpoints and specific stromal-immune crosstalk in TNBC immunotherapy.

Glioblastoma (GBM), the most common and aggressive primary brain tumor in adults, remains a formidable therapeutic challenge. Within the immunosuppressive tumor microenvironment, regulatory T cells (Tregs) have attracted increasing attention for their pivotal role in facilitating tumor immune evasion and sustaining immunosuppression. Through diverse mechanisms, Tregs potently inhibit anti-tumor immunity, thereby driving tumor progression and contributing to therapeutic resistance, which collectively correlates with poor clinical outcomes. This review systematically outlines the biological features and regulatory networks of Tregs in GBM, with particular emphasis on emerging strategies designed to target these cells. We discuss approaches such as Treg depletion, interference with their recruitment, functional reprogramming, and combination immunotherapies. Furthermore, we critically assess the translational progress and clinical limitations of these approaches, including challenges related to target specificity, immune adaptation, and treatment-related toxicities. By synthesizing mechanistic insights with therapeutic prospects, this review aims to inform future directions in precision immunotherapy and inspire multidisciplinary efforts toward effective Treg-targeting regimens for GBM.

Glioblastoma (GBM) is the most malignant primary brain tumor, with treatment resistance tightly linked to the intricate regulation of the tumor immune microenvironment (TME). In recent years, the complement system-especially its central component C3 and its cleavage products C3a/C3aR signaling-has drawn increasing attention for its roles in GBM initiation and progression. This review systematically delineates the expression patterns of C3 in GBM, its regulatory mechanisms, and its connections to key biological processes such as hypoxia, immunosuppression, and angiogenesis. We provide a comprehensive analysis of the potential of targeting C3/C3aR signaling as a novel GBM therapy, including the application of small-molecule antagonists, synergistic effects with radiotherapy, and the prospects for biomarker development based on liquid biopsy. All therapeutic claims are based predominantly on preclinical evidence; clinical translation remains to be validated. By integrating the latest findings, this work aims to offer new perspectives and theoretical support for understanding GBM immune evasion and for the development of precise immunotherapies.