A self-enhancing Cu-TBAPy MOF was synthesized, which serves as both an electrochemiluminescence (ECL) emitter and a dual coreactant accelerator. It was then employed as an ECL probe to construct a highly sensitive ECL immunosensor for the sensitive determination of the lung cancer marker Cyfra 21 - 1. Benefiting from its rigid framework structure and the spatial confinement of the TBAPy ligand imposed by Cu²⁺ coordination, thermal dissipation of the excited-state energy from the ligand is effectively suppressed, resulting in a strong ECL signal that renders this material suitable as a probe for ECL immunosensors. Moreover, the Cu²⁺ sites within the MOF catalyze the reduction of K₂S₂O₈ at the electrode to produce the coreactant SO₄^•‒. Meanwhile, the MOF exhibits peroxidase-like activity, catalyzing the reduction of H₂O₂ to generate hydroxyl radicals (OH^•), which further react with K₂S₂O₈ to yield additional SO₄^•‒. Through the dual promotion mechanism, the ECL signal of the MOF is substantially enhanced. The Cu-TBAPy MOF was employed as a probe, and secondary antibody‑labeled polydopamine nanospheres (PDA NPs) were introduced as signal regulators in a sandwich immunoassay. The ECL quenching was achieved through the dual effects of ECL resonance energy transfer between PDA and the MOF, combined with the scavenging of hydroxyl radicals by PDA. Based on the changes in the ECL signal, an ultrasensitive determination of Cyfra 21 - 1 was realized, with a linear range from 10 fg/mL to 10 ng/mL and a detection limit as low as 2.04 fg/mL. The sensor has been successfully applied to the determination of Cyfra 21 - 1 in serum samples.

Cutaneous melanoma is a highly aggressive malignancy characterized by marked biological heterogeneity and variable clinical outcomes. Reliable biomarkers for prognostic stratification and biological characterization remain limited. This study aimed to investigate the expression pattern, prognostic significance, immune associations, and functional relevance of Forkhead box M1 (FOXM1) in melanoma.

Multi-omics analyses were performed using TCGA, GTEx, GEO, and Human Protein Atlas datasets. Survival analysis, Cox regression, nomogram construction, functional enrichment, immune infiltration, genomic alteration, and drug sensitivity analyses were conducted. FOXM1 expression was further validated by immunohistochemistry. Functional experiments, including qRT-PCR, Western blotting, CCK-8 proliferation assays, and Transwell migration and invasion assays, were performed following FOXM1 knockdown in A375 melanoma cells.

FOXM1 was significantly overexpressed in melanoma and independently associated with poor overall survival. A FOXM1-based prognostic model demonstrated satisfactory predictive performance. Functional analyses indicated that FOXM1 was primarily involved in cell-cycle progression and mitotic regulation. High FOXM1 expression was associated with an immunosuppressive microenvironment characterized by reduced cytotoxic immune infiltration and altered immune scores. Genomic analysis suggested copy-number amplification as a major contributor to FOXM1 overexpression. In vitro experiments confirmed efficient FOXM1 silencing and demonstrated that FOXM1 knockdown significantly inhibited melanoma cell proliferation, migration, and invasion.

FOXM1 is a prognostically relevant and immune-associated biomarker in melanoma. Its overexpression is associated with aggressive tumor behavior, and functional inhibition suppresses malignant phenotypes, highlighting its potential value for risk stratification and therapeutic targeting.

Early diagnosis of extraluminal locoregional recurrence (LRR) near the anastomosis after surgery for gastrointestinal malignancies is challenging. This study evaluated the diagnostic performance of endoscopic ultrasound (EUS), EUS-guided fine-needle aspiration (EUS-FNA), and an integrated diagnostic pathway in this context.

We retrospectively analyzed patients who underwent EUS at our hospital between April 2014 and April 2025 for suspected extraluminal LRR. We collected clinical, procedural, and pathological data. Each patient had at least 6 months of clinical-imaging follow-up. The final diagnosis was based on pathology (surgical or EUS-FNA) or confirmed disease progression and served as the reference standard for calculating diagnostic performance.

Seventy-seven patients were included. EUS identified suspicious extraluminal lesions in 37 patients; 35 of these underwent EUS-FNA. EUS alone demonstrated a sensitivity of 94.6% (95% CI 81.8-99.3%), specificity of 95.0% (95% CI 83.1-99.4%), and accuracy of 94.8%. The corresponding values for EUS-FNA were 93.9% (95% CI 79.8-99.3%), 100.0% (95% CI 15.8-100.0%), and 94.3%, respectively, while the integrated diagnostic strategy achieved 89.2% (95% CI 74.6-97.0%), 100.0% (95% CI 91.2-100.0%), and 94.8%, respectively. The subgroup analysis showed the high sensitivity of EUS-FNA in all recurrence patterns, tumor types, and anastomotic sites (≥ 83.3%). According to the surgical pathological findings of the primary tumor, the recurrence rate was significantly higher in patients with elevated-risk (57.1% vs 23.8%; OR 4.27, 95% CI 1.38-13.2; P = 0.011), but EUS-FNA still achieved a sensitivity of 92.9%.

Combining EUS with selective EUS-FNA provides an accurate and safe strategy for detecting extraluminal LRR. This approach uses EUS's high sensitivity for lesions and definitive pathology from EUS-FNA, significantly enhancing the accuracy of postoperative surveillance for extraluminal anastomotic LRR.

The global incidence of rectal cancer (RC) is increasing at an alarming rate, with over 50% of cases still diagnosed at advanced stages, despite improvements in early detection. While neoadjuvant (chemo)radiotherapy regimens remain a cornerstone of treatment, up to 20-40% of tumours exhibit or develop resistance to ionising radiation, limiting therapeutic options and leading to disease evolution. This review offers a comprehensive insight into the complex biological and molecular mechanisms underlying RC radioresistance within the fundamental 6Rs of radiobiology: Repair, Reoxygenation, Redistribution, Radiosensitivity, Repopulation, and Reactivation. More specifically, DNA damage repair pathways, cell cycle regulation, hypoxia, transcriptional plasticity regulators such as cancer stem cells, and non-coding RNAs are comprehensively reviewed. Additionally, the critical roles of tumour-infiltrating lymphocytes, cancer-associated macrophages, and inflammatory cancer-associated fibroblasts in radioresistance are also dissected, which collectively shape an immunosuppressive and pro-metastatic niche following radiotherapy. Furthermore, a less explored mechanism, namely the metabolic rewiring of cancer cells after radiotherapy, is proposed as a new 7th R of Radiobiology, namely "Reprogramming", that enables tumour survival and promotes aggressive phenotypes. This new perspective adds a new layer of complexity to the molecular understanding of RC resistance and provides a mechanistic insight currently missing in radiobiology research. Additionally, advanced experimental models, such as spheroids, patient-derived organoids, and animal models, are discussed as valuable platforms for pre-clinical research and therapeutic testing. This review also integrates mechanistic insights with biomarker-guided clinical decision-making to support RC management. By unravelling these multifactorial mechanisms, we highlight opportunities to develop predictive biomarkers and tailored therapeutic strategies to overcome resistance and improve patient outcomes.

Ovarian cancer (OC) is a highly lethal gynecological malignancy owing to late-stage diagnosis, high recurrence and metastasis rate. Spondin-1 (SPON1), a secreted extracellular matrix protein, has been demonstrated to be over-expressed in multiple tumors. However, the carcinogenic mechanism of SPON1 in OC remains unclear. Differential expression analysis was employed to identify SPON1-related genes from public databases. Immunohistochemistry (IHC) was utilized to detect SPON1 protein expression. Kaplan-Meier analysis was applied to evaluate the survival differences. Least absolute shrinkage and selection operator and Cox analysis were used to construct risk model. The C-index, receiver operating characteristic curve, calibration curve and decision curve analysis were performed to evaluate the predictive efficacy. Enrichment analysis revealed biological processes. Additionally, the relationships between risk score and tumor microenvironment (TME), somatic mutations and drug sensitivity were assessed. SPON1 was significantly upregulated in OC samples, and high SPON1 expression was associated with worse survival rate. Then a six-gene risk model was conducted in training set. The prognostic accuracy of model was validated using multiple external cohorts. Functional analysis indicated that multiple cancer progression and immune-related pathways were markedly associated with the risk score. The infiltration levels of most immune cells were decreased in the high-risk subgroup. High-risk patients displayed poor response to common drugs for chemotherapy and decreased tumor mutation burden in OC. In summary, we developed and validated a SPON1-based risk model for predicting the prognosis of OC patients and explored the differences in the TME and response to chemotherapy.

SH3 Domain Binding Glutamate Rich Protein Like 3 (SH3BGRL3) plays a crucial part in regulating tumor necrosis factor (TNF)-induced effects and was involved in the onset and progression of various cancers. However, its role at pan-cancer level remains unclear.

Firstly, SH3BGRL3 expression and its correlation with patients' survival, and other clinical variables were explored in our clinical cohort of 370 kidney neoplasm patients. Subsequently, differential expression analysis, competing endogenous RNA and protein-protein interaction network analysis, correlation analysis with clinical characteristics, tumor purity, gene alteration, immune landscape and signaling pathways were performed to evaluate the role of SH3BGRL3 in pan-cancer. Drug sensitivity analysis, molecular docking and in vitro experiments were also conducted to explore its possible pharmaceutical significance.

In our clinical cohort of kidney neoplasms, SH3BGRL3 was downregulated in tumor tissues (p < 0.001). Higher tumor SH3BGRL3 was linked to decreased overall survival (p = 0.022), advanced stages and was an independent risk factor for progression-free survival (hazard ratio = 2.11, 95%confidence interval = 1.05-4.2, p = 0.037). Further pan-cancer analysis revealed that SH3BGRL3 expression was upregulated in most tumors, and correlated with unfavorable outcomes and advanced tumor stages of various cancers. It was also associated with tumor purity, tumor genomics, tumor immunity, pathway enrichment, and drug sensitivity at pan-cancer level. Dasatinib was found to effectively suppress SH3BGRL3.

SH3BGRL3 was an independent prognostic factor in our kidney neoplasm cohort. At the pan-cancer level, it served as a promising prognostic and immunological biomarker exhibiting cancer-type-specific variations.

Despite advancements in therapeutic cancer vaccines, clinical translation has been hindered by limited efficacy, with Sipuleucel-T remaining the only FDA-approved therapeutic cancer vaccine to date. However, recent advances in personalized mRNA vaccines, such as Moderna's mRNA-4157 and BioNTech's autogene cevumeran, have demonstrated significant reductions in recurrence risk and improved survival across several cancer types, renewing optimism in the field. Personalized cancer vaccines leverage patient-specific tumor antigens to initiate potent and targeted immune responses. This review outlines various classes of personalized vaccines, including DNA-, mRNA-, peptide-, dendritic cell-, and whole-cell-based platforms, and examines the immunological challenges they face, such as tumor heterogeneity, immunosuppressive microenvironments, and inadequate immune memory. To address these limitations, both conventional and nanotechnology-enhanced delivery systems have been developed. Notably, nanovaccines constructed from lipid-polymer hybrids, biomimetic membranes, and stimulus-responsive materials enable codelivery of neoantigens and immunostimulatory agonists, promoting enhanced lymph node targeting, dendritic cell activation, and antigen cross-presentation. Furthermore, biomimetic formulations incorporating autologous tumor membranes preserve native antigenic diversity and allow dynamic adaptation to evolving tumors. When integrated with artificial intelligence for antigen selection and multiomics for patient stratification, these platforms accelerate vaccine design and improve precision. Combination regimens with immune checkpoint inhibitors or other agents further potentiate efficacy and promote durable antitumor immunity. Increasing clinical evidence, especially in melanoma and pancreatic cancer, underscores the potential of these strategies to induce long-term protection and reduce recurrence. Overall, next-generation personalized cancer vaccines are advancing the transition from reactive treatment to proactive, precision-controlled cancer immunotherapy.

Inflammatory myofibroblastic tumour (IMT) is a rare mesenchymal neoplasm of intermediate biological potential, most commonly affecting children and young adults, with the lung being one of the the most common sites. Its variable clinical, radiological and pathological features often mimic malignancy, making diagnosis challenging. We report a middle-aged man in his early 50s presenting with life-threatening haemoptysis and found to have a right main bronchus mass causing central airway obstruction. Emergency rigid bronchoscopy with cryo-debulking was performed for airway stabilisation and tissue diagnosis. Histopathology confirmed IMT. Immunohistochemistry was anaplastic lymphoma kinase negative, while molecular analysis demonstrated ROS proto-oncogene 1, receptor tyrosine kinase (ROS1) positivity, highlighting the molecular heterogeneity of IMT. Following multidisciplinary tumour board discussion, the patient was initiated on targeted therapy with crizotinib, with planned reassessment for surgical resection. This case emphasises the importance of early tissue diagnosis, molecular profiling and multidisciplinary decision-making in achieving personalised and potentially lung-sparing treatment.

Neurofibromatosis type 1-associated diffuse lung disease (NF-DLD) is characterised by upper lobe predominant emphysematous changes and cystic lesions. However, its radiological features are heterogeneous, particularly with respect to the presence or absence of fibrosis. NF-DLD is associated with complications such as spontaneous pneumothorax, pulmonary hypertension and secondary infections, and, although rare, the coexistence of lung cancer has also been documented. We report the case of a man in his 50s with NF-DLD complicated by non-small cell lung cancer with mediastinal invasion. Although the clinical course was complicated by radiation pneumonitis and bacterial pneumonia, the patient achieved a complete response following multidisciplinary treatment, which has been sustained for 10 years. This case highlights a rare but clinically significant presentation with a favourable long-term outcome.