Meningiomas are a common intracranial neoplasm, accounting for the majority of primary brain tumors. Resection of these tumors is a mainstay of treatment; however, the time to discharge from the hospital might vary depending on patient-level factors. In particular, the relationship between race, socioeconomic status, and hospital length of stay (LOS) in this population remains understudied. The aim of this study was to assess the association between demographic and medical characteristics, social vulnerability index (SVI) scores, and LOS after meningioma resection.

A retrospective review of patients who underwent resection of meningiomas at a single tertiary-care academic institution between 2018 and 2023 was completed. Data pertaining to patient demographics, medical comorbidities, tumor grade, postoperative complications, and LOS were recorded. SVI scores were recorded from the Agency for Toxic Substances and Disease Registry.

Ninety-nine patients (68 female, mean age 62.8 years) were included in the analysis. Self-identified race was Black for 37 patients, White for 20 patients, Asian for 3 patients, and other for 31 patients. Twenty-nine patients were Hispanic. The median overall SVI score was 0.943 (IQR 0.575-0.987). The median hospital LOS was 6 days (3.0-11.0 days). Black race was the only demographic variable associated with a prolonged time to discharge in the multiple linear regression analysis. Postoperative intracranial hemorrhage and pneumonia were the only clinical factors associated with a significantly delayed time to discharge after controlling for confounding factors.

These findings demonstrate that Black race is a significant risk factor for delayed hospital discharge among patients undergoing resection of meningiomas. Due to the increased morbidity and mortality rates associated with prolonged hospital stays, continued efforts to understand the relationship between race, socioeconomic status, and LOS is warranted.

We found epidermal growth factor-containing fibulin-like extracellular matrix protein 1 (EFEMP1) is up-regulated in liver cancer cells exposed to sorafenib for a long time using a bioinformatic tool. Here, the mechanism of EFEMP1 in sorafenib resistance of hepatocellular carcinoma (HCC) cells was explored.

Human HCC cell lines Huh7 and HCCLM3 received low concentrations of sorafenib for a long time to construct sorafenib-resistant Huh7 and HCCLM3 (Huh7-SR and HCCLM3-SR) cells. HCCLM3, HCCLM3-SR, Huh7 and Huh7-SR cells received sorafenib, and the cell viability was assayed by CCK-8 method. HCCLM3-SR and Huh7-SR cells were transfected before sorafenib treatment, and these cells apoptosis was determined with flow cytometry assay. Ferroptosis-related index, EFEMP1, phosphorylated PI3K (p-PI3K), p-AKT level in HCCLM3, HCCLM3-SR, Huh7 and Huh7-SR cells was detected using flow cytometry assay, colorimetry, qRT-PCR and Western blot analysis, respectively.

Following sorafenib treatment, HCCLM3-SR (8/16 μM) and Huh7-SR (4/8/16/32 μM) cell viability was higher than HCCLM3 and Huh7 cell viability. HCCLM3-SR and Huh7-SR cells presented higher IC50 of sorafenib. Following sorafenib (7 μM) treatment, ROS, MDA, TBARS, Fe2+ level in HCCLM3-SR and Huh7-SR cells was lower, and SLC7A11, GPX4, EFEMP1, p-AKT and p-PI3K level in Huh7-SR and HCCLM3-SR cells was higher than those in HCCLM3 and Huh7 cells. Under sorafenib (7 μM) treatment, EFEMP1 silencing promoted apoptosis, up-regulated ROS, MDA, TBARS, Fe2+ level and inhibited SLC7A11, GPX4, p-AKT and p-PI3K expression in Huh7-SR and HCCLM3-SR cells.

Knockdown of EFEMP1 promotes ferroptosis by inactivating PI3K/AKT to resensitize sorafenib-resistant HCC cells to sorafenib.

Isocitrate dehydrogenase 1 (IDH1) mutations are well-established oncogenic drivers in several malignancies, including gliomas and hematologic neoplasms, but are rarely reported in melanoma and remain poorly characterized in this tumor type. Their clinicopathological and molecular significance in cutaneous melanoma is not well-defined. We retrospectively analyzed 9 cases of cutaneous melanoma harboring IDH1 mutations identified by next-generation sequencing from a larger institutional cohort. Clinicopathological characteristics, immunohistochemical profiles (including p16, PRAME, Ki-67, and PD-L1), and associated molecular alterations were evaluated. Eight tumors carried the pathogenic IDH1 p.R132C mutation and one harbored p.V178I. Most cases corresponded to nodular melanomas with epithelioid morphology, increased Breslow thickness (median 2.87 mm), high mitotic activity, and frequent ulceration. Tumor-infiltrating lymphocytes were weak or absent in most tumors. All cases expressed S100 and Melan-A; PRAME was strongly positive in 6 cases, while partial or complete loss of p16 expression was observed in all tumors. PD-L1 expression (tumor proportion score 1%-49%) was detected in 3 cases. Co-occurring mutations in the MAPK pathway were identified in 8 tumors, and 5 cases also harbored TERT promoter mutations (c.-146C>T, C228T). Comparable variant allele frequencies of IDH1 and associated mutations suggest an early oncogenic role. IDH1-mutated melanomas represent a rare molecular subset frequently associated, in this limited series, with established high-risk clinicopathological features. The recurrent coexistence of IDH1 mutations with MAPK pathway and TERT promoter alterations supports a potential cooperative role within melanoma oncogenesis. These findings are descriptive and hypothesis-generating, and further studies with larger cohorts are required to clarify the biological and clinical relevance of IDH1 mutations in melanoma.

Chronic myelomonocytic leukemia (CMML) is a rare myeloid neoplasm characterized by clinical heterogeneity and is associated with poor outcomes. To date, limited molecular information has been incorporated into disease classification and risk stratification. We aimed to integrate genomic features into the clinical decision-making process for CMML.

We analyzed a retrospective cohort of 3013 patients with CMML (training set) and a prospective population of 516 patients (validation set). Using an innovative framework for multimodal data analysis, we developed molecular-based disease taxonomy and prognostication.

Unsupervised clustering identified nine entities with distinct genomic features and outcomes (P < .001), including splicing machinery, transcription factors, signal transduction and tyrosine kinase pathways aberrations, and high-risk molecular signatures. Notably, 15% of patients showed molecular/clinical overlap with other myeloid neoplasms. We integrated molecular and clinical information to build the international CMML Prognostic Scoring System (iCPSS), incorporating mutations in nine genes together with hematologic parameters and cytogenetic abnormalities. The iCPSS identified five groups with distinct probability of overall and leukemia-free survival in both training and validation cohorts (P < .001), outperforming existing prognostic models. Importantly, 55% of patients were reassigned to higher or lower risk groups by the iCPSS. Decision analysis demonstrated that iCPSS could refine the optimal timing of allogeneic transplantation at the individual level; compared with conventional prognostic tools, iCPSS-based decision modeling changed transplantation strategy in 31% of cases, resulting in a significant gain-in-life expectancy for eligible patient population (P < .001). A federated learning platform was implemented to enable continuous, privacy-preserving model update across multiple centers.

Molecular information improves CMML classification and prognostication, supports more effective clinical decision making, and potentially refines the design of clinical trials.

Cancer immunotherapy remains limited by insufficient antigen presentation and immunosuppressive tumor microenvironment. Here, we present a vaccine strategy based on cold atmospheric plasma (CAP)-engineered tumor cell-derived immune reprogramming nanovesicles (CAPTURE) that integrates spatiotemporal sequential immunization to potentiate antitumor immunity. CAPTURE is engineered from tumor cells pretreated with CAP, which up-regulates major histocompatibility complex class I expression via p62-mediated autophagy to promote full-spectrum epitope antigen presentation, and surface-functionalized anti-CD28 (αCD28) on CAPTURE provides costimulatory signals to directly activate T cells through αCD28-CD28, bypassing B7-CTLA-4-mediated T cell inhibition. Under spatiotemporal sequential immunity, CAPTURE exhibits homologous tumor targeting and lymph node accumulation, enhancing antigen presentation for CD8⁺ T cell activation and tumor immunogenic remodeling. In mouse models, CAPTURE achieved near-complete tumor suppression, driven by amplified cytotoxic T cell responses, increased T cell clonal diversity, and CXCR3-mediated tumor infiltration. This study presents a universal biomimetic nanovaccine strategy that can reshape both T cells' immunity and tumor cells' immunogenicity, induce broad-spectrum immune responses to overcome immune evasion, and offer unique insights and innovative technologies for precision cancer immunotherapy.

This study evaluated the effectiveness of the Attitude, Definition, Open mind, Planning, Try it out (ADOPT) nursing model during the perioperative period in patients with esophageal cancer, focusing on self-management efficacy, self-care ability, and symptom clusters. Seventy-six patients undergoing radical resection between November 2024 and September 2025 were assigned to either the ADOPT group or the conventional care group (38 patients each) according different. Both groups received routine perioperative nursing, while the ADOPT group additionally implemented systematic interventions based on the 5 components of ADOPT. Patient outcomes were assessed using the Strategies Used by People to Promote Health, Exercise of Self-Care Agency, and MD Anderson Symptom Inventory scales on day 2 of admission, postoperative day 1, and prior to discharge. Baseline characteristics and surgical parameters were comparable between groups. At discharge, patients in the ADOPT group demonstrated significantly greater improvements in self-management efficacy and self-care ability, as well as reduced symptom severity and functional limitations, compared with the conventional group (P < .05). These findings indicate that the ADOPT nursing model effectively enhances patient self-management and self-care capacity while alleviating symptom burden, providing a systematic and individualized framework to optimize perioperative care for esophageal cancer.

Upper tract urothelial carcinoma (UTUC) is a rare and highly aggressive malignancy primarily occurring in the upper urinary tract, including the renal pelvis and ureter. Despite recent advancements in treatment strategies, the diagnosis and management of this disease remain challenging. This study proposes a systematic bibliometric evaluation of collaborative networks and scholarly impact across national, institutional, individual author, and journal levels within UTUC research. The goal is to evaluate the evolution of knowledge structure clusters and identify trending topics and emerging issues.

A topic-based search strategy was employed to retrieve articles and reviews related to UTUC from the Web of Science core database bibliometric analysis was conducted using Citespace and VOSviewer.

This investigation analyzed 3621 publications spanning 83 countries, where American and Japanese researchers demonstrated the highest productivity. Publications related to UTUC have been increasing year by year. The primary research institutions include the Medical University of Vienna, UT MD Anderson Cancer Center, Kaosiung Medical University, and Université de Montréal. Publication analysis reveals "UROL ONCOL-SEMIN ORI" as the predominant outlet for article dissemination in this field, while citation networks identify "Journal of Urology" as the most influential reference source. The author network encompasses 14,918 researchers, among whom Shariat SF, Rouprêt M, Margulis V, and Lotan Y have shown exceptional productivity, with Rouprêt M achieving particular prominence through co-citation frequency. Through co-citation analysis, a macro sketch and micro characterization of the entire knowledge domain are achieved. Current and developing research areas include FGFR3 mutations, molecular immunotherapy targeting, and tumor localization. "Pembrolizumab," "multicenter," "survival," and "transitional-cell carcinoma" may also represent new trends and focal points for future research.

The analysis reveals a clear trajectory toward more rigorous scientific inquiry in UTUC investigations, with particular emphasis on developing standardized protocols for tumor localization, surgical approaches, and novel treatment modalities. This evolving paradigm reflects the discipline's dedication to advancing therapeutic precision while minimizing risks, suggesting significant potential for subsequent research to refine clinical decision-making and improve prognostic results.

Cytomegalovirus (CMV) and/or Epstein-Barr virus (EBV) infection or reactivation is widely recognized in immunocompromised individuals, particularly those undergoing transplantation or those with acquired immune deficiency syndrome. There are reports of EBV-CMV co-infection or reactivation; however, this co-infection-induced pneumonitis has rarely been seen in patients outside these settings.

A 64-year-old male with previously treated pulmonary tuberculosis, positive hepatitis B surface antigen and a squamous cell carcinoma of the esophagus underwent 5 cycles of concurrent radiochemotherapy with weekly carboplatin and paclitaxel. Following treatment completion, the patient developed reactivated hepatitis B, requiring antiviral therapy initiation. Six weeks after completing radiochemotherapy, the patient experienced fever and dyspnea.

The initial chest computed tomography scan revealed honeycomb-like, triangular, mixed alveolar-interstitial opacification in both lungs. Due to a poor clinical response to empiric antibiotics and negative results for both blood and sputum cultures, a bronchoalveolar lavage sample was obtained and revealed high viral loads of EBV and CMV, suggesting EBV-CMV pneumonitis.

Treatment with ganciclovir and corticosteroids resulted in significant clinical improvement, with marked resolution of lesions observed on computed tomography scans.

The patient was discharged in stable condition. However, 4 weeks later, while still on corticosteroid taper, the patient developed a recurrence of fever that progressed to respiratory failure, and was subsequently diagnosed with respiratory aspergillosis. The patient passed away after 1 week.

This case highlights the importance of suspecting CMV and/or EBV pneumonitis in patients undergoing chemotherapy and no response to empiric antibiotics. Timely detection of causative pathogens is important, as prompt intervention can markedly improve patient outcomes.

This study investigated whether the active ingredients of Pinellia pedatisecta Schott extract (PE) inhibit colorectal cancer (CRC) by targeting the Warburg effect, a common cancer hallmark, and to elucidate the involved mechanism.

The active ingredients of PE were identified by high performance liquid chromatography (HPLC). The efficacy of the beta-sitosterol (BS), baicalein, and guanosine (Guo) combination was then evaluated in vivo. In vitro, cell viability, migration, and invasion capabilities were investigated by CCK-8, scratch assay, and Transwell assays, respectively. Network pharmacology was employed to identify potential targets related to the Warburg effect, which were subsequently validated in vitro.

HPLC identified three active ingredients in PE: BS, baicalein, and Guo. The mice exhibited tumor weight loss and volume reduction after BS-baicalein-Guo treatment. In addition, BS-baicalein-Guo elevated apoptosis of HCT-116 cells, while significantly reducing their proliferation in vivo. Besides, BS-baicalein-Guo diminished glucose uptake, lactate and ATP, as well as the expression of glycolysis-related proteins (HK2 and PKM2) and extracellular signal-regulated kinase (ERK) and epidermal growth factor receptor (EGFR) phosphorylation in HCT-116 cells, while NSC228155 (EGFR activator) ameliorated these phenomena.

The BS-baicalein-Guo combination synergistically alleviates the Warburg effect in CRC by suppressing the EGFR/ERK pathway, highlighting its potential as a therapeutic target.

Desmoid tumours are a locally invasive neoplasm that can exhibit unpredictable clinical behaviour. While treatment options are numerous, few are supported by level 1 evidence. A recent phase 3 trial evaluated the efficacy of long-used pegylated liposomal doxorubicin in patients with progressive desmoid tumours.