Lymph node metastasis (LNM) is frequent in patients with thymic neuroendocrine neoplasms (T-NENs), but detailed studies on metastatic patterns remain limited. This study integrates surgical, imaging, and pathologic data to characterize nodal spread, providing reference data to optimize lymph node dissection (LND) and radiotherapy planning.

Patients with pathologically confirmed T-NENs at our institution were included. Medical records were reviewed to obtain patient characteristics, treatment modalities, failure patterns, and survival outcomes. These data were subsequently analyzed.

Between September 2008 and December 2022, 72 patients (55 males, 17 females; median age 55 years, range 25-70 years) were included. Pathologic subtypes comprised typical carcinoid (TC, n = 9), atypical carcinoid (AC) (n = 50), and neuroendocrine carcinomas (NEC) (n = 13). During a median follow-up of 53 months, cumulative lifetime nodal involvement (including baseline and recurrence) was observed in 67 patients (93.06%). Cumulatively, the most frequently involved stations were right lower paratracheal (51.39%), left perijugular (47.22%), and subcarinal (43.06%), with additional, less frequent involvement at other stations. The cumulative LNM rate was 100% in TC, 92.00% (46/50) in AC, and 92.31% (12/13) in NEC. The median progression-free survival was 23 months, and the 5-year overall survival was 63.31%.

This study summarizes detailed patterns of LNM and highlights the importance of locoregional treatment. The findings provide a reference for defining the extent of surgical dissection and designing radiotherapy clinical target volumes (CTV), and a basis for future prospective studies.

Chemotherapy-induced neutropenia is a frequent complication in patients with cancer that can lead to severe outcomes like sepsis, hospitalizations, and treatment delays. A neutropenic sepsis care bundle was implemented in an.

At diagnosis and throughout treatment of acute myeloid leukemia, oral leukemic infiltrates from malignant blast cell invasion and mucosal ulcerations (i.e., mucositis as a side effect of antineoplastic therapy) are common. Ma.

The mutant isocitrate dehydrogenase 1/2 inhibitor (mIDHi) vorasidenib was recently incorporated into clinical treatment guidelines for IDH-mutant gliomas, although its impact on chemoradiation is unclear. Specifically, it is unknown whether upfront mIDHi exposure alters subsequent chemoradiation efficacy. Addressing this critical question has been challenging because of limited clinical data and a paucity of mIDHi-responsive preclinical glioma models. We first established that a genetic mouse model of IDH-mutant astrocytoma developed by our group was responsive to vorasidenib monotherapy. We then used this mouse to address whether mIDHi alters the response to chemoradiation after progression on mIDHi. Mice that received upfront vorasidenib followed by chemoradiation at progression had improved survival compared with control mice receiving vehicle followed by chemoradiation. We then compiled real-world data and early outcomes from 29 patients who were among the first to receive mIDHi followed by radiation with or without chemotherapy. Our study directly addresses uncertainty surrounding therapy sequencing that has emerged after introduction of vorasidenib as a first-line treatment for IDH-mutant glioma. Our empirical preclinical data demonstrate that prior mIDHi treatment enhances chemoradiation sensitivity of IDH-mutant glioma.

Single-cell-level resolution tumor therapy represents an advanced strategy against glioblastoma but lacks suitable theranostic agents. Here, we developed a spatiotemporal-switchable, two-dimensional (2D), bismuthene-based second near-infrared window (NIR-II) nanozyme. In this platform, the bismuthene scaffold simultaneously directed the assembly of indocyanine green (ICG) into ordered J-aggregates and anchored monodispersed platinum (Pt) atoms. The resulting J-aggregates acted as an optical antenna with a long-wavelength absorption peak at 895 nanometers and high photobleaching resistance of 78.0%, enabling the identification of single tumor cells with a resolution of 44.3 micrometers at 1350 nanometers for precise glioma resection. Postoperatively, the spatiotemporal-switchable function was activated for therapeutic intervention, in which the photothermal effect amplified the original efficiency of the catalase-like activity of Pt atoms by threefold, driving a surge in intracellular oxygen to combat tumor hypoxia. Upon 808-nanometer irradiation, the induced oxygen release in the tumor microenvironment amplified ICG-mediated photodynamic therapy, and combined with bismuthene-mediated photothermal therapy, it effectively inhibited residual tumors. In an orthotopic glioma mouse model, this approach minimized recurrence and achieved increased survival without inducing neurological or motor deficits. This work provides an atomic-level and molecular-level design blueprint for NIR-II nanotheranostic agents, paving the way toward clinical translation of single-cell-level precision medicine for brain malignancies.

Conventional receptor-targeted fluorescent probes have shown promise in tumor imaging, yet achieving a high tumor-to-normal (T/N) tissue ratio in vivo remains challenging due to limited biomarker density on tumor cell membranes. Here, we present an in situ assembly strategy of bioorthogonal-functionalized chimeric artificial receptors (BCARs) that locally constructs BCARs on tumor surfaces, which amplify fluorescence signals and enable high-contrast imaging. Rapid, selective membrane engineering under physiological conditions increases effective receptor density, enhancing fluorophore binding and tumor visualization. Mechanistic studies reveal that BCARs exhibit exceptional membrane retention and spatial precision, sustaining signal amplification in heterogeneous tumor microenvironments. In air-pouch and orthotopic bladder cancer models, BCARs notably improve the T/N imaging ratio and tumor boundary delineation. Translational validation with surgical specimens from 14 patients with bladder cancer confirms clinical feasibility. This work establishes a versatile platform for on-site receptor reprogramming and signal amplification, offering a powerful tool for high-contrast tumor margin detection.

Therapeutic resistance remains a major challenge in cancer treatment, driven by compensatory signaling and stress response pathways that sustain tumor survival. Topoisomerase IIβ-binding protein 1 (TopBP1), a multifunctional scaffold protein with nine BRCT domains, integrates replication stress signaling with oncogenic networks and is frequently overexpressed in aggressive cancers. Its BRCT7/8 domains mediate critical interactions with E2F1, mutant p53, MIZ1, PLK1, and CIP2A, making TopBP1-BRCT7/8 an attractive therapeutic target. Using docking-guided screening and structure-activity relationship-driven optimization, we developed CS18 as a potent and selective BRCT7/8 inhibitor that disrupts oncogenic TopBP1 complexes without interfering with DNA replication. CS18 suppresses MYC transcriptional programs, restores E2F1-mediated apoptosis, and induces mitotic catastrophe. It exhibits broad-spectrum anticancer activity and synergizes with poly(ADP-ribose) polymerase (PARP) inhibitors in multiple cancer types and enhances osimertinib sensitivity in EGFR-mutated non-small cell lung cancer (NSCLC) cells. CS18 demonstrates efficacy in patient-derived breast cancer xenografts and overcomes osimertinib resistance in refractory NSCLC in vivo. These findings establish CS18 as a chemically distinct TopBP1 inhibitor with translational potential to overcome therapeutic resistance and advance precision oncology.

Background and objectives Drug resistance and off-target toxicity remain major challenges in cancer therapy. Due to rapid proliferating nature of malignant cells, microtubule-targeting agents (MTAs) are widely used for chemotherapy, although their clinical efficacy is often limited by drug resistance and adverse effects. Objective of this study was to identify a novel therapeutic agent capable of selectively targeting microtubules in cancer cells while minimising toxicity to normal cells. Present study evaluates the chemotherapeutic potential of Vibrio cholerae haemagglutinin protease (HAP) as a novel MTA for gastric and colon cancers by investigating its role in microtubule degradation and apoptosis induction. Methods Effects of HAP were evaluated in human gastric and colon cancer cells using cellular and molecular assays. Time-dependent live-cell imaging was employed to assess HAP internalisation and co-localisation within intracellular organelles. Explant cultures derived from human tumour tissues were used to replicate the tumour microenvironment and validate therapeutic responses. Results HAP treatment activated protease-activated receptor 1 (PAR1), which is overexpressed in malignant cells, leading to an increase in intracellular reactive oxygen species (ROS) and facilitated HAP internalisation. Once internalised, HAP induced microtubule degradation through four mechanisms: ROS-mediated degradation of MAP2 and tau, destabilising microtubule network; enhancing tubulin-PARKIN interaction, enabling microtubule ubiquitination; and activation of lysosomal and proteasomal pathways to degrade microtubules. Collectively these events triggered apoptotic cascades in cancer cells and explant tissues, while normal healthy cells remained unaffected. Interpretation and conclusions HAP demonstrates strong potential as a selective anticancer therapeutic by inducing microtubule degradation and apoptosis without compromising viability of normal cells.

Massage is widely used in cancer survivors. However, formal assessment of potential harms is lacking. The aim of this study is to assess harms related to massage.

This systematic review and meta-analysis included studies that compared massage with control conditions, in people with- and/or receiving treatment for cancer. The primary outcome was adverse events. Ten databases and trials registries were searched up to 22 October 2024. Quality of adverse events reporting was assessed as adherence to the CONSORT statement extension for reporting of harms. Studies reporting on adverse events were assessed for risk of bias using the PEDro scale (randomized controlled/ cross-over trials) and ROBINS-I (quasi-experimental and cohort) and were eligible for meta-analysis (random-effect). The study was registered at PROSPERO (CRD42023352993).

Sixty-three intervention studies were included, of which 53% (n = 34 studies) did not report on adverse events. Twenty-nine studies (n = 2699) reported on adverse events explicity and/or as study discontinuation. Of these, no studies assessed deep massage, with most interventions using light massage. Meta-analyses indicated no evidence of a higher risk of adverse events related to massage compared to usual care/attention control. Three cohort studies (n = 1406) were included, two of which (both with critical risk of bias) found significant associations between massage over tumor site and negative survival outcomes, in patients with osteosarcoma. Overall, the quality of adverse events reporting was poor, and certainty of evidence considered very low.

Results indicate that light to moderate intensity massage in people living with- and/or receiving treatment for cancer can be performed without increased risk of harms. Contraindications for massage should be applied as per the general population. Due to uncertainty as to whether massage over tumor in osteosarcoma constitutes an increased risk of negative survival outcomes, massage directly on tumor is discouraged, though definitive evidence is lacking.

Diffuse large B-cell lymphoma (DLBCL) is the most prevalent form of non-Hodgkin lymphoma, exhibiting significant molecular and clinical heterogeneity. Advances in classification integrating phenotypic, genetic, and transcriptomic features have improved diagnosis and prognosis. However, a comprehensive and integrated molecular characterization of DLBCL cell lines is still lacking, which limits their optimal use as reliable experimental models. We employed fluorescence in situ hybridization, immunohistochemistry, and targeted DNA and RNA sequencing to identify genetic subtypes and determine the cell of origin, providing a comprehensive characterization of 29 DLBCL cell lines through the integration of phenotypic, genomic, and transcriptomic data. Principal component analysis, gene set enrichment analysis (GSEA), differential expression profiling, and regulon analysis enabled us to dissect molecular heterogeneity. We achieved high concordance in genetic subtype assignment using multiple classification algorithms (2-S, LymphGen, and DLBclass). The DHIT/DZ signature and transcriptional profiling further revealed additional molecular complexity. Some DLBCL-NOS cases exhibited high-grade features, suggesting that gene expression signatures may capture biological aggressiveness better than cytogenetic methods. GSEA confirmed the relevance of signaling pathways across DLBCL subtypes, and regulatory network analysis identified specific transcription-factor activities that support these pathways. MCD cell lines showed increased NF-κB and STAT signaling, while EZB/MYC+ cell lines demonstrated increased proliferation and cell cycle regulation, along with decreased NF-κB/STAT activity. Our study offers a detailed molecular overview of DLBCL cell lines, underscoring their relevance for mechanistic and therapeutic research. The data highlights how integrating genetic and transcriptomic analyses can refine disease classification and guide personalized therapy strategies.