TMB-L

Immunotherapy with atezolizumab (1200 mg every 3 weeks [Q3W]) combined with targeted therapy with bevacizumab (600 mg Q3W) was initiated in July 2021.A substantial temporal gap of approximately 21 months followed, after which electroacupuncture-based rehabilitation (5-Hz continuous-wave, stimulating Jiaji acupoints, Zusanli, etc) was started in May 2023. Targeted immunotherapy combined with electroacupuncture may influence neural remodeling by modulating a pro-reparative inflammatory microenvironment, which could potentially support functional reconstruction in patients with spinal metastases. However, there is no direct evidence that immunotherapy accelerates neural recovery, and these observations should be interpreted as hypothesis-generating findings requiring rigorous testing in prospective studies.

This ADP-ribosylation-based prognostic model reliably predicts LUAD survival and identifies potential biomarkers for tailored therapy.

Multidisciplinary team approaches are essential for individualized care. Future progress depends on biomarker-driven trials, integration of novel strategies such as Chimeric Antigen Receptor T-Cell (CAR-T) therapy, and stronger international collaborative research to improve outcomes in this challenging malignancy.

In summary, the 6 PANoptosis-related lncRNAs can well predict the prognosis of LUAD patients, which may provide new insight for survival prediction and clinical immunotherapy of LUAD patients.

The predominance of PD-L1 negativity together with MSS/low-TMB features suggests a generally immunologically "cold" phenotype in most reported tumors, while exploratory fusion partner-specific enrichment patterns may help refine diagnostic suspicion and generate hypotheses for future biomarker-guided stratification. These findings provide a translational basis for rare-cancer immunobiology research and for the rational design of biomarker-integrated prospective studies.

CT-based radiological features are significantly correlated with TMB status in lung adenocarcinoma. A composite model incorporating these features demonstrates high diagnostic accuracy for identifying high TMB, offering a valuable non-invasive tool for guiding personalized treatment strategies.

We present a case of a 68-year-old woman with metastatic functional PanNET (VIPoma) who developed a treatment-associated hypermutated, microsatellite instability-high (MSIhigh) phenotype following capecitabine-temozolomide (CAPTEM) therapy. Treatment with pembrolizumab resulted in a robust clinical, biochemical, and radiographic response. This case highlights dynamic genomic evolution in PanNETs and underscores the importance of serial molecular profiling in guiding therapeutic decisions.

SMARCA4 restoration or pharmacologic inhibition of p300 suppresses SCCOHT growth, an effect reversed by p53 deletion and accompanied by reactivation of these cell cycle progression genes. Our findings uncover a chromatin-based mechanism whereby SMARCA4 loss subverts p53-mediated transcriptional repression through reprogramming p300 genomic occupancy to sustain oncogenic growth, highlighting p300 as a potential therapeutic target in SCCOHT.

The successful development of immunotherapeutics for GBM requires generating a robust antitumor immune response while overcoming T-cell anergy and tolerance. The immune system has various checkpoint pathways; thus, targeting multiple checkpoints simultaneously will have potential survival benefits.

Whole-exome sequencing revealed low tumor mutational burden (median 1.28 Muts/Mb), recurrent mutations in AK1, ARHGAP39, KRT24, MICAL3, SLC6A9 (27.3%), KRAS, and KMT2C (18.2%), alongside MUC2 copy gain (63.6%) and bidirectional Y_RNA alterations (gain 54.5%/loss 45.5%). Collectively, HPV-associated CPCC represents a distinct and aggressive subtype characterized by distinctive histopathological features, a predominant association with HPV18, frequent presentation at advanced stages, and marked molecular and biomarker heterogeneity.

Despite high cytotoxicity, however, NF-YAx selects a resistant subpopulation with mesenchymal/neural crest stem cell-like identity, unveiling a doxorubicin-induced NF-YAx-dependent resistance mechanism, with potential to influence post-therapeutic relapse and disease progression. Therefore, evaluating alternative NF-YA splicing, and especially NF-YAx expression, in advanced stage and post-therapeutic relapsed NBs, may be of both prognostic and therapeutic significance.

This case represents a rare duodenal MGT confirmed by histopathology and immunohistochemistry, with novel FOXP1 and KDM5A mutations identified for the first time. These findings broaden the molecular spectrum of MGT and highlight the importance of integrating molecular profiling into the diagnosis and management of rare tumors, while surgical resection remains the cornerstone of therapy.