TMB-H

This molecular signature implies potential synergistic effects between chromatin instability, compromised DNA damage repair mechanisms, and augmented immunogenicity. Through comprehensive genomic analysis, we elucidate the biological significance of this mutational landscape and discuss its therapeutic implications, aiming to advance precision diagnosis and guide innovative treatment strategies for SMARCA4-DNSCLC.

This case highlights the role of genomic profiling test for clinical decision-making as tumor mutational burden predicts the efficacy of immune checkpoint inhibitor therapy in SCCB. This case also underscores the urgent need for novel treatment approaches for SCCB.

The melanocytes in skin from tanning bed users had higher mutation burdens and higher proportions of cells with pathogenic mutations-these differences were most prominent over body sites that experience comparatively less exposure to natural sunlight. We conclude that tanning bed radiation induces melanoma by increasing the mutation burden of melanocytes and by mutagenizing a broader field of melanocytes than are typically exposed to natural sunlight.

Cell experiments revealed that interference of UBE2Q1-AS1 significantly inhibited the proliferation and migration of 786-O cells. The migrasome-associated lncRNA model accurately predicts ccRCC patient prognosis, offering new insights for immunotherapy and clinical applications.

Radiology plays a central role in the management of these therapies, as phenomena such as pseudoprogression challenge the classic RECIST (response evaluation criteria in solid tumors) system, and early detection of immune-mediated side effects often precedes clinical manifestation in imaging. The growing complexity of therapy requires radiologists to possess precise image interpretation, interdisciplinary collaboration, and knowledge of immunological principles, thus, enabling an improved prognosis for many tumor types.

This study systematically reveals that EDCs promote HCC initiation and progression by perturbing cell cycle, metabolic, and immune homeostasis through multi-target, multi-pathway mechanisms. The nine-gene risk model demonstrates superior performance in HCC diagnosis and prognosis and shows potential clinical translational value in drug-sensitivity prediction and pan-cancer analyses. This work provides a new perspective at the intersection of environmental toxicology and precision oncology and informs individualized therapeutic strategies.

Our comprehensive genomic characterization of patient-derived LCOs provides valuable insights into the mutational landscape and evolutionary dynamics of lung cancer. These well-annotated organoid models serve as a powerful resource for investigating tumor biology and developing genomically informed therapeutic strategies.

Research hotspots include multidisciplinary treatment (MDT), diagnostic tumor markers (e.g., CA125, CA19-9, and carcinoembryonic antigen (CEA)), imaging (e.g., MRI, ultrasound), and novel approaches such as immunotherapy and targeted therapy (Microsatellite Instability-High (MSI - H), Tumor Mutational Burden-High (TMB - H). Future directions call for multicenter clinical trials and interdisciplinary collaboration to improve patient outcomes.

Patients with NSCLC and low TPS/high IC scores may benefit more from Nivo+Ipi than from Pembro due to distinct genomic and immunological features, including high TMB and Treg fraction.

Sintilimab failed to improve PFS-6 in both grade 1 and grade 2/3 recurrent/progressive meningiomas in this single-arm, single-center, and small-sample trial. When evaluating PD-1 inhibitor treatment for recurrent/progressive meningioma patients, who generally have a longer expected survival and high TMB, the use of the Immunotherapy Response Assessment in Neuro-Oncology (iRANO) criteria may be more appropriate to avoid overlooking potential clinical benefits.

Palmitoylation-related genes, particularly ZDHHC18, serve as promising prognostic biomarkers and predictive indicators for immune therapy in ccRCC. These findings offer new insights into ccRCC biology and highlight potential therapeutic targets for improving patient outcomes.

Lastly, EBVaGC is more likely to express the PI3K and ARID1A mutations, which can potentially be treated using PI3K/mTOR dual inhibitors and Akt/PARP inhibitors. These six subtypes could aid the selection of more successful treatments for EBVaGC, thereby improving the current overall survival and prognosis of patients.