TMB (Tumor Mutational Burden)

This study delineates the expression landscape of LSMRGs in GC and clarifies their associations with molecular subtypes, prognosis, and immune regulation. The findings provide novel prognostic biomarkers and a molecular basis for targeting lipid-soluble signaling pathways in GC therapy.

This work set up a prognostic model for LUAD based on 8 MDRGs, pinpointing promising biomarkers and targets for LUAD treatment.

The revised tumor burden score (rTBS) provides a clinically actionable, cost-effective tool to enhance prognostic stratification in patients with metastatic colorectal cancer (mCRC) receiving immunotherapy. By integrating routinely available metrics (CEA, metastatic organ count, and target lesions), rTBS achieves superior prognostic discrimination (AUC = 0.768) compared to traditional biomarkers such as TMB (AUC = 0.656) and consistently stratifies outcomes across molecular subtypes. Of particular clinical relevance, rTBS identifies patients with more favorable prognosis within the MSI-L/MSS/TMB-Low subgroup, addressing a major unmet need in this biomarker-limited population. It also refines risk stratification in MSI-H/TMB-High patients by identifying those with high tumor burden and poor prognosis. By leveraging readily accessible clinical and imaging data, rTBS circumvents the need for costly molecular profiling, bringing pragmatic risk stratification within reach even in resource-constrained settings. These findings position rTBS as a useful decision-support tool for prognostic evaluation, assisting clinicians in personalizing management strategies for mCRC.

Polymorphism co-occurrence patterns indicate a relatively low mutational burden, with epigenetic dysregulation and oncogenic signaling representing central mechanisms in iCCA development. Further large-scale studies integrating tissue and circulating DNA analyses are warranted to validate these findings and identify clinically actionable biomarkers in iCCA.

In vivo xenograft experiments confirmed that DSTN knockdown significantly inhibited HNSCC tumor growth. In conclusion, this study demonstrates that DSTN is a key driver promoting the malignant progression of HNSCC; high DSTN expression indicates poor prognosis, while its downregulation exerts tumor-suppressive effects through multiple mechanisms, including inhibiting the secretion of MMPs, suppressing glucose metabolism, blocking the Wnt/β-catenin signaling pathway, and inducing disulfidptosis.

However, current standard of care treatments such as surgical resection, radiotherapy, temozolomide, and tumor treating fields have reached a therapeutic plateau, highlighting the urgent need for new therapeutic strategies...We further synthesize recent advances in spatial and longitudinal profiling technologies to describe the dynamic tumor immune ecosystem. We discuss how spatial compartmentalization and evolutionary processes collectively drive immune escape and therapeutic resistance, and highlight emerging strategies including adaptive immunotherapy, precision targeted delivery, and multimodal monitoring to overcome these challenges.

In our analysis of post-MPN AMLs, we identified nine mutated loci across six genes (JAK2, IDH1/2, TP53, SRSF2, U2AF1) and linked these mutations to specific transcriptional phenotypes. Overall, LOTR-Seq provides novel insights into the evolution of post-MPN AML.

Future directions emphasize next-generation ICIs, optimized combination regimens, and AI-driven biomarker integration to achieve durable, personalized treatments. This review underscores the potential of immunotherapy to redefine TNBC management while highlighting the imperative for continued innovation to address unmet clinical needs.

This study reveals aberrant TRIP13 expression across multiple cancers and its association with immune modulation and tumor aggressiveness. The elevation of TRIP13 in palbociclib resistant prostate cancer, together with the regulatory E2F1-TRIP13-HECTD3 axis, highlights its potential as a prognostic biomarker and therapeutic target.

The expression level of YKT6 was correlated with tumor-infiltrating immune cells in breast cancer. It may offer potential value for the treatment of breast cancer patients.

Crucially, to bridge the translational gap between computational inference and clinical reality, we emphasize the mandatory integration of orthogonal ex vivo validation (e.g., patient-derived organoids and microphysiological systems). Ultimately, by transforming static spatial snapshots into testable dynamic trajectories, this computation-experiment closed-loop aims to generate actionable insights and prioritize rational combination strategies safely under expert oversight.

PTEN loss occurred frequently (59% 12/22 mice), and contributed to osteosarcomagenesis, as demonstrated by tumor initiation with in vivo CRISPR/Cas9-mediated deletion experiments (2 mice). Together, these results demonstrate that a preclinical model of osteosarcoma can generate the genomic heterogeneity and complexity of the human disease, thereby facilitating research into mechanisms of tumor initiation and drivers of progression and relapse.