TP53 (Tumor protein P53)

Integrated clinicopathologic and molecular assessment reclassified most HEPU cases as reactive or clonal, with only 39% remaining idiopathic. Myeloid NGS frequently identifies clonal variants critical for refining HE classification, although results require cautious interpretation within the WHO-HAEM5 and ICC 2022 context.

1 Article types. Original Research.

Sevoflurane demonstrated comparatively weaker effects. Overall, our results indicate that volatile anesthetics may directly influence cancer cell biology; however, their clinical implications require further validation in in vivo and clinical studies.

This, in turn, activates the DAZ-associated protein 2 (DAZAP2)/homeodomain-interacting protein kinase 2 (HIPK2)/tumor protein 53 (TP53) signaling cascade, resulting in enhanced cell cycle progression and increased BRCA cell proliferation. In summary, our findings suggest that chimeric PLEKHB2::FAM168B mRNA may serve as a potential biomarker in BRCA.

This review comprehensively examines the role of ubiquitination modification in HCC and its clinical relevance. Future research directions include the exploration of novel ubiquitination modifications, their interactions with other post-translational modifications, and the development of precision medicine strategies based on multi-omics technologies to improve HCC treatment outcomes.

The mitophagy scoring system serves as a robust prognostic biomarker and predictor of immunotherapy response in HCC, offering insights into tumor heterogeneity and clinical decision-making.

Our study identified key gene-based genotypes (Type II/III) of distinct GEPNEC patients and yielded their prognosis and therapeutic utility.

Survival differed significantly among the three etiological groups (χ2=11.53, P=0.003). AEL is a subtype of acute myeloid leukemia with extremely poor prognosis that is highly associated with TP53 gene abnormalities.

Early integration of tumor volumetry and ctDNA profiling refines advanced PDAC prognosis. The combined TTV-TF score offers greater prognostic value than either parameter alone, to be validated in a larger prospective cohort.

This case suggests that AML harboring rare FLT3-JMD point mutations may exhibit transient dependence on FLT3 signaling and may respond to FLT3 inhibition despite the absence of canonical FLT3 alterations. These findings highlight the potential value of extended molecular profiling and longitudinal genomic assessment to identify potential therapeutic targets and mechanisms of resistance in relapsed AML.

By analyzing plasma DNA from individuals harboring germline TP53 mutations, patients receiving radiotherapy, and liver transplantation recipients, we demonstrate that ctDNA shortening can be distinguished from phagocytosis-associated cfDNA shortening through differences in the amplitude and scale parameters of intra- and inter-nucleosomal components. Moreover, leveraging tumor-related fragmentomic alterations, characterized by increased fragmentation entropy identified through cfDNA size deconvolution, significantly enhances cancer detection.

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.