TP53 mutation

We also discuss methodological advances and limitations in isoform detection at transcript and protein levels, including isoform-specific quantitative reverse-transcription polymerase chain reaction, antibody panels, capillary nanoimmunoassays, and targeted liquid chromatography-tandem mass spectrometry. Comprehensive profiling of p53 isoforms may eventually help refine biological classification and risk assessment, but its clinical utility will depend on assay standardization and prospective validation.

Thereby, we establish the first patient-level single-cell map of ED and provide a curated resource for future work on ED, SDS, and TP53-driven leukemogenesis. Overall, our findings in pre-malignant ED offer a window into early alterations leading to high-risk leukemia.

HMG proteins exhibit context-dependent roles in breast cancer, with HMGA1, HMGB2-3, and HMGN1/4 driving tumors, while HMGA2, HMGB1, HMGB4, and HMGN2 show protective or paradoxical effects. These findings position HMG proteins as both biomarkers and therapeutic targets, particularly HMGA1 in TNBC angiogenesis and HMGN2 in the induction of apoptosis.

© 2026 The Author(s). The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland

uSMTs exhibit a broad morphologic spectrum in LFS, and multiple molecular alterations may drive tumorigenesis, including MED12, FH, TP53, RB1, ATRX, and a novel ACTG2::BRAF fusion. Although some may be incidental, uSMT in this setting appears enriched for atypical morphology, FH deficiency, and aberrant p53 expression, suggesting an interplay between p53 and FH pathways in tumorigenesis.

p53 IHC, particularly using a ≥40% cut-off at 3+ intensity, is an accurate and accessible surrogate for TP53 mutation detection in LUAD patients. This method facilitates rapid molecular stratification, optimal resource utilization and informed prognostic and therapeutic decision-making in routine pathology practice.

Furthermore, static magnetic fields have been reported to increase apoptosis, inhibit proliferation, and may offer a complementary treatment with low toxicity. These findings suggest that magnetic-field-based approaches offer an innovative strategy for GBM treatment.

Importantly, we constructed a nomogram using PDGFA, age, tumor, and node. Furthermore, high PDGFA expression was associated with HNSCC progression through multiple pathways and processes, suggesting PDGFA as a promising target for therapeutic intervention to modulate anti-tumor responses.

Future integration with multi-omics data, radiomics, and artificial intelligence (AI) promises to enhance its clinical utility. Overcoming current hurdles through standardization and technological innovation is essential for its routine clinical adoption.

This study reveals that the R267W variant drives cell cycle dysregulation and malignant phenotypes in lung cancer by disrupting TP53's transcriptional functions. These findings establish a molecular basis for the pathogenic classification of TP53 variants of uncertain clinical significance.

Tumor tissue and serial plasma samples were collected from 15 patients with aUC treated with dose-dense methotrexate, vinblastine, doxorubicin, and cisplatin (ddMVAC). While the NOIR-SS-based assay proved sensitive and informative, limitations include the cost and time required for sequencing, potential temporal discordance between tissue and plasma sampling, and the absence of correction for clonal hematopoiesis of indeterminate potential. Overall, ctDNA profiling using this targeted panel and NOIR-SS suggested the feasibility of sensitive, non-invasive molecular monitoring in aUC, and may have future clinical applicability if validated prospectively in larger cohorts.

It elaborates on the structure and function of p53 and its mutation-induced carcinogenic mechanisms, then focuses on analyzing the research history and clinical translation status of small-molecule drugs (e.g., APR-246), discusses the application prospects of gene therapy and immunotherapy strategies, and introduces emerging therapies based on CRISPR and PROTAC technologies. By integrating the latest research findings, this article aims to provide theoretical basis and directional guidance for the precise development and clinical translation of p53-targeted drugs.