TP53 mutation

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.

Treatment with low-dose Len in transfusion-independent del(5q) MDS reduced the mutational burden of most genes and did not promote the expansion of preexisting clones or AML progression, especially TP53-mutated clones. Early administration of Len in del(5q) MDS patients without TD may be an effective therapeutic approach with a manageable safety profile regarding clonal evolution.

Ropeginterferon alfa-2b-njft (ropeg), a mono-PEGylated interferon-α, showed efficacy and safety in patients with hydroxyurea-intolerant/resistant essential thrombocythemia (ET) in the phase 3 SURPASS-ET largely conducted in Asia. Ropeg showed efficacy and substantial molecular responses with good overall tolerability across a broad ET population. PharmaEssentia.

P1/2, N=220, Recruiting, Nutshell Therapeutics (Shanghai) Co., LTD. | Not yet recruiting --> Recruiting

Both HPV status and p53 profile can be reliably assessed by immunohistochemistry with substantial agreement. Patients with a mutated p53 profile showed significantly worse survival, irrespective of the mutated profile variant.

This study represents the latest investigation of resistance mechanisms to afatinib in NSCLC patients with nonclassical mutations. The mechanism of resistance to EGFR-TKI in this study was discovered different from that of patients with classical mutations.

Notably, low-dose Capivasertib, an AKT inhibitor targeting tumors with PIK3CA/AKT1/PTEN mutation(s), induced senescence selectively in FUCA2-high LUAD irrespective of PIK3CA/AKT1/PTEN/TP53 mutational status, and its combination with the nutraceutical senolytic procyanidin C1 achieved potent and low-toxicity suppression of LUAD across multiple preclinical models. Together, our results uncover the FUCA2-ErbB3 fucosylation-AKT pathway as a central regulator of senescence and propose a FUCA2-guided drug repurposing strategy for LUAD.