TP53 (Tumor protein P53)

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.

Furthermore, emerging platforms such as RNA interference (RNAi), messenger RNA (mRNA) therapy, and genome editing offer new opportunities to modulate apoptotic signaling. In this review, we summarize the molecular mechanisms of apoptosis in cancer, discuss targeted therapeutic strategies according to their signaling pathways and developmental stages, and outline future directions for apoptosis-based cancer therapy.

Additionally, co-treatment with the autophagy inhibitor chloroquine (CQ) attenuated MA-induced FTH1 downregulation and rescued MA-induced inhibition of cell viability in MDA-MB-231 cells...Bioinformatics analysis identified key hub genes associated with MA-induced autophagy, including tumor protein p53 (TP53), heat shock protein 90 alpha family class a member 1 (HSP90AA1), AKT serine/threonine kinase 1 (AKT1), mTOR, tumor necrosis factor (TNF), interleukin 6 (IL6), epidermal growth factor receptor (EGFR) and BCL2 apoptosis regulator (BCL2), as well as hub genes related to ferroptosis, such as mitogen-activated protein kinase 3 (MAPK3), RELA proto-oncogene (RELA), epidermal growth factor receptor (EGFR), prostaglandin-endoperoxide synthase 2 (PTGS2), SRC proto-oncogene (SRC), interleukin 1 beta (IL1B), interleukin 6 (IL6), and peroxisome proliferator activated receptor gamma (PPARG). In MDA-MB-231 cells, MA triggered autophagy through p53 upregulation and mTOR signaling inhibition, and induced ferroptosis by reprogramming GSH metabolism and activating the NCOA4-mediated ferritinophagy pathway, lead to FTH1 degradation.

The nomogram based on HER2 status shows promising preliminary predictive performance in predicting pCR. Given the lack of external validation and single‑center design, this model remains exploratory and hypothesis‑generating.

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.

Notably, the combination of TQ and PTX was shown to support a greater senotherapeutic effect. Findings indicated that TQ and PTX acted as senotherapeutic agents in 5-FU-induced senescent CRC spheroids and may have potential as adjuvants to enhance CRC therapy.

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.

This study comprehensively reveals YGJ's pharmacological properties against thyroid cancer, identifying its core targets and multi-pathway mechanisms.