TP53

Where the papers sit

64 papers from the last 6 months study TP53 directly · updated from PubMed 8 Oct 2026

• Molecular Cancer Drug Discovery

  Cancer drug discovery combines molecular docking with synthesis, cell-based cytotoxicity, and apoptosis assays. Natural products, metal complexes, nanomaterials, and engineered peptides are screened against pathways involving p53, Akt/MDM2, GSK3β, BAX, and COP1. Reported endpoints are mainly binding predictions, growth inhibition, ROS, and apoptotic signaling rather than clinical efficacy. The field is moving from broad compound screening toward mechanism-linked validation of candidate agents.

  21 papers · 32.8%

• p53 and Cellular Senescence

  p53-linked senescence and cell-cycle control recur across cancer progression, tissue repair, diabetes, and reproductive disease. Studies examine p21, PTEN/AKT, RUNX1-p53, and unfolded-protein-response pathways that determine whether cells arrest, die, or remain dysfunctional. Exosomes, microneedle patches, pathway-directed compounds, and metabolic agents are being used to modify these outcomes. The work highlights a context-dependent balance between suppressing tumor growth and preserving tissue or β-cell function.

  13 papers · 20.3%

• Ferroptosis in Cancer and Disease

  Ferroptosis research is linking p53, redox balance, and treatment response across cancer and degenerative disease. In breast cancer, p53 suppresses HIF-1α/TFRC-mediated ferroptosis and contributes to doxorubicin resistance, while trastuzumab produces ferroptosis-related changes in HER2-positive organoids. Other studies manipulate Nrf2, SLC7A11, GPX4, glutathione, and ROS to restore or block ferroptosis. Mutant-p53 stabilization and ferroptosis-modulating compounds remain promising but context-dependent strategies.

  11 papers · 17.2%

• Therapy in Acute Leukemia

  Treatment work centers on biologically selected strategies for acute leukemia and related myeloid disease. Selective CK1α degradation, HSP90 inhibition in TP53-mutant AML with ribosomal loss, and the MDM2/MDMX inhibitor ALRN-6924 broaden targeted options. Lower-intensity therapy, ASXL1 status, MRD, and complex karyotype recur as tools for risk and treatment allocation. NTX-301 and CAR-T resistance studies keep epigenetic, metabolic, and immune vulnerabilities in focus.

  9 papers · 14.1%

• Molecular Stratification in Carcinoma

  Carcinoma studies increasingly combine TP53 and other driver alterations with clinical staging to refine prognosis and treatment selection. FGFR3, KRAS, HRAS, and TP53 classification adds only modestly to TNM prediction in urothelial disease, while accessible biomarker testing is emphasized in oral cancer. Targeted MDM2 degradation seeks to restore p53 signaling in Merkel cell carcinoma, and SETD2-mediated metabolic control may improve sunitinib response in renal carcinoma. The evidence remains heterogeneous across tumor types and requires prospective validation.

  7 papers · 10.9%

• Others — Genome Editing and Hereditary Cancer

  Prime-editing studies focus on improving delivery, screening throughput, and replacement of large DNA segments. Engineered extracellular vesicle-like particles and microhomology are presented as ways to expand editing efficiency. A separate clinical report links Li-Fraumeni syndrome with recurrent glioma and chondroblastic osteosarcoma. The cluster therefore has no single research direction beyond its connection to TP53-related genetic disease and engineering.

  3 papers · 4.7%