TP53 (Tumor protein P53)

The senescence-ferroptosis-related genes TP53, HIF1A, and CDKN2A demonstrated potential as diagnostic and prognostic biomarkers in HCC. The developed nomogram may support individualized prognostic assessment and inform early diagnostic and therapeutic strategies in patients with HCC.

CCNG1 protein may promote TP53 degradation. When TP53 is downregulated, hepatocyte apoptosis increases significantly, resulting in atypical RILD.

As a result, three repurposed drugs were identified as priorities: (i) mefloquine (reference drug: vorasidenib citrate), (ii) clofibric acid (reference drug: carmustine), and armillarisin A (reference drug: lomustine). These results also suggest repurposing candidates for synergistic combinations across different brain tumors. The two applications developed in this work are freely accessible and in the public domain at https://assay.smallmoles.com/escorwin.

P1, N=26, Active, not recruiting, University of Chicago | Trial completion date: Dec 2025 --> Dec 2027 | Trial primary completion date: Dec 2025 --> Dec 2027

P2, N=17, Active, not recruiting, National Cancer Institute (NCI) | Trial completion date: Jan 2026 --> Jan 2027

Co-administration of the immune checkpoint inhibitor αPD-L1 further improved therapeutic efficacy. These findings suggest that targeted tumor starvation probes boost radiosensitivity and anti-tumor immunity, and this strategy shows improved efficacy in combination with αPD-L1 therapy.

In conclusion, this multicenter study suggests that most MS are of myelomonocytic/monoblastic origin, a high proportion of them are NPM1 mutated, and may lack expression of MPO and CD34. NPM1 mutation-specific antibodies should be integrated into the diagnostic panels for MS or LC, while IRF8 and PU.1 are not recommended as they cannot distinguish MS from histiocytic neoplasms.

In particular, the dynamic interplay between tumor cell metabolic reprogramming and the immune suppressive tumor microenvironment, collectively termed the "metabolic-immune axis", constitutes a major challenge underlying drug resistance. This review summarizes how this axis, through mechanisms such as enhanced glycolysis and abnormal amino acid/lipid metabolism, influences bladder cancer progression and treatment responsiveness, thereby establishing a theoretical framework for future research directions.

In summary, this study identifies STAT3, TP53, and MMP9 as central mediators of BaP-induced progression along the Correa cascade via a synergistic regulatory network. These findings provide new insights into environmental gastric carcinogenesis and highlight potential therapeutic strategies, including dual STAT3/MDM2 inhibition or MMP9 blockade.

P2, N=100, Not yet recruiting, Peking University People's Hospital

Common CHIP mutations, including TET2, TP53, and SF3B1 mutations, were not associated with risk of incident RA when restricted to those with most complete general outpatient and hospital record follow-up in the UK Biobank.

Cell cycle analysis showed 71.82% of cells in the G0/G1 phase and it decreases further, confirming cell cycle arrest. These findings demonstrate that M. tridentata extract exerts potent anticancer activity by inducing apoptosis and inhibiting proliferation in HepG2 cells.