TP53 (Tumor protein P53)

Understanding the biology and clinical impact of TP53 mutations is vital for risk stratification and treatment selection. This review summarises the molecular function of p53, the clinical relevance of TP53 mutations in haematological malignancies, and emerging therapeutic approaches.

In this review, we discuss the genetic evolution of CRC and highlight how emerging functional models, including PDOs and organoid-on-a-chip platforms, bridge the gap between genomic alterations and tumor behavior. We propose that integrating these platforms offers a promising framework for advancing functional precision medicine and improving our understanding of CRC biology.

This multinational registry-based analysis highlights evolving global treatment patterns, supports newer TKIs' effectiveness, and identifies clinical and molecular factors associated with treatment duration.

Initial therapy with 'pemetrexed + carboplatin + tislelizumab' was administered...The RA flare was managed with methylprednisolone 1 mg/kg/day followed by a slow prednisone taper and sulfasalazine. Treatment was switched to 'pemetrexed + carboplatin + bevacizumab'...It may create a potential opportunity for conversion surgery in well-responding patients, enabling long-term disease control. This case underscores the critical importance of highly individualized, multidisciplinary treatment decision-making.

Transcriptomic profiling of CD34+ bone marrow cells revealed unique, homogeneous gene expression patterns, particularly within the AML-like, biTET2, SF3B1, and TP53-complex subgroups. Further integration of multi-omics data may refine MDS classification, improving clinical decision-making and guiding the development of targeted therapies.

DSS exerts anti-RA effects through synergistic interactions of alisol C, myricanone, kaempferol, and mandenol with core targets, modulating oncogenic, metabolic, and inflammatory pathways. This integrative strategy deciphers DSS's polypharmacology and provides a mechanistic foundation for clinical application.

In line with previous reports, this case further suggests that ICPN may represent a common precursor lesion with the potential for divergent differentiation to GB MiNEN. The discordant p53 profiles observed across tumor components may be further explained by clonal evolution and intratumoral heterogeneity.

A 19-gene signature derived from the virtual tumor framework stratified patients most likely to benefit from radiotherapy, which was validated using TCGA data. These results demonstrate the utility of virtual tumors to predict effective therapeutic combinations and present a computational resource for large-scale screening of personalized therapies to guide clinical decision-making in NSCLC patients.

Targeted next-generation sequencing demonstrated high tumor mutational burden (>10 mutations/Mb) and 2 common driver mutations [TP53 (c.853G>A) and TERT (c.-146C>T)]. This is the first report of an HPV-independent cervical SCC with choriocarcinomatous differentiation, supporting a clonal origin with divergent differentiation, and suggesting comprehensive therapies combining immunotherapy and pathway inhibitors for this aggressive cancer.

P2, N=118, Completed, Institut für Klinische Krebsforschung IKF GmbH at Krankenhaus Nordwest | Active, not recruiting --> Completed

The mOS of the EGFR-TP53 co-mutant group who received second-line TKIs combined with platinum-containing double-drug chemotherapy and bevacizumab after the progression of first-line single-drug TKIs was 27.0 months versus 6.0 months compared with those who did not receive second-line therapy (P = .019). In first-line EGFR-TKIs monotherapy in patients with EGFR-TP53 co-mutation, osimertinib was clearly superior to gefitinib. In first-line EGFR-TKIs monotherapy progression, TKIs combined with chemotherapy and antiangiogenesis therapy could prolong patients' survival.

Overall, this integrative analysis suggests that TLXZF may exert its effects on HCC through a synergistic "multi-component-multi-target-multi-pathway" regulatory pattern, primarily involving oncogenic, inflammatory, and survival-related signaling networks. These findings are hypothesis-generating and provide an initial basis for the identification and screening of core bioactive components, key targets, and relevant pathways to support future experimental validation and clinical research.