TP53 wild-type

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.

Rescue experiments and xenograft studies further verified this regulatory axis. KDM4D enhances ESCC radiosensitivity through the SRBD1/RPL11/c-Myc/WIP1/CHK1 pathway, highlighting its potential as both a diagnostic biomarker and a therapeutic target.

In this review, we summarize the biological roles of p53, examine how TP53 gene alterations drive therapeutic resistance in myeloid neoplasms, and compare contemporary classification frameworks, including their limitations and proposed refinements. We also highlight standard and emerging therapeutic strategies aimed specifically at TP53-mutated myeloid neoplasms.

Our findings suggest that the effects of thymoquinone may vary depending on the cellular genetic background and are shaped by multidimensional mechanisms under conditions of metabolic stress, and detailed studies on this subject are needed. The online version contains supplementary material available at 10.1007/s10616-026-01009-4.

P2, N=110, Recruiting, Dana-Farber Cancer Institute | N=180 --> 110

Although TP53 mutations are associated with poor prognosis in patients treated with chemotherapy, their adverse prognostic impact appears to be attenuated in the context of CAR-T cell therapy. These findings suggest that CAR-T therapy may partially mitigate the negative impact of TP53 alterations.

An IHC panel incorporating p53, MMR, and β-catenin effectively stratifies EC risk. Nuclear β-catenin identifies a higher-risk subset within the prognostically heterogeneous NSMP group, supporting its integration into routine prognostic protocols to guide adjuvant therapy and surveillance, particularly in resource-limited settings.

This case expands the anatomic spectrum of DEK::AFF2 fusion-associated nonkeratinizing squamous cell carcinoma by demonstrating noncontiguous middle ear and sinonasal involvement. Recognition of its characteristic morphologic, immunophenotypic, and molecular features is essential to avoid misdiagnosis.

uSMTs exhibit a broad morphologic spectrum in LFS, and multiple molecular alterations may drive tumorigenesis, including MED12, FH, TP53, RB1, ATRX, and a novel ACTG2::BRAF fusion. Although some may be incidental, uSMT in this setting appears enriched for atypical morphology, FH deficiency, and aberrant p53 expression, suggesting an interplay between p53 and FH pathways in tumorigenesis.

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.

Although the null pattern has limited PPV for nonsense mutations, its high NPV supports its use in excluding such variants. p53 IHC may serve as a practical and cost-effective approach for inferring TP53 mutation status, particularly in settings where molecular testing is restricted.

Our in vitro findings indicate that TP53 deficiency in B-ALL cells downregulates adhesion networks and impairs immunogenic signaling, which correlates with accelerated CAR-T cell exhaustion. These transcriptomic and cellular observations suggest a potential link between TP53-mediated adhesion loss and CAR-T resistance, warranting further in vivo validation and biophysical investigations.