TP53 wild-type

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.

These cell lines harbor wild-type p53, which, in response to treatment with doxorubicin or Nutlin-3, promoted the expression of well-known p53 target genes (CDKN1A, MDM2). Treatment with adenoviral vectors encoding canine p14ARF and interferon-β (IFNβ) resulted in cell death with liberation of immunogenic cell death markers in vitro and reduction of tumor progression when subcutaneous tumors in nude mice were treated with in situ gene therapy. These results indicate that adenovirus-mediated delivery of p14ARF and IFNβ is effective in a canine model of oral melanoma, supporting the feasibility of applying comparative oncology approaches to the development of this gene therapy strategy.

While progression in the central nervous system did not impact clinical outcomes in this patient population, the high rate of disease in the central nervous system does warrant consideration and tailoring treatment with central nervous system penetration. This subgroup continues to behave as a distinct population and as such requires unique treatment and treatment strategies.

SMARCA4 restoration or pharmacologic inhibition of p300 suppresses SCCOHT growth, an effect reversed by p53 deletion and accompanied by reactivation of these cell cycle progression genes. Our findings uncover a chromatin-based mechanism whereby SMARCA4 loss subverts p53-mediated transcriptional repression through reprogramming p300 genomic occupancy to sustain oncogenic growth, highlighting p300 as a potential therapeutic target in SCCOHT.

This case demonstrates the diagnostic value of USG-FNAC as a reliable and safe method for confirming metastasis in anatomically challenging locations. Additionally, it emphasises the importance of incorporating molecular profiling and recognising histological features such as squamous differentiation and MELF patterns as markers of aggressive behaviour in a subset of low-to-intermediate grade EC.

Molecular docking predicted a binding affinity of -7.1 kcal/mol, with baicalin occupying the p53-binding pocket of MDM2, whereas the known inhibitor Nutlin-3 showed a docking-predicted binding energy of -7.5 kcal/mol...In vitro assays showed that baicalin inhibited proliferation and induced morphological changes more prominently in MCF-7 cells compared to MDA-MB-231 cells, supporting a possible p53-dependent response. Overall, this study provides computational and preliminary cellular evidence that baicalin may interact with MDM2 and contribute to p53-mediated anticancer activity.

These findings suggest that the prognostic impact of p53 is context-dependent and largely mediated by established clinical factors, particularly tumor burden. Integrated clinicopathologic and molecular assessment remains essential for accurate risk stratification in endometrial cancer.

The combined L1CAM/β-catenin IHC profile categorized patients into prognostically distinct categories and offers pragmatic prognostic refinement, particularly for pMMR/p53wt tumors in centers lacking POLE sequencing. This approach doesn't replace comprehensive molecular testing and requires prospective validation before clinical implementation.

P1, N=24, Active, not recruiting, National Cancer Institute (NCI) | Trial completion date: Jun 2026 --> Jun 2027 | Trial primary completion date: Jun 2026 --> Jun 2027