TP53 wild-type

SMILE is often associated with invasive carcinoma and may be a harbinger of neoplasia similar to its cervical counterpart. Close examination is necessary for accurate diagnosis, and further study is warranted to determine the potential benefits of closer follow-up.

Our findings support the Exon Regulon model of MDM2 splicing, regulated by distal elements analogous to distal enhancer elements that control transcription. These finding sheds light on intricacies in the splicing code that could have significant implications for developing splice variant targeting cancer therapies.

Relevant to the sequential inactivation of each p53 allele during cancer progression, the lung cancer mutants block the activity of a wild-type p53 allele when co-expressed in a dominant negative manner. Identification of this loss-of-function mechanism has key implications for therapeutic strategies aimed at restoring p53 function in lung cancer.

UL88 emerged as the most strongly expressed HCMV gene across MB samples. These findings suggest a potential prognostic and therapeutic role for HCMV in MB, warranting validation in larger, prospective cohorts.

Mutations in p53 have been implicated in poor prognosis and reduced sensitivity to 5-fluorouracil (5-FU) treatment in colon cancer...The expression levels of these genes were associated with overall survival in patients with colon cancer. These findings highlight proteomic alterations linked to p53 deficiency and support a proposed model in which differential regulation of specific proteins may be associated with reduced sensitivity to 5-FU, providing a basis for future mechanistic and functional studies.

TP53 DBD-involved alterations define a high-risk subgroup with inferior PFS, particularly in treatment settings using first- or second-generation EGFR-TKIs. Incorporation of TP53 domain-based classification, together with EGFR mutation subtype, may improve risk stratification and help guide treatment planning in EGFR-mutant NSCLC.

The combination enhanced the p53 expression. Our findings elucidate the mechanism underlying this synergistic interaction and underscore the potential of p53 status as a predictive biomarker for identifying patients most likely to benefit from HHT and gilteritinib combination therapy.

Recent progress in small molecule MDM2 inhibitors is discussed, with a focus on non-covalent agents such as rhein-derived anthraquinone analogs, including AQ-101, which demonstrate promising anti-cancer activity with reduced toxicity. These findings support the continued development of non-covalent MDM2 inhibitors as a novel therapeutic approach for cancers involving both wild-type and mutant p53.

Despite significantly prolonged progression-free survival, the mutant IDH1 inhibitor ivosidenib achieved only a 3% response rate in clinical trials, highlighting the need for new therapeutic options for IDH1mut iCCA...The combination of mIDH1 and MDM2 inhibitors synergistically suppressed the proliferation of IDH1wt iCCA cells. Our study delineated a novel mIDH1-MDM2-wtTP53 axis and its potential application of wtTP53 reactivation therapy in IDH1mut iCCA.

Furthermore, we discuss the potential of next-generation selective estrogen receptor degraders (SERDs) and the importance of refining patient selection through robust predictive biomarkers. Driven by molecular insights, endocrine therapy is transitioning from a secondary palliative option into a definitive cornerstone of precision oncology, offering a personalized and effective treatment for patients with advanced or recurrent endometrial carcinoma.

Tumor cell CEBPB expression, up-regulated by TP53 mutation, can increase CTLA4 expression in T cells and negatively affect patient outcomes. These findings suggested a central role of tumor cell CEBPB in shaping an immunosuppressive TME.

Median OS from time of TP53 detection was 0.5 years in high-risk patients, compared to 2.3 years for patients with intermediate risk and 6.3 years for patients with low risk. This scoring system may help refine risk stratification for chronic phase MPN patients harboring TP53 aberrations.