TP53 (Tumor protein P53)

UPK2 marks a distinct subset of CRCs with poor prognosis, epithelial-mesenchymal transition, micropapillary growth, and squamous differentiation. These findings may affect the development of targeted therapies in precision medicine.

Our new unique mouse model will allow further studies of the effects of Trp53 nonsense mutation in a multi-organ system and serve as a model for the Li-Fraumeni syndrome (LFS). It will also be valuable for preclinical evaluation of novel therapeutic strategies for targeting TP53 nonsense mutations in cancer.

In vitro experiments further demonstrated that ITGB2 knockdown led to inactivation of Akt and ERK signaling and suppression of cell aggressiveness in ER+/HER2- breast cancer cells. ITGB2 gain represents an unfavorable prognostic marker for early recurrence in luminal HER2-negative high proliferative breast cancer, with potential therapeutic implications.

Wnt1-Cre2; Cse1lCRISPR/flox embryos exhibited consistently increased apoptosis at E9.5 in the affected tissues along with an increase in p53 expression. These data together show a previously unknown critical function of CSE1L in neural crest cell survival during development.

This study first demonstrates juglone's anti-OS efficacy via the ROS/PI3K/AKT pathway. In vivo studies confirm potent tumor suppression with short-term safety, supporting its clinical promise for OS treatment.

In patients with Richter transformation, epcoritamab monotherapy showed clinically meaningful antitumour activity, although the investigator-assessed overall response rate was below the alternative hypothesis of 50%, with a safety profile consistent with previous studies. These findings support further investigation of epcoritamab as a potential treatment option for patients with Richter transformation.

Moreover, KMT2A silencing significantly reduced GOF p53, YAP, phosphorylated AKT, and their downstream targets, suggesting that KMT2A may cooperate with GOF p53 to promote HGSOC progression via YAP, AKT, and p21 signaling pathways. In conclusion, our data indicate that KMT2A contributes to HGSOC-associated cellular phenotypes in the OVCAR3 model; however, further studies are needed to clarify its broader role in HGSOC and its potential as a therapeutic target.

Additionally, we explore the potential of targeting these molecules to enhance the efficacy of radiation therapy and improve patient outcomes. Our study contributes to the comprehension of the molecular processes underlying oral cancer and provides insights into the development of novel therapeutic strategies based on personalized medicine.

In the subgroup analysis, SAMD4B mean expression was the highest in the TP53 mutation group, which showed the worst OS. SAMD4B may serve as a novel prognostic biomarker for patients with EC.

Patients with advanced NSCLC and refractory MPE have a poorer prognosis after first-line targeted therapy than those with non-refractory MPE. More aggressive systemic and local treatment approaches may offer better survival benefits in these patients.

Secondary endpoints include patient-reported quality of life (FACIT-Fatigue scale), response rate at 3 months posttreatment (Lugano criteria), local control, relapse-free survival, and overall survival. Exploratory analyses will evaluate financial toxicity (COST-FACIT questionnaire), health care expenditure, late toxicity, and the prognostic value of preradiation metabolic imaging parameters, including metabolic tumor volume, total lesion glycolysis, and maximum standardized uptake value, as well as molecular biomarkers such as TP53, MYC, and Ki-67.

The cooperative GOG 281/LOGS trial showed that trametinib, an MEK inhibitor (MEKi), was significantly more effective than standard-of-care options (including chemotherapy or hormonal therapy) in increasing progression-free survival (median PFS 13.0 months vs. 7.2 months; hazard ratio 0.48, p < 0.001)...Genomic and multi-omic profiling have revealed actionable vulnerabilities and precision oncology approaches. The advent of biomarker-directed trials, molecular subtyping incorporation, and innovative computational strategies is likely to gradually ameliorate therapy selection and, thereby, finally improve long-term outcomes for patients with this complex disease.