PTEN mutation

To investigate therapeutic options, we utilized patient-derived xenograft (PDX) and tumoroid models established from PDX tumors derived from UDEC patient samples to evaluate everolimus (an mTOR inhibitor) and palbociclib (a CDK4/6 inhibitor), alone and in combination. In a clinical cohort of 29 UDEC patients, higher survivin expression showed a trend toward shorter overall and progression-free survival, supporting its role as a prognostic biomarker. These findings highlight dual PI3K/AKT/mTOR and CDK4/6 inhibition as a promising strategy for UDEC and demonstrate the translational value of PDX and tumoroid models in aggressive gynecologic cancers.

In thymic lymphomas expressing Grb10, enhanced interferon signaling and Pten mutations, along with activation of the PI3K-AKT-mTOR signaling pathway, were suggested to promote cell proliferation and survival. These results suggest that extensive genomic deletions caused by high-LET carbon-ion irradiation may contribute to carcinogenesis by altering the expression of multiple genes located in the deleted region.

Both lines displayed undifferentiated iPSC morphology, robust expression of undifferentiated iPSC state markers, trilineage differentiation capacity, normal karyotypes, and validated PTEN variants. These iPSC lines provide a patient-specific platform for studying PTEN-associated developmental and signaling abnormalities.

Tumour Immune Dysfunction and Exclusion analysis suggested that individuals with high-risk scores are not suited for immunotherapeutic intervention. Based on bioinformatic analyses, this research offers a novel framework for the classification and therapeutic direction of EEC.

The combination of genetics and MRD allows accurate identification of adult Ph- ALL patients candidates to alloHSCT or chemotherapy. The trial was registered at www.ClinicalTrials.gov: NCT04179929.

Understanding their shared and divergent mechanisms aids risk stratification, individualized therapy, and improved quality of life. Further prospective studies are needed to optimize patient-specific management and translate mechanistic insights into clinical practice.

This study identified uric acid-related genes as potential independent indicators of clinical outcomes in glioblastoma progression. A novel prognostic UARG-associated signature was developed and validated, which showed potential in predicting GBM patient outcomes.

Our analysis demonstrates that genomic alterations in PTEN, TP53, or RB1 are not only prognostic for poor outcomes but are also associated with a unique, immunologically complex TME in this Brazilian cohort.

The introduction of immune checkpoint inhibitors (anti-PD-1/PD-L1) has revolutionized first-line treatment, but second-line options remain largely dependent on older chemotherapies such as docetaxel or pemetrexed...Innovative strategies are under investigation: antibody-drug conjugates (anti-TROP-2, anti-CEACAM-5), cancer vaccines (TEDOPI), external electric fields (TTFields), oncolytic viruses, and PROTACs. While some of these show promise in progression-free survival, global survival benefit remains modest. The identification of robust predictive biomarkers is essential for tailoring future therapies.

TP53 mutations were more prevalent in males (p = 0.03) and associated with squamous cell carcinomas (p = 0.007), whereas EGFR mutations were more common in females (p < 0.001) and associated with lung adenocarcinomas (p = 0.029). Our findings suggest that a high TMB combined with a heterozygous HLA-I genotype serves as an effective biomarker for predicting the efficacy of immunotherapy in Chinese patients with NSCLC.

P1, N=39, Active, not recruiting, National Cancer Institute (NCI) | Trial completion date: Sep 2026 --> Dec 2026

Our machine-learning algorithm accurately recognized the over-elongated PTENG132D/WT gastruloids and morphological reversal with AKT inhibitor treatment. Our data suggest a potential link between the mutant PTEN allele-specific early developmental alterations and the clinical outcomes of PHTS, and provide a platform for pathogenic mutation and drug screening.