PTEN mutation

The patient therefore underwent adjuvant carboplatin/paclitaxel chemotherapy followed by vaginal brachytherapy and has remained recurrence-free for five years. This case demonstrates molecular classification of an unusual histological type of EC exhibiting an extremely short-term risk of early distant metastasis and its implication on aggressive adjuvant therapeutical approach. It, furthermore, exemplifies the pronounced heterogeneity of the NSMP subgroup.

P2, N=35, Active, not recruiting, National Cancer Institute (NCI) | Trial completion date: Dec 2025 --> Dec 2026

Clinically significant mutations (KIT: Asp816Val, Ala829Pro; and KRAS: Gln61Leu) suggest potential therapeutic targets for GCT, while MTOR, PIK3CA, and AKT2 emerge as candidates for targeted therapy. These findings provide insights into the genomic alterations of pediatric GCTs and emphasize the potential for targeted therapies.

Together, these findings reveal a critical epigenetic-metabolic axis in EC, wherein NSD1-mediated methylation of PPARγ at K98 orchestrates tumor-suppressive metabolic control via PTEN. These insights not only elucidate a regulatory pathway in EC pathogenesis but also highlight potential therapeutic targets for intervention in metabolically driven tumors.

Additionally, the review addresses key genetic alterations implicated in prostate carcinogenesis, including mutations in BRCA1/2, HOXB13, and PTEN deletions, as well as changes in the androgen receptor pathway. By evaluating recent advancements and applications of these biomarkers, this review aims to enhance understanding of their role in improving early diagnosis, prognosis, and personalised management of prostate cancer.

P1/2, N=30, Suspended, M.D. Anderson Cancer Center | Recruiting --> Suspended

Particular emphasis is placed on delivery technologies, viral and non-viral vectors, including lipid nanoparticles, polymeric systems, inorganic nanocarriers and DNA nanostructures, which are rapidly evolving to improve precision, safety and CNS penetrance. Collectively, this review highlights CRISPR/Cas9 as a powerful tool whose integration with molecular neuro-oncology and precision medicine may ultimately shift GBM treatment toward more personalized and durable therapeutic interventions.

Gene Ontology analysis indicated that SCLC-BM and LCLC-BM were associated with deregulated glial proliferation processes. These findings provide a comprehensive genomic characterization of BM from various lung cancer histologies.

In this article, the genetics and molecular pathogenesis, clinical manifestations, imaging features, and most up-to-date surveillance recommendations of CS are reviewed.

The identification of MLA in atypical locations such as the mesentery and cervical mucosa expands the histologic spectrum of this tumor and provides further support for the hypothesis of a Müllerian epithelial origin. The findings of this study broaden the known morphologic and anatomic distribution of MLA and contribute to a better understanding of its pathogenesis.

These age-specific molecular subtypes correlated with significant survival differences. Our study identifies conserved age-specific molecular subtypes of EC and reveals population-specific genomic features, underscoring the need for age-tailored and ethnicity-aware therapeutic strategies.

This study represents the largest genomic cohort to date of FGFR alterations in GBM, IDH-wt. FGFR::TACC fusion-positive and FGFR1 mutation-positive GBMs exhibited distinct genetic profiles, highlighting the clinical relevance of molecular subclassification and providing insight for future therapeutic strategies.