PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha)

While A-1331852 was cytotoxic yet weakly immunogenic, its combination with OT-55 enhanced DAMP release, increased CD8⁺ effector functions, and, with PD-1/Tim-3 blockade, achieved local and distant tumor control with low toxicity. These findings identify OT-55 as an immunogenic adjuvant converting tolerogenic BH3 mimetic-driven apoptosis into ICD, providing a proof-of-concept immunogenic treatment for myelomonocytic AML.

Our findings support a monoclonal origin for ASC, with smoking influencing divergent evolutionary trajectories and immune microenvironment characteristics between ACC and SCCC. These insights provide a molecular framework for personalized ASC therapies.

Given the challenges in diagnosis and the potential for rapid recurrence or metastasis, early detection is crucial. Comprehensive genomic profiling is highly desirable, as genomic analysis may direct the development of targeted therapeutic agents to treat relapse.

Continuous oncogene expression was required for lesion maintenance, as doxycycline withdrawal reversed the proliferative phenotype, indicating a dynamic and reversible process...These findings demonstrate that identical oncogenic signals-HPV16 E6/E7 expression and PI3K activation-produce distinct premalignant outcomes depending on epithelial context. This work highlights the critical role of local microenvironmental factors in HPV-driven carcinogenesis and provides a platform to identify tissue-specific therapeutic vulnerabilities in HPV-associated cancers.

ER-negative and triple-negative effusions demonstrate more aggressive molecular features including enrichment of TP53 mutations and earlier effusion development. Effusion-based molecular testing yields clinically relevant genomic information in advanced breast cancer.

Western blot experiments further verified that shikonin modulated the expression of core target proteins and suppressed the HIF-1 signaling pathway. This study systematically elucidates the pharmacological mechanism of shikonin against renal cell carcinoma, providing a theoretical basis for the development and application of shikonin as a novel anti-RCC agent.

By seamlessly bridging real-world pharmacovigilance with advanced structural biology and single-cell transcriptomics, this study delineates the comprehensive safety landscape of capivasertib. Our findings provide crucial clinical alerts for AE monitoring and offer deep mechanistic insights to optimize personalized therapeutic management in breast cancer.

Overall, alpelisib combined with capecitabine demonstrated modest antitumor activity in a molecularly selected subset of patients with metastatic colorectal cancer. However, frequent treatment-limiting toxicities may limit the future clinical applicability of this regimen and highlight the need for improved toxicity management and optimized patient selection.

Molecular-risk stratification and integrated modeling identify clinically meaningful prognostic groups in CRLM. These findings support incorporation of genomic profiling into precision surgical and transplant evaluation, while emphasizing the need for prospective validation.

Using our RCA protocol, we detected mutant circRNAs derived from the TP53 gene in EVs from the plasma of ovarian cancer-bearing animals. In this study, we present a new model of mutant circRNA amplification from EVs, which may provide a basis for a diagnostic test for ovarian cancer patients.

Alpelisib plus paclitaxel was tolerable and pharmacologically feasible with a defined RP2D but showed limited efficacy in PIK3CA-altered GC.