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

This observation highlights the potential clinical benefit of repeating NGS even in late stages of breast cancer treatment. Furthermore, NGS may expand our ability to utilize targeted agents in not only early phase but also later phase breast cancer treatment.

KRAS mutations and p-ERK1/2 expression support a potential role of MAPK/ERK signaling in AOT pathogenesis. The absence of PIK3CA mutations despite p-mTOR expression may in part suggest mutation-independent activation of the PI3K/mTOR pathway. The lack of nuclear β-catenin accumulation may suggest that canonical Wnt signaling is less likely to significantly contribute to AOT tumorigenesis. Further studies with larger cohorts and investigations of additional molecules related to these pathways are warranted.

Overexpression of KAT6A or PIK3CA alleviateS the promoting effect of TRERNA1 knockdown on ferroptosis of NSCLC cells. In conclusion, TRERNA1 represses ferroptosis in NSCLC via the KAT6A/H3K23ac/TRIM24-PIK3CA pathway, representing a promising therapeutic strategy for NSCLC.

Collectively, these findings identify E545A as a functionally active and therapeutically consequential PIK3CA variant. Our study expands the current understanding of PIK3CA-driven oncogenic diversity beyond canonical hotspot mutations and underscores the need for variant-resolved stratification to improve the efficacy of PI3K-targeted therapies.

We established a novel lactylation-related risk signature that effectively stratifies CRC patients by prognosis and TME characteristics. By elucidating the crosstalk between metabolic dysregulation, stromal barriers, and immune exclusion, this study provides potential biomarkers and stratified therapeutic strategies-ranging from standard chemotherapy to targeted metabolic and stromal interventions-to optimize precision medicine for CRC patients.

Specific genomic alterations may help stratify immunotherapy outcomes in recurrent or metastatic cervical cancer. The proposed genomic risk model remains exploratory and requires validation in larger, independent cervical cancer cohorts.

Our findings highlight the potential of cisplatin-alpelisib treatment in a subset of HGSOC patients with PIK3CA overexpression, mediated either through gene amplification or transcriptional modulation, reflecting the wider application of alpelisib in PIK3CA-non-mutated ovarian cancer.

This study demonstrates that wogonin acts as a key bioactive constituent of SBG and suppresses GBM progression through AKT1-centered PI3K-Akt pathway inhibition, with rescue experiments supporting a causal contribution of AKT suppression to the observed phenotypes. By integrating multi-omics analysis with functional and rescue-based validation, this work provides mechanistic evidence supporting wogonin as a promising compound for further preclinical evaluation in GBM.

Using clinical samples, we show that the DNAe panel with analysis using DNAe's pipeline detects mutations comparably to the commercial Oncomine-Assay. This paves the way for development of the DNAe panel into a test for the LiDia-SEQ platform.

In survival analysis using the Cox proportional hazards model, the presence of PIK3CA mutations was identified as being potentially associated with adverse prognosis (hazard ratio: 2.73, 95% confidence interval: 1.15-6.49, and p = 0.023). To enhance the prognosis of gynecologic cases, earlier CGP testing to expand the opportunities for GMT and the proactive introduction of PIK3CA-related clinical trials might be crucial.

Treatment of metastatic, castration-resistant prostate cancer (mCRPC) remains clinically challenging due to tumor heterogeneity and resistance to standard microtubule-targeting agents, such as docetaxel and cabazitaxel. The top upregulated proteins, TTLL3, ANAPC7, PIK3CA, ARID4B, and COL16A1, are linked to microtubule dynamics and cell cycle regulation; the main downregulated, namely KDM2B, PTOV1, YWHAQ, PSMB6, and PRKCB, are involved in cell survival, protein homeostasis and mitotic checkpoint control. These findings provide proteomic evidence that (+)-PTC interferes with cytoskeletal protein dynamics and promotes apoptosis in mCRPC and so warranting its further investigation as a candidate anti-cancer scaffold.

In addition, pathogenic germline variants in MITF, NTRK1, and BAP1 were identified in three patients; notably, the NTRK1 germline variant was accompanied by an independent somatic mutation in the same gene. Overall, these findings support liquid biopsy as a valuable approach for molecular profiling of CUP and highlight the critical importance of paired ccfDNA/gDNA analysis, including CHIP assessment, to accurately distinguish somatic, germline, and hematopoiesis-related variants.