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

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.

Anlotinib demonstrated promising responses with manageable toxicity in a heavily pretreated R/M HNSCC population. Integration of genomic and immune microenvironment features may provide hypothesis-generating insights into patient selection.

ctDNA represents a transformative tool in CC care, enabling real-time, tumor-specific insights with broad diagnostic and prognostic implications. Future efforts should focus on prospective validation, integration with imaging and artificial intelligence, and development of cost-effective ctHPV DNA screening panels, particularly for underserved populations.

Epigenetic dysregulation and recent applications of single-cell and spatial transcriptomics highlighted tumour heterogeneity. Despite progress, evidence remains uneven across cancer types, with limited exploration of germline variants beyond colorectal, pancreatic, and select liver cancers.

In a small-sample-size test, the ESEA system achieved 100% sensitivity and specificity in pleural effusion samples (n=5) and a 100% ctDNA detection rate in patients with extracranial lesions and disease progression (n=6). These results highlight its potential as a cost-effective, highly sensitive, and robust platform for dynamic, real-time companion diagnostics, as well as non-invasive monitoring of treatment response and tumor evolution.

Together, these structure-informed alleles show that discrete PI3K structural perturbations can differentially uncouple lifespan, growth, and developmental outcomes in vivo. By combining structural modeling with genome editing in a tractable aging model, this work establishes a framework for dissecting conserved signaling enzymes at single-residue resolution and uncovers unexpected organismal roles for PI3K structure in coordinating growth and longevity.