PIK3R2 (Phosphoinositide-3-Kinase Regulatory Subunit 2 )

Clinically, PIK3R2 is significantly upregulated in gastric cancer, with elevated expression levels correlating with poor prognosis specifically in female patients, whereas no significant prognostic association was observed in male patients. These findings underscore the critical role of the ERβ/PIK3R2 signaling axis in estrogen-related gastric cancer, providing a potential therapeutic strategy for this subset of patients.

HNSCC after HSCT typically develops after prolonged latency and shows favorable outcomes with curative therapy. However, recurrence is marked by rapid progression and poor systemic treatment response, underscoring the prognostic relevance of chronic GVHD and the need for novel therapeutic strategies.

The action of L-carnitine against PCOS was mechanistically and pharmacologically implicated with major biological pathways, such as the HIF-1A, PI3K-Akt, and other signaling pathways. These primary predictive biotargets might be used to manage PCOS in the clinical setting after further development.

TLG-5 exerts a therapeutic effect on CAG by regulating β-alanine metabolism, pyrimidine metabolism pathways, and inhibiting the PI3K-AKT signaling pathway and HIF-1 signaling pathways.

FOLFOX (folinic acid, fluorouracil, and oxaliplatin) is a standard first-line therapy for microsatellite stable (MSS) CRC lacking actionable driver mutations; however, its efficacy and genomic impact in EOCRC, particularly in underrepresented groups, remain poorly understood. By integrating clinical, molecular, and treatment variables, the AI-HOPE and AI-HOPE-PI3K platforms enabled rapid, reproducible, and fine-grained analysis of complex datasets. These findings underscore the need for ancestry-informed molecular profiling to optimize therapeutic strategies and highlight AI-guided interrogation as a powerful tool for advancing precision oncology in underrepresented and disproportionately affected CRC populations.

PIK3R2 ectopic expression overcame the cellular effects of CyKILRb downregulation, but not PI 3 K or AKT inhibition orienting the signaling pathway from CyKILRb→↑PIK3R2→PI3K→AKT→↓CyKILRa→enhanced oncogenicity. These findings highlight the critical role of CyKILRb in tumorigenesis and define a novel feed-forward regulatory mechanism linked to alternative RNA splicing.

In patients with UCS, TSC2 loss is linked to poorer PFS, highlighting its utility as a prognostic marker. The association between TSC2 loss and increased recurrence risk highlights the potential therapeutic advantage of targeting the mTOR pathway in TSC2-deficient tumors.

Furthermore, we found that inhibiting the apoptosis-related gene CTTN suppresses the anti-apoptotic capacity of HNSCC. Results from HNSCC-PDOs suggest that CTTN may represent a key target for HNSCC invasion and treatment.

We also observed the upregulation of matrix metalloproteinase (MMP) genes and components of the glycosaminoglycan degradation pathway in glioma cells on the collagen matrix compared with those on HA matrix. This study reveals the effect of collagen and HA on glioma cells at the transcriptional level and contributes to the understanding of potential targets for therapy.

Our results reveal a distinct mutational profile in Saudi CRC patients, characterized by novel and enriched somatic variants affecting key oncogenic pathways. These findings underscore the necessity of including underrepresented populations in cancer genomics to support globally equitable precision oncology.

Notably, in vivo studies further indicated that either silencing circSCAP or co-administering the PIK3R2 inhibitor SAR-260301 with platinum significantly improves treatment efficacy in resistant TNBC models. These findings establish circSCAP and SCAP-129aa as promising biomarkers and potential therapeutic targets for overcoming platinum resistance in TNBC.

The DNAm episignatures of MAPK10, PLCG1, PLCβ3 and PIK3R2 have a significant influence on radon-induced lung cancer. This brings a new perspective to understanding the pathways involved in radon-induced lung cancer and offers potential targets for developing blood-based biomarkers and epigenetic therapeutics.