International Clinical and Medical Case Reports Journal (ISSN: 2832-5788) | Volume 4, Issue 8 | Case Report | Open Access
Houhong Wang*
Department of General Surgery, The Affiliated Bozhou Hospital of Anhui Medical University, China
*Correspondence to: Houhong Wang
Fulltext PDFThe phosphatidylinositol 3-Kinase (PI3K) pathway is a key regulator of cell survival, proliferation, and metabolism, and its dysregulation is frequently observed in Gastric Cancer (GC). This retrospective study aimed to systematically evaluate the expression profiles, clinicopathological associations, and prognostic significance of PI3K pathway components in GC using data from the PubMed database. We analyzed 42 eligible studies published between 2016 and 2024, involving 7,856 patients. Results showed that PI3K overexpression/activation was detected in 46.8% of GC cases (95% Confidence Interval [CI]: 42.1%-51.5%). PIK3CA mutations were identified in 18.3% of patients (95% CI: 15.2%-21.4%), with hotspot mutations in exon 9 (E545K) and exon 20 (H1047R) accounting for 62.7% of total mutations. PI3K pathway activation was significantly associated with advanced TNM stage (Odds Ratio [OR] = 2.53, 95% CI: 2.06-3.11, P < 0.001), lymph node metastasis (OR = 2.78, 95% CI: 2.25-3.44, P < 0.001), and poor differentiation (OR = 2.19, 95% CI: 1.80-2.66, P < 0.001). Moreover, PI3K overexpression predicted shorter overall survival (Hazard Ratio [HR] = 1.76, 95% CI: 1.51-2.05, P < 0.001). In patients receiving PI3K inhibitors, PIK3CA mutation status was associated with a higher objective response rate (34.2% vs. 16.5%, OR = 2.61, 95% CI: 1.87-3.64, P < 0.001). These findings highlight the PI3K pathway as a critical oncogenic driver and potential therapeutic target in GC.
Houhong Wang. Retrospective Analysis of Phosphatidylinositol 3-Kinase (PI3K) Pathway in Gastric Cancer. Int Clinc Med Case Rep Jour. 2025;4(8):1-4.