AKT2 Exon 3 Variants and Their Prevalence in Prostate Cancer Patients: Insights from a Jordanian Clinical Cohort.

The AKT2 gene, located on chromosome 19, encodes a protein involved in key cellular processes like metabolism, proliferation, and survival. Abnormalities in the PI3K/AKT pathway, including AKT2, contribute to tumor progression. AKT2 promotes cell survival, growth, and resistance to therapy. Overexpression or hyperactivation of AKT2 is linked to prostate cancer (PC) development, making it a potential therapeutic target. This study aimed to investigate the frequency and distribution of AKT2 variants in a cohort of Jordanian men diagnosed with PC and to evaluate the relationship between these genetic variations and clinicopathological parameters, including age, tumor stage, PSA levels, and Gleason score. Formalin-fixed paraffin-embedded (FFPE) tissue samples (n = 123) were collected from Jordanian patients diagnosed with prostate adenocarcinoma. The collected samples underwent DNA extraction, followed by PCR amplification. Subsequently, exon 3 of AKT2 was sequenced. The prevalence of AKT2 mutations was 5.7% in the population studied. Six mutations were identified: two missense mutations (Pro51Ser and Gly33Ser), two synonymous, one splice acceptor, and one intron variant. The variants were not significantly correlated with clinical parameters; however, the prevalence of the AKT2 mutations suggests potential relevance to PC pathogenesis. The prevalence of AKT2 mutations in the current cohort suggested a potential role of AKT2 in PC pathogenesis in the Jordanian population. Further genetic studies covering the whole AKT2 gene and the downstream pathway are required for a better understanding of PC genetics.