although individual treatments provided benefits, their combined use enhanced therapeutic outcomes through modulation of oxidative stress, inflammation, and androgenic activity in BPH management.
Through integrated multi-omics analysis, we established that oxidative stress pathways may drive pNET progression through a coordinated mechanism involving metabolic reprogramming (via BCL2L1 and PHGDH downregulation), immune microenvironment remodeling (through altered dendritic cell and NK cell function), and complex regulatory networks. BCL2L1 and PHGDH represent potential diagnostic biomarkers and candidate therapeutic targets that require experimental validation, providing new directions for precision medicine in pNET.
In the xenograft study, tumor size, body weight, and organ weight were significantly attenuated by the test drugs compared with the standard cisplatin. KRAS and ERK2 are components of EGFR-associated signaling pathways. Hence, acenocoumarol and silodosin can be further explored as repurposed candidates in future preclinical and clinical studies.