From Genes to Therapy: Pituitary Adenomas in the Era of Precision Medicine

Abstract

This review presents a comprehensive analysis of pituitary adenomas, a type of brain tumor with diverse behaviors and complexities. We cover various treatment approaches, including surgery, radiotherapy, chemotherapy, and their integration with newer treatments. Key to the discussion is the role of biomarkers in oncology for risk assessment, diagnosis, prognosis, and the monitoring of pituitary adenomas. We highlight advances in genomic, epigenomic, and transcriptomic analyses and their contributions to understanding the pathogenesis and molecular pathology of these tumors. Special attention is given to the molecular mechanisms, including the impact of epigenetic factors like histone modifications, DNA methylation, and transcriptomic changes on different subtypes of pituitary adenomas. The importance of the tumor immune microenvironment in tumor behavior and treatment response is thoroughly analyzed. We highlight potential breakthroughs and innovations for a more effective management and treatment of pituitary adenomas, while shedding light on the ongoing need for research and development in this field to translate scientific knowledge into clinical advancements, aiming to improve patient outcomes.

Genome-Wide DNA Methylation Profiling as a Prognostic Marker in Pituitary Adenomas—A Pilot Study

“…While we located none of the same genes as Silva-Junior et al [ 13 ], Mosella et al [ 14 ], or Hallen et al [ 21 ], we did identify similar signaling pathways (cell junction, metabolic process, and neuronal system development). Interestingly, cluster 2 showed higher regrowth potential compared to the other clusters, and also showed links with the VEGF and Ras signaling pathways, both of which are associated with aggressive regrowth for pituitary adenomas according to a review by Serioli et al [ 35 ], with VEGF as a potential target [ 36 ]. One DMR for cluster 1 was associated with the CREB5 gene, which has previously been associated with the regulation of cell growth and proliferation in glioma stem cells [ 37 ].…”