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Prostate cancer is a multifactorial disease that mainly occurs due to the accumulation of somatic, genetic and epigenetic changes, resulting in the inactivation of tumor-suppressor genes and activation of oncogenes. Mutations in genes,
specifically those that control cell growth and division or the repair of damaged DNA, make the cells grow and divide uncontrollably to form a tumor. The risk of developing prostate cancer depends upon the gene that has undergone the mutation. Identifying such genetic risk factors for prostate cancer pose a challenge for the researchers. Besides genetic mutations,
many epigenetic alterations including DNA methylation, histone modifications (methylation, acetylation, ubiquitylation,
sumoylation, and phosphorylation) nucleosomal remodelling, and chromosomal looping, have been significantly contributed
to the onset of prostate cancer as well as the prognosis, diagnosis, and treatment of prostate cancer. Chronic inflammation
also plays a major role in the onset and progression of human cancer, via. modifications in the tumor microenvironment by
initiating epithelial-mesenchymal transition and remodelling the extracellular matrix. In this article, the authors present a
brief history of the mechanisms and potential links between the genetic aberrations, epigenetic changes, inflammation and
inflammasomes that are known to contribute to the prognosis of prostate cancer. Furthermore, the authors examine and discuss clinical potential of prostate carcinogenesis in relation to epigenetics and inflammation for its diagnosis and treatment.
LC–QTOF- ESI(+)/MS Metabolomic Profile Analysis Applied to Identify Blood Biomarkers of Benign Hyperplasia and Prostate Cancer
