Review Article
The second most common cause of cancer-related fatalities in men is prostate cancer, which is also the most prevalent non-skin cancer. A lot of patients with prostate cancer display an aggressive disease with metastasis and progression, whereas some patients display an indolent illness with little potential to advance. Intraepithelial neoplasia, androgen-dependent adenocarcinoma, androgen-independent adenocarcinoma, sometimes known as castration-resistant adenocarcinoma, are the three phases of development of human prostate malignancies. Our understanding of the genetic events involved for the onset and progression of prostate cancer has advanced very quickly because to developments in molecular technologies. These investigations have demonstrated that, in comparison to other malignancies, the prostate cancer genome has a comparatively low mutation rate and little chromosomal losses or gains. Prostate cancer pathways saw an accumulation and convergence of genomic and epigenomic aberrations as the disease progressed, creating a highly diverse transcriptome landscape that was dominated by an overactive androgen receptor signalling axis. This review emphasises the present level of knowledge and lists options for reducing prostate cancer morbidity and death.
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