Prostate Cancer: A Continuous Evolutionary Search for Molecular Therapy Targets

Marcia Mashianoke Lekganyane and Lesetja Raymond Motadi

Department of Biochemistry, University of Johannesburg, Auckland Park, Johannesburg, 2050, South Africa

^*Correspondance to: Lesetja Raymond Motadi 

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Abstract:

Prostate Cancer (PCa) is the most frequently diagnosed carcinoma in males and one of the leading causes of death in men around the globe [1]. Recent studies estimate that over a million males are diagnosed with prostate cancer on an annual basis, with approximately 0.3 million prostate cancerrelated deaths per annum. Development of Castration-Resistant Prostate Cancer (CRPC) culminates from over-expression of the Androgen Receptor (AR) gene; mostly through amplification of the AR gene, AR gene mutations and elevated synthesis of androgens in prostate cancer tumors. Advanced CRPC eventually develops to metastatic Castration-Resistant Prostate Cancer (mCRPC) in all patients. On the other hand, TP53 gene has the highest frequency of mutations across all variations of human cancer, with well over 50% of alterations found on various regions of the protein. Missense mutations of p53 frequently result in the loss of wild-type p53 (wtp53) which plays a very vital role in tumour suppression. In prostate cancer, Tp53 is one of the most common mutated or in activated protein which results in cancer development and progression. This review aims to look at progress made to date on both Tp53 targeted therapy in relation to all existing therapy both in clinical trials and those that still at initial phases.

Keywords:

Prostate cancer; Cisplatin; RGX-104; p53; Nutlin-3

Cite the Article:

Lekganyane MM, Motadi LR. Prostate Cancer: A Continuous Evolutionary Search for Molecular Therapy Targets. Clin Oncol. 2019; 4: 1630.