Drivers of Radioresistance in Prostate Cancer.
Liam KingNijole BernaitisDavid Robert Harry ChristieRuss Chess-WilliamsDonna SellersCatherine McDermottWendy DareShailendra Anoopkumar-DukiePublished in: Journal of clinical medicine (2022)
Prostate cancer (PCa) is the second most commonly diagnosed cancer worldwide. Radiotherapy remains one of the first-line treatments in localised disease and may be used as monotherapy or in combination with other treatments such as androgen deprivation therapy or radical prostatectomy. Despite advancements in delivery methods and techniques, radiotherapy has been unable to totally overcome radioresistance resulting in treatment failure or recurrence of previously treated PCa. Various factors have been linked to the development of tumour radioresistance including abnormal tumour vasculature, oxygen depletion, glucose and energy deprivation, changes in gene expression and proteome alterations. Understanding the biological mechanisms behind radioresistance is essential in the development of therapies that are able to produce both initial and sustained response to radiotherapy. This review will investigate the different biological mechanisms utilised by PCa tumours to drive radioresistance.
Keyphrases
- prostate cancer
- radical prostatectomy
- dna damage response
- early stage
- gene expression
- cancer stem cells
- locally advanced
- radiation induced
- radiation therapy
- dna methylation
- papillary thyroid
- randomized controlled trial
- stem cells
- metabolic syndrome
- blood pressure
- adipose tissue
- squamous cell carcinoma
- mesenchymal stem cells
- clinical trial
- blood glucose
- dna damage
- free survival
- young adults
- replacement therapy
- smoking cessation