Abstract
Prostate cancer is the second most commonly diagnosed cancer in American men over the age of 45 years and is the third most common cause of cancer related deaths in American men. In 2012 it is estimated that 241,740 men will be diagnosed with prostate cancer and 28,170 men will succumb to prostate cancer. Currently, radiation therapy is one of the most common definitive treatment options for localized prostate cancer. However, significant number of patients undergoing radiation therapy will develop locally persistent/recurrent tumours. The varying response rates to radiation may be due to 1) tumor microenvironment, 2) tumor stage/grade, 3) modality used to deliver radiation, and 4) dose of radiation. Higher doses of radiation has not always proved to be effective and have been associated with increased morbidity. Compounds designed to enhance the killing effects of radiation, radiosensitizers, have been extensively investigated over the past decade. The development of radiosensitizing agents could improve survival, improve quality of life and reduce costs, thus benefiting both patients and healthcare systems. Herin, we shall review the role and mechanisms of various agents that can sensitize tumours, specifically prostate cancer.
Highlights
In 2012 it is estimated that 241,740 men will be diagnosed with prostate cancer and 28,170 men will succumb to prostate cancer [1]
The majority of men with newly diagnosed localized prostate cancer may be eligible for active surveillance, surgery, or radiation therapy either alone or in combination with androgen deprivation therapy
This review will focus on radiation therapy, which is a common treatment option for localized prostate cancer
Summary
In 2012 it is estimated that 241,740 men will be diagnosed with prostate cancer and 28,170 men will succumb to prostate cancer [1]. Resveratrol (RSV), a natural polyphenol compound, was shown to enhance prostate cancer cell response to irradiation by 1) inhibiting activation of Akt, 2) enhancing activation of ATM and AMPK pathways, and 3) effecting pathways encompassing p53, p21, and p27, which are associated with early cell cycle arrest Perturbation of these molecules result in an increase in radiation induced DNA damage and apoptosis [148]. Selenite, another naturally occurring compound, can inhibit cell growth and induces apoptosis through p53 Ser-15 phosphorylation and caspase-mediated pathway in LNCaP cells [161] This antiproliferative effect is associated with a decrease in the Bcl-2/Bax expression ratio and a decrease in the ratio of GSH/GSSG (essentially an oxidative state) in LAPC-4 prostate cancer cells. A more concerted effort must be made to bring promising targeted therapeutics to clinical trial in order to determine treatment efficacy
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