C Alberti1. 1. L.D. of Surgical Semeiotics, Parma, Italy. eneide94@gmail.com.
Abstract
OBJECTIVES: Though the external beam radiation therapy is a standard treatment option for both organ-confined and regionally advanced prostate cancer, unluckily, despite more and more effective advances in radiation delivery procedures, the prostate cancer radioresistance still occurs in a significant amount of patients undergone radiotherapy. This review aims to highlight the molecular aberrations of prostate cancer cell growth- and apoptosis signaling pathways that might induce, together with both prostate cancer cell/cancer stem cells gene- and surrounding microenvironment crucial implications, the tumor radioresistance. METHODS: An up-dated review of several thorough studies on such matter. RESULTS: The plenty of intriguing knowledge acquisitions about the prostate cancer radioresistance depending on cancer cell growth/ apoptosis signaling pathway-related molecular aberrations together with prostate cancer cell/cancer stem cell abnormal gene profile, may be the premise leading--on the basis of preclinical research in animal models--to clinically overcome the tumor radioresistance. CONCLUSIONS: Current developments of radiosensitizer agents focusly targeting prostate cancer cell radioresistance-associated specific molecular/gene aberrations are directed to improve, by implementing customized tumor radiosensitization modalities, the radiation therapy outcomes.
OBJECTIVES: Though the external beam radiation therapy is a standard treatment option for both organ-confined and regionally advanced prostate cancer, unluckily, despite more and more effective advances in radiation delivery procedures, the prostate cancer radioresistance still occurs in a significant amount of patients undergone radiotherapy. This review aims to highlight the molecular aberrations of prostate cancer cell growth- and apoptosis signaling pathways that might induce, together with both prostate cancer cell/cancer stem cells gene- and surrounding microenvironment crucial implications, the tumor radioresistance. METHODS: An up-dated review of several thorough studies on such matter. RESULTS: The plenty of intriguing knowledge acquisitions about the prostate cancer radioresistance depending on cancer cell growth/ apoptosis signaling pathway-related molecular aberrations together with prostate cancer cell/cancer stem cell abnormal gene profile, may be the premise leading--on the basis of preclinical research in animal models--to clinically overcome the tumor radioresistance. CONCLUSIONS: Current developments of radiosensitizer agents focusly targeting prostate cancer cell radioresistance-associated specific molecular/gene aberrations are directed to improve, by implementing customized tumor radiosensitization modalities, the radiation therapy outcomes.
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