Radiation Endocrine Action in Prostate Cancer
Authors: PG Cornes, M Shahidi
Journal: Journal of Clinical Oncology (2000)

Article Tools SPECIAL DEPARTMENTS Article Tools OPTIONS & TOOLS Export Citation Track Citation Add To Favorites Rights & Permissions COMPANION ARTICLES No companion articles ARTICLE CITATION DOI: 10.1200/JCO.2000.18.23.4004 Journal of Clinical Oncology - published online before print September 21, 2016 PMID: 11099341 Radiation Endocrine Action in Prostate Cancer Paul G. S. CornesxPaul G. S. CornesSearch for articles by this author , Mehdi ShahidixMehdi ShahidiSearch for articles by this author Larry L. KestinxLarry L. KestinSearch for articles by this author , Alvaro A. MartinezxAlvaro A. MartinezSearch for articles by this author Show More Royal Marsden Hospital Surrey, United KingdomWilliam Beaumont Hospital Royal Oak, MI https://doi.org/10.1200/JCO.2000.18.23.4004 First Page Full Text PDF Figures and Tables © 2000 by American Society of Clinical OncologyjcoJ Clin OncolJournal of Clinical OncologyJCO0732-183X1527-7755American Society of Clinical OncologyResponse01122000In Reply:We sincerely thank Dr Beitler and Drs Cornes and Shahidi for taking the time to address important issues regarding our article.1 As Beitler implies, high-dose-rate (HDR) brachytherapy clearly offers some enticing radiobiologic and technical advantages. Recent studies have indicated a relatively low alpha:beta ratio in prostate cancer for which hypofractionated HDR brachytherapy would seem ideal.2,3 In fact, we have also begun a prospective study evaluating the use of HDR brachytherapy alone (as monotherapy) for the treatment of low-risk prostate cancer. Since 1999, we have already treated 43 patients using this technique. The preliminary report is currently in press.4Although we believe that the HDR brachytherapy boost is primarily responsible for the improved outcome in our study, treatment of the pelvis in the implant group versus the prostate only in the external-beam radiation therapy (EBRT)-alone group may be a confounding factor, as pointed out in our Discussion. The use of pelvic fields in the treatment of prostate cancer has remained controversial for many years. Although the majority of studies have not demonstrated improved outcome with treating the whole pelvis, some studies have indicated a potential benefit in certain subgroups with high-risk prostate cancer.5 Although a scattered dose to the testicles could possibly cause a reduction in androgen levels, we are confident that slight hormonal changes were not responsible for the difference in outcome between the two treatment groups. According to the thorough study cited by Cornes and Shahidi, the distance from the testis to the lower field border is the most important factor influencing testicular dose.6 The second most important factor is the number of port films obtained. In our study, regardless of whether a whole-pelvis or prostate-only field was used, the inferior field edge was identical for the two treatment groups (1.5 cm inferior to the urethral cone). In addition, port films were consistently acquired at a rate of one film per week per treatment field. Based on the data from Amies et al,6 approximately 0.7 Gy (0.025 Gy × 28 port films) was delivered to the testes via filming for the prostate-only patients, versus 0.5 Gy (0.025 Gy × 20 port films) for the pelvis group. Most importantly, variation in field size is only a minor factor influencing testicular dose. According to the data published by Amies et al, an 8-cm equivalent-square field contributed approximately 1.4% of the relative dose at isocenter to the testicles, versus 2.2% for a 15-cm equivalent-square field. Extrapolating this data for our study, this would mean a testicular dose of 0.93 Gy (0.014 × 66.6 Gy) in the prostate-only group versus 1.01 Gy (0.022 × 46.0 Gy) in the pelvis group. Combining this with the dose received from port films, the prostate-only group received a total of 1.63 Gy, versus 1.51 Gy for the pelvis group. Thus, the prostate-only patients may have received more testicular dose than the pelvis patients in our study. Furthermore, while some studies have indicated reduced androgen levels after testicular radiation, we know of no data demonstrating that the resultant minor fluctuation in hormonal levels translated into an improved clinical outcome. We realize that there is a considerable error margin and a wide range in the estimation of testicular dose from EBRT. Regardless, we are relatively certain that the clinical impact of testicular dose in our matched-pair analysis is negligible. It seems a bit more plausible that the additional 29 Gy (median) in total dose to the prostate (equivalent dose in 2-Gy fractions based on an alpha:beta ratio of 1.5 Gy) was the primary reason for improved outcome with an HDR brachytherapy boost.1. Kestin LL, Martinez AA, Stromberg JS, et al: A matched-pair analysis of conformal high-dose-rate brachytherapy boost versus external-beam radiation therapy alone for locally advanced prostate cancer. J Clin Oncol 18:: 2869,2000-2880, Link, Google Scholar2. Brenner DJ, Hall EJ: Fractionation and protraction of radiotherapy of prostate carcinoma. Int J Radiat Oncol Biol Phys 43:: 1095,1999-1101, Crossref, Medline, Google Scholar3. Brenner DJ: Toward optimal external-beam fractionation for prostate cancer. Int J Radiat Oncol Biol Phys 48:: 315,2000-316, Medline, Google Scholar4. Martinez AA, Pataki I, Edmundson G, et al: Phase II prospective study of the use of conformal high dose rate brachytherapy as monotherapy for the treatment of favorable stage prostate cancer: A feasibility report. Int J Radiat Oncol Biol Phys (in press) Google Scholar5. Stock RG, Ferrari AC, Stone NN: Does pelvic irradiation play a role in the management of prostate cancer? Oncology (Huntingt) 12:: 1467,1998-1472, Medline, Google Scholar6. Amies CJ, Mameghan H, Rose A, et al: Testicular doses in definitive radiation therapy for localized prostate cancer. Int J Radiat Oncol Biol Phys 32:: 839,1995-846, Crossref, Medline, Google Scholar