2ND PRIMARY MALIGNANCIES IN T1-3N0 PROSTATE-CANCER PATIENTS TREATED WITH RADIATION-THERAPY WITH 10-YEAR FOLLOW-UP

Citation
Pas. Johnstone et al., 2ND PRIMARY MALIGNANCIES IN T1-3N0 PROSTATE-CANCER PATIENTS TREATED WITH RADIATION-THERAPY WITH 10-YEAR FOLLOW-UP, The Journal of urology, 159(3), 1998, pp. 946-949
Citations number
21
Categorie Soggetti
Urology & Nephrology
Journal title
ISSN journal
00225347
Volume
159
Issue
3
Year of publication
1998
Pages
946 - 949
Database
ISI
SICI code
0022-5347(1998)159:3<946:2PMITP>2.0.ZU;2-V
Abstract
Purpose: The risk of patients with prostate cancer to have second prim ary malignancies is unclear. Population and autopsy based studies have shown no increased risk, which is at variance with several institutio nal analyses. A retrospective review was performed With comparison to expected cancer data from the Connecticut Tumor Registry. Materials an d Methods: Records of a cohort of prostate cancer patients treated wit h staging pelvic lymphadenectomy and definitive radiotherapy between N ovember 1, 1974 and July 7, 1987 were reviewed. Median potential follo wup from date of diagnosis was 10.9 years. Results: Of the 164 patient s 150 (91.5%) had followup to death or to August 1995, with data avail able in part on 4 of the remaining patients. In 43 patients 51 second primary malignancies developed. Increased frequency of lymphomas, and kidney, bladder and rectal lesions (all p <0.001) was observed concurr ently with diagnosis of prostate cancer, although this may be due to b ias since full staging for the prostate cancer mag have led to their d iagnosis. An increased frequency of renal lesions in the 1 to 4-year f ollowup period (p = 0.032) also was observed. Two sarcomas and a leuke mia were putatively radiation induced but their frequency was not sign ificantly different from the comparison baseline. Conclusions: Much of the apparent increase in second primary malignancies associated with prostate cancer noted by some authors may be attributed to bias in the staging process. Renal cancers may occur more frequently in patients with prostate cancer but the distribution of these lesions is inconsis tent with a field defect mechanism of cancer induction.