2ND PRIMARY CANCERS FOLLOWING CANCERS OF THE KIDNEY AND PROSTATE IN NEW-SOUTH-WALES (AUSTRALIA), 1972-91

Citation
M. Mccredie et al., 2ND PRIMARY CANCERS FOLLOWING CANCERS OF THE KIDNEY AND PROSTATE IN NEW-SOUTH-WALES (AUSTRALIA), 1972-91, CCC. Cancer causes & control, 7(3), 1996, pp. 337-344
Citations number
32
Categorie Soggetti
Oncology,"Public, Environmental & Occupation Heath
ISSN journal
09575243
Volume
7
Issue
3
Year of publication
1996
Pages
337 - 344
Database
ISI
SICI code
0957-5243(1996)7:3<337:2PCFCO>2.0.ZU;2-G
Abstract
Data from the New South Wales (NSW) (Australia) Central Cancer Registr y for the period 1972-91 were examined to determine the risk of second primary cancers following an initial invasive cancer of the renal par enchyma (ICD-9 code 189.0), renal pelvis (code 189.1), or prostate (co de 185). Eligible cases were restricted to those who had survived for at least two months after diagnosis of the first primary cancer. Expec ted numbers of cancers were obtained by assuming that subjects experie nced the same cancer incidence as prevailed in the corresponding gener al population and applying gender-, age-, and calendar-specific rates to the appropriate person-years at risk. The relative risk (RR) of a s econd primary cancer was taken to be the ratio of observed to expected numbers of second cancers. Following prostatic cancer, there was an o verall deficit of cancers at all sites combined (RR = 0.79, 95 percent confidence interval [CI] = 0.75-0.84), and no site had a significantl y raised RR. Taking this into consideration, there appeared to be a re ciprocal relationship of increased risk of prostatic cancer (RR = 1.7, CI = 1.2-2.3) following an initial cancer of the renal parenchyma and of renal parenchymal cancer (RR = 1.2, CI = 0.8-1.7) after cancer of the prostate. An increased risk of bladder cancer occurred following r enal parenchymal (RR = 3.4, CI = 1.1-8.0, for women only) as well as a fter renal pelvic cancer (men: RR = 8.7, CI = 5.4-13; women: RR = 39, CI = 26-56). A tobacco-related pattern of excess risk was seen after r enal pelvic cancer but not after cancer of the renal parenchyma. These data illustrate that an excess of second primary cancers may reflect shared etiologic factors or increased medical surveillance.