Non-steroidal anti-inflammatory drugs (NSAIDs) interfere with the growth of mammary tumours (Lala et al, 1997;Robertson et al, 1998) and prevent distant metastasis (Hubbard et al, 1988;Khoo et al, 1992) in rodents. The epidemiologic evidence for similar effects in women is limited and inconsistent (Isomäki et al, 1978;Friedman and Ury, 1980;Gridley et al, 1993;Thun et al, 1993;Schreinemachers and Everson, 1994;Harris et al, 1995Harris et al, , 1996Egan et al, 1996).To study the effects of NSAID use on breast cancer risk we carried out a nested case-control study, using the records of the Saskatchewan Cancer Agency (SCA) and data collected routinely by the Saskatchewan Prescription Drug Plan (SPDP), which has provided full or partial outpatient drug coverage to the Saskatchewan population since 1975.To study the effects of NSAID use on breast cancer growth and spread we carried out analyses using the drug exposure histories of the cases and attributes of the stage of their tumours at diagnosis, as assessed by the international tumour-lymph node-metastasis (TNM) system (Spiessl et al, 1992). SUBJECTS AND METHODS Study populationsThe source population was the open population of women aged ≥ 35 years, eligible to receive benefits from the SPDP during 1981 to mid-1995 with no history of cancer since 1970 other than nonmelanoma skin cancer or cervical carcinoma in situ.Subjects entered the source population on 1 January 1981, their 35th birthday, or on the date of immigration to Saskatchewan, whichever occurred latest. Subjects left the source population on 30 June 1995, or on the date of diagnosis of breast cancer, death or emigration, whichever occurred first.The SPDP has provided coverage for outpatient prescription drugs for 94% of the Saskatchewan population (1.01 million people in mid-1991; Rawson et al, 1992). Excluded are aboriginals, military personnel, members of the Royal Canadian Mounted Police, and inmates of federal penitentiaries: they are covered by federal agencies. The accuracy of the identifying and recorded prescription information both exceed 99% (Risch and Howe, 1994).The cases were subjects in the source population who were diagnosed with histologically proven invasive female breast cancer and reported to the SCA. Registration of cancer cases was nearly complete (Parkin et al, 1997). To be in our study, cases must have been eligible to benefit from the SPDP for ≥ 5 years before diagnosis. Hereafter, the date of diagnosis will be designated as the 'index date'. Summary We carried out a nested case-control study to measure the rate ratio (RR) for invasive female breast cancer in relation to nonsteroidal anti-inflammatory drug (NSAID) use. The source population consisted of the female beneficiaries of the Saskatchewan Prescription Drug Plan from 1981 to 1995 with no history of cancer since 1970. Four controls/case, matched on age and sampling time, were randomly selected. Dispensing rates during successive time periods characterized NSAID exposure. RRs associated with exposure during each period we...

To test the hypothesis that tricyclic antidepressant use increases invasive female breast cancer incidence, we carried out a case -control study within the population of female beneficiaries of the Saskatchewan Prescription Drug Plan aged 535 years from 1981 -1995 with no history of cancer since 1970. This agency has provided full or partial coverage for outpatient prescriptions to Saskatchewan residents since 1975. We accrued 5882 histologically proven cases and 23 517 controls, randomly selected from the source population and individually matched on age and sampling time. Heavy exposure to any tricyclic antidepressants was associated with an elevated rate ratio for breast cancer 11 -15 years later (2.02, 95% confidence interval: 1.34 -3.04). Post hoc analyses based on the results of genotoxicity studies carried out using Drosophila melanogaster suggested that the increased risk could be attributed to the use of the six genotoxic tricyclic antidepressants, and not to the use of the four nongenotoxic tricyclic antidepressants. However, our results may have been confounded by the effects of other determinants of breast cancer associated with tricyclic antidepressant use.

Although the association between antidepressant drug use and risk of cancer has received considerable attention in the past years, no work has been done specifically on prostate cancer. We carried out a population-based case -control study to assess the risk of prostate cancer in association with exposure to tricyclic antidepressants (TCAs) and selective serotonin reuptake inhibitors (SSRIs). 7767 prostate cancer cases diagnosed between 1981 and 2000 were accrued through the Saskatchewan Cancer Agency. Saskatchewan Health identified a total of 31 068 male controls who were matched on age and calendar time. Data on exposure to TCAs and SSRIs were compiled from the Saskatchewan outpatient prescription drug database, and covered a period upto 24 years. A positive significant association was found between TCA use and risk of prostate cancer, when exposure took place 2-5 years before diagnosis, with rate ratios of 1.31, 1.58, and 2.42 at the low, medium and high average daily dose levels, respectively. Exposure to SSRIs was not found to be significantly associated with the risk of prostate cancer. TCA use 2-5 years in the past was associated with a small dose-dependent increase in the risk of prostate cancer. Nevertheless, detection bias could have contributed to the observed association.

The aim of this study was to examine the effects of oral and transdermal oestrogen replacement therapy on the risk of colorectal cancer. Data from a nested case -control study, designed to investigate the effect of hormone replacement therapy (HRT) on colorectal cancer were analysed. New cases of colorectal cancer, diagnosed between 1992 and mid-1998 (N ¼ 1197), were identified using the Saskatchewan Cancer Agency cancer registry. Women X50 years of age, eligible for coverage by the Saskatchewan Prescription Drug Plan, were included in the study. Four controls per case were age matched to cases, using incidence density sampling. The outpatient prescription drug plan database was used to ascertain oestrogen prescriptions. Women were classified according to history of transdermal (TDE) and oral (OE) oestrogen use. Conditional logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs). Compared with women who had never used HRT, ORs for o3 and X3 years of TDE use and colorectal cancer were 0.69 (95% CI: 0.43 -1.10) and 0.33 (95% CI: 0.12 -0.95), and for OE use were 0.90 (95% CI: 0.73 -1.01) and 0.75 (95% CI: 0.60 -0.93), respectively. The risk reduction for colorectal cancer with TDE may be greater in magnitude than that which has been reported for oral HRT.

No abstract