Our study aimed to examine why individuals withdraw from genetic testing for breast and ovarian cancer susceptibility. We explored the characteristics of 334 individuals from high-risk breast and ovarian cancer families who declined genetic testing for BRCA1/2 mutations, when, and why they did so. Individuals who declined genetic testing were older, and a greater proportion had never developed breast or ovarian cancer. Fifty one per cent (51.1%) of individuals withdrew after the first genetic counseling session. Most of those who declined were afraid of the psychological effects of genetic testing (36.3%). The next most-cited explanations concerned logistic problems such as a limited ability to travel, lack of time, personal issues, advanced age, or health problems (21.7%). The third category included individuals who did not see any advantage in being tested (14.5%). Insurability was a concern (5.9%), mainly for men. Surprisingly, confidentiality was not a frequently reported issue (1.3%). Sixty eight per cent (68%) of individuals belonging to a family in which at least one individual has been tested withdrew after the presence of a deleterious BRCA1/2 mutation in a relative was disclosed, compared to 42% after the disclosure of a nonconclusive test result in at least one relative. Concern about the psychological effects of the result was still one of the major reasons. Several factors may influence an individual's decision to decline genetic testing; a greater understanding of these issues may help health professionals to better meet the needs and concerns of individuals from high-risk families, thus possibly improving their health outcomes.

Emerging evidence opens new possibilities to improve current breast cancer mammography screening programs. One promising avenue is to tailor mammography screening according to individual risk. However, some factors could challenge the implementation of such approach, specifically its potential impact on the equitable delivery of services. This study aims to identify the barriers and facilitators to the equitable delivery of services within a future integration of a personalized approach in the Québec screening program. We then propose different means to address them. We conducted 16 semi-structured interviews with stakeholders with a role in the management, implementation or assessment of the Québec screening program. The barriers and facilitators identified by respondents were regrouped in two themes: 1) Reproduction of social inequities, and 2) Amplification of regional disparities in access to services. We consider that fostering inclusion through communication strategies and relying on electronic communication technologies could help in addressing these issues.

After 3 h of incubation at room temperature, hydroxyFlutamide, the active metabolite of Flutamide (Eulexin), and Casodex (bicalutamide), an analog of Flutamide, have comparable potency to displace [3H]R1881 from the human prostate and rat ventral prostate androgen receptors contrary to the previous claims that Casodex was four times more potent using different incubation conditions. Binding data, in fact, must be interpreted with caution, since they are very much dependent upon the duration and temperature of incubation. In the more appropriate intact cell situation, hydroxyFlutamide is approximately three times more potent than Casodex at inhibiting dihydrotestosterone-stimulated proliferation of androgen-sensitive mouse Shionogi carcinoma cells in vitro. Under in vivo conditions, in the orchiectomized rat supplemented with androstenedione implants, Flutamide is about three times more potent than Casodex at inhibiting ventral prostate and seminal vesicle weight. When both compounds were administered for 7 days to intact rats, Flutamide and Casodex showed similar apparent potency. However, taking into account the much higher plasma levels of testosterone and dihydrotestosterone in intact animals treated with Flutamide compared with those treated with Casodex, the estimated potency of Flutamide in the intact rat is also at least three times higher than that of Casodex. The present data, contrary to previous claims based upon the inappropriate intact rat model clearly show that Flutamide is at least three times more potent than Casodex in rat and mouse tissues.These data are opposite to those obtained in the inappropriate intact rat model where Casodex was reported to be five to ten times more potent than Flutamide. Using more appropriate models of androgen action, the present data thus indicate a 15-to 30-fold lower estimate of the potency of Casodex. Since the choice of the dose of Casodex to be used for the treatment of prostate cancer patients is based upon such a large overestimate of the true potency of Casodex, the present data should help the choice of a more appropriate dose of this antiandrogen for the treatment of prostate cancer.

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