Risk Of Advanced Cancer Research Articles

Breast cancer risk characteristics of women undergoing whole-breast ultrasound screening versus mammography alone.

There are no consensus guidelines for supplemental breast cancer screening with whole-breast ultrasound. However, criteria for women at high risk of mammography screening failures (interval invasive cancer or advanced cancer) have been identified. Mammography screening failure risk was evaluated among women undergoing supplemental ultrasound screening in clinical practice compared with women undergoing mammography alone. A total of 38,166 screening ultrasounds and 825,360 screening mammograms without supplemental screening were identified during 2014-2020 within three Breast Cancer Surveillance Consortium (BCSC) registries. Risk of interval invasive cancer and advanced cancer were determined using BCSC prediction models. High interval invasive breast cancer risk was defined as heterogeneously dense breasts and BCSC 5-year breast cancer risk ≥2.5% or extremely dense breasts and BCSC 5-year breast cancer risk ≥1.67%. Intermediate/high advanced cancer risk was defined as BCSC 6-year advanced breast cancer risk ≥0.38%. A total of 95.3% of 38,166 ultrasounds were among women with heterogeneously or extremely dense breasts, compared with 41.8% of 825,360 screening mammograms without supplemental screening (p<.0001). Among women with dense breasts, high interval invasive breast cancer risk was prevalent in 23.7% of screening ultrasounds compared with 18.5% of screening mammograms without supplemental imaging (adjusted odds ratio,1.35; 95% CI, 1.30-1.39); intermediate/high advanced cancer risk was prevalent in 32.0% of screening ultrasounds versus 30.5% of screening mammograms without supplemental screening (adjusted odds ratio,0.91; 95% CI, 0.89-0.94). Ultrasound screening was highly targeted to women with dense breasts, but only a modest proportion were at high mammography screening failure risk. A clinically significant proportion of women undergoing mammography screening alone were at high mammography screening failure risk.

Volumetric breast density and risk of advanced cancers after a negative screening episode: a cohort study

BackgroundWe evaluated the association between volumetric breast density (BD) and risk of advanced cancers after a negative screening episode.MethodsA cohort of 16,752 women aged 49–54 years at their first screening mammography in the Florence screening programme was followed for breast cancer (BC) incidence until the second screening round. Volumetric BD was measured using fully automated software. The cumulative incidence of advanced cancer after a negative screening episode (including stage II or more severe cancer during the screening interval - on average 28 months - and at the subsequent round) was calculated separately for Volpara density grade (VDG) categories.ResultsBC incidence gradually increased with the increas in BD: 3.7‰, 5.1‰, 5.4‰ and 9.1‰ in the VDG categories 1–4, respectively (p trend < 0.001). The risk of advanced cancers after a negative screening episode was 1.0‰, 1.3‰, 1.1‰, and 4.2‰ (p trend = 0.003). The highest BD category, compared with the other three together, has double the invasive BC risk (RR = 2.0; 95% CI 1.5–2.8) and almost fourfold risk of advanced cancer (RR = 3.8; 95% CI 1.8–8.0).ConclusionBD has a strong impact on the risk of advanced cancers after a negative screening episode, the best early surrogate of BC mortality. Therefore, our results suggest that screening effectiveness is quite different among BD categories.

Changes in mortality and incidence of prostate cancer by risk class in different periods in Italy: the possible effects of PSA spread.

In Italy, the spread of prostate-specific antigen (PSA) testing varies in different areas. A peak of incidence was reached in 2003-2004 in some areas, while in others the incidence is still increasing. Mortality has declined since 1999 in some areas, while it remains stable in others. We compared mortality and the risk of advanced cancer over 2 periods (1996-1998; 2005-2007) and by geographic area characterized by a different spread of PSA, to understand the possible impact of PSA on the epidemiology of prostate cancer. In 8 Italian Cancer Registries (CRs), 4,632 cases diagnosed over 2 periods, 1996-1998 and 2005-2007, were sampled to assess risk class. The CRs were classified into late and early phase of PSA testing depending on whether an incidence peak had been reached by 2008. Incidence by risk class was estimated based on overall incidence in each CR and on risk class distribution in the sample. We calculated standardized mortality (MRR) and risk class-specific incidence rate ratios (IRR) to compare the 2 periods. Incidence increased from 1996-1998 to 2005-2007 (IRR 1.5; 95% CI 1.4, 1.6). High-risk and metastatic cancer incidence decreased only in late-phase areas (IRR 0.78; 95% CI 0.69, 0.88; and 0.40; 95% CI 0.30, 0.54, respectively), while in early-phase areas, incidence remained virtually stable (IRR 1.2; 95% CI 1.0, 1.4; and 0.77; 95% CI 0.59, 1.0, respectively). Mortality decreased only in late-phase areas (MRR 0.81; 95% CI 0.85, 0.97; vs 1.1; 95% CI 0.92, 1.2) in early-phase areas. Mortality reduction and a decrease in high-risk and metastatic cases occurred simultaneously only in areas in late phase of PSA spread.

Use of aspirin, but not other non-steroidal anti-inflammatory drugs is associated with decreased prostate cancer risk at the population level

The cyclooxygenase 2 (COX-2) enzyme overexpression in prostate cancer has led to the hypothesis that COX-2 inhibition may reduce prostate cancer growth. Some previous studies have linked the usage of COX-2 inhibiting non-steroidal anti-inflammatory drugs (NSAIDs) with a decreased prostate cancer risk. We estimated the association between cumulative COX-2 inhibition by NSAID usage and prostate cancer risk at population level.All new prostate cancer cases in Finland during 1995–2002 and matched controls (24,657 case–control pairs) were identified from national registries. Detailed information on medication purchases was obtained from a national prescription database. A total cumulative COX-2 inhibition value was calculated based on total cumulative mg amount of each NSAID drug and the drug-specific COX-1/COX-2 inhibition ratio. Prostate cancer risk was analysed with propensity score-matched conditional logistic regression model.In total, 53.8% of the cases and 46.5% of the controls had any prescription-use of NSAIDs, while 8.1% and 7.9%, respectively, had used aspirin. Compared to the non-users, any NSAID use was associated with an elevated overall prostate cancer risk (46.4% versus 53.6%, respectively; odds ratio [OR] 1.3, 95% confidence interval [CI] 1.3, 1.4) and risk of advanced cancer (11.8% versus 14.1%; OR 1.6, 95% CI 1.5, 1.8). The risk remained elevated despite the amount of cumulative COX-2 inhibition. In a separate analysis, the risk increase was similar for each NSAID with the exception of aspirin, which was associated with a decreased overall prostate cancer risk (OR 0.90, 95% CI 0.84, 0.96) in a dose-dependent fashion.NSAID use is associated with an increased prostate cancer risk at the population level regardless of the COX-2 inhibition. This may be explained by systematic differences between prescription NSAID users and non-users. In contrast, aspirin use is associated with a decreased overall prostate cancer risk. Further studies on aspirin and prostate cancer will be needed.

Abstract B107: A pooled analysis of 14 prospective cohort studies on the association between red meat, poultry, fish, and egg intake and risk of prostate cancer

Abstract Background: Findings from epidemiological studies that have examined the association between intakes of red meat, poultry, fish and eggs and prostate cancer risk are inconsistent. Methods: We examined the associations of these dietary factors with risk of prostate cancer in an international collaboration of 14 cohort studies. The primary data from each study were analyzed using standardized criteria for the exposure and outcome variables. During the follow-up ranging from up to 10 to 22 years across studies, 51,896 incident prostate cancer cases were identified among 806,969 participants. Of these, 5,061 cases were advanced stage cases (equivalent to T4, N1 or M1 or fatal). The majority of advanced cases (n=3,692) were fatal cases. There were 37,006 low-grade cases (defined as Gleason score &amp;lt;8 or well/moderately differentiated) and 9,414 high-grade cases (Gleason score&amp;gt;=8 or poorly differentiated/ undifferentiated). A Cox proportional hazard model was used to calculate multivariate study-specific relative risks (RR) and then these results were pooled employing a random effects model. Results: Higher unprocessed red meat and processed meat intakes were not associated with a substantially increased risk of prostate cancer regardless of stage or grade, e.g. pooled RR (95% confidence interval (CI)) for advanced cancers when comparing highest versus lowest category was 0.96 (0.77–1.19) for unprocessed red meat and 1.05 (0.91–1.20) for processed meat intake. Poultry and egg intakes were not associated with risk of localized, low-grade or high-grade cancers. However, higher poultry intake was associated with a non-significant 16% decreased risk of advanced cancer when comparing the highest (≥40 g/day, equivalent to ≥1.4 ounces/day) with the lowest intake category (&amp;lt;5 g/day, equivalent to &amp;lt;0.18 ounces/day) (pooled RR, 95% CI: 0.84, 0.70–1.00, p-value test for common effects, localized vs. advanced: 0.009). Associations for poultry intake were slightly stronger and statistically significant for fatal cancers (pooled RR, 95% CI: 0.74, 0.62–0.88). Participants in the highest category of egg intake (≥25 g/day, equivalent to at least half an egg per day) had a 14% increased risk of advanced cancers when compared to participants in the lowest intake category (&amp;lt;5 g/day) (pooled RR, 95% CI: 1.14, 1.03–1.26, p-value test for common effects, localized vs. advanced: &amp;lt;0.001). However, the positive association between egg intake and risk of advanced prostate cancer was restricted to studies in North America (≥ 25g/day vs. &amp;lt;5 g/day: pooled RR, 95% CI: 1.23, 1.10–1.37) whereas egg intake was not associated with risk of advanced cancer in studies in other continents (pooled RR, 95% CI: 0.95, 0.79–1.14). Intake of seafood (i.e. fish and other types of seafood including shellfish) was not associated with risk of prostate cancer regardless of stage and grade. Conclusion: Our results do not support a substantial association between unprocessed red meat, processed meat or seafood intake and risk of prostate cancer regardless of stage or grade. Higher poultry intake was associated with a modest decreased risk of fatal prostate cancer. The positive association between egg intake and risk of advanced cancers warrants further investigation given the observed differences in associations by geographical region. Citation Information: Cancer Prev Res 2011;4(10 Suppl):B107.

Abstract A106: Coffee consumption and risk of lethal and advanced prostate cancer

Abstract Background: Coffee is a commonly consumed beverage which contains many biologically active compounds. It is a major source of caffeine and antioxidants, and it has effects on insulin and glucose metabolism as well as sex hormone levels. This suggests that coffee may have a beneficial effect on risk of prostate cancer; however, this association has not been studied in depth. Methods: We prospectively investigated the association between coffee intake and prostate cancer risk in the Health Professionals' Follow-Up Study. From 1986 to 2006, 4975 cases of prostate cancer were identified. Intake of regular and decaffeinated coffee was assessed in 1986 and every four years thereafter. We used Cox proportional hazards models to assess the association between coffee intake and risk of prostate cancer. To investigate possible mechanisms, we used linear regression to examine the cross-sectional association between coffee intake and levels of circulating hormones in blood samples collected between 1993 and 1995 from a subset of men in the cohort. Results: There was a weak inverse association between total coffee intake and overall prostate cancer risk, with an adjusted relative risk of 0.81 (95% CI: 0.67–0.97, p-value for linear trend=0.08) for men consuming six or more cups of coffee (regular or decaf) per day compared to non-drinkers. The association was stronger for lethal and advanced (fatal, T3b or T4, or N1 or M1) prostate cancers. Compared to non-drinkers, the highest consumers had a relative risk of 0.41 (CI: 0.22–0.77, p-trend=0.02) for lethal cancer and 0.41 (CI: 0.24–0.71, p-trend=0.002) for advanced cancer. The association with lethal and advanced cancers was more pronounced in never smoking men (RR=0.11; CI: 0.02–0.83, p-trend=0.001 for advanced cancer). The inverse association was seen in both the pre-PSA and PSA screening eras. Results were similar for regular and decaffeinated coffee. For the highest versus lowest groups of intake, the relative risk of advanced cancer was 0.67 (CI: 0.34–1.33, p-trend=0.03) for regular coffee and 0.72 (CI: 0.46–1.13, p-trend=0.03) for decaffeinated coffee. There was an inverse association between caffeine intake and risk of lethal and advanced disease, but this association was weaker than that seen for coffee, and it became non-significant when total coffee intake was also included in the model. Coffee intake was inversely associated with plasma levels of C-peptide (p-trend=0.003) and positively associated with testosterone (p-trend=0.03) and SHBG (p-trend=0.04). Coffee intake was not related to circulating levels of IGF-1, IGFBP3, free testosterone, or estradiol. Conclusion: The strong inverse association between coffee consumption and risk of lethal and advanced prostate cancers is potentially important and should be confirmed in other populations. The association appears to be related to non-caffeine components of coffee and may be mediated through effects on insulin metabolism and/or sex hormone levels. Citation Information: Cancer Prev Res 2010;3(1 Suppl):A106.

Antidiabetic Medication and Prostate Cancer Risk: A Population-based Case-Control Study

Decreased risk of prostate cancer in diabetic men has been reported. The authors evaluated the association between antidiabetic medication use and prostate cancer at the population level. All incident prostate cancer cases in Finland during 1995-2002 were identified from the Finnish Cancer Registry. Matched controls were provided by the Population Register Center (24,723 case-control pairs). Information on medication use was obtained from a comprehensive prescription database. Multivariable-adjusted odds ratios were computed by using conditional logistic regression. The authors found that prostate cancer risk was decreased for antidiabetic medication users (odds ratio = 0.87, 95% confidence interval: 0.82, 0.92). The decrease was observed for most drug groups. The odds ratio decreased in a dose-dependent fashion by quantity of use. Duration of antidiabetic treatment was inversely associated with overall prostate cancer risk and risk of advanced cancer. Similar risk reduction for users of different antidiabetic drugs suggests that diabetes, instead of the medication itself, is behind the association. This finding is unlikely to be secondary because of differential uptake of the prostate-specific antigen test or different prostate-specific antigen levels between medication users and nonusers; prevalence of testing in Finland is low. Dose and time dependency of the relation probably indicates that duration of diabetes is negatively associated with risk.

Cholesterol-Lowering Drugs and Prostate Cancer Risk: A Population-based Case-Control Study

Previous studies have shown that statin use may reduce prostate cancer risk. In the current study, we evaluated the association between serum cholesterol-lowering medication use and prostate cancer risk at the population level. All newly diagnosed prostate cancer cases in Finland during 1995 to 2002 and matched controls (24,723 case control pairs) were identified from the Finnish Cancer Registry and the Population Register Center, respectively. Detailed information on cholesterol-lowering drug purchases during the study period was obtained from the prescription database of the Social Insurance Institution of Finland. After adjustment for potential confounders, having ever-use of any statin was associated with marginally elevated overall prostate cancer risk [odds ratio (OR), 1.07; 95% confidence interval (95% CI), 1.00-1.16]. However, none of the statins was associated with the overall prostate cancer risk when analyzed separately. On the other hand, the risk of advanced prostate cancer was decreased among users of atorvastatin, lovastatin, and simvastatin (OR 0.61, 95% CI 0.37-0.98; OR 0.61, 95% CI 0.43-0.85; and OR 0.78, 95% CI 0.61-1.01, respectively). The risk was not affected among users of other cholesterol drug groups. Our large population-based study showed no evidence for reduced overall prostate cancer risk among users of cholesterol-lowering drugs, whereas the risk of advanced cancer was decreased among statin users.

Diet and Nutrition: A Spoonful of Risk?

Vol. 115, No. 7 EnvironewsOpen AccessDiet and Nutrition: A Spoonful of Risk? Valerie J. Brown Valerie J. Brown Search for more papers by this author Published:1 July 2007https://doi.org/10.1289/ehp.115-a350aAboutSectionsPDF ToolsDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InReddit Soy foods are rich in isoflavones such as genistein and daidzein, strong antioxidants that bind to cells’ estrogen receptors. For years, soy products have presented intriguing hints that they may confer protection against some cancers. For example, the incidence of prostate cancer among Asian males is far below that of U.S. males, with the former eating far more soy products than the latter. Now a large study offers more intriguing—and more confusing—evidence than ever.Norie Kurahashi and colleagues at Japan’s National Cancer Center used data from a 1995 cohort of the Japan Public Health Center-Based Prospective Study on Cancer and Cardiovascular Diseases to analyze diet and prostate cancer data for 43,509 Japanese men. Participants aged 45–74 had answered questions on medical history, lifestyle factors such as smoking, and how often they ate each of 147 foods. At the end of 2004, there were 307 recently diagnosed cases of prostate cancer in the cohort, of which 74 were advanced, 220 were localized to the prostate gland, and 13 were of undetermined stage.The Kurahashi group found a dose-dependent lowering of risk of localized prostate cancer with increasing consumption of soy foods. However, further analysis showed that consumption of miso soup was associated with increased risk of advanced prostate cancer—men over age 60 who ate two or more bowls of miso soup a day were at twice the risk of advanced cancer as those who ate less than one bowl. And for men under 60, the risk for both localized and advanced prostate cancer rose with consumption of genistein, daidzein, and soy foods in general. The findings were published in the March 2007 Cancer Epidemiology, Biomarkers and Prevention.Richard Hoffman, an associate professor of medicine at the University of New Mexico, points out that the Kurahashi study did not adjust for family history, a known risk factor for prostate cancer. Men with a family history of prostate cancer might try to prevent cancer by increasing their isoflavone intake. Therefore, he says, family history could confound the study results, producing a spurious association between higher isoflavone consumption and increased risk of advanced cancer.Another possible confounder is that isoflavones, which are weakly estrogenic, inhibit testosterone production, thus limiting tumor growth but only as long as cells have estrogen receptors. However, as tumor cells develop, they lose those receptors, freeing up testosterone and making the tumors more aggressive.Regarding the apparent protective effect against localized cancer, Kurahashi says, “Isoflavones might delay the progression from latent to clinical[ly] significant prostate cancer in Japanese [men]. However, when or how isoflavones affect latent or localized prostate cancer development and whether isoflavones can be used in the treatment or chemoprevention of this cancer are not yet clear.” Kurahashi and colleagues will follow the cohort through two full decades and conduct nested case–control studies using archived blood samples in hopes of solving this puzzle.FiguresReferencesRelatedDetails Vol. 115, No. 7 July 2007Metrics About Article Metrics Publication History Originally published1 July 2007Published in print1 July 2007 Financial disclosuresPDF download License information EHP is an open-access journal published with support from the National Institute of Environmental Health Sciences, National Institutes of Health. All content is public domain unless otherwise noted. Note to readers with disabilities EHP strives to ensure that all journal content is accessible to all readers. However, some figures and Supplemental Material published in EHP articles may not conform to 508 standards due to the complexity of the information being presented. If you need assistance accessing journal content, please contact [email protected]. Our staff will work with you to assess and meet your accessibility needs within 3 working days.

Height-related risk factors for prostate cancer.

Previous studies have reported that adult height is positively associated with the risk of prostate cancer. The authors carried out a population-based case–control study involving 317 prostate cancer cases and 480 controls to further investigate the possibility that height is more strongly associated with advanced, compared with localized forms of this disease. Since the inherited endocrine factors, which in part determine height attained during the growing years, may influence the risk of familial prostate cancer later in life, the relationship with height was also investigated for familial versus sporadic prostate cancers. Adult height was not related to the risk of localized prostate cancer, but there was a moderate positive association between increasing height and the risk of advanced cancer (relative risk (RR) = 1.62; 95% confidence interval (CI) 0.97–2.73, upper versus lowest quartile, P -trend = 0.07). Height was more strongly associated with the risk of prostate cancer in men with a positive family history compared with those reporting a negative family history. The RR of advanced prostate cancer for men in the upper height quartile with a positive family history was 7.41 (95% CI 1.68–32.67, P -trend = 0.02) compared with a reference group comprised of men in the shortest height quartile with a negative family history. Serum insulin-like growth factor-1 levels did not correlate with height amongst men with familial or sporadic prostate cancers. These findings provide evidence for the existence of growth-related risk factors for prostate cancer, particularly for advanced and familial forms of this disease. The possible existence of inherited mechanisms affecting both somatic and tumour growth deserves further investigation. © 2000 Cancer Research Campaign