| 1. |
|
|
| 2. |
|
|
| 3. |
- Loeb, S., et al.
(författare)
-
Testosterone Replacement Therapy and Risk of Favorable and Aggressive Prostate Cancer
- 2017
-
Ingår i: Journal of Clinical Oncology. - : American Society of Clinical Oncology (ASCO). - 0732-183X .- 1527-7755. ; 35:13, s. 1430-1436
-
Tidskriftsartikel (refereegranskat)abstract
- Purpose The association between exposure to testosterone replacement therapy (TRT) and prostate cancer risk is controversial. The objective was to examine this association through nationwide, population-based registry data. We performed a nested case-control study in the National Prostate Cancer Register of Sweden, which includes all 38,570 prostate cancer cases diagnosed from 2009 to 2012, and 192,838 age-matched men free of prostate cancer. Multivariable conditional logistic regression was used to examine associations between TRT and risk of prostate cancer (overall, favorable, and aggressive). Two hundred eighty-four patients with prostate cancer (1%) and 1,378 control cases (1%) filled prescriptions for TRT. In multivariable analysis, no association was found between TRT and overall prostate cancer risk (odds ratio [OR], 1.03; 95% CI, 0.90 to 1.17). However, patients who received TRT hadmore favorable-risk prostate cancer (OR, 1.35; 95% CI, 1.16 to 1.56) and a lower risk of aggressive prostate cancer (OR, 0.50; 95% CI, 0.37 to 0.67). The increase in favorable-risk prostate cancer was already observed within the first year of TRT (OR, 1.61; 95% CI, 1.10 to 2.34), whereas the lower risk of aggressive disease was observed after > 1 year of TRT (OR, 0.44; 95% CI, 0.32 to 0.61). After adjusting for previous biopsy findings as an indicator of diagnostic activity, TRT remained significantly associated with more favorable-risk prostate cancer and lower risk of aggressive prostate cancer. The early increase in favorable-risk prostate cancer among patients who received TRT suggests a detection bias, whereas the decrease in risk of aggressive prostate cancer is a novel finding that warrants further investigation. (C) 2017 by American Society of Clinical Oncology.
|
|
| 4. |
|
|
| 5. |
|
|
| 6. |
|
|
| 7. |
- Van Hemelrijck, M, et al.
(författare)
-
Lipid profiles and the risk of kidney cancer in the Swedish AMORIS study
- 2011
-
Ingår i: JOURNAL OF CLINICAL ONCOLOGY. - : American Society of Clinical Oncology (ASCO). - 0732-183X .- 1527-7755. ; 29:7
-
Konferensbidrag (övrigt vetenskapligt/konstnärligt)abstract
- 342 Background: Since multiple epidemiologic studies showed a link between obesity and kidney cancer (KCa), the lipid metabolism is thought to play a role in development of KCa. With the exception of cholesterol and total fat intake, the association between changes in lipid biomarkers and KCa has not often been researched. We assessed the link between lipid profiles and KCa risk in a large prospective cohort study. Methods: A cohort based on 85,261 persons (> 20 years old) with baseline measurements of glucose, triglycerides (TG), total cholesterol, HDL, LDL, apolipoprotein A-I and apoB was selected from the Swedish Apolipoprotein Mortality Risk (AMORIS) study. Multivariate Cox proportional hazards models were used to analyze associations between quartiles and dichotomized values of these lipid components and KCa risk. All models were adjusted for age, gender, socioeconomic status, fasting status, history of kidney disease prior to baseline (ICD9: 580-93), and glucose, cholesterol, and TG levels (depending on the covariate of interest). Results: During a mean follow-up of 12 years, 161 persons developed KCa (58% men). The mean age at baseline was 46 years. TG were the only lipid component for which a statistically significant association was found with risk of KCa (Hazard Ratio (HR): 1.05 (95%CI: 0.59-1.87), 1.77 (1.05-2.98), and 1.77 (1.04-3.02) for the second, third, and fourth quartile, compared to the first, with p-value for trend: 0.008). The lipid ratio of TG and HDL also showed a statistically significant positive association with risk of KCa (HR: 1.21 (0.71-2.08), 1.56 (0.94-2.58), and 1.92 (1.17-3.17) for the second, third, and fourth quartile, compared to the first, with p-value for trend: 0.004). No other associations were found between lipid components and KCa risk. Conclusions: This detailed analysis of lipid components and risk of KCa found a relation between levels of TG and KCa risk. In contrast to previous studies, we did not find an association between cholesterol levels and KCa risk. Lipid profiles based on the markers used in this study do not seem to reflect the etiological pathway that has previously been shown between obesity and KCa. Further mechanistic studies are required to assess the link between lipid deregulation and KCa. No significant financial relationships to disclose.
|
|
| 8. |
- Van Hemelrijck, M, et al.
(författare)
-
Serum calcium and incident and fatal prostate cancer in the Swedish AMORIS study
- 2012
-
Ingår i: JOURNAL OF CLINICAL ONCOLOGY. - : American Society of Clinical Oncology (ASCO). - 0732-183X .- 1527-7755. ; 30:5
-
Konferensbidrag (övrigt vetenskapligt/konstnärligt)abstract
- 36 Background: Many observational studies have shown a positive association between intake of dairy products and prostate cancer (PCa) risk. From a biological point of view it is of interest to study this association as bone was recently shown to be a positive regulator of male fertility which suggests that regulation of bone remodeling and reproduction are linked. Since androgens promote cell proliferation and inhibit prostate cell death, it is possible that calcium (Ca) is linked to PCa risk via its link with the reproductive system. We studied the association between serum Ca and PCa while also accounting for levels of albumin, a protein to which Ca is bound. Methods: A cohort based on 192,183 men with baseline information on Ca (mmol/L) and albumin (g/L) was selected from the Swedish Apolipoprotein MOrtality RISk (AMORIS) study. Age-stratified multivariable Cox proportional hazard models were used to analyze associations between Ca and incident and fatal PCa risk. All models were adjusted for fasting status, glucose levels, socio-economic status, season at time of Ca measurement, Charlson comorbidity index, and history of fractures. Results: A 6,202 men were diagnosed with PCa and 672 died of PCa during mean follow-up of 12 years. A weak negative association was found between PCa risk and Ca (HR per SD: 0.97 (95%CI: 0.95-1.00)). A similar association was also found between albumin-corrected Ca and PCa risk (HR: 0.96 (0.89-1.03), 0.94 (0.87-1.01), and 0.92 (0.86-0.99) for the 2nd, 3rd, and 4th quartile compared to the 1st; P for trend: 0.02). No association was found with fatal PCa, nor was there effect-modification by overweight. A strong positive association between Ca and death was observed when censoring for PCa (HR per SD: 1.13 (95%CI: 1.12-1.15)). Conclusions: Serum levels of Ca were weakly negatively associated with PCa risk in our study when adjusted for age and history of comorbidities and fractures. A negative association between Ca and PCa risk is likely explained by the strong relation between Ca and non-PCa death. These competing risks need to be handled in order to define whether Ca is causally involved in PCa aetiology or whether it only acts a marker of other metabolic events in the causal pathway.
|
|
| 9. |
|
|
