What is the risk of prostate cancer mortality following negative systematic TRUS-guided biopsies? A systematic review.

OBJECTIVE: To investigate the risk of prostate cancer-specific mortality (PCSM) following initial negative systematic transrectal ultrasound-guided (TRUS) prostate biopsies. DESIGN: Systematic review. DATA SOURCES: PubMed and Embase were searched using a string combination with keywords/Medical Subject Headings terms and free text in the search builder. Date of search was 13 April 2020. STUDY SELECTION: Studies addressing PCSM following initial negative TRUS biopsies. Randomised controlled trials and population-based studies including men with initial negative TRUS biopsies reported in English from 1990 until present were included. DATA EXTRACTION: Data extraction was done using a predefined form by two authors independently and compared with confirm data; risk of bias was assessed using the Newcastle-Ottawa Scale for cohort studies when applicable. RESULTS: Four eligible studies were identified. Outcomes were reported differently in the studies as both cumulative incidence and Kaplan-Meier estimates have been used. Regardless of the study differences, all studies reported low estimated incidence of PCSM of 1.8%-5.2% in men with negative TRUS biopsies during the following 10-20 years. Main limitation in all studies was limited follow-up. CONCLUSION: Only a few studies have investigated the risk of PCSM following initial negative biopsies and all studies included patients before the era of MRI of the prostate. However, the studies point to the fact that the risk of PCSM is low following initial negative TRUS biopsies, and that the level of prostate-specific antigen before biopsies holds prognostic information. This may be considered when advising patients about the need for further diagnostic evaluation. PROSPERO REGISTRATION NUMBER: CRD42019134548.

Educational level and the risk of depression after prostate cancer.

Background: The risk of depression is inversely associated with socioeconomic position in the general population; however, studies on the association in cancer populations are limited. The aim was to investigate if shorter education was associated with a higher risk of depression following prostate cancer diagnosis. Material and methods: This is a cohort study among participants in the Danish prospective Diet, Cancer and Health (DCH) study including 2337 men diagnosed with prostate cancer between 1997 and 2014. Primary outcome was indication of moderate to severe depression, defined as either a first hospital contact for depression or first use of antidepressants. The main indicator of socioeconomic position was education categorized into short (<9 years of education), medium (9-12 years) and long (>12 years). We retrieved information on education, depression and cohabitation status from Danish National Registries. Information on stage, primary treatment, lifestyle and anthropometry was obtained from medical records and questionnaires. Data were analyzed using Cox proportional hazards models adjusted for possible confounders and mediators. Results: The hazard of first depression was 1.86-fold higher (95% CI, 1.36-2.54) in prostate cancer patients with short education compared to those with long education. Adjustment for stage and primary treatment did not change the HRs, while adding comorbidity and lifestyle factors resulted in an HR of 1.65 (95% CI, 1.19-2.29). Men with medium education had a non-statistically significant 1.23-fold higher hazard of depression (95% CI, 0.95-1.59) than men with long education in the fully adjusted model. Educational differences were present in the cumulative incidence of first depression among cancer-free DCH study participants, but the level of first depression was substantially lower in this population than in prostate cancer patients. Conclusions: We found indication of social inequality in depression following prostate cancer. Patients and particularly men with short education might benefit from psychosocial intervention and support.

Interaction between ADH1C Arg(272)Gln and alcohol intake in relation to breast cancer risk suggests that ethanol is the causal factor in alcohol related breast cancer.

Alcohol is a risk factor for breast cancer. We wanted to determine if ADH polymorphisms which modify the rate of ethanol oxidation to acetaldehyde, were associated with breast cancer risk. We matched 809 postmenopausal breast cancer cases with 809 controls, nested within the prospective Diet, Cancer and Health study. Among variant allele carriers of ADH1C Arg(272)Gln, alcohol intake increased the risk of breast cancer with 14% (95% CI: 1.04-1.24) per 10g alcohol/day, but not among homozygous wild type carriers (p for interaction=0.06). Thus, slow oxidation of ethanol seemed to be associated with breast cancer risk.