Mean sojourn time, overdiagnosis, and reduction in advanced stage prostate cancer due to screening with PSA: implications of sojourn time on screening.
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ABSTRACT:
SUBMITTER: Pashayan N
PROVIDER: S-EPMC2670005 | biostudies-other | 2009 Apr
REPOSITORIES: biostudies-other
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Project description:Prostate-specific antigen (PSA) screening for prostate cancer in men of average risk remains controversial. Patients' ability to incorporate risk reduction data into their decision-making may depend on their numeracy. We assessed the impact of patients' numeracy on their understanding of the risk reduction benefits of PSA screening. Men attending a general internal medicine clinic were invited to complete a survey. Four versions of the survey each included a three-item numeracy test and PSA risk reduction data, framed one of four ways: absolute (ARR) versus relative risk reduction (RRR), with or without baseline risk (BR). Respondents were asked to adjust their perceived risk of prostate-cancer mortality using the data presented. Accuracy of risk reduction was evaluated relative to how risk data were framed. Among a total of 200 respondents, a majority incorrectly answered one or more of the numeracy items. Overall accuracy of risk adjustment was only 20%. Accuracy varied with data framing: when presented with RRR, respondents were 13% accurate without BR and 31% accurate with BR; when presented with ARR, they were 0% accurate without BR and 35% accurate with BR. Including BR data significantly improved accuracy for both RRR (P = 0.03) and ARR groups (P < 0.01). Accuracy was significantly related to numeracy; numeracy scores of 0, 1, 2, and 3 were associated with accuracy rates of six, five, nine, and 36 percent, respectively (P < 0.01). Overall, numeracy was significantly associated with the accuracy of interpreting quantitative benefits of PSA screening. Alternative methods of communicating risk may facilitate shared decision-making in the use of PSA screening for early detection of prostate cancer.
| S-EPMC5746255 | biostudies-literature
Project description:BackgroundThe benefits and harms of population-wide mammography screening have been long debated. This study evaluated the impact of screening frequency and age range on breast cancer mortality reduction and overdiagnosis.MethodsWe developed a Markov simulation model for the evaluation of mammography screening in a cohort of British women born in 1935-40.ResultsFor triennial screening in women aged 47-73, breast cancer mortality reduction and overdiagnosis was 18.1% (95% confidence interval: 17.3%, 19.0%) and 5.6% (5.1%, 6.1%), of all breast cancer deaths and diagnoses, respectively, from age 40 to 85 years. For annual screening in the same age range, estimates for both outcomes increased considerably to 35.0% (34.2%, 35.7%) and 7.6% (7.1%, 8.1%), respectively. For the age extension of triennial screening from 50-70 to 47-73, we estimated 5 (3, 7) incremental breast cancer deaths avoided and 14 (9, 19) incremental cases overdiagnosed per 10?000 women invited for screening.ConclusionsEstimates of mortality reduction and overdiagnosis were highly dependent on screening frequency, age range, and uptake, which may explain differences between some previous estimates obtained from randomised trials and from service screening.
| S-EPMC4021535 | biostudies-literature
Project description:Abstract This is a protocol for a Cochrane Review (Intervention). The objectives are as follows: To assess the effect of screening mammography for breast cancer on overdiagnosis in women aged 40 years and older at average risk of breast cancer.
| S-EPMC6513440 | biostudies-literature
Project description:Prostate-specific antigen (PSA) screening for prostate cancer remains controversial because it increases overdiagnosis and overtreatment of clinically insignificant tumors. Accounting for genetic determinants of constitutive, non-cancer-related PSA variation has potential to improve screening utility. In this study, we discovered 128 genome-wide significant associations (P < 5 × 10-8) in a multi-ancestry meta-analysis of 95,768 men and developed a PSA polygenic score (PGSPSA) that explains 9.61% of constitutive PSA variation. We found that, in men of European ancestry, using PGS-adjusted PSA would avoid up to 31% of negative prostate biopsies but also result in 12% fewer biopsies in patients with prostate cancer, mostly with Gleason score <7 tumors. Genetically adjusted PSA was more predictive of aggressive prostate cancer (odds ratio (OR) = 3.44, P = 6.2 × 10-14, area under the curve (AUC) = 0.755) than unadjusted PSA (OR = 3.31, P = 1.1 × 10-12, AUC = 0.738) in 106 cases and 23,667 controls. Compared to a prostate cancer PGS alone (AUC = 0.712), including genetically adjusted PSA improved detection of aggressive disease (AUC = 0.786, P = 7.2 × 10-4). Our findings highlight the potential utility of incorporating PGS for personalized biomarkers in prostate cancer screening.
| S-EPMC10287565 | biostudies-literature
Project description:PurposeThis study aimed to quantify the probability of overdiagnosis of prostate cancer by polygenic risk.MethodsWe calculated the polygenic risk score based on 66 known prostate cancer susceptibility variants for 17,012 men aged 50-69 years (9,404 men identified with prostate cancer and 7,608 with no cancer) derived from three UK-based ongoing studies. We derived the probabilities of overdiagnosis by quartiles of polygenic risk considering that the observed prevalence of screen-detected prostate cancer is a combination of underlying incidence, mean sojourn time (MST), test sensitivity, and overdiagnosis.ResultsPolygenic risk quartiles 1 to 4 comprised 9, 18, 25, and 48% of the cases, respectively. For a prostate-specific antigen test sensitivity of 80% and MST of 9 years, 43, 30, 25, and 19% of the prevalent screen-detected cancers in quartiles 1 to 4, respectively, were likely to be overdiagnosed cancers. Overdiagnosis decreased with increasing polygenic risk, with 56% decrease between the lowest and the highest polygenic risk quartiles.ConclusionTargeting screening to men at higher polygenic risk could reduce the problem of overdiagnosis and lead to a better benefit-to-harm balance in screening for prostate cancer.
| S-EPMC4430305 | biostudies-literature
Project description:Evaluating the performance of serum prostate-specific antigen (PSA) test in population-based screening with receiver operating characteristics (ROC) curve often neglects the time dimension. Asymptomatic cases with negative PSA test would have been missed if sojourn time is not taken into account to allow for cases surfacing into the clinical phase. Data included 20,796 men with PSA test at the first screening round was used from population-based Finnish prostate cancer screening trial during 1996-1999. Cancers detected at the first screen, together with interval cancers ascertained during 4-year follow-up were expediently used to estimate sensitivity and specificity. A sojourn-time-corrected model was applied to estimating the possible false negative cases for those with PSA?<?4 ng/ml for correcting the ROC curve. The estimated sensitivity estimate was reduced from 94.4% without correction to 68.8% with correction but the estimated specificity was identical (89.4% vs. 89.2%) at cutoff of 3 ng/ml. The corrected area under curve (AUC) [77.0% (74.9-79.1%)] of the PSA test was significantly lower than the uncorrected AUC [95.9% (95.3-96.6%)]. The failure of considering the time since last negative screen due to incomplete ascertainment for asymptomatic cancer led to the overestimation of PSA test performance that further affects the cut-off value of PSA tests for population-based prostate cancer screening.
| S-EPMC7691355 | biostudies-literature
Project description:ObjectivesTo quantify the risk of overdiagnosis associated with prostate cancer screening in Australia using a novel lifetime risk approach.DesignModelling and validation of the lifetime risk method using publicly available population data.SettingOpportunistic screening for prostate cancer in the Australian population.ParticipantsAustralian male population (1982-2012).InterventionsProstate-specific antigen testing for prostate cancer screening.Primary and secondary outcome measuresPrimary: lifetime risk of overdiagnosis in 2012 (excess lifetime cancer risk adjusted for changing competing mortality); Secondary: lifetime risk of prostate cancer diagnosis (unadjusted and adjusted for competing mortality); Excess lifetime risk of prostate cancer diagnosis (for all years subsequent to 1982).ResultsThe lifetime risk of being diagnosed with prostate cancer increased from 6.1% in 1982 (1 in 17) to 19.6% in 2012 (1 in 5). Using 2012 competing mortality rates, the lifetime risk in 1982 was 11.5% (95% CI 11.0% to 12.0%). The excess lifetime risk of prostate cancer in 2012 (adjusted for changing competing mortality) was 8.2% (95% CI 7.6% to 8.7%) (1 in 13). This corresponds to 41% of prostate cancers being overdiagnosed.ConclusionsOur estimated rate of overdiagnosis is in agreement with estimates using other methods. This method may be used without the need to adjust for lead times. If annual (cross-sectional) data are used, then it may give valid estimates of overdiagnosis once screening has been established long enough for the benefits from the early detection of non-overdiagnosed cancer at a younger age to be realised in older age groups.
| S-EPMC6429722 | biostudies-literature
Project description:Exposure measurement error is a pervasive problem for epidemiology research projects designed to provide valid and precise statistical evidence supporting postulated exposure-disease relationships of interest. The purpose of this commentary is to highlight an important real-life example of this exposure measurement error problem and to provide a simple and useful diagnostic tool for physicians and their patients that corrects for the exposure measurement error. More specifically, prostate-specific antigen doubling time (PSADT) is a widely used measure for guiding future treatment options for patients with biochemically recurrent prostate cancer. Numerous papers have been published claiming that a low calculated PSADT value (denoted PSADT^) is predictive of metastasis and premature death from prostate cancer. Unfortunately, none of these papers have adjusted for the measurement error in PSADT^, an estimator that is typically computed using the popular Memorial Sloan Kettering website very often visited by both physicians and their patients. For this website, the estimator PSADT^ of the true (but unknown) PSADT for a patient (denoted PSADT∗) is computed as the natural log of 2 (i.e., 0.6931) divided by the estimated slope of the straight-line regression of the natural log of PSA (in ng/mL) on time. We utilize PSADT^ to derive an expression for the probability that the unknown PSADT∗ for a patient is below a specified value C (>0) of concern to both the physician and the patient. This probability is easy to interpret and takes into account the fact that PSADT^ is a statistical estimator with variability. This variability introduces measurement error, namely, the difference between a computed value PSADT^ and the true, but unknown, value PSADT∗. We have developed an Excel calculator that, once the [time, ln(PSA)] values are entered, outputs both the value of PSADT^ and the desired probability. In addition, we discuss problematic statistical issues attendant with PSADT∗ estimation typically based on at most three or four PSA values. We strongly recommend the use of this probability when physicians are discussing PSADT^ values and associated treatment options with their patients. And, we stress that future epidemiology research projects involving PSA doubling time should take into account the measurement error problem highlighted in this Commentary.
| S-EPMC10724542 | biostudies-literature
Project description:We defined prostate-specific antigen (PSA) thresholds from a well calibrated risk prediction model for identifying and excluding advanced prostate cancer (PCa). We retrieved 902 biopsied patients with a pre-biopsy PSA determination (Roche assay). A logistic regression model predictive for PCa including the main effects [i.e., PSA, age, histological evidence of glandular inflammation (GI)] was built after testing the accuracy by calibration plots and Hosmer-Lemeshow test for goodness of fit. PSA thresholds were derived by assuming a diagnostic sensitivity of 95% (rule-out) and 80% (rule-in) for overall and advanced/poorly differentiated PCa. In patients without GI, serum PSA concentrations ≤ 4.1 (<65 years old) and ≤3.7 μg/L (≥65 years old) excluded an advanced PCa (defined as Gleason score ≥ 7 at biopsy), with a negative predictive value of 95.1% [95% confidence interval (CI): 83.0-98.7] and 88.8% (CI: 80.2-93.9), respectively, while PSA > 5.7 (<65) and >6.1 μg/L (≥65) should address biopsy referral. In presence of GI, PSA did not provide a valid estimate for risk of advanced cancer because of its higher variability and the low pre-test probability of PCa. The proposed PSA thresholds may support biopsy decision except for patients with asymptomatic prostatitis who cannot be pre-biopsy identified.
| S-EPMC8305281 | biostudies-literature
Project description:ObjectiveTo investigate the efficacy and safety of prostate-specific antigen (PSA) testing to screen for prostate cancer.DesignSystematic review and meta-analysis.Data sourcesElectronic search of Cochrane Central Register of Controlled Trials, Web of Science, Embase, Scopus, OpenGrey, LILACS, and Medline, and search of scientific meeting abstracts and trial registers to April 2018.Eligibility criteria for selecting studiesRandomised controlled trials comparing PSA screening with usual care in men without a diagnosis of prostate cancer.Data extractionAt least two reviewers screened studies, extracted data, and assessed the quality of eligible studies. A parallel guideline committee (BMJ Rapid Recommendation) provided input on the design and interpretation of the systematic review, including selection of outcomes important to patients. We used a random effects model to obtain pooled incidence rate ratios (IRR) and, when feasible, conducted subgroup analyses (defined a priori) based on age, frequency of screening, family history, ethnicity, and socioeconomic level, as well as a sensitivity analysis based on the risk of bias. The quality of the evidence was assessed with the GRADE approach.ResultsFive randomised controlled trials, enrolling 721?718 men, were included. Studies varied with respect to screening frequency and intervals, PSA thresholds for biopsy, and risk of bias. When considering the whole body of evidence, screening probably has no effect on all-cause mortality (IRR 0.99, 95% CI 0.98 to 1.01; moderate certainty) and may have no effect on prostate-specific mortality (IRR 0.96, 0.85 to 1.08; low certainty). Sensitivity analysis of studies at lower risk of bias (n=1) also demonstrates that screening seems to have no effect on all-cause mortality (IRR 1.0, 0.98 to 1.02; moderate certainty) but may have a small effect on prostate-specific mortality (IRR 0.79, 0.69 to 0.91; moderate certainty). This corresponds to one less death from prostate cancer per 1000 men screened over 10 years. Direct comparative data on biopsy and treatment related complications from the included trials were limited. Using modelling, we estimated that for every 1000 men screened, approximately 1, 3, and 25 more men would be hospitalised for sepsis, require pads for urinary incontinence, and report erectile dysfunction, respectively.ConclusionsAt best, screening for prostate cancer leads to a small reduction in disease-specific mortality over 10 years but has does not affect overall mortality. Clinicians and patients considering PSA based screening need to weigh these benefits against the potential short and long term harms of screening, including complications from biopsies and subsequent treatment, as well as the risk of overdiagnosis and overtreatment.Systematic review registrationPROSPERO registration number CRD42016042347.
| S-EPMC6283370 | biostudies-literature