We describe changes in prostate cancer incidence, survival and mortality and the resulting impact in additional diagnoses and avoided deaths in European areas and the United States.
Using data from 12 European cancer registries and the Surveillance, Epidemiology and End Results program, we describe changes in prostate cancer epidemiology between the beginning of the PSA era (USA: 1985-1989, Europe: 1990-1994) and 2002-2006 among patients aged 40-64, 65-74, and 75+. Additionally, we examine changes in yearly numbers of diagnoses and deaths and variation in male life expectancy.
Incidence and survival, particularly among patients aged <75, increased dramatically, yet both remain (with few exceptions in incidence) lower in Europe than in the United States. Mortality reductions, ongoing since the mid/late 1990 s, were more consistent in the United States, had a distressingly small absolute impact among patients aged 40-64 and the largest absolute impact among those aged 75+. Overall ratios of additional diagnoses/avoided deaths varied between 3.6 and 27.6, suggesting large differences in the actual impact of prostate cancer incidence and mortality changes. Ten years of remaining life expectancy was reached between 68 and 76 years.
Policies reflecting variation in population life expectancy, testing preferences, decision aids and guidelines for surveillance-based management are urgently needed.
"Further urological evaluation is offered when PSA levels exceed 3 ng/ml. Although the European Randomized study of screening for prostate cancer (ERSPC) demonstrated a potential for mortality decline  , the very long lead time of cancer detection , the potentially very serious side-effects of the treatment and large variation in the life expectancy of different populations , as well as concern about the overall validity of the ERSPC results  keep PSA-based early detection highly controversial   . "
"Thus, an estimate of the complete prevalence is often derived from observed data using statistical models, which can also be extended to estimate future prevalence. Estimating future prostate cancer prevalence is particularly complicated due to the changes in patterns of incidence and survival that have occurred since the introduction of prostatespecific antigen (PSA) testing in the late 1980s . These marked changes mean that historical data are a relatively unreliable foundation for modelling prevalence. "
[Show abstract][Hide abstract] ABSTRACT: Background:
Information on the current and future numbers of Australian men living with prostate cancer is limited. We describe a method for estimating complete prevalence of prostate cancer to provide a measure of the burden of prostate cancer in Australia.
Prostate cancer data from the New South Wales (NSW) Central Cancer Registry were used with PIAMOD (Prevalence and Incidence Analysis MODel) software to estimate future prostate cancer prevalence in NSW. We first fitted parametric incidence and survival models then used the modelled incidence and survival estimates to calculate complete prevalence. The estimated and projected prevalence incorporate past observed trends and take into account different assumptions about future survival trends. These models were validated against observed prevalence from the counting method.
Based on data for 1996-2007, the number of men living with prostate cancer in NSW was estimated to rise by 59% to 73%, from 38,322 in 2007 to 60,910-66,160 in 2017. The increasing incidence rates and the ageing population were the major contributors to this estimated increase. Validation suggested that these projections were reasonable, as the estimated prevalence in 1996-2007 was in good agreement with the corresponding prevalence calculated using the direct counting method, and the incidence models were supported by the recent data on prostate-specific antigen testing.
As the number of men living with prostate cancer is expected to increase dramatically in the next decade in Australia, representing a significant challenge to the health system, careful planning and development of a healthcare system able to respond to this increased demand is required. These projections are useful for addressing the challenge in meeting the cancer care needs of men with prostate cancer.
Cancer Epidemiology 12/2014; 39(1). DOI:10.1016/j.canep.2014.11.009 · 2.71 Impact Factor
"Further, this disease carries substantial morbidity and mortality in European countries. (Shibata and Whittemore, 2001; Neppl-Huber et al, 2012) Although therapeutic choices for castration-resistant prostate cancer (CRPC) have expanded recently beyond docetaxel-based chemotherapy, median survival remains suboptimal at less than 2 years. (de Bono et al, 2010; Kantoff et al, 2010; de Bono et al, 2011; Scher et al, 2012). "
[Show abstract][Hide abstract] ABSTRACT: Background:
The mammalian target of rapamycin (mTOR) pathway is deregulated in castration-resistant prostate cancer (CRPC). We investigated the efficacy and toxicity of temsirolimus, an mTOR inhibitor, in chemotherapy-naïve CRPC.
In this phase II open label study, eligible patients received IV temsirolimus at 25 mg weekly until objective disease progression, unacceptable toxicity or investigator's discretion. Toxicity was assessed every 4 weeks and responses every 8 weeks. Primary end point was calculating the overall response (OR) rate as well as measuring stable disease (SD) to assess the overall clinical benefit calculated as OR+SD. Secondary end points included prostatic-specific antigen (PSA) changes and time to progression biochemically and radiographically. Correlative studies included prospective assessment of quality of life (QoL) using two previously validated scales.
Although the sponsor halted the study early, 21 patients were enrolled of which, 15 were evaluable for efficacy and OR. Median age was 74 (range: 57–89), median PSA was 237.5 ng ml−1 (range: 8.2–2360), visceral disease present in 11 patients (52%), and 17 patients (81%) patients had Gleason score (7–10). Two patients had a partial response (PR) and eight had SD. The OR was 13% (2/15) and the overall clinical benefit (OR+SD) was 67% (10/15). Median time to radiographic disease progression was 2 months (range 2–10 months). Biochemical response assessment was available for 14/15 patients. Any PSA decline was observed in four patients (28.5% 4/14) with one patient (7%) having >50% PSA decline. Median time to progression by PSA was 2 months (range 1–10 months). With a median follow-up of 32 months, median overall survival (OS) was 13 months (range: 2–37) and three patients remain alive at the data cutoff (5/2013) for an OS of 14% at 4 years on an intent-to-treat analysis. Major non-haematologic toxicities included fatigue (19%) and pneumonia (14%). Main laboratory toxicities included hyperglycaemia (24%) and hypophosphatemia (14%). Also, 52% of enrolled patients had serious adverse events. Other toxicities were consistent with previously reported adverse events with temsirolimus. Despite these observed adverse events, temsirolimus did not adversely impact QoL.
Temsirolimus monotherapy has minimal activity in chemotherapy-naïve CRPC.
British Journal of Cancer 09/2013; 109(7). DOI:10.1038/bjc.2013.530 · 4.84 Impact Factor
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