Prostate cancer screening has no effect on prostate cancer specific mortality over 20 years of follow-up of Swedish men

2011 ◽  
Vol 17 (1) ◽  
pp. 25-26
Author(s):  
Pim J van Leeuwen
Keyword(s):  
Prostate Cancer ◽  
Cancer Screening ◽  
Prostate Cancer Screening ◽  
Specific Mortality ◽  
Cancer Specific Mortality

scholarly journals Furthering the prostate cancer screening debate (prostate cancer specific mortality and associated risks)

2011 ◽  
Vol 5 (6) ◽  
pp. 416-421 ◽  
Author(s):  
G. Michael Allan ◽  
Michael P. Chetner ◽  
Bryan J. Donnelly ◽  
Neil A. Hagen ◽  
David Ross ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Screening ◽  
Prostate Cancer Screening ◽  
Specific Mortality ◽  
Cancer Specific Mortality

scholarly journals Furthering the prostate cancer screening debate (prostate cancer specific mortality and associated risks)

2013 ◽  
Vol 5 (6) ◽  
pp. 416
Author(s):  
G. Michael Allan ◽  
Michael P. Chetner ◽  
Bryan J. Donnelly ◽  
Neil A. Hagen ◽  
David Ross ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Screening ◽  
Prostate Cancer Screening ◽  
Poor Quality ◽  
Good Evidence ◽  
Screening Programs ◽  
Fecal Occult ◽  
Actual Compliance ◽  
Specific Mortality ◽  
Cancer Specific Mortality

Screening for prostate cancer remains a contentious issue. As withother cancer screening programs, a key feature of the debate isverification of cancer-specific mortality reductions. Unfortunatelythe present evidence, two systematic reviews and six randomizedcontrolled trials, have reported conflicting results. Furthermore, halfof the studies are poor quality and the evidence is clouded by keyweaknesses, including poor adherence to screening in the interventionarm or high rates of screening in the control arm. In highquality studies of prostate cancer screening (particularly prostatespecificantigen), in which actual compliance was anticipated inthe study design, there is good evidence that prostate cancer mortalityis reduced. The numbers needed to screen are at least as goodas those of mammography for breast cancer and fecal occult bloodtesting for colo-rectal cancer. However, the risks associated withprostate cancer screening are considerable and must be weighedagainst the advantage of reduced cancer-specific mortality. Adverseevents include 70% rate of false positives, important risks associatedwith prostate biopsy, and the serious consequences of prostatecancer treatment. The best evidence demonstrates prostate cancerscreening will reduce prostate cancer mortality. It is time for thedebate to move beyond this issue, and begin a well-informed discussionon the remaining complex issues associated with prostatecancer screening and appropriate management.

Costs and effects of prostate cancer screening in SwedenA 15-year follow-up of a randomized trial

2004 ◽  
Vol 38 (4) ◽  
pp. 291-298 ◽  
Author(s):  
Karin Sennfält ◽  
Gabriel Sandblom ◽  
Per Carlsson ◽  
Eberhard Varenhorst
Keyword(s):  
Prostate Cancer ◽  
Cancer Screening ◽  
Randomized Trial ◽  
Prostate Cancer Screening

The association of very low PSA with increased cancer-specific death in men with high-grade prostate cancer.

2015 ◽  
Vol 33 (7_suppl) ◽  
pp. 62-62
Author(s):  
Brandon Arvin Virgil Mahal ◽  
Ayal Aaron Aizer ◽  
Jason Alexander Efstathiou ◽  
Paul Linh Nguyen
Keyword(s):  
Prostate Cancer ◽  
Reference Group ◽  
High Grade ◽  
Specific Mortality ◽  
National Cohort ◽  
Poorly Differentiated ◽  
Cancer Specific Mortality ◽  
Prostate Cancers ◽  
Very High

62 Background: It has been hypothesized that very low PSAs in men with high-grade prostate cancer could reflect dedifferentiation and a poorer prognosis, but clinical evidence to support this is limited. We sought to determine whether a very low-presenting PSA was associated with greater prostate cancer-specific mortality (PCSM) among men with Gleason score (GS) 8-10 disease. Methods: The Surveillance, Epidemiology and End Results Program was used to identify a national cohort of 328,904 men diagnosed with cT1-4N0M0 prostate cancer between 2004 and 2010. Multivariable Fine-Gray competing-risks regression analysis was used to determine PCSM as a function of PSA level (<2.5 ng/mL, 2.6-4 ng/mL, 4.1-10 ng/mL, 10.1-20 ng/mL, 20.1-40 ng/mL, or >40ng/mL) and GS (8-10 vs. <=7). Results: Median follow-up was 38 months. Among men with GS 8-10 disease, using PSA 4.1-10 as the reference group, the Adjusted HR (AHR) for PCSM for men with PSA level <2.5 was 1.86 (95% CI 1.51-2.29; P<0.001), PSA 2.6-4 was1.44 (1.17-1.78; P<0.001), PSA 10.1-20 was 1.58 (1.39-1.78; P<0.001), PSA 20.1-40 was 2.04 (1.78-2.33; P<0.001), and PSA>40 was 3.19 (2.83-3.59; P<0.001), suggesting a U-shaped distribution. There was a significant interaction between PSA level and GS (Pinteraction<0.001) such that PSA <2.5 only significantly predicted for poorer PCSM among patients with high grade GS 8-10 disease. Conclusions: Among patients with high grade GS 8-10 disease, patients with PSA <2.5 and 2.6-4 appear to have a higher risk for cancer-specific death compared to patients with a 10.1-20 PSA level, supporting the notion that low PSA in GS 8-10 disease may be a sign of underlying aggressive and extremely poorly differentiated or anaplastic low PSA-producing tumors. Patients with low PSA GS 8-10 disease should be considered for clinical trials studying the use of chemotherapy and other novel agents in very-high risk prostate cancers.

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