This guideline addresses prostate cancer early detection for the purpose of reducing prostate cancer mortality with the intended user as the urologist. This document does not make a distinction between early detection and screening for prostate cancer. Early detection and screening both imply detection of disease at an early, pre-symptomatic stage when a man would have no reason to seek medical care –an intervention referred to as secondary prevention.1 In the US, early detection is driven by prostate specific antigen (PSA)-based screening followed by prostate biopsy for diagnostic confirmation. While the benefits of PSA-based prostate cancer screening have been evaluated in randomized-controlled trials, the literature supporting the efficacy of DRE, PSA derivatives and isoforms (e.g. free PSA, -2proPSA, prostate health index, hK2, PSA velocity or PSA doubling time) and novel urinary markers and biomarkers (e.g. PCA3) for screening with the goal of reducing prostate cancer mortality provide limited evidence to draw conclusions. While some data suggest use of these secondary screening tools may reduce unnecessary biopsies (i.e. reduce harms) while maintaining the ability to detect aggressive prostate cancer (i.e. maintain the benefits of PSA screening), more research is needed to confirm this. However, the likelihood of a future population-level screening study using these secondary screening approaches is highly unlikely at least in the near future. Therefore, this document focuses only on the efficacy of PSA screening for the early detection of prostate cancer with the specific intent to reduce prostate cancer mortality and not secondary tests often used after screening to determine the need for a prostate biopsy or a repeat prostate biopsy (e.g., PSA isoforms, PCA3, imaging).
At the Florida Center for Prostate Care, you have access to a , expert in the treatment of all stages of prostate cancer, including . Our physicians have treated 10,000 men with prostate cancer, and have performed more than 5,000 prostate seed implants, making us one of the world's premier centers. We have patented medical devices, been awarded national research grants, and published 200 papers in medical journals. Our new center offers , the most advanced technology for the most precise delivery of radiation therapy. Based on our experience, we have trained hundreds of doctors across the United States, Europe, Asia and Africa on our treatment technique.
The two largest screening trials have provided some indirect evidence about the likely benefits of more versus less frequent screening. In the ERSPC, a comparison between the Rotterdam section (interscreening interval four years) and the Swedish section (interscreening interval two years) suggested that a two year screening interval significantly reduced the incidence of advanced disease.108 Evidence on the comparison of a two-year screening interval with annual screening was provided by the PLCO trial. This trial compared annual screening with a control group that had screening rates similar to those in the US population which corresponded to screening on average every two years.20 Prostate cancer mortality rates were similar in the two groups through 13 years of follow-up, suggesting little benefit from screening more frequently than every two years. In addition, data from a randomized trial (Goteborg) and a case-control study suggest that a rescreening interval of four years is not likely to miss a curable prostate cancer among men with a PSA below 1.0ng/ml.99,101
Any discussion of the benefits and harms of prostate cancer screening in men age 55 to 69 years should consider the man's individual life expectancy. Prior studies have documented that men with less than a 10 to 15 year life expectancy are unlikely to realize a benefit from aggressive treatment for localized prostate cancer96 and as such, it follows that the earlier disease detection associated with screening in these men likely will be less beneficial, if beneficial at all. To this end, shared decision making should include a discussion of the man's baseline mortality risk from other co-morbid conditions, their individual risk for prostate cancer, given their race/ethnicity and family history, and the degree to which screening might influence their overall life expectancy and chance of experiencing morbidity from prostate cancer or its treatment.
Evidence for screening benefit in this setting is moderate and is derived from large RCTs. Specifically, results from ERSPC document a relative risk reduction of prostate cancer-specific death of 21% at a median follow-up of 11 years17 While the absolute reduction in prostate cancer-specific mortality was relatively small (0.10 deaths per 1,000 person-years or 1.07 deaths per 1,000 men randomized), this may represent an underestimate of benefit given the length of follow-up of the study and the degree of non-compliance in the intervention arm. The Panel acknowledges that the prostate component of PLCO failed to show a benefit to screening with a median follow-up of 13 years,18 but attributes this finding to high rates of screening in the control arm biasing the study to the null.
Research presented at the 2009 ASCO (American Society of Clinical Oncology)meeting presented newer findings about the androgen dependence of prostatecancers -- rather than being totally dependent on the androgens producedby the testes and adrenal glands, some prostate cancers can produce their owntestosterone and drive their own growth.
Nilandron(R) is a nonsteroidal anti-androgen indicated for use in combination with surgical castration for the treatment of men with metastatic prostate cancer.
As discussed above, prostate cells and prostate cancer cells need themale hormone dihydrotestosterone (DHT) to function and survive, for the mostpart.
But this is truefor all side effects of all the treatments discussed here, and, I wouldventure, all other medical interventions.)Walsh and his colleagues note that "Dose-escalated radiation with the use of conformal techniques causes intermittent rectal bleeding of grade 2 or higher (requiring transfusions, interventional radiology, or endoscopic or operative intervention) in 1.5 to 18% of patients and causes impotence in 40 to60% of patients." (See and references therein.)
Radiation can be delivered to the prostate gland locally, with less probabilityof damage to external tissue, the theory goes, if a radioactive substanceis emplanted within the prostate.
It is often the tack taken for men whose cancer is not very large or aggressive and who either are in a state of health where many of the standard medical treatments are not feasible or it is likely they will die of something else before the prostate cancer will give them symptoms.
The Memorial Sloan Kettering Cancer Center providesprostate cancer nomograms (as well as nomograms for some other typesof cancer) that relate Gleason score, PSA and other factors to probabilitiesof survival for various medical treatment options.
There is no commonly effective treatment for metastatic prostate cancerexcept for hormonal blockade although other chemotherapies are used as well,especially for hormone refractory prostate cancer.
In general, the population of prostate cancer cells needs a form of testosterone, the male hormone produced 95% in the testes and 5% in theadrenal glands, in order to live and thrive and grow.
"This genetic evidence suggests that MSR1 may play an important role in prostate cancer susceptibility in both African American men and men of European descent," says Jianfeng Xu, M.D., Dr.