Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1519176 (PSA)
 5,490 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Screening for prostate cancer represents a clinical dilemma with no clear evidence to suggest decreased mortality from any diagnostic test. We now possess new knowledge regarding optimal combinations of DRE, TRUS, and PSA. While DRE and TRUS may be too subjective and PSA too nonspecific, their combined predictive values identify not only men at high risk but also those for whom continued frequent screening may not be cost effective. A monoclonal PSA decision level of no more than 4.0 ng/ml should be used, since 40 percent of cancers detected from 4.0 to 10.0 ng/ml already have extracapsular extension. Assuming that DRE is performed by experienced examiners, the combination of PSA and DRE should produce cost-effective early detection and minimize missed cancers below 4.0 ng/ml. TRUS should be reserved for those patients with either PSA elevations and/or DRE abnormalities. The use of TRUS gland volume data to further modify PSA decision levels, such as the "predicted" PSA concept, may also improve TRUS biopsy criteria and predictive values. Prostate cancer detection can then be objectively limited to a small percentage of the population and better selected for earlier, more localized disease. The ultimate decrease in mortality from screening remains to be demonstrated in randomized trials or observed only after decades of increased public awareness about prompt early detection combined with effective, definitive therapy.
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PMID:Prostate cancer screening: current trends and future implications. 137 79

No screening test has been proven to reduce prostate cancer mortality. DRE has been the traditional method of screening, and it is often used to detect other diseases in addition to prostate cancer. Newer modalities, such as TRUS and PSA, can identify patients with nonpalpable prostate cancer, but the use of these tests will also result in many false-positives. In addition, it is not known whether the use of these tests will reduce prostate cancer mortality, or instead cause harm to those patients screened. Given the potential for harm, and the extraordinary expense, routine screening of asymptomatic men with newer modalities should be considered experimental.
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PMID:Prostate cancer screening. 138 77

Although PSA is considered to be the true serum marker of prostatic tissue and a valuable indicator for cancer in the gland, knowledge of its significance and limitations is essential to its use for screening, staging, and monitoring CAP. PSA may be used in conjunction with DRE for early detection of CAP. Men with abnormal DRE should have a TRUS with or without biopsy. In men older than 50 years and with negative DRE and PSA < 4 ng/mL, annual evaluations are prudent. In patients with a PSA range of 4.0 to 9.9 ng/mL, high-risk groups such as black males and those with a positive family history should have TRUS. Males with negative DRE in the PSA range of 4.0 to 9.9 ng/mL should have TRUS to evaluate prostate volume and PSAD. Biopsy should be considered in those with PSAD > 0.15. Men with PSA > 10 ng/mL, even in the presence of an enlarged benign prostate, should have multiple directed biopsies under TRUS guidance.
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PMID:The current role of prostatic acid phosphatase and prostate-specific antigen in the management of prostate cancer. 138 63

The goal of an early detection program is not to detect all prostate cancers, but only to detect those that are potentially morbid or lethal (clinically important cancers). The prevalence of such cancers in the population of 50-year-old men can be estimated to be about 6%, using both epidemiologic and pathologic data. Screening trials using PSA and/or TRUS instead of or in addition to DRE have approached this rate of detection. As Fig 1 illustrates, screening appears to detect almost all of the clinically important cancers in the study population. The fear that these tests will detect a high proportion of latent, or clinically unimportant, cancers appears to be unfounded. Our studies and those of others support the concept that 85% to 90% of cancers detectable with current tests are clinically important. The detection of nonpalpable cancers by PSA or TRUS reduces the proportion of cancers detected at an advanced stage without increasing significantly the detection of latent or clinically unimportant cancers. Despite this analysis, we still lack definitive data to show that screening and treating early stage cancers will decrease the mortality rate of this disease. Such a conclusion will require a long-term, randomized screening trial or a comparison of mortality rates among large populations of men differing primarily in the extent of screening for prostate cancer.
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PMID:Early detection of prostate cancer: the nature of cancers detected with current diagnostic tests. 752 52

In 1993, medical therapy for BPH is a reality. Androgen deprivation therapy (LHRH agonists, antiandrogens, and 5 alpha-reductase inhibitors) has been shown to be effective by reducing the static component of BPH. Of these agents, the 5 alpha-reductase inhibitors have the greatest promise because of their low toxicity profile. Aromatase inhibitors, which function via a different mechanism, however, have not been demonstrated, as monotherapy, to be effective in the treatment of symptomatic BPH. It is still theoretically possible that aromatase inhibitors could have a role in the management of prostatism if they are utilized in conjunction with an antiandrogen or 5 alpha-reductase inhibitor. Although the early results for this endocrine therapies are encouraging, several issues relating to medical treatment remain unanswered. Not everyone with significant prostatism will respond to androgen deprivation therapy. How does the physician identify pre-treatment the patient most likely to achieve a significant improvement in voiding function with 5 alpha-reductase inhibitor therapy? At the present time, there is no method--based on symptoms, DRE findings, serum hormone and PSA levels, or histopathologic criteria--for recognizing the ideal patient for androgen deprivation therapy. Without question, it is a subjective decision. As a result, the benefits and risks of these medical approaches as well as those of the minimally invasive and surgical therapies must be discussed with the patient so that he can participate in the management decision. In this manner, the expectations and needs of the patient will be best served.
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PMID:Endocrine therapies for BPH: scientific rationale, clinical results, and patient selection. 752 91

With the inevitable increase in non-surgical management of the many thousands of patients with assumed benign prostatic enlargement, the issue of undiagnosed prostatic cancer needs to be addressed. Currently our knowledge is incomplete in many areas, especially that pertaining to the outcome of therapy of incidentally discovered prostate cancers. Nonetheless common sense dictates that all patients presenting with clinical BPH should undergo DRE and those with palpable induration or asymmetry should be biopsied in the knowledge that around a third will prove positive. Ideally all patients with clinical BPH should also have a PSA determination, however, the result should be interpreted with care, taking into account the age and estimated life-expectancy of the patient. Patients younger than 75 with a PSA > 10 ng/ml should probably be biopsied routinely--around half will have cancer. Patients with PSA values between 4 and 10 (around 50% of cases of BPH) may legitimately be carefully observed for a period. Biopsy should be performed if an increase of > 20% in the PSA occurs during the year of follow-up especially in younger patients. Evidence is mounting that TRUS has serious deficiencies in identifying prostate cancers, nonetheless it does provide the most effective means of accomplishing transrectal prostatic biopsy. Further studies are required to critically evaluate the competing claims for improved diagnostic accuracy of PSAD, PSAV and age-adjusted PSA, the last of which does have the advantage of practicability.
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PMID:BPH: when to rule out carcinoma of the prostate. 752 2

The first problem to be solved in the evaluation of BPH patients is surely the differential diagnosis with prostate carcinoma. We evaluated the impact of a combined approach for prostate cancer detection using DRE, PSA, TRUS and ultrasound-guided biopsy, determining the sensitivity and specificity of different tools, in order to obtain a diagnostic algorithm to be used for pretreatment differential diagnosis between prostate cancer and BPH.
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PMID:Prostate cancer detection in BPH patients. 753 Sep 42

PSA is a 34-kDa 240-amino-acid glycoprotein produced exclusively by prostatic epithelial cells. PSA is a serine protease, is a member of the kallikrein gene family, and has a high sequence homology with human glandular kallikrein. It has chymotrypsin-, trypsin-, and esterase-like activities. In the serum it is present mainly in a complex form with alpha 1-antichymotrypsin. It is secreted in the seminal plasma and is responsible for liquefaction of the seminal coagulum. The production of PSA proteins appears to be under the control of circulating androgens acting through the androgen receptors. The PSA gene is up-regulated predominantly by androgens at both the protein and mRNA levels. DRE causes minimal changes in the PSA level, while prostate massage, ultrasonography, systoscopic examination, and prostate biopsy can all cause clinically significant elevations. Other conditions, such as prostatitis, prostate intraepithelial neoplasia, acute urinary retention, and renal failure can also elevate the PSA level. The value of PSA as a screening tool is questionable because of the great deal of overlap in PSA levels between BPH and prostate cancer. However, if used in men over 50, in conjunction with DRE and/or ultrasonography, it may become a vital part of the early detection program. PSA's role in determining the clinical and pathological stage is also limited, in spite of the direct correlation between the pathological stage and the PSA level, because of great overlap in the PSA levels in various stages. The most important clinical utility of PSA is in monitoring patients after definitive therapy. PSA is most sensitive and reliable in the detection of a residual tumor, possibly recurrence, or disease progression following treatment, irrespective of the treatment modality. PSA can accurately predict the tumor status and can detect recurrence several months before its detection by any other method. PSA is also a very sensitive and specific immunohistochemical marker for tumors of prostatic origin. Compared to PAP, PSA is a more precise and meaningful marker in all clinical situations. With the development of ultrasensitive assays and the adoption of an international standard PSA calibrator, so that results from multicenter studies can be compared, PSA could become one of the most useful tumor marker in cancer biology.
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PMID:Prostatic specific antigen. 753 74

The Authors report their experience in the diagnosis of prostatic carcinoma by means of DRE, TRUS and PSA. They emphasize the improvement of diagnosis given by these exams when used in association, despite a high rate of false positives. In the years 92-93, 182 patients underwent ecoguided prostatic biopsy after DRE and PSA evaluation. PSA density value was calculated as proposed by Benson (PSAD = PSA/V); this parameter should screen between PSA elevation due to BPH and those due to prostatic carcinoma. After their experience, even if limited, they conclude that TRUS should not be used as a "first-line test" but only in patients with abnormal findings in DRE and/or PSA. PSAD may be useful to improve specificity of PSA even if a precise cut-off can not be determined.
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PMID:[Current role of echography, of PSA and of PSAD in the diagnosis of prostatic carcinoma]. 753 69

Several common misconceptions have fueled the debate over the early detection and treatment of prostate cancer. While prostate cancer is often described as a common cancer that older men die with rather than of, the reality is that the incidence, mortality, and mean age and stage at diagnosis of prostate cancer are very similar to those of breast cancer, which is rarely the subject of similar concerns. Many studies have confirmed that given enough time, all clinically detected prostate cancers will inexorably progress locally and eventually metastasize to regional lymph nodes as well as to distant sites. The relatively slow doubling time compared to that of other cancers and the wide spectrum of biologic activity of prostate cancer have made retrospective studies reporting the long-term survival of conservatively treated patients highly suspect due to selection bias and inadequate follow-up. While it is accepted that a large number of men harbor clinically insignificant cancers in their prostate glands, these estimates have been based on careful pathologic step-sectioning studies of prostates obtained either at autopsy or after cystoprostatectomy for bladder cancer. Several studies have now demonstrated that currently available diagnostic modalities for detecting prostate cancer, DRE, PSA, and TRUS, are not able to detect a significant proportion of small, clinically unimportant cancers. Rather, studies have shown that while the traditional DRE has been largely unsuccessful in detecting prostate cancers at a sufficiently early stage for effective treatment with either radical prostatectomy or radiation therapy, a combination of the DRE and PSA followed by TRUS and ultrasound-guided biopsy in those with abnormal results can detect an increased proportion of clinically significant prostate cancers while they are still confined to the prostate gland and thus more likely to be eradicated by treatment. Several randomized trials are now under way in this country and in Europe that may settle many of these issues over the next decade. However, currently available data suggest that prostate cancer screening holds the promise of decreasing the considerable morbidity and mortality caused by this disease.
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PMID:Screening for prostate cancer: an analysis of the early experience. 753 41


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