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)

The use of PSA-density (PSAD) as an indicator for prostate biopsy at intermediate PSA values has generated controversy. There are investigators who consider that the determination of PSAD is futile, and that it is better to do a prostate biopsy based on PSA values alone, TRUS (Transrectal Ultrasound) findings and/or DRE examinations. Asian countries, especially in the Far East, are considered to have a low incidence of prostate cancer (PCa). However, based on western references, we still measure PSA-density with a cut-off level of 0.15 to promote prostate biopsy in patients with intermediate PSA values (4.1-10.0 ng/ml). Our study aims to evaluate the usefulness of PSAD as an indication for biopsy in patients with intermediate serum PSA values. To evaluate the usefulness of this indicator, we conducted a retrospective study of 132 uncatheterized (to minimize potential bias) BPH and PCa cases that were hospitalized in our department between 1995-1997 (3 years). This group comprised 127 BPH and 5 PCa patients. Mean age was 66.1 +/- 7.69 years; mean PSA was 7.92 +/- 9.289 ng/ml; mean prostate volume was 54.1 +/- 26.72 cc; mean PSAD was 0.15 +/- 0.185. More specifically, there were 49 patients with intermediate PSA values (47 BPH & 2 PCa). The receiver operator characteristic (ROC) curve revealed an optimum cut-off level of 0.19. At this level of PSA density, the measured sensitivity was 100% with a specificity of 79%. We concluded that, in our uncatheterized patients (without retention) series, the PSAD cut-off level for prostate biopsy (0.19) was higher than that in the western world (0.12 or 0.15).
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PMID:A higher PSA-density cut-off level in patients with intermediate PSA values for the early detection of prostate cancer. 1089 3

Primary prostate transitional cell carcinoma is a very rare tumour originating in the transitional epithelial cells of the intraprostate periurethral ductus. Only 17 of 829 patients diagnosed with prostate carcinoma were found to have the transitional cell variety. Eight (8) of those had pure transitional cell carcinoma and 9 a mixed presentation of acinar adenocarcinoma and transitional cell ductal carcinoma. Bladder origin of the tumour was ruled out in all cases. We report a retrospective study on the clinical behaviour of prostate transitional cell carcinoma. Compared to acinar carcinomas, few differences were found when age, symptoms, physical findings and imaging diagnosis were evaluated. Clinical presentation, DRE, PSA, metastatic spread and presence of supravesical obstructive uropathy where also studied to establish a diagnosis. Radiotherapy was the most frequently used therapeutical approach. Mean survival is 26.6 months (4-60 months) and there has been 11 death up to now. Compared to acinar forms, this tumour shows a hormone-resistant, aggressive biological behaviour with poor prognosis. Early diagnosis and radical surgery are the only options available to increase life expectancy for these patients.
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PMID:[Primary transitional carcinoma of the prostatic ductus]. 1096 77

Early diagnosis of prostate cancer is best achieved using a combination of DRE and PSA as first-line tests to detect signs of prostate cancer. Because DRE and PSA do not always detect the same cancer, the tests are complementary. Among men with elevated PSA who are negative on DRE, the chance of cancer ranges from 12 to 32%. Most men with PSA elevations do not have cancer. This high false-positive rate among men without cancer has led to many approaches to decrease the incidence of false-positive test results, including PSA density, transition zone PSA density, PSA velocity, age-specific PSA reference ranges and percent free PSA.
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PMID:[Prostate specific antigen: a role of PSA in the diagnosis of prostate cancer]. 1176 72

DRE has been used as a diagnostic and screening tool for prostate cancer for decades. However these are based on Western data and its local applicability has yet to be verified. We held a Prostate Health Awareness Week in August 1998 and a total of 2086 men were screened. All men aged 50 years old and above were included for the study. The subjects were evaluated on DRE findings, PSA levels and if indicated a TRUS-guided biopsy results. We concluded that DRE per se might have limited role in the screening of prostate cancer in Malaysia. Screening using DRE and PSA combined are still recognized as the most cost-effective means. Neither DRE nor PSA alone has high enough specificity for diagnosis of prostate cancer cases. Combining DRE and PSA will definitely increase the specificity significantly.
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PMID:The role of DRE in the diagnosis of prostate carcinoma. 1177 Oct 76

Our study was performed to evaluate the diagnostic usefulness of %fPSA alone and combined with an ANN at different PSA concentration ranges, including the low range 2-4 ng/ml, to improve the risk assessment of prostate cancer. A total of 928 men with prostate cancer and BPH without any pretreatment of the prostate in the PSA range 2-20 ng/ml were enrolled in the study between 1996 and 2001. An ANN with input data of PSA, %fPSA, patient's age, prostate volume and DRE status was developed to calculate the individual's risk before performing a prostate biopsy within the different PSA ranges 2-4, 4.1-10 and 10.1-20 ng/ml. ROC analysis and cut-off calculations were used to estimate the diagnostic improvement of %fPSA and ANN in comparison to PSA. At the 90% sensitivity level, %fPSA and ANN performed better than PSA in all ranges, enhancing the specificity by 15-28% and 32-44%, respectively. For the low PSA range 2-4 ng/mL, we recommend a first-time biopsy at an ANN specificity level of 90%. For PSA 4-10 ng/mL, we recommend a first-time biopsy based on the ANN at the 90% sensitivity level. Use of an ANN enhances the %fPSA performance to further reduce the number of unnecessary biopsies within the PSA range 2-10 ng/ml.
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PMID:An artificial neural network considerably improves the diagnostic power of percent free prostate-specific antigen in prostate cancer diagnosis: results of a 5-year investigation. 1199 19

Prostate cancer is the commonest non-skin malignancy in the United States and has a substantial mortality rate despite the use of PSA-based screening. Furthermore, therapy for prostate cancer by surgery, radiotherapy or hormonal manipulation carries a significant risk of treatment-related morbidity. Recent analysis of secondary endpoints of several large-scale randomized prospective clinical trials for other malignancies has suggested that selenium or vitamin E may result in a decreased incidence and mortality from prostate cancer. In vitro and preclinical studies of these antioxidants support this hypothesis. This review outlines the rationale and design of SELECT, the Selenium and Vitamin E Cancer Prevention Trial, designed to test the hypothesis that selenium or vitamin E alone or in combination can reduce the clinical incidence of prostate cancer in a population-based cohort of men at risk. SELECT is a phase III, randomized, double-blinded, prospective, 2x2 factorial clinical trial which will randomize 32,400 healthy men with normal DRE and serum PSA to one of four study arms: selenium alone, vitamin E alone, selenium+vitamin E, or placebo. Study agents will be taken orally for a minimum of 7 and maximum of 12 y with assessments of general health, incident prostate cancer and toxicity performed at 12 month intervals. Under the assumptions described, the detectable risk reduction is 25% for an effective single agent relative to placebo, with an additional 25% reduction for the combination relative to an effective single agent. The estimated power for the comparison of a single agent vs placebo is 96% and the power for the comparison of an effective single agent vs combination is 89%. Secondary endpoints will include prostate cancer-free survival, all-cause mortality, and the incidence and mortality of other cancers and diseases potentially impacted by the chronic use of selenium and vitamin E. Other trial objectives will include periodic quality of life assessments, assessment of serum micronutrient levels and prostate cancer risk, and studies of the evaluation of biological and genetic markers with the risk of prostate cancer. Prostate Cancer and Prostatic Diseases (2000) 3, 145-151
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PMID:SELECT: the Selenium and Vitamin E Cancer Prevention Trial: rationale and design. 1249 90

A family history is one of the strongest risk factors for prostate cancer (PC). We evaluated the detection rate of PC in relatives of 119 German PC families that took part in ongoing linkage analyses. Brothers of patients with sporadic prostate cancer aged < 55 years at onset were included as well. Responses were received from 120/196 (61.2%) individuals of the familial and 67/120 (55.8%) of the sporadic group. Findings (DRE, TRUS, PSA) were more often suspicious for carcinoma in the PC families. Prostate cancer was diagnosed in 6 (5.0%) and 2 (2.99%) participants of the familial and the sporadic group, respectively. These detection rates tended to be higher than that of an age-matched subgroup of an unselected population in other European screening studies. The most important risk factor for the diagnosis of PC was a low average age at onset within the family. These data imply that prostate cancer screening in the high-risk group of men with familial predisposition cannot be assessed by population-based studies and should be evaluated separately.
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PMID:[Preventing prostate carcinoma in men with familial disposition]. 1252 47

PSA continues to be one of the most effective and widely used cancer screening tools available. Its popularity in prostate cancer screening, however, has eroded its usefulness in the staging of this disease. As more men are screened every year on a routine basis with DRE and PSA, the average PSA at diagnosis has drifted down to well below 10 ng/mL in many centers, including ours. This trend is likely to accelerate, as a PSA cut off for prompting biopsy of the prostate of 2.5 ng/mL gains more widespread acceptance. The recent realization that, at these levels, serum PSA is more reflective of the presence of BPH than of the extent of cancer and, therefore, does not provide additional staging information, has renewed the search for new biochemical markers that are capable of predicting prostate cancer stage and prognosis. Because of the heterogeneity of this disease, it is unlikely that a single biochemical marker that is capable of accurately staging all prostate cancer patients will be found. For this reason, nomograms that are capable of integrating various parameters to predict stage and prognosis will remain indispensable. As new biochemical markers that provide independent predictive information about stage or prognosis are identified, they can be incorporated into currently available nomograms. Of the biochemical markers discussed in this article, IL-6sR and TGF-beta1 are the most promising. By incorporating them into a preoperative nomogram designed to predict PSA recurrence, we found that they improved the ability to predict biochemical recurrence by a statistically and clinically significant margin. The ability to stage prostate cancer and predict response to therapy has improved dramatically over the last 3 decades. Nevertheless, there is still a need for new biochemical markers that will improve the ability to predict an individual patient's stage and response to therapy. Incorporating these new markers into nomograms will enhance the ability to provide optimal care for each prostate cancer patient.
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PMID:Biochemical staging of prostate cancer. 1273 3

BCR is the most clinically used endpoint for identification of treatment failure. Approximately 15% to 53% of patients undergoing primary curative therapy will develop BCR. BCR often precedes clinically detectable recurrence by years. It does not necessarily translate directly into PCa morbidity and mortality, nor does it always reflect the desired endpoint. Furthermore, it has not been validated as a surrogate endpoint, in that interventions that have been shown to alter the PSA level have not been shown to also alter survival. The utility of PSA level as a surrogate endpoint is brought into question by the knowledge that the overall survival rate of patients at 10 years is similar in patients with and without BCR, and that in a significant proportion of men, the only evidence of disease during their lifetime will be a detectable PSA level. The likelihood of developing BCR post-therapy can be predicted by using multiple clinical and pathologic variables. With the development of nomograms that incorporate several markers, the accuracy of prediction has improved. Until recently, the natural history of BCR post-RRP has not been well understood. Pound et al showed the heterogenous and prolonged natural history of BCR. In this large series of men with BCR following RRP, only 34% of men developed metastatic disease. The median time from development of BCR to identification of metastases was 8 years, and the median time from the development of metastatic disease to death was just under 5 years. These data highlight the extremely variable and potentially indolent nature of BCR. The risk of metastatic disease following BCR has been relatively well defined and relates to PSADT and time to PSA recurrence. It generally is accepted that a PSADT of less than 6 to 10 months and a time to PSA recurrence of less than 1 to 2 years relates to a higher risk of developing metastatic disease. Local recurrence, however, remains poorly understood with respect to its true incidence, clinical significance, and natural history. The significance of BCR post-RT remains unclear due to the lack of data on its natural history. Attempts have been made to identify patients at high risk for metastatic progression by looking at time to PSA recurrence and PSADT. A PSADT of less than 6 to 12 months and a time to PSA recurrence of less than 12 months reflects a higher risk of developing metastatic disease. Accurate risk stratification by means of an algorithm similar to that produced by Pound et al has not been performed on a large cohort, thus making risk assessment for an individual patient difficult. The major dilemma for clinicians in the management of BCR is the identification of the site of disease recurrence, which ultimately guides therapy decisions. Clinicopathologic features allow for risk stratification for recurrence, and multiple investigations have attempted to localize the site of recurrence. Time to biochemical progression, Gleason score, and PSADT are predictive of the probability and time to development of metastatic disease, and allow for stratification of patients into different risk groups (see Table 2). TRUS, CT, PET, and DRE all have limited utility in the identification of local recurrence. ProstaScint and MRI have demonstrated encouraging initial results: however, they require further investigation. Bone scintigraphy is of little value for the initial investigation of BCR. In patients with a PSA level of less than 10 ng/mL, the risk of having a positive bone scan is less than 1% and, until the PSA level rises above 40 ng/mL, the risk of having a positive bone scan is less than 5%. Therefore, bone scintigraphy should be reserved for patients with a PSA level greater than 10 to 20 ng/mL or patients with a rapidly rising PSA level. Using new MRI sequences, there is some evidence that MRI is better for the detection of bony metastatic disease; however, this technique requires further investigation. BCR causes anxiety for the patient and the treating doctor, because the best way to manage patients with PSA-only progression is unknown. Currently, there are no validated treatment recommendations for the management of BCR. The information in this review provides the framework for assignment of patients into clinical trials based on different risk categories. Patients at high risk for metastatic progression could be identified early and thus entered into appropriate clinical trials for systemic therapies. Similarly, patients with a low risk of progression could be placed into observation protocols, potentially sparing them from exhaustive and inappropriate investigations.
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PMID:Markers and meaning of primary treatment failure. 1273 13

Family history is one of the strongest epidemiological risk factors for the development of prostate cancer. The impact on the clinical presentation and prognosis, however, is controversial. In the present study, we analyzed 464 familial and 492 sporadic prostate cancer patients following radical prostatectomy. The average age at onset was 62.1 years in the familial group and 64.2 years in the sporadic controls (p<0.001). The screening attitude, DRE findings and the PSA values at diagnosis the pT- and pN-stages, and the tumor grade did not differ between both groups. With a median follow-up of 3.3 years, the 5- and 10-year progression-free survival rates were 76.2% and 56.5% in familial and 70.8% and 55.5% in sporadic patients, respectively (n.s.). A multiple logistic regression analysis revealed that family history did not have an influence on disease recurrence. In our population there was no association between a familial predisposition and clinical features or clinical course of the disease. Whether hereditary prostate cancer is distinct from sporadic forms cannot be determined before the underlying genetic alterations are identified.
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PMID:[Familial versus sporadic prostate cancer in the German population. Clinical and pathological characteristics in patients after radical prostatectomy]. 1289 39


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