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Public awareness of prostate cancer and the prostate-specific antigen test.

Prostate cancer and prostate-specific antigen (PSA) testing have been the focus of significant media attention. This study examines the public's knowledge of prostate cancer, knowledge of the PSA test, and among men, the use of the test. The data are from the 1993 Kentucky Health Survey, an annual probability-based statewide telephone survey of adult (18 years of age and older) Kentucky residents (n = 661). Although 92% of the sample reported hearing of prostate cancer, the respondents were basically uninformed about the outcomes of prostate cancer. Men 50 years of age and older were no more informed than was the rest of the sample about prostate cancer or PSA testing. However, 94% of the men who had the test recommended by their physician had undergone the test. These findings indicate that adults remain poorly informed about prostate cancer and possible case-finding strategies. If the American Cancer Society's (ACS) early detection recommendations are to succeed, attention should focus on improving the public's awareness of currently available methods for early detection of prostate cancer.

Health Knowledge, Attitudes, Practice↗

Advanced prostate cancer with normal serum prostate-specific antigen values.

Prostate-specific antigen is a specific and sensitive marker of prostate cancer, and most patients with advanced prostate cancer have elevated serum prostate-specific antigen values. Over a period of 45 months, 976 cases of advanced prostate cancer (stages C and D) were investigated to determine the serum prostate-specific antigen level at presentation. Eight cases of advanced prostate cancer are documented in which the serum prostate-specific antigen values were within normal limits. Six of the eight cases showed the features of invasive moderately differentiated acinar carcinoma; one case of small-cell carcinoma and one of cribriform carcinoma were noted. Direct immunohistochemical assessment of tumor tissue was performed, and the correlation between monoclonal and polyclonal antibody staining was assessed. In seven of the eight cases, monoclonal antibodies showed no convincing staining, while all but one (small cell) were positive for polyclonal stains.

Adenocarcinoma↗

[The significance of prostate markers in the orthology of the female prostate].

In addition to knowledge gained in the first half of the 8th decade, the evidence of cross-antigenicity between male prostate and Skene's glands by means of PSA and PSAcP demonstrations in Skene's glands and ducts justifies utilization of the term prostate in both sexes. The authors compared the results of immunohistochemical examination of prostatic markers by means of the PAP method which was used at the beginning of the 8th decade, with that of BSAP technique. Prostatic tissues of 11 females and children at the age ranging from 5 to 71 years were examined. The results gained by means of the BSAP method were identical with those gained by means of the PAP method. Prostatic markers PSA and PSAcP were expressed on the surface and in apical cytoplasm of cells lining the prostatic ducts, and in prostatic glands. The authors proved the expression also in membranes of the stratified cylindrical epithelial cells of the ducts, and in female prostatic fluid in ducts and glands, especially PSAcP. Even though both immunohistochemical methods brought identical results, the authors recommend to prefer the BSAP method to the PAP method due to optically more contrast expression. (Fig. 8, Ref. 36.)

Acid Phosphatase↗

The incidence of unsuspected metastases from clinically benign prostate glands with latent prostate carcinoma.

OBJECTIVE: To determine how many latent prostate gland carcinomas (unsuspected carcinomas in clinically benign prostate glands) metastasize. DESIGN: The prostate glands and the pelvic and paraaortic lymph nodes were removed at autopsy from 209 consecutive patients with clinically benign prostate glands. The prostate glands were completely sectioned and examined microscopically using full cross sections. Pelvic and para-aortic lymph nodes were identified and examined microscopically for metastases. RESULTS: Seventy-nine (38%) of the prostate glands had latent prostate carcinomas. None of the pelvic or paraaortic lymph nodes contained metastases. CONCLUSION: This study suggests that few latent prostate-gland carcinomas metastasize.

Aged↗

Demonstration of a progestin receptor in human benign prostatic hyperplasia and prostatic carcinoma.

Cytosol from human benign hyperplastic and carcinomatous prostatic tissue has been shown to contain a progestin receptor with a dissociation constant of approximately 10(-9) M. The receptor was measured using 3H-labeled R 5020 (17 alpha, 21-dimethyl-19-nor-4,9-pregnadiene-3,20-dione) as ligand. Progesterone, cyproterone acetate, and R 1881 (methyltrienolone) were efficient competitors to R 5020 for binding sites on the receptor whereas testosterone, 5 alpha--dihydrotestosterone, estradiol, cortisol, and several hydroxylated and saturated derivatives of progesterone did not compete. The [3H]R 2020-receptor-complex had a sedimentation coefficient of approximately 4 S, an isoelectric point of approximately 5, was heat-labile, and was destroyed by treatment with trypsin but not with deoxyribonuclease or ribonuclease. Seventeen of 21 patients with benign prostatic hyperplasia and three patients with prostatic carcinoma had 1 to 40 fmoles of specific R 5020-binding sites per mg of cytosol protein. One sample of normal prostatic tissue did not contain significant amounts of progesting receptor. Tissue specimens removed by transvesical adenoma enucleation displayed a larger number of specific R 5020-binding sites than electroresected specimens. The progestin receptor in hyperplastic prostate may be involved in the mechanism of the action of progestins used in the medical treatment of benign prostatic hyperplasia. Quantitation of progestin receptor in cancer of the prostate may form part of the basis of a predictive test program for endocrine therapy of prostatic malignancy.

Aged↗

Autocrine regulation of prostate-specific antigen gene expression in a human prostatic cancer (LNCaP) subline.

Prostate-specific antigen (PSA), a M(r) 34,000 serine protease, is recognized as a useful marker for the detection and prognosis of patients with prostate cancer. Although serum PSA is an excellent prognostic indicator, an increasing number of factors were found to regulate the PSA expression of prostatic cancer cells, which include androgenic steroids, the growth factors (GFs) and the extracellular matrix. The purpose of this study is to define a novel protein factor that may be responsible for regulating PSA expression by androgen-independent (AI) human prostate cancer cells. We have established a LNCaP subline (C4) from a parental LNCaP tumor grown in a castrated host. The C4 subline overexpressed PSA mRNA and protein. Serum-free conditioned medium (CM) isolated from the C4 subline is able to stimulate PSA gene expression in parental LNCaP cells in a concentration-dependent manner. This autocrine PSA-inducing activity was found to be organ specific because CMs from other fibroblast cell lines (such as bone, prostate, kidney, and lung fibroblasts) and the CMs from several prostatic carcinoma cell lines (such as parental LNCaP, PC-3, DU-145) and a bladder transitional carcinoma cell line (WH) fail to exhibit similar activity. The activity of the CM from the C4 subline cannot be substituted by GFs such as TGF-alpha, TGF-beta, bFGF, HGF, KGF, or NGF; neuropeptide (bombesin/GRP); secondary messenger analogue (dibutyryl cAMP); beta 2-adrenergic agonist (isoproterenol); or alpha 1-adrenergic agonist (phenylephrine), indicating that the factor(s) may be a novel prostate-specific autocrine factor (PSAF). Both androgen and PSAF exhibit an additive effect on up-regulating PSA gene expression, suggesting that the signal transduction pathway elicited by PSAF may differ from that mediated by the androgen receptor. Further characterization of PSAF by heat, acid, and trypsin digestion revealed that the PSAF may be a protein factor with a unique amino acid composition. These observations suggest that a novel autocrine pathway mediated by PSAF may be responsible for the overexpression of PSA mRNA and protein in a human prostatic cancer cell line. The potential clinical significance of this factor will be discussed.

Castration↗

[Role of CT in patients with prostatic disease: usefulness of depiction of prostatic zonal anatomy].

The purpose of this study was to evaluate the role of CT in patients with and without prostatic disease. CT and MR findings were reviewed in 25 patients without known prostatic disease, 11 patients with benign prostatic hyperplasia and 11 patients with prostatic cancer. Differential attenuation allowed for distinction of the peripheral zone and inner gland of the prostate by CT in 72% of normal patients. The distinction rate of prostatic zonal anatomy by CT decreased to 30% in the diseased group. When zonal anatomy of the prostate is not visualized on pelvic enhanced CT, the presence of prostatic disease might be considered.

Adolescent↗

Plasminogen activator activities in short-term tissue cultures of benign prostatic hyperplasia and prostatic carcinoma.

The high prevalence of prostatic carcinoma (PRCA) and the limited therapeutic possibilities provide a strong stimulus for exploring new approaches in experimental research that ultimately may lead to improved therapy. Indeed, methods for assessing carcinoma prognosis, such as clinical staging (clinical examination, ultrasound, and plasmatic levels of prostatic acid phosphatase and prostate specific antigen) and histopathological grading according to the Gleason score, usually fail to provide consistent predictive information regarding the clinical outcome of single tumors. Increased plasminogen activator (PA) activities have been associated with high-grade malignancies and with the potential for invasion/metastasis in many tumors. Urokinase-type plasminogen activator (uPA) is present in prostatic secretion, and an increased uPA activity has been noted in human prostatic cell lines with metastatic behavior. Unfortunately, any study of uPA production or gene regulation in primary tumors is complicated by the inherent mixture of host stromal cells, infiltrating macrophages, and subpopulations of tumor cells that may have variable metastatic capacity and ability to synthesize uPA. In short-term tissue culture of prostatic samples, it is possible to grow in vitro cancer prostatic epithelial cells and thus exclude the presence of contaminant cells. We have shown elsewhere that the levels of a type IV collagenase, 92-kDa matrix metalloproteinase, a protease involved in tumor progression and invasion, are increased in PRCA primary cell cultures if compared with benign prostatic hyperplasia (BPH) cell cultures (C. Festuccia et al., manuscript in preparation). Activation of matrix metalloproteinases also can be correlated with uPA expression; therefore we studied the expression of uPA in serum-free culture media of primary cultures of PRCA or BPH tissue samples.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗

Retroviral transduction of transforming growth factor-beta1 induces pleiotropic benign prostatic growth abnormalities in mouse prostate reconstitutions.

Transforming growth factor-beta1 (TGF-beta1) plays an important role in the normal growth and differentiation of the mouse prostate with accumulations of extracellular TGF-beta1 in fetal and neonatal prostate tissues particularly at epithelial-mesenchymal interfaces. We have demonstrated increased accumulation of TGF-beta1 in areas of human prostates with benign prostatic hyperplasia and adenocarcinoma by immunohistochemistry. To study the role of TGF-beta1 in pathologic processes, we constructed retroviruses that express the cDNA for murine TGF-beta1 along with either a dominant selectable geneticin (G418) resistance (Neo) gene, BabeTGF-beta1Neo, or a histochemically detectable beta-galactosidase gene, BabeTGF-beta1Gal. The biologic activity of these retroviruses was evaluated in vitro in NIH3T3 fibroblasts and in vivo using the mouse prostate reconstitution (MPR) model. Expression of the retrovirus in MPR was confirmed by beta-galactosidase staining and by reverse transcription followed by PCR for the virus-encoded RNA. Pathologic evaluation of hematoxylin and eosin-stained sections was complemented by immunohistochemical analysis of cytokeratin and neuronal markers. TGF-beta1 transducing retrovirus infection did not have an effect on total growth of the MPR; however, changes in the growth and distribution of specific cell types were observed. A phenotype of benign hyperplasia that involved increased numbers of cytokeratin 14-positive cells characteristic of basal epithelial cells was observed. Immunohistochemical studies colocalized an increased accumulation of extracellular TGF-beta1 with these cytokeratin 14 expressing hyperplastic lesions, An increase in stromal abnormalities was also observed and included a significant increase in the density of neuronal cells. The TGF-beta1-induced hyperplastic response involving basal epithelial cells may be the result of paracrine stimulation of growth of specific cell types in the prostate and may represent a divergence of normal growth processes. Benign growth abnormalities of basal epithelial cells in the human prostate have also been reported. An increased density of neuronal cells and other stromal abnormalities in response to TGF-beta1 retroviral transduction is also consistent with benign growth abnormalities in the human prostate.

3T3 Cells↗

Recommended prostate-specific antigen testing intervals for the detection of curable prostate cancer.

OBJECTIVE: To evaluate prostate-specific antigen (PSA) testing intervals that maintain the detection of curable cancer and reduce unnecessary testing. DESIGN AND PATIENTS: Historical prospective study of serial PSA measurements at 2- and 4-year intervals from frozen serum samples of 40 men who eventually developed prostate cancer and 272 men without prostate cancer who were participants in a prospective aging study (Gerontology Research Center of the National Institute on Aging, the Baltimore Longitudinal Study of Aging) and the case series of 389 consecutive men treated surgically for nonpalpable prostate cancer. MAIN OUTCOME MEASURES: Probability of a PSA conversion to 4.1 to 5.0 ng/mL and to greater than 5.0 ng/mL at 2 and 4 years and probability of detecting curable prostate cancer by age and PSA level. RESULTS: When the pretreatment PSA level was less than or equal to 4.0 ng/mL, nonpalpable prostate cancers were highly likely (34/36, 94%) to be curable (organ-confined or capsular penetration with Gleason score < 7 and negative margins), and the majority (25/36, 69%) were small cancers (confined tumor < or = 0.5 cm3 with no Gleason pattern 4 or 5). When the pretreatment PSA level was greater than 4.0 ng/mL and less than or equal to 5.0 ng/mL, cancers were highly likely to be curable (32/36, 89%), and a minority were small cancers (12/36, 33%). When the pretreatment PSA level was greater than 5.0 ng/mL, 96 (30%) of 317 cancers were noncurable. The PSA conversion (for cancer cases) to a level at which cure is less likely (> 5.0 ng/mL) is rare (0%) after 2 or 4 years when the initial PSA is less than 2.0 ng/mL. PSA conversion to a range at which cancers are likely to be curable and less likely to be small (4.1-5.0 ng/mL) is rare after 2 years (0%-4%) when the baseline PSA level is less than 2.0 ng/mL but common when the baseline PSA level is between 2.1 and 3.0 ng/mL (27%) or 3.1 and 4.0 ng/mL (36%). CONCLUSIONS: These data suggest that for men with no cancer suspected on digital rectal examination, a PSA level of 4.0 to 5.0 ng/mL is an acceptable range for maintaining the detection of curable prostate cancer and a 2-year PSA testing interval is not likely to miss a curable prostate cancer when the initial PSA level is less than 2.0 ng/mL. Recognizing that 70% of a screened population between the ages of 50 years and 70 years have PSA levels less than 2.0 ng/mL, elimination of annual PSA testing for these men would result in large health care cost savings.

Aged↗

Stratification of prostate-specific antigen level and results of transrectal ultrasonography and digital rectal examination as predictors of positive prostate biopsy.

OBJECTIVE: To determine which of several variables--age, serum level of prostate-specific antigen (PSA), findings of transrectal ultrasonography (TRUS) and findings of digital rectal examination (DRE)--are the best predictors of positive prostate biopsy results. SETTING: An urban, university-affiliated tertiary care hospital. PATIENTS: a cohort of 1330 consecutive men referred to the diagnostic imaging department for TRUS and TRUS-guided prostate biopsy. Each patient was referred after examination by a urologist because of clinical suspicion of prostate cancer. METHODS: All of the men had undergone prior determination of serum level of PSA. Repeat DRE was performed at the time of imaging. The variables age, PSA level, TRUS findings and DRE findings were tested aline and in combination as predictors of positive biopsy results by means of logistic regression analysis. A summary of percentage risk for positive biopsy results was constructed for each combination of statistically significant variables, stratified for age. RESULTS: Cancer was detected in 541 men (40.7%). A strong correlation was observed between serum PSA level and the likelihood of positive biopsy result (p < 0.001). Of 402 men with normal age-specific PSA, 109 (27.1%) had positive biopsy results. Of 403 men with PSA of 10 ng/mL or more, 233 (57.8%) had cancer. The level of serum PSA was also related to the number of prostate sextants harbouring cancer (p < 0.001). TRUS findings at the time of biopsy were a strong predictor of cancer of the PSA level was abnormal (p < 0.001). DRE results alone did not correlate with positive biopsy results, regardless of age, PSA level of TRUS findings. CONCLUSIONS: Men in whom there is a clinical concern for prostate cancer should undergo prostate biopsy if there is any elevation of age-specific PSA, particularly if the findings of TRUS are also abnormal. Because DRE alone was not predictive of biopsy outcome, algorithms for prostate cancer detection that rely on abnormal DRE results to identify men who should undergo biopsy will miss a significant number of cancers.

Aged↗

[The role of prostate specific antigen and its derivatives (age-specific PSA, PSA density, velocity, free/total PSA) in the diagnosis of prostate cancer].

PSA is the most useful tumor marker for the diagnosis and treatment of prostate cancer. Its clinical use, however, still lacks the necessary sensitivity and specificity to be considered as ideal. In fact PSA is not specific for adenocarcinoma of the prostate: an elevated serum level of the marker does not necessarily mean malignant growth and normal levels too often hide an occult and potentially lethal cancer. With the discovery of different molecular PSA forms in the serum, an improved discrimination between benign prostate hyperplasia (BPH) and prostate cancer appears possible. This may be particularly useful in cases with equivocal PSA values and unpalpable prostate neoplasm to reduce the number of unnecessary prostate biopsies and increase the number of biopsies in cases without palpable or ultrasonic visible anomalies. The clinical use of PSA age-referenced levels is discussed. Their use is invaluable in screening programs where the routine adoption of age-specific values can help to pick-up younger patients with potentially curable prostate cancer and older patients with BPH where additional tests would be unnecessary. The role of PSA velocity (PASAV) s also discussed. An elevation rate of PSA of 0.75 ng/ml over 18 months on 3 serial samples appears to be the best cut-off to distinguish BPH from prostate cancer. However, the use of PSAV seems to be less useful in patients with elevated PSA levels and negative biopsy results. Free to total PSA ratio is probably the best parameter to reduce the number of unnecessary biopsies in men with a serum total PSA of 4 to 10 ng/ml. The advantages and limitations for different levels of cut-off are shown. A flow chart illustrating the role of various PSA "derivatives" in screening and subsequent evaluation of men over 50 years of age is also presented.

Age Factors↗

Simultaneous radiotherapy for prostate cancer: 125I prostate implant followed by external-beam radiation.

PURPOSE: Using a rigorous prostate-specific antigen definition of disease-freedom, the 10-year disease-free survival rates after simultaneous radiation of prostate cancer are presented. PATIENTS AND MATERIALS: From January 1984 through December 1996, 1020 men with clinical stage T1T2N0 prostate cancer were treated by simultaneous radiation: radioactive 125I prostate implantation followed by external-beam radiation. The median pretreatment prostate-specific antigen was 7.5 ng/mL (range, 0.2-188 ng/mL). Implantation was performed by both the retropubic and the transperineal technique, always followed by external-beam radiation. None received hormone treatment. Disease freedom is defined as achieving and maintaining a posttreatment prostate-specific antigen of < or = 0.5 ng/mL. The median follow-up is 3 years (range, 1-14 years). RESULTS: The overall 5- and 10-year disease-free survival rates are 79% and 72%, respectively, after which a plateau is reached. At 5 years posttreatment, significantly better disease-free survival results are documented with simultaneous radiation by the ultrasound technique (92%) compared with the retropubic implant technique (73%). On multivariate analysis, pretreatment prostate-specific antigen is the most significant factor associated with disease-free survival, followed by implant technique. DISCUSSION: The 10-year disease-free survival rate after simultaneous radiation is comparable to the 10-year results after radical prostatectomy. Disease freedom is defined by the same prostate-specific antigen criteria used for surgery. A plateau in the disease-free curve suggests cure. Of equal importance, the information described in this report should form only a baseline relative to future results as men treated with simultaneous radiation using the transperineal implant technique reach longer follow-up.

Aged↗

[Significance of bacterial prostatic colonization for nosocomial urinary tract infections after transurethral prostate resection].

Nosocomial urinary tract infections (UTI) are frequent complications after transurethral prostatectomy. The resection itself, postoperative catheterization and the prostate are possible causes of these infections. In this prospective study we investigated the influence of bacterial prostatic colonization on the incidence of postoperative urinary tract infections and inflammatory complications. In 78 patients we observed in 42 cases (53.8%) a bacterial prostatitis. In 14 patients (17.9%) we found nosocomial UTI's and in 12 patients (15.4%) inflammatory complications. The incidence of postoperative UTI's increase significantly in patients with positive prostate-cultures. On the other hand we only found corresponding prostate- and postoperative urine-cultures in less than 50%. The presented data are not sufficient to conclude the kind of relevance of bacterial prostatic colonization for postoperative UTI's in transurethral prostatectomy. Under consideration of the significant increase of nosocomial UTI's in patients with positive prostate cultures a perioperative antibiotic prophylaxis seems to be required in general.

Aged↗

Discrimination of benign from malignant prostatic disease by selective measurements of single chain, intact free prostate specific antigen.

PURPOSE: Free prostate specific antigen (PSA) in serum consists of heterogeneous molecular subforms. Recently we developed an immunoassay for selective measurement of a subfraction of free PSA called intact PSA, which has been shown to be closely associated with prostate cancer. We assessed the ability of serum intact PSA to discriminate between benign and malignant prostatic disease. MATERIALS AND METHODS: In serum of 178 men with benign disease and 255 men with prostate cancer we measured total PSA and free PSA using a commercially available immunoassay. Intact PSA levels were analyzed by a newly developed assay specific for noncleaved, that is single chain forms of free PSA. Internally cleaved "nicked" PSA was calculated by subtracting intact from free PSA. We also calculated ratios of intact PSA-to-free PSA (intact-to-free PSA) and nicked PSA-to-total PSA (nicked-to-total PSA). We compared means, medians and ranges of all analytes and ratios in patients with and without cancer for the entire total PSA range and in a subset with total PSA ranging from 2 to 10 ng./ml. Furthermore, various combinations of PSA forms were tested for their predictive ability. For statistical comparison we used the Mann-Whitney U test and ROC analysis. RESULTS: The ratio intact-to-free PSA was significantly higher in cancer (median 48.5%) compared to noncancer cases (median 41.8%, p <0.0001). Conversely, the ratio nicked-to-total PSA was significantly higher in men without compared to those with prostate cancer (median 11.0% and 6.0%, respectively, p <0.0001). Highest discriminative ability was observed for a combination of intact, total and free PSA (log [intact, free, total], AUC = 0.773) followed by nicked-to-total PSA (AUC 0.755). In the subgroup of patients with total PSA levels from 2 to 10 ng./ml. only the AUC of log intact, free, total (AUC 0.706, p = 0.0017) and nicked-to-total PSA (AUC 0.704,p = 0.0019) were significantly larger compared to the AUC of total PSA (AUC 0.602). CONCLUSIONS: By contrast to measuring crude free PSA concentration, selective determination of specific free PSA subforms, intact PSA and nicked PSA proved to be useful to discriminate men with benign from malignant prostatic disease. These markers may serve to generate specific serum profiles of PSA for improved specificity and early detection of prostate cancer. To translate the encouraging statistical advantage shown in this study into a clinically applicable tool warrants further investigation.

Biomarkers, Tumor↗

Prostate specific antigen: a critical assessment of the most useful tumor marker for adenocarcinoma of the prostate.

PSA is a kallikrein-like, serine protease that is produced exclusively by the epithelial cells of all types of prostatic tissue, benign and malignant. Physiologically, it is present in the seminal fluid at high concentration and functions to cleave the high molecular weight protein responsible for the seminal coagulum into smaller polypeptides. This action results in liquefaction of the coagulum. PSA is also present in the serum and can be measured reliably by either a monoclonal immunoradiometric assay or a polyclonal radioimmunoassay. The calculated half-life of serum PSA ranges from 2.2 to 3.2 days and the metabolic clearance rate of this tumor marker follows first-order kinetics. Digital rectal examination, cystoscopic examination and prostate biopsy all can cause spurious elevations of the serum PSA concentration. Conditions such as bacterial prostatitis and acute urinary retention also can falsely elevate the serum PSA level. Because approximately 25% of the patients with BPH only will have an elevated serum PSA concentration and BPH tissue contributes to this PSA value in a variable manner from patient to patient, it is unlikely that PSA by itself will become an effective screening tool for the early diagnosis of prostate cancer. However, if combined with digital rectal examination and/or transrectal ultrasound it may become a vital part of any early detection program. Prostatic intraepithelial neoplasia also may be associated with moderately elevated serum PSA levels. Although there is a direct correlation between the serum PSA concentration and clinical stage, PSA is not sufficiently reliable to determine the clinical stage on an individual basis. This finding also applies to pathological stage. As a result, the preoperative serum PSA concentration cannot be used to decide whether to recommend radical prostatectomy for potential cure. Low preoperative serum PSA concentrations in patients with previously untreated prostate cancers are predictive of a negative bone scan. Thus, in these select patients a staging bone scintigram may not be necessary. With respect to monitoring patients after definitive therapy, PSA is an exquisitely sensitive tumor marker. Irrespective of the treatment modality (radical prostatectomy, radiation therapy or antiandrogen treatment), PSA reflects accurately the tumor status of the patient and is prognostic of eventual outcome; this tumor marker is capable of predicting tumor recurrence months before its detection by any other method. PSA is also a most useful immunocytochemical marker. Its sensitivity and specificity to identify tissue of prostatic origin approach 100%. When compared to PAP, PSA is a more precise and meaningful marker in all clinical situations.(ABSTRACT TRUNCATED AT 400 WORDS)

Acid Phosphatase↗

Exfoliative cytology of prostatic carcinoma using a prostatic fluid collecting catheter.

In 152 patients who were suspected to have prostatic disease prostatic fluid obtained by a specially designed catheter was examined cytologically. Cytology was positive in 16 of 20 patients who initially were diagnosed clinically as having prostatic carcinoma, in 10 of 41 patients with suspected carcinoma and in 3 of 91 patients with clinical prostatic hypertrophy or other benign diseases. All but one of these cytologically positive cases finally were confirmed histologically to have prostatic carcinoma. In 4 patients initially diagnosed as having prostatic carcinoma cytology was not positive but in one the initial clinical diagnosis was incorrect and only 3 were false negative. This method of diagnosis is simple and highly effective in detecting prostatic carcinoma.

Adenocarcinoma↗

New concepts in tissue specificity for prostate cancer and benign prostatic hyperplasia.

Of the hundreds of species of mammals, all of which have prostate glands, only humans and dogs are known to suffer from benign prostatic hyperplasia (BPH) and prostate carcinoma. In humans, prostate carcinoma is common, yet carcinomas of other sex accessory tissues are rare. In addition, different anatomic regions within the prostate gland have very different rates of BPH and carcinoma. In this article, we explore ideas and potential mechanisms relating to these paradoxical findings that may help explain the species, organ, and zone specificity of BPH and prostate cancer. We present an evolutionary argument that attempts to relate a high-fat diet, with its potential for generating oxidative DNA damage, to the species selectivity of prostate cancer. In addition, we outline an argument based on our preliminary studies indicating that chronic inflammation and the associated increase in cell turnover in the setting of increased oxidative stress may help to account for the organ selectivity of genitourinary carcinomas.

Animals↗