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At least 1,099 records · Page 61Linked to original sources
PubMed1999

Promatrilysin expression is induced by fibroblast growth factors in the prostatic carcinoma cell line LNCaP but not in normal primary prostate epithelial cells.

BACKGROUND: It has been determined that prostate cancer cells overexpress the matrix metalloprotease matrilysin (MMP-7), but the factors regulating this expression have not been identified. Fibroblast growth factors (FGF), which are expressed in the prostate, might participate in paracrine regulation of matrilysin expression by prostate cancer cells. METHODS: We tested the ability of recombinant FGF proteins and prostate fibroblast-conditioned media (PFCM) to induce promatrilysin expression in the prostate carcinoma cell line, LNCaP, and in normal prostate epithelial (PrEC) cells. We also characterized prostate fibroblast FGF expression by reverse transcriptase-polymerase chain reaction (RT-PCR). An inhibitor of FGF receptor activation (SU5402) was used to determine the role of FGF proteins in the induction of promatrilysin expression by PFCM. RESULTS: Recombinant FGF-1, FGF-2, FGF-9, FGF-10, and PFCM significantly induced promatrilysin expression in LNCaP cells but not in PrEC cells. Prostate fibroblasts express mRNAs for these FGF proteins, and inhibition of LNCaP cell FGF receptors with SU5402 substantially reduced the induction of promatrilysin expression by PFCM. CONCLUSIONS: Stromally expressed FGF proteins induce promatrilysin expression in a prostate carcinoma cell, and may provide a mechanism for the overexpression of promatrilysin observed in prostate cancer.

Carcinoma↗
PubMed2000

Prostate-specific antigen: A surrogate endpoint for screening new agents against prostate cancer?

BACKGROUND: An endpoint for clinical trials of prostate cancer which simplifies traditional endpoints (response of measurable lesions, progression rates, and death) is urgently needed. This is especially true for hormone-unresponsive disease, for which many new drugs are presently in a development phase. This paper presents a rationale for the use of prostate-specific antigen (PSA) in clinical trials of progressive prostate cancer under endocrine treatment. METHODS: The study is based on 84 patients who progressed after radical prostatectomy or node dissection, of whom 24 showed increasing PSA levels under subsequent endocrine treatment. An average linear relationship between (log-transformed) PSA and time and a subject-specific deviation from this average relationship were assessed. The predictive value of the subject-specific parameters of the linear fit with respect to time to prostate cancer-specific death was determined. The outcomes of the fitting procedure were used to calculate sample sizes for future studies (duration, 6 months) using PSA increase over time in hormone-unresponsive prostate cancer as a marker for treatment efficacy. RESULTS: The average PSA doubling time in this population was 4 months (corresponding time constant = 0.25). The assessed variance of the time constants equalled 0.04; the overall residual variance equalled 0.265. The subject-specific rate of change of the log-transformed PSA value in hormone-unresponsive prostate cancer was a highly significant predictor of prostate cancer-specific death. This suggests the potential usefulness of PSA as an endpoint in trials of hormone-unresponsive prostate cancer. Depending on conditions chosen (e.g, desired power and changes in log PSA slope), 18-70 participants per arm will be necessary in future phase III studies. A suggestion (algorithm) for the use of PSA in drug development is presented. CONCLUSIONS: Relatively small PSA-based trials in patients with hormone-unresponsive prostate cancer are possible if a similar patient population is utilized. As long as surrogacy is not established, such studies cannot be considered conclusive with respect to effectiveness of treatment, but are likely to be useful as a screening tool for new drugs. Experimental confirmation in human prostate cancer model systems of synergism between PSA decrease and tumor control by a given test treatment is likely to enhance the level of certainty of PSA-based drug evaluation.

Biomarkers, Tumor↗
PubMed1997

Eight years of "Prostate Cancer Awareness Week": lessons in screening and early detection. Prostate Cancer Education Council.

BACKGROUND: Prostate Cancer Awareness Week began in 1989 to raise public awareness of the disease and impact on its clinical dynamics. Prior to 1990, prostate carcinoma was usually diagnosed in symptomatic men as advanced and ipso facto incurable. METHODS: A 5-year longitudinal study of screening and early detection was initiated in 1992, involving 250 centers that tested over 50,000 men annually. The study analyzed the following: 1) the efficacy of digital rectal examination and prostate specific antigen (PSA) tests for the early detection of prostate carcinoma, 2) the impact of serial screening on stage of disease at diagnosis and cancer detection, 3) age and race specific reference ranges for PSA, 4) prostate carcinoma risk factors, and 5) psychosocial variables that influence the appropriateness and acceptability of both screening and treatment. RESULTS: Community-based screening for prostate carcinoma is as effective as programs conducted at academic centers, but annual testing may not be necessary for all men. Participants in community screening programs may require more prescreening information and education regarding the potential risks and benefits of screening, and also regarding the cascade of diagnostic and treatment decisions that follow an abnormal digital rectal examination or an elevated PSA finding. CONCLUSIONS: Community-based prostate carcinoma screening programs have contributed to the shift in the diagnosis of prostate carcinoma at an earlier stage. They provide data that are useful in studying the natural course of prostate carcinoma and in designing studies of the effect that prostate carcinoma screening has on mortality from the disease.

Community Medicine↗
PubMed2000

Evaluation of prostatic specific antigen and digital rectal examination as screening tests for prostate cancer.

BACKGROUND: The 11,811 first visits and 46,751 annual follow-up visits performed since 1988 were analyzed in order to assess the efficacy of serum prostatic specific antigen (PSA) and digital rectal examination (DRE) for diagnosis of prostate cancer. METHODS: At first visit, screening included DRE and measurement of PSA using 3.0 ng/ml as upper limit of normal, demonstrated as optimal value in the course of the study. Transrectal echography of the prostate (TRUS) was performed only if PSA and/or DRE was abnormal. For elevated PSA, biopsy was performed only if PSA was above the value predicted from prostatic volume measured by TRUS. At follow-up visits, it was decided during the course of the study to use PSA alone. RESULTS: PSA was above 3.0 ng/ml in 16.6% and 15.6% of men at first and follow-up visits, respectively. Prostate cancer was found in 2.9% of men invited for screening at first visit and in only 0.4% of men at follow-up visits for a 7.1-fold decrease at follow-up visits done up to 11 years. PSA alone allowed to find 90.5% and 90. 0% of cancers at first and follow-up visits, respectively, compared to 41.1% and 25.0% by DRE alone. In the presence of normal PSA, 344 and 1,919 DREs are needed to find one prostate cancer at first and follow-up visits, respectively. A significant improvement in stage of the disease is found at follow-up (215 cancers) compared to first visits (337 cancers). Comparison made between men invited for screening and those who were not invited but screened showed no significant difference in terms of incidence and prevalence of prostate cancer as well as diagnosis of cancer as a function of age or as a function of PSA, DRE, and TRUS data. The cost for finding one case of prostate cancer is estimated at Can $2,420 and Can $7, 105 (first and follow-up visits, respectively, when PSA is used as prescreening). CONCLUSIONS: PSA used as prescreening and followed by DRE and TRUS when PSA is abnormal is highly efficient in detecting prostate cancer at a localized (potentially curable) stage since 99% of the cancers diagnosed were at such a localized stage, thus practically eliminating the diagnosis of metastatic and noncurable prostate cancer. The approach used is highly reliable, sensitive, efficient, and acceptable by the general population. The detection of clinically nonsignificant cancer is an exception.

Age Factors↗
PubMed2001

Perioperative prediction by MRI of prostate volume six to twelve months after laser-induced thermotherapy of benign prostatic hyperplasia.

The purpose of this study was to predict prostate volume outcome 6-12 months after interstitial, laser-induced thermotherapy (LITT) for benign prostatic hyperplasia (BPH) on the basis of prostate magnetic resonance (MR) images obtained within 48 hours before and after LITT. Twenty patients (age, 64.2 +/- 7.4 years) with symptomatic BPH had LITT of the transitional zone of the prostate. MRI was performed within 48 hours before and after LITT, and 6-12 months after LITT (late follow-up). MRI included axial and sagittal T2-weighted fast spin-echo (FSE) images and contrast-enhanced, axial T1-weighted images. Volumes of different prostatic compartments (total prostate, transitional zone, peripheral zone, LITT lesions) were measured by planimetry. Subtraction of LITT lesion volume less than 48 hours after LITT from total and transitional zone volume before LITT, respectively, predicted respective prostatic volumes at late follow-up. Pearson correlations of predicted and measured total prostate and transitional zone volumes were 0.972 and 0.975, respectively. Total prostate volume at late follow-up was accurately predicted (difference, -0.5 +/- 5.7 cc; P = 0.6981, two-tailed paired t-test). Transitional zone volume was underestimated (difference, -3.1 +/- 4.7 cc; P = 0.0075). Peripheral zone volume was overestimated (difference, 2.6 +/- 3.5 cc; P = 0.0034). Perioperative MRI allows accurate prediction of prostate volume 6-12 months after LITT for BPH. Underestimation of transitional zone volume may be due to ongoing growth of BPH. LITT appears to affect peripheral zone tissue outside the target region. J. Magn. Reson. Imaging 2001;13:64-68.

Follow-Up Studies↗
PubMed2003

Advanced age at diagnosis is an independent predictor of time to death from prostate carcinoma for patients undergoing external beam radiation therapy for clinically localized prostate carcinoma.

BACKGROUND: Whether age at diagnosis is predictive of time to prostate carcinoma specific death after external beam radiation therapy (RT) for patients who are diagnosed with clinically localized prostate carcinoma during the prostate specific antigen (PSA) era has not been investigated previously. METHODS: A multivariate Cox regression analysis was used to evaluate the ability of pretreatment risk group and age at diagnosis to predict time to all causes of death and time to death from prostate carcinoma for 381 patients who underwent RT for clinically localized prostate carcinoma. RESULTS: Age at diagnosis, as a continuous variable (P(continuous) = 0.04), and risk group (P(categorical) = 0.02) were independent predictors of time to death from prostate carcinoma, whereas only age at diagnosis (P(continuous) = 0.01) was a predictor of time to all causes of death. When analyzed as a categorical variable, beginning at age 73 years, age at diagnosis was an independent predictor (P(categorical) < 0.04) of time to death from prostate carcinoma. Upon further analysis, this finding was limited to high-risk patients. For example, age > or = 75 years at diagnosis predicted for a shorter median time to death from prostate carcinoma (6.3 years vs. 9.7 years; P = 0.002) in high-risk patients. CONCLUSIONS: Patients with clinically localized, high-risk prostate carcinoma who were diagnosed at age > or = 73 years and were treated with RT had a worse prognosis compared with patients who were diagnosed age < 73 years, raising the possibility that a more aggressive prostate carcinoma biology may develop during andropause.

Age Factors↗
PubMed2006

Association of vitamin D receptor FokI polymorphism with prostate cancer risk, clinicopathological features and recurrence of prostate specific antigen after radical prostatectomy.

To investigate the effect of vitamin D receptor (VDR) FokI polymorphism on susceptibility to prostate cancer and the outcome of the disease in a Taiwanese population, we genotyped a total of 416 prostate cancer patients, 502 age-matched male controls and 189 non age-matched symptomatic benign prostatic hyperplasia. Although we did not find a significant association between VDR FokI genotypes and overall prostate cancer risk, we found that in men aged less than or equal to the median age of 73 years with VDR FokI F allele specifically had an increased risk of prostate cancer with a marginal significant trend (OR, 2.08; 95% CI, 1.00-4.34, p for trend = 0.056). The FF genotype was also highly associated with more aggressive prostate cancer (Gleason score 8-10) (OR, 2.47; 95% CI, 1.20-5.08) than did the Ff and ff genotypes. After adjusting other covariates, we found that in patients who had localized prostate cancer for which a radical prostatectomy was performed (n = 131), the VDR FokI FF genotype was associated with worse prostate-specific antigen (PSA) recurrence-free survival (hazard ratio = 3.25, 95% CI = 1.32-8.00, p = 0.010). Our findings suggest that the VDR FF genotype may increase the risk of early-onset prostate cancer and is associated with more aggressive disease. Furthermore, the VDR polymorphism could be used as a prognostic marker for localized prostate cancer after radical prostatectomy.

Aged↗
PubMed2002

Detection of human polyomaviruses and papillomaviruses in prostatic tissue reveals the prostate as a habitat for multiple viral infections.

BACKGROUND: To determine whether human polyomavirus (hPy) genomes are present in prostate tissues, we have carried out a polymerase chain reaction (PCR) screening in two sets of prostate samples, archival and fresh frozen, as well as performing in situ hybridization (ISH). The frozen prostate samples as well as the urine from the same patients were also screened for human papillomavirus (HPV) sequences. METHODS: Highly sensitive nested-PCR assays were used. The detection of subpopulations of JC virus (JCV) -transcriptional control regions (TCRs) was also evaluated by Southern analysis and by direct DNA sequencing. An in situ hybridization technique was also used to detect JCV DNA in prostatic tissue. RESULTS: The paraffin-embedded archival samples gave variable, unsatisfactory results. Results from the fresh frozen samples, however, were consistent and were frequently positive for JCV and less frequent for BK virus DNA. ISH confirmed the presence of JCV DNA in prostatic glandular epithelium. The TCR region of JCV from prostate tissue and urine from prostate cancer patients showed the presence of both archetypal and rearranged TCRs, including several new sequence variants. HPV DNA was also frequently detected and in some cases also mixed with hPy DNA from frozen tissue and urine. CONCLUSION: The use of fresh frozen samples proved to be essential for consistent and reproducible detection of HPV and hPy viral DNAs. The presence of JCV DNA by ISH and the occurrence of a subpopulation of JCV TCR regions suggests that the prostate is a site for virus replication. The prostate is a complex habitat where mixed infections with oncogenic DNA viruses frequently occur and opens the discussion to the potential role of these viruses in the cancer of the prostate.

Aged↗
PubMed2001

Caspase 3 expression in benign prostatic hyperplasia and prostate carcinoma.

BACKGROUND: Apoptotic resistance to androgen ablation represents a significant problem in the treatment of prostate cancer. Over expression of antiapoptotic proteins such as Bcl-2 and mutations in p53 contribute to this resistance. The caspase family of proteases are central executioners of the cell death pathway. They are expressed in normal prostate secretory epithelial cells. Altered expression may represent an additional component leading to cell resistance. The aim of this study was to determine by immunohistochemistry caspase 3 expression in benign prostatic hyperplasia and prostate cancers. METHODS: Twenty-two patients with histologically determined prostate cancer and benign prostatic hyperplasia (BPH) were investigated. All specimens were obtained from patients undergoing surgical resection of the prostate. Immunohistochemical analysis was performed on formalin fixed paraffin embedded sections to assess caspase 3 expression. RESULTS: Caspase 3 was expressed in 18/22 (81.1%) samples, with high expression in BPH which demonstrated staining in both basal and secretory epithelial cells. Increasing grades of prostatic cancer showed a significant loss of expression in secretory epithelial layers and little staining in epithelial cells in high-grade prostatic carcinoma. CONCLUSIONS: Altered caspase 3 expression may represent an additional mechanism of apoptotic resistance to androgen ablation. Prostate 47:183-188, 2001.

Apoptosis↗
PubMed2004

Prostatic intraepithelial neoplasia and intestinal metaplasia in prostates of probasin-RAS transgenic mice.

BACKGROUND: Activation of the RAS pathway has been implicated in the pathogenesis of many types of human cancers, including prostate cancer. Here we employed a transgenic approach to assess the potential contribution of RAS to prostate carcinogenesis. METHODS: Probasin-RAS (Pb-RAS) transgenic mice were generated and shown to express high levels of activated RAS in the prostate lobes. Transgenic prostates were compared to normal controls by histology and immunohistochemistry with relevant markers. RESULTS: Pb-RAS transgenic prostates exhibit neoplastic changes including low-grade prostatic intraepithelial neoplasia, and metaplastic changes towards an intestinal goblet cell phenotype. The finding of high levels of the goblet cell-specific peptide Itf/Tff3 in these transgenic prostates is in accordance with recent microarray studies showing that ITF/TFF3 is upregulated in human prostate cancer samples. CONCLUSIONS: The Pb-RAS mouse model could be useful for elucidating the early events in prostate carcinogenesis, as well as for studying the mechanisms and potential prostate cancer relevance of intestinal metaplasia.

Androgen-Binding Protein↗
PubMed2004

Up-regulation of cathepsin X in prostate cancer and prostatic intraepithelial neoplasia.

BACKGROUND: Evidence is accumulating that several proteases are involved in prostate cancer progression. A locus which is often amplified in prostate cancer is the chromosomal region 20q13. Interestingly, one of the genes encoding the cysteine protease cathepsin X maps to this region. The aim of this study was to assess the expression pattern of cathepsin X in malignant and non-malignant prostatic tissue samples. METHODS: Matched malignant and non-malignant tissue specimens were obtained from 56 men after radical prostatectomy. Cathepsin X was quantified at both protein and mRNA levels using several detection methods: Western blotting, immunohistochemistry, quantitative RT-PCR, and in situ hybridization. Furthermore, genomic DNA was analyzed by PCR for possible gene amplification. RESULTS: Immunohistochemical analysis of formalin-fixed, paraffin-embedded sections of radical prostatectomy specimens was performed utilizing a polyclonal antibody against human procathepsin X and revealed staining of acinar basal cells in normal prostate glands. Prostatic intraepithelial neoplasias (PINs) and prostate carcinomas stained highly positive for cathepsin X, showing a significant difference to the staining of normal prostate glands. In contrast, relatively weak and heterogeneous staining was observed for cathepsins F, B, and L. Up-regulation of cathepsin X at the protein level was confirmed by Western blotting. No statistically significant difference was observed at the mRNA level. PCR of genomic DNA revealed that cathepsin X up-regulation most likely occurs in the absence of genomic amplification. CONCLUSIONS: The high expression levels of cathepsin X both in PIN and invasive adenocarcinomas of the prostate suggest that cathepsin X may play a role in the early tumorigenesis of prostate cancer. Further studies are needed to define the utility of this cysteine protease as a diagnostic marker for the early detection of prostate cancer.

Aged↗
PubMed2004

Induction and function of CYR61 (CCN1) in prostatic stromal and epithelial cells: CYR61 is required for prostatic cell proliferation.

BACKGROUND: CYR61 is an extracellular matrix-associated protein that promotes adhesion, migration, and proliferation of endothelial cells and fibroblasts. Prostate enlargement, which frequently causes the urethral compression, is often histologically observed as stromal and epithelial hyperplasia in an enlarged gland. To determine whether or not CYR61 has relevance to the progression of benign prostatic hyperplasia (BPH), we investigated the induction of CYR61, and also examined its function in both prostatic stromal and epithelial cells. METHODS: Recombinant CYR61 protein was used for the examination of the activity of CYR61 as to cell adhesion and proliferation. Quantitative reverse transcription-polymerase chain reaction (RT-PCR) was utilized to screen for inducers of the CYR61 gene in prostatic cells. Finally, the effects of an anti-sense oligonucleotide, which could reduce the production of CYR61, on the morphology and growth of prostatic cells were also examined. RESULTS: Recombinant CYR61 protein promotes prostatic cell adhesion and proliferation. The mRNA for CYR61, a growth factor-inducible immediate early gene, was markedly induced by fetal bovine serum (FBS) within 1 hr, and strongly induced by transforming growth factor-beta1 (TGF-beta) for at least 19 hr following stimulation. The suppression of CYR61 production with an anti-sense oligonucleotide causes obvious morphological changes of prostatic cells. Furthermore, we have shown that CYR61 is necessary, at least in part, for FBS-induced prostatic cell proliferation, because dramatic inhibition of cellular growth was caused by the suppression of CYR61 production with the addition of the anti-sense oligonucleotide before FBS stimulation. CONCLUSIONS: In this study, we demonstrate that serum growth factors induce the CYR61 gene in both stromal and epithelial cells, and that CYR61 plays functional roles in cell adhesion, morphology, and proliferation, supporting its involvement in benign prostatic enlargement. These results strongly suggest that CYR61 is a key molecule, and therefore could be a potential therapeutic target in prostatic hyperplastic growth.

Cell Adhesion↗
PubMed1999

In utero exposure to antiandrogens alters the responsiveness of the prostate to p,p'-DDE in adult rats and may induce prostatic inflammation.

DDE is an environmental pollutant with antiandrogenic properties. Following administration to pregnant rats, DDE was shown to cause feminization in the male offspring at the neonatal stages but did not affect the pubertal growth of accessory sex organs. In this study, we examined the potential of in utero exposure to antiandrogens to alter the responsiveness of the male rats to subsequent DDE challenge. Pregnant Long-Evans rats were dosed by gavage from Gestation Day 14 to 18 at 0, 10 (low dose), or 100 (high dose) mg DDE, or 40 mg flutamide/kg body wt (bw)/day (in utero treatment). At approximately 80 days of age, the male offspring from each of the four in utero treatment groups were divided into two groups. One group received the adult treatment of four daily gavage administrations of DDE at 70 mg/kg bw (adult treatment), while the second group served as the adult treatment control (adult control). The in utero treatment resulted in 18, 31, and 53% reductions of ventral prostate weights at approximately 85 days of age compared to the control for the low- and high-dose DDE and flutamide groups, respectively. These results suggest that the in utero antiandrogen treatments produced a latent effect on prostate growth that became pronounced only in the postpubertal stage. The in utero treatment also altered the responsiveness of the prostate to the adult treatment, indicated by a significant reduction in ventral prostate weight that was seen only in the control group of the in utero treatment but not in the other groups. The in utero treatment was also associated with expression of testosterone-repressed prostatic message-2 in the adult ventral prostate. In addition, a few prostates in the high-dose DDE- and flutamide-treated groups of the in utero treatment were found to have chronic suppurative prostatitis. While other types of hormonal manipulations have been shown to incite similar responses in rat prostate, the possible linkage between in utero antiandrogen treatment and prostatic inflammation needs to be further evaluated.

Adipose Tissue↗
PubMed2005

Immunohistochemical analysis of Omi/HtrA2 expression in prostate cancer and benign prostatic hyperplasia.

To study the expression and significance of the serine protease Omi/HtrA2 in prostate cancer and benign prostatic hyperplasia. The expression of Omi/HtrA2 was assayed by means of immunohistochemical technique in 41 prostate cancer (Cap), 20 benign prostatic hyperplasia (BPH) and 10 normal prostate (NP) specimens. Omi/HtrA2 expression was positive in 30 (73.17%) prostate cancer specimens, and the positive rate of Omi/HtrA2 was lower in well differentiated than in poorly and moderately differentiated groups (P < 0.05). By contrast, the cells in normal prostate and benign prostatic hyperplasia groups showed no or weak expression of Omi/HtrA2. Prostate cancer cells in vivo may need Omi/HtrA2 expression for apoptosis, and that Omi/HtrA2 expression might be involved in prostate cancer development.

Adult↗
PubMed2004

Clinical outcome of transrectal ultrasound-guided prostate biopsy, targeting eight cores, for detecting prostate cancer in Japanese men.

BACKGROUND: The objective of this study was to evaluate the clinical usefulness of transrectal ultrasound (TRUS)-guided eight-core prostate biopsy for detecting prostate cancer in Japanese men. METHODS: Between January 1998 and September 2002, a total of 628 consecutive patients underwent TRUS-guided biopsy of the prostate. As a rule, eight cores were taken from each patient; that is, standard sextant cores from the peripheral zone and two additional cores from the bilateral anterior lateral horns (ALHs). The present study included 428 patients who underwent an initial biopsy, whose age was between 50 and 79 years, and whose prostate-specific antigen (PSA) value was less than 20.0 ng/ml. The cancer detection rate was calculated according to age, PSA, digital rectal examination (DRE) and TRUS findings, prostate volume, and PSA density (PSAD). We also assessed whether the sampling of the two extra cores from the ALHs increased the cancer detection rate. RESULTS: Of the 428 patients, 101 (23.6%) were diagnosed as having cancer by eight-core prostate biopsies. The cancer detection rate was significantly associated with the PSA value (ng/ml; < or =4 versus 4-10, versus 10-20), DRE findings (normal versus abnormal), TRUS findings (normal versus abnormal), and PSAD (ng/ml2; < or =0.15 versus >0.15). but not with age (years: < or =70 versus >70) on prostate volume (ml; < or =30 versus 30-50, versus >50). Of the 101 patients diagnosed as having prostate cancer, 11 had positive cores only in the ALH; that is, the increase in the cancer detection rate yielded by obtaining two extra cores from the ALHs was 10.9%. CONCLUSION: Despite the reasonable strategy, systematic prostate biopsy targeting eight cores did not significantly improve the cancer detection rate compared with that of standard sextant biopsy in Japanese men. However, the increased cancer detection rate yielded by additional sampling from the ALHs was comparatively prominent in the subgroup whose PSA value was in the gray zone (4-10 ng/ml) or whose prostate volume was greater than 50 ml.

Adult↗
PubMed1989

Determination of prostatic volume by ultrasonography. A useful procedure in patients with prostatism?

Digital palpation is rather unreliable for estimating the volume of the prostate. Ultrasonographic measurements have been advocated as a more appropriate method. We examined 47 patients ultrasonographically. Of these, 34 underwent a transurethral resection of the prostate (TURP) (ultrasonographic volume 29 patients: prostate less than 60 cm3, 5 patients with cardiovascular problems: prostate greater than 60 cm3) and 13 an open prostatectomy according to Hryntschak (prostate greater than 60 cm3). In all patients ultrasonically determined volumes were compared with the operatively removed volume of prostatic tissue. If the size of the prostate had been estimated by digital palpation only, 12 patients would have undergone the wrong procedure (TURP instead of Hryntschack procedure). Ultrasonographic calculation of the prostatic volume demonstrated that all of these patients could be treated with less risk. After resection or abdominal prostatectomy some prostatic tissue remains. We concluded that there is no clear difference in the incidence of secondary prostatic obstruction (in need of re-TURP) either after abdominal prostatectomy or after TURP.

Adult↗
PubMed1993

Value of transrectal prostate ultrasonography pre-transurethral prostatectomy in screening for occult prostate carcinoma.

A total of 311 patients who underwent consecutive transurethral resection of prostate (TURP) for obstructive voiding symptoms were reviewed. All patients had benign prostate glands by digital rectal examination. Results of preoperative ultrasound screening of the prostate in 65 of 311 patients showed 41 with nonmalignant prostate, but pathologic examination showed cancer in 11 and benign hyperplasia in 30. Of seven ultrasounds interpreted as suspicious for cancer, pathologic examination revealed benign hyperplasia in all seven. Of 17 patients with ultrasound interpretations consistent with prostate cancer, 14 had transrectal ultrasound-guided prostate biopsies prior to TURP. Biopsy specimens revealed benign hyperplasia without carcinoma in all 14 patients. Two of 17 patients refused biopsies, and 1 underwent TURP without biopsy for urinary retention and did have cancer. Sensitivity of prostate ultrasound in evaluation of occult prostate carcinoma in this group of patients was 8.3 percent and specificity was 56.6 percent. Our results indicate that transrectal prostate ultrasound performed on men with obstructive voiding symptoms and benign glands as evidenced by digital rectal palpation has little value in predicting the presence or absence of occult prostate cancer.

Aged↗
PubMed1981

Expression of prostatic acid phosphatase in human prostate cancer.

By a specific immunochemical measurement, the activity of prostatic acid phosphatase (PAP) in prostate cancer was found to be about 25%, on average, based on micrograms DNA or per cell, of that in normal prostate or benign prostatic hypertrophy (BPH). The reduction of PAP in prostate cancer was further revealed by a decrease in PAP protein. The 125I-labeled anti-PAP IgG specifically bound to nascent peptides on PAP-synthesizing polysomes showed no qualitative differences among cancerous prostate, normal prostate and BPH. However, the quantitative binding of 125I-labeled anti-PAP IgG to polysomes of cancerous prostate was half that of normal prostate of BPH. These data suggest that a significant amount of PAP and its synthesizing polysomes was reduced in prostate cancer as a result of PAP gene suppression.

Acid Phosphatase↗