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PubMed2004

Controversies in prostate cancer screening.

PURPOSE: Prostate cancer is the most common cancer in men and the second most common cause of cancer death in men, and yet controversy continues to surround the practice of prostate cancer screening. Despite recent studies that have cast doubt over the true efficacy of breast cancer screening programs, the National Cancer Institute continues to support breast cancer screening and it has withheld endorsement of widespread prostate cancer screening. Criticisms of prostate cancer screening include the financial burden of screening, the morbidity of prostate biopsy, the low positive predictive value of screening, the over treatment of an indolent disease and the lack of evidence demonstrating a mortality benefit due to screening. MATERIALS AND METHODS: We formulated a comprehensive discussion addressing the criticisms of prostate cancer screening. RESULTS: In an effort to highlight the importance of prostate cancer screening we noted how concerns regarding cost, morbidity and low positive predictive value are common to widely accepted screening programs for other common malignancies. We also draw attention to the danger of abandoning prostate cancer screening, a practice that is called into question by watchful waiting series and Markov modeling of prostate cancer treatment. Finally, we observed how the implementation of prostate cancer screening in the United States has led to the phenomenon of stage migration and paralleled the decrease in the prostate cancer mortality rate. CONCLUSIONS: The prostate specific antigen era has brought great promise for improving the prognosis of prostate cancer. We must continue to seek support for widespread prostate cancer screening.

Humans↗

PubMed2000

Prostate specific antigen bounce after radioactive seed implantation followed by external beam radiation for prostate cancer.

PURPOSE: Prostate specific antigen (PSA) may temporarily increase following radiotherapy for prostate cancer without signaling cancer recurrence. We describe this phenomenon which is called PSA bounce. MATERIALS AND METHODS: From 1984 to 1995, 779 stage T1T2N0 cancer cases were treated with simultaneous radiotherapy with a 125iodine prostate implant followed by external beam radiation. Median pretreatment PSA was 7.7 ng./ml. (range 0.3 to 188). PSA bounce was defined as an increase of 0.1 ng./ml. or greater above the preceding PSA level after simultaneous radiation followed by a subsequent decrease below that level. Disease-free status was defined as the ability to achieve and maintain posttreatment PSA 0.2 ng./ml. or less. RESULTS: PSA bounce was observed in 35% of men (273 of 779). Median time to PSA bounce was 18 months from the time of implant and 92% of bounces were observed within 36 months. Median pre-bounce PSA was 0.7 ng/ml. (range 0.1 to 8.9) and median bounce height (increase above the pre-bounce level) was 0.4 ng./ml. (range 0.1 to 15.8). No distinguishing characteristics were observed between men with PSA bounce and those with cancer recurrence, and bounce had no prognostic significance relative to recurrence. CONCLUSIONS: PSA bounce is common following seed implantation for prostate cancer. It produces anxiety in men previously treated for prostate cancer and confounds the diagnosis of recurrence.

Brachytherapy↗

PubMed1999

Highly metastatic human prostate cancer growing within the prostate of athymic mice overexpresses vascular endothelial growth factor.

Angiogenesis is essential for tumor progression and metastasis. It is mediated by the release of angiogenic factors by the tumor or host. We analyzed the expression of angiogenic factors by the prostate cancer cell line LNCaP and two derived variants, in vitro and in vivo, to determine whether metastatic cell lines express higher levels of these factors. The production of three angiogenic factors, vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), and interleukin 8 (IL-8), by LNCaP and its variants, LNCaP-LN3 (highly metastatic) and LNCaP-Pro5 (slightly metastatic), was measured by ELISA. VEGF, bFGF, and IL-8 mRNA expression was determined in vitro by Northern blot analysis. VEGF mRNA expression was determined in vivo by in situ hybridization. VEGF and flk-1 protein expression and microvessel density of LNCaP cell tumors were quantified by immunohistochemistry. In vitro, VEGF production by LNCaP-LN3 (3.15+/-0.04 pg/ml/10(3) cells) was significantly higher than those of both LNCaP (2.38+/-0.34 pg/ml/10(3) cells) and LNCaP-Pro5 (1.67+/-0.37 pg/ml/10(3) cells; P = 0.049 and 0.001, respectively). None of the three cell lines produced detectable levels of bFGF or IL-8 in vitro. In vivo, LNCaP-LN3 tumors exhibited higher levels of VEGF mRNA and protein (152.2+/-28.5 and 200.5+/-28.3) and of flk-1 protein (156.5+/-20.6) and had higher microvessel density (16.4+/-4.2) than either LNCaP tumors (89+/-17.5, 173.3+/-23.0, 124.6+/-21.6, and 12.4+/-3.5, respectively) or LNCaP-Pro5 tumors (63+/-14.7, 141.2+/-38.1, 126.1+/-20, and 5.8+/-2.2, respectively). In conclusion, metastatic human prostate cancer cells exhibited enhanced VEGF production and tumor vascularity compared with prostate cancer cells of lower metastatic potential. Thus, VEGF may play an important role in prostate cancer metastasis.

Animals↗

PubMed2003

The usefulness of serum human kallikrein 11 for discriminating between prostate cancer and benign prostatic hyperplasia.

Prostate-specific antigen (PSA) is the most useful tumor marker for diagnosis and monitoring of prostate cancer (CaP). Recently, we developed a specific immunoassay for human kallikrein 11 (hK11), one of the kallikrein gene family members, and found that hK11 was highly expressed in prostatic tissue and could be detected in seminal plasma (E. P. Diamandis et al., Cancer Res., 62: 295-300, 2002). The aim of this study was to investigate whether serum hK11 levels could be used to discriminate CaP from benign prostatic hyperplasia (BPH). We analyzed for hK11, total PSA, and percentage of free PSA, 150 serum samples from men with histologically confirmed BPH (n = 64) or CaP (n = 86). Total and free PSA levels were measured by the Immulite PSA assay, and hK11 levels were measured by our previously published immunofluorometric assay. Serum hK11 levels and the hK11:total PSA ratio were both significantly lower in CaP patients than in BPH patients. In the subgroup of patients with percentage of free PSA less than 20, an additional 54% of BPH patients could have avoided biopsies by using the hK11:total PSA ratio. Receiver operating characteristic (ROC) curve analysis demonstrated that the hK11:total PSA ratio [area under the curve (AUC), 0.83] and percentage of free PSA (AUC, 0.83) were much stronger predictors of CaP than total PSA (AUC, 0.69). These preliminary data suggest that the hK11:total PSA ratio could be a useful tumor marker for CaP and could be combined with percentage of PSA to further reduce the number of unnecessary prostatic biopsies.

Aged↗

PubMed2000

Cancer surveillance series: interpreting trends in prostate cancer--part I: evidence of the effects of screening in recent prostate cancer incidence, mortality, and survival rates.

Explore the source record for details and available documents.

Humans↗

PubMed2005

[Congress of the Association Française d'Urologie (AFU) 2004: prostate cancer management].

Prostate cancer was the subject of communications, round tables and plenary sessions at the 98th congress of the Association française d'urologie (AFU). We report the whole of the meetings on the subject by classifying them by categories: epidemiology and biological diagnosis, information to patients included in screening (recommendations of the ANAES), biopsies and IRM, radiotherapy, radical prostatectomy, brachytherapy, HIFU (High Intensity Focused Ultrasound), functional consequences and quality of life, treatment of PSA elevation, advanced cancer of the prostate, place of surgery in T3 cancers of the prostate, research.

Biopsy↗

PubMed1993

[Radioimmunodetection of prostatic cancer: in vivo 131I-gamma-seminoprotein for diagnosis of prostatic cancer by nuclear imaging].

69 patients with prostatic cancer were subjected to radioimmunodetection (RAID) with 131I-labeled antibody against gamma-seminoprotein (gamma-Sm), the images of malignant tumor sites was obtained by single photon emission computed tomography (SPECT) with dual radionuclide and computer processing. Of the 69 patients 66 were confirmed by RAID. The ratio of tumor tissue to normal tissue (T/N) 6.9 and the best time for incaging was 96 hours after injection of anti-gamma-Sm. The diameter of the minimum tumor in RAID was 0.5 cm. metastatic prostatic cancer in the pelvis or bone location as well as the origin tumors were also detected in 13 cases. Anti-gamma-SmRAID can differentiate benign from malignant prostatic neoplasms. In 37 cases of benign prostate hyperplasia, only two were positive. The positive detective rate of B-ultrasound and CT was 70.8% and 73.1% respectively.

Dextrans↗

PubMed2006

Magnetic resonance spectroscopy in patients with locally confined prostate cancer: association of prostatic citrate and metabolic atrophy with time on hormone deprivation therapy, PSA level, and biopsy Gleason score.

This study was undertaken to determine respective associations between prostatic citrate or metabolic atrophy (no detectable citrate, choline, and creatine) at magnetic resonance spectroscopy (MRS) and time on hormone-deprivation therapy, serum PSA, and biopsy Gleason score. Clinical data, histopathology reports and PSA levels of 36 patients on hormone-deprivation therapy (age, 64+/-9 years, pre-therapeutic biopsy Gleason sum, median 6, range 3-8, antiandrogens only, n=3, LHRH-analogues only, n=4, combined hormone-deprivation therapy, n=29, duration, 27+/-19 weeks) for locally confined prostate cancer (PCA) were retrospectively correlated with findings in the peripheral zone of the prostate at 3D-MRS (endorectal coil, PRESS, TR 1,000 ms, TE 130 ms). The results show that citrate was usually detected after 13 weeks or less of hormone-deprivation therapy (10/12 vs. 6/24 patients, chi-square-test, p=0.002). All patients with PSA levels exceeding 0.20 ng/ml had detectable metabolites (citrate, n=12, choline without citrate, n=6), while 9/18 patients with PSA 0.20 ng/ml or less showed metabolic atrophy (Fisher-exact-test, p=0.001). There were no significant associations between citrate, metabolic atrophy, pre-therapeutic PSA, and biopsy Gleason sum, respectively. It has been concluded that hormone-deprivation therapy for locally confined PCA has not reached its full deprivation potential after 13 weeks. MRS detects prostate metabolism in patients with PSA exceeding 0.20 ng/ml after hormone-deprivation therapy.

Aged↗

PubMed1999

Predicting extracapsular extension of prostate cancer in men treated with radical prostatectomy: results from the population based prostate cancer outcomes study.

PURPOSE: We investigated whether clinical information routinely available in community practice could predict extracapsular extension of clinically localized prostate cancer in men undergoing radical prostatectomy. MATERIALS AND METHODS: We examined prostate cancer outcomes in a population based sample of 3,826 patients with primary prostate cancer in 6 regions of the United States covered by the Surveillance, Epidemiology, and End Results program. Stratified and weighted logistic regression was used to identify predictors of and probabilities for extracapsular extension of clinically localized tumors treated with radical prostatectomy. RESULTS: Nearly 47% of men undergoing radical prostatectomy had extraprostatic extension. The strongest predictors were elevated prostate specific antigen (PSA) greater than 20 versus less than 4 ng./ml. (odds ratio 5.88, 95% confidence interval 2.90 to 11.15), Gleason score greater than 8 versus less than 6 (1.73, 1.04 to 2.87) and age greater than 70 versus less than 50 years (1.91, 0.98 to 3.70). Ethnicity and region were not associated with increased risk of extraprostatic extension. A nomogram developed from our model predicts extracapsular extension ranging from 24% in men younger than 50 years with PSA less than 4 ng./ml. and a Gleason score of less than 7 to 85% in those 70 years old or older with PSA greater than 20 ng./ml. and a Gleason score of 8 or more. If prostatectomy were limited to patients with less than 60% probability of extraprostatic extension based on the nomogram, 95% of those with organ confined cancers would undergo definitive surgery and 18% of those with extracapsular extension would be spared the morbidity of surgery. CONCLUSIONS: In a population based analysis of prostate cancer practice patterns PSA, Gleason score and age are clinically useful predictors of extracapsular extension. Although extracapsular extension may be an imperfect predictor of cancer outcomes, our nomogram provides more realistic probabilities for extracapsular extension than those based on institutional series.

Aged↗

PubMed1990

Prostate specific antigen for assessing response to ketoconazole and prednisone in patients with hormone refractory metastatic prostate cancer.

Serial prostate specific antigen levels were assessed in 15 patients with hormone refractory metastatic prostate cancer treated with ketoconazole and prednisone. Of the men 12 (80%) with continually increasing prostate specific antigen levels before treatment had a decrease in prostate specific antigen with a median duration of response of 3 months. Three patients (20%) had a prolonged response (greater than or equal to 8 months) as seen by a persistently decreasing prostate specific antigen and improvement in bone pain. There appears to be a small subgroup of patients with progressive prostate cancer despite androgen ablation who will benefit from ketoconazole and glucocorticoid treatment. The use of serial prostate specific antigen levels appears to help define this subgroup and avoid the need for multiple radiological procedures to assess response.

Adenocarcinoma↗

PubMed1997

Management of progressive metastatic prostate cancer.

Metastatic prostate cancer is a growing health problem and is the second leading cause of cancer death in men. While the response of patients with metastatic prostate cancer to initial hormonal manipulation is excellent, the majority of patients eventually progress. As a result, a growing number of patients and their physicians need-to-find acceptable therapeutic alternatives. Fortunately, the number of therapies in the management armamentarium is growing and includes: alternative hormonal therapies, chemotherapy, radioisotopes, and investigational agents. The major focus of treatment has shifted to palliation and quality of life. The decline of prostate-specific antigen (PSA) has become another important end point as evidence supporting a correlation with prolonged survival mounts. Enrolling eligible patients in clinical trials is critical to the development of new treatment strategies for this difficult disease.

Androgen Antagonists↗

PubMed1990

[Correlation between histologic grading and prognosis of prostatic cancer--comparing the grading system of the Japanese general rules of prostatic cancer with Gleason's grading].

To evaluate the correlation between the histological grade and the prognosis, we reviewed 100 cases of prostatic cancer according to the Japanese General Rules of Prostatic Cancer (JGRPC) and Gleason grading system. The study led to the following results: (1) There was a close relation between the JGRPC grade and Gleason score (GS). (2) The JGRPC grade and Gleason score were equally concerned with the clinical stage. (3) There were significant differences in survival rate between well and moderately, well and poorly differentiated groups by the JGRPC grading system, and between GS 2-4 and GS 5-7, GS 2-4 and GS 8-10 groups by Gleason score. (4) In proportion to the JGRPC grade, the cancer death rate increased linearly in each stage. (5) When the patients were grouped according to their JGRPC grades of main lesion and accompanied lesion, the cancer death rate increased in the cases with lower differentiated elements. We conclude that the JGRPC grading system is easily comprehensible, and equal with the Gleason grading system to predict the prognosis of prostatic cancer.

Adenocarcinoma↗

PubMed1996

There are multiple forms of glyceraldehyde-3-phosphate dehydrogenase in prostate cancer cells and normal prostate tissue.

We analyzed glyceraldehyde-3-phosphate dehydrogenase (GAPDH) expression in normal and malignant human prostate tissues, normal rat prostate, and Dunning R-3327 rat prostate cancer cell lines. We detected multiple forms of GAPDH in Dunning cell lines by two-dimensional protein electrophoresis and Western analysis. Five forms of GAPDH that differed by isoelectric point were detected for each of the two metastatic Dunning cell lines, while four or fewer forms were detected for Dunning cell lines with low metastatic ability. We also detected multiple forms of GAPDH in normal and malignant human prostate specimens by two dimensional protein electrophoresis and immunohistochemical analysis. GAPDH was undetectable in normal human prostate secretory epithelium by immunohistochemistry, but was abundant in nuclei of normal basal cells and stromal cells. In human prostate cancer specimens, there was a rough correlation between cytoplasmic staining for GAPDH and tumor grade, but GAPDH staining was extremely heterogeneous. GAPDH was abundant in nuclei of some high-grade human prostate tumors. Both of the human prostate cancer bone metastases analyzed with immunohistochemistry had markedly elevated cytoplasmic GAPDH expression. We conclude that multiple forms of GAPDH may play diverse roles in normal prostate tissue and in prostate cancer.

Adenocarcinoma↗

PubMedDate not supplied

Placental growth factor gene expression in human prostate cancer and benign prostate hyperplasia.

BACKGROUND: Angiogenesis plays a crucial role in normal development and carcinogenesis of prostate glands. Placental growth factor (PlGF) belongs to the same family as the vascular endothelial growth factor. The presence of PlGF in human prostate has not been studied. In the current study, we investigated the gene expression profiles of PlGF in human prostate. MATERIALS AND METHODS: Gene expression of PlGF-1 and PlGF-2 was assessed by RT-PCR and direct sequencing. Gene expression levels were quantified by real-time PCR, and we compared the transcript levels among benign prostate hyperplasia (BPH), prostate caner (CAP) and CAP after androgen deprivation therapy (CAP-Tx). RESULTS: Human prostate cancer cells, LNCaP, PC-3 and DU-145, expressed both PlGF-1 and -2 mRNAs. Human prostate tissues, BPH, CAP and CAP-Tx, also expressed both types of PlGF mRNA. BPH and CAP-Tx expressed similar levels of PlGF, however, CAP expressed significantly lower levels of PlGF than BPH or CAP-Tx (p < 0.01). CONCLUSION: PlGF mRNA was expressed in human prostate. Significantly lower levels of PlGF in CAP in comparison with those in BPH or CAP-Tx suggested that PlGF might have effects on vasculogenesis and angiogenesis in prostate disease.

Alternative Splicing↗

PubMed1986

Evaluation of prostate-specific antigen and prostatic acid phosphatase as prostate cancer markers.

Prostate-specific antigen (PSA) and prostatic acid phosphatase (PAP) have been evaluated in patients with prostate cancer, benign prostatic hypertrophy (BPH), and prostatitis. PSA has proved to be diagnostically more sensitive than PAP for the detection of prostate cancer: 95.0 per cent vs 60.0 per cent for 40 newly diagnosed cancer cases, and 97.1 per cent vs 65.7 per cent for 35 relapsed cases. This also holds true for those patients with early-stage disease: 71.4 per cent vs 0 per cent for 7 Stage A1 cases. The specificities of PSA and PAP are comparable, 96.8 per cent vs 98.9 per cent, respectively. PSA is also more sensitive for monitoring therapy, since it usually rises before PAP and always precedes clinical signs of relapse. Although PSA may be elevated more frequently than PAP in some patients with BPH and prostatitis, it is postulated that these patients with elevated serum PSA and normal serum PAP may fall into a high-risk sub-population which may have early prostate cancer or precancerous conditions not easily detectable by current clinical and diagnostic techniques. Our data suggest PSA is a sensitive useful tumor marker for the diagnosis and management of prostate cancer. In addition, PAP, in combination with PSA, may serve as a useful adjunct for differential diagnosis and confirmation of advanced stage prostate cancer.

Acid Phosphatase↗

PubMed2004

Long-term survival rates of patients with prostate cancer in the prostate-specific antigen screening era: population-based estimates for the year 2000 by period analysis.

PURPOSE: In the era of widespread prostate specific antigen (PSA) screening, a large proportion of older men have to live with a diagnosis of prostate cancer. In this study, we applied a new method for up-to-date analysis of long-term survival to evaluate if and to what extent these patients still have any excess mortality compared to the general population. METHODS: Five- and 10-year absolute and relative survival rates for the year 2000 were derived from the 1973 to 2000 database of the Surveillance, Epidemiology and End Results Program using the recently introduced period analysis methodology. RESULTS: Overall, 5- and 10-year relative survival rates were approximately 99% and 95%; that is, excess mortality compared with the general population was as low as 1% and 5% within 5 and 10 years following diagnosis, respectively. Two-thirds of patients were diagnosed with well or moderately differentiated localized/regional prostate cancer, and among these patients, 5- and 10-year relative survival rates were above 100% (indicating the lack of any excess mortality) at all ages. CONCLUSION: While the value of PSA screening for lowering mortality due to prostate cancer remains to be shown by randomized clinical trials, the majority of patients diagnosed with prostate cancer in the PSA screening era do not have excess mortality compared to the general population under current patterns of medical care. This information may be important for both clinical management of, and for patients' coping with, the disease.

Aged↗

PubMed2001

Brachytherapy for clinically localized prostate cancer: thirteen-year disease-free survival of 769 consecutive prostate cancer patients treated with permanent implants alone.

OBJECTIVE: To report 13-year biochemical disease-free survival results on 769 consecutive prostate cancer patients treated with brachytherapy alone. MATERIAL AND METHODS: Seven hundred sixty-nine patients with stage T1-T3, low to high Gleason grade prostate cancer underwent transperineal prostate implants with Iodine-125 (I-125) or Palladium-103 (Pd-103) as the sole treatment between January 1, 1987 and January 1, 1997. Median age was 69 years (range 43-92) and median follow-up was 71 months (range 18-156). Study cohort characteristics are summarized in Tables I and II and Figures 4-6. The patients were divided into two risk groups (low and high risk for extra-prostatic disease) based mainly on clinical stage and Gleason score. Group 1 consisted of 542 patients, who were considered at low risk and were treated with I-125. Group 2 comprised 227 patients, who were considered higher risk and were treated with Pd-103. No patient underwent pathological staging and none received androgen ablative therapy. Treatment failure was based on our modification of the American Society for Therapeutic Radiology and Oncology's (ASTRO) recommended failure criteria, defined as 3 consecutive serum Prostate Specific Antigen (PSA) rises (1). A critical component in our modification is that the value of the third PSA rise be above 0.5 ng/mL. RESULTS: One hundred thirty-seven patients were lost to follow-up. Thirteen patients expired of non-cancer causes within 18 months of the implant. This left 619 patients for evaluation, 441 in Group 1 and 178 in Group 2. The biochemical disease-free survival rates of the 619 patients at 3, 5, 10, and 13 years were 85%, 80%, 77%, and 77%, respectively (Fig. 1). The biochemical disease-free survival rates of the 441 "lower risk" I-125 treated patients at 3, 5, 10, and 13 years were 84%, 79%, 76%, and 76%, respectively (Fig. 2). The biochemical disease-free survival rates of the 178 "higher risk" Pd-103 treated patients at 3, 5, 10, and 13 years were 87%, 82%, 80%, and 80%, respectively (Fig. 3). CONCLUSION: The excellent long-term results presented here, as well as the many advantages of prostate brachytherapy over other common treatments, demonstrate that brachytherapy is an effective treatment for clinical organ-confined prostate cancer in the long term.

Adult↗

PubMed1992

Prostate-specific antigen and prostate-specific acid phosphatase in neuroendocrine cells of prostate cancer.

Prostate-specific antigen is a specific immunohistochemical marker of benign prostatic epithelium and prostate cancer. A subpopulation of neuroendocrine cells seen in 50% of cancers do not produce this protein marker. These cells appear to secrete prostate-specific acid phosphatase. This finding may explain the marked variation in serum prostate-specific antigen levels in all stages of prostate cancer.

Acid Phosphatase↗