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PubMed1995

Prostate-specific antigen and prognosis in patients with metastatic prostate cancer--a multivariable analysis of prostate cancer mortality.

OBJECTIVE: To analyse the prognostic significance of pre- and post-treatment serum prostate-specific antigen (PSA) levels, together with a variety of other factors, in a multivariable analysis of survival in men with stage D2 prostate cancer. PATIENTS AND METHODS: Cox's proportional hazards model was used to compare survival in 134 men with stage D2 metastatic prostate cancer followed prospectively over a 4 year period, using both univariable and multivariable models. The influence of the following factors on survival was analysed: pre- and post-treatment PSA (both absolute and percentage values), age, treatment, testosterone, pre- and post-treatment alkaline phosphatase (absolute and percentage values), acid phosphatase, haemoglobin, symptom score and performance status and extent of disease on bone scan. RESULTS: Pre-treatment PSA levels did not significantly influence survival. Similarly, a low absolute post-treatment PSA level at 3 months after the start of treatment conferred no survival advantage relative to patients with a high PSA level at this time. A post-treatment percentage PSA of < 10% at 2, 3 and 6 months after commencement of treatment was associated with prolonged survival. Low pre-treatment alkaline phosphatase (less than the upper limit of normal) and high pre-treatment testosterone levels (> or = 10 nmol/L) were similarly associated with prolonged survival. CONCLUSIONS: The strong influence of post-treatment percentage PSA on survival in patients with stage D2 prostate cancer suggests that the percentage change in bulk of metastatic deposits is more important in determining survival than the absolute volume of tumour. Pre-treatment alkaline phosphatase seems to be a better indicator of tumour activity than pre-treatment PSA. These findings have important implications for the design and analysis of clinical trials of new therapies in men with stage D2 prostate cancer and for the future selection of alternative treatments for patients with this stage of the disease.

Aged↗

PubMed1998

Transition zone volume-adjusted prostate-specific antigen value predicts extracapsular carcinoma of the prostate in patients with intermediate prostate-specific antigen levels.

OBJECTIVE: The aim of the present study was to examine the efficacy of the volume-adjusted prostate-specific antigen (PSA) density as a predictor of pathological stage. Among patients who underwent radical prostatectomy for clinically organ-confined prostate cancer, we selected patients with PSA levels of 4-10 ng/ml. In these patients with borderline PSA value extent of disease is most difficult to predict. Using the transition zone (TZ) volume instead of the total prostate volume, we compared the ability of PSA to predict the tumor extent. METHODS: From April 1992 to November 1996, we examined 61 consecutive patients who underwent radical prostatectomy. Their age ranged from 52 to 78 years. The PSA densities for the total prostate volume (PSAD) and for the TZ volume (PSAT) were calculated by transrectal ultrasound examinations. To compare the usefulness of PSA, PSAD, and PSAT, the area under the receiver-operator characteristic (ROC) curve was calculated for each parameter. RESULTS: The final pathological stage was pT2N0M0 in 34 patients, pT3N0M0 in 20 patients, and pT3N1M0 in 7 patients. Accordingly, 34 patients (55.7%) had organ-confined prostate cancer. In patients with capsular perforation, the areas under the ROC curve were 0.686 for PSA, 0.665 for PSAD, and 0.860 for PSAT, while in those with seminal vesicle invasion the respective values were 0.712, 0.703, and 0.882. Thus, PSAT was superior to PSA and PSAD in differentiating extracapsular disease. CONCLUSION: PSAT provides superior preoperative prediction of extracapsular tumor invasion, which appears to be useful in treatment selection (e.g. total prostatectomy).

Aged↗

PubMed1996

Clinical use of prostate-specific antigen and prostate-specific antigen density in the staging of patients with cancer of the prostate.

OBJECTIVE: To examine the efficacy of prostate-specific antigen (PSA) and prostate-specific antigen density (PSAD) in staging patients undergoing radical prostatectomy for clinically localized prostate cancer (CaP). PATIENTS AND METHODS: Prostate gland volumes were estimated in patients with clinically localized CaP (n = 119) performing transrectal ultrasound and employing the prolate ellipse formula. PSA was determined using an enzyme immunoassay. All patients underwent laparoscopic pelvic lymphadenectomy followed by radical perineal prostatectomy in No disease. The PSA density was calculated relating the Serum PSA to the sonographically estimated prostate volume. RESULTS: The pathological examination of the prostatectomy specimens revealed a pT2 tumor in 52 cases (43.7%) and a pT3 tumor in 41 cases (34.5%). In 26 patients (21.8%) the histological examination demonstrated metastases to the lymph nodes. Patients with a pT2No CaP demonstrated a median PSA level of 8.95 ng/ml and a median PSAD of 0.3, those with a pT3No CaP demonstrated a median PSA level of 12.3 ng/ml and a median PSAD of 0.38 and those with a T2-3pN + revealed a median PSA level of 22.9 ng/ml and a median PSAD of 0.7. CONCLUSIONS: Both marker, serum PSA as well as PSAD, did not sufficiently distinguish patients with organ-confined cancer from those with extracapsular tumor extension. In contrast, PSAD levels seem to provide useful additional information in the staging of patients with clinically localized CaP with regard to the lymph node status.

Aged↗

PubMed1999

Consensus statements on radiation therapy of prostate cancer: guidelines for prostate re-biopsy after radiation and for radiation therapy with rising prostate-specific antigen levels after radical prostatectomy. American Society for Therapeutic Radiology and Oncology Consensus Panel.

PURPOSE: To develop evidence-based guidelines for (1) prostate re-biopsy after radiation and (2) radiation therapy with rising prostate-specific antigen (PSA) levels after radical prostatectomy in the management of patients with localized prostatic cancer. DESIGN: The American Society of Therapeutic Radiology and Oncology (ASTRO) challenged a multidisciplinary consensus panel to address consensus on specific issues in each of the two topics. Four well-analyzed patient data sets were presented for review and questioning by the panel. The panel sought criteria that would be valid for patients in standard clinical practice as well as for patients enrolled in clinical trials. Subsequent to an executive session that followed these presentations, the panel presented its consensus guidelines. RESULTS AND CONCLUSIONS: Based on the data presented, the prostate re-biopsy negative rates ranged from 62% to 80% for patients with stage T1-2 tumors. The panel judged that prostate re-biopsy is not necessary as standard follow-up care and that the absence of a rising PSA level after radiation therapy is the most rigorous end point of total tumor eradication. Further, the panel judged that re-biopsy may be an important research tool. Based on the data presented, the long-term (5 years or more) PSA remission rate after salvage radiation therapy ranges from 27% to 45%. The panel requested results from prospective randomized trials to evaluate optimally this information. The panel judged that the total dose of radiation should be 64 Gy or slightly higher and that, in patients with or without radiation therapy, there is no standard role for androgen suppressant therapy for rising PSA values after prostatectomy.

Biopsy↗

PubMed2002

Percent free prostate specific antigen in the total prostate specific antigen 2 to 4 ng./ml. range does not substantially increase the number of biopsies needed to detect clinically significant prostate cancer compared to the 4 to 10 ng./ml. range.

PURPOSE: Percent free prostate specific antigen (PSA) is useful to select patients for prostate biopsy with total PSA 4 to 10 ng./ml. However, 20% of men with PSA between 2.6 and 4 ng./ml. harbor significant prostate cancer and percent free PSA has been suggested to aid in the decision to biopsy in this total PSA range as well. Concerns exist that the number of biopsies needed to detect 1 cancer in this range may be inappropriately high. In a prospective referral population we evaluated sensitivity and specificity of various percent free PSA cutoffs and determined the biopsy-per-cancer ratio in the PSA 2 to 4 ng./ml. range in men with a benign digital rectal examination, and report on the biological nature of the detected cancers based on Gleason score. Results were compared to those obtained from a reference group of patients (PSA 4 to 10 ng./ml., benign digital rectal examination) from the same prospective referral cohort. MATERIALS AND METHODS: Total PSA and free PSA were measured and percent free PSA was calculated. Of the initial 1,602 men 756 had a benign digital rectal examination and PSA 4 to 10 ng./ml., and 219 had a benign digital rectal examination and PSA 2 to 4 ng./ml. Sensitivity, specificity, the number of true positive (evidence of cancer) and false-positive (no evidence of cancer) biopsies were determined. The ratio of true positive biopsies-to-all biopsies performed was used to determine the biopsy-per-cancer ratio. Gleason score of the detected cancers was evaluated. The procedure was repeated for the PSA 4 to 10 ng./ml. range. RESULTS: In the PSA 4 to 10 ng./ml. range a sensitivity of 63.7% to 92.5% with a specificity of 57.5% to 18.7% was found when percent free PSA was 18% to 25%. On average 3 biopsies were needed to detect 1 cancer. When PSA was 2 to 4 ng./ml. sensitivity was 46.3% to 75.6% and specificity was 73.6% to 37.6% when the same percent free PSA cutoff was examined. Calculation of the biopsy-per-cancer ratio for various percent free PSA cutoffs revealed that 3 to 5 biopsies were needed to find 1 cancer. Of 41 cancers detected in the PSA 2 to 4 ng./ml. range 6 had a Gleason score 5. The majority (28 of 41) of cases had a Gleason score of 6. Gleason score was 7 in 5 patients and 8 in 1. CONCLUSIONS: In the PSA 4 to 10 ng./ml. range high sensitivity for prostate cancer detection is critical and 3 biopsies are needed to detect 1 cancer. In the PSA 2 to 4 ng./ml. range a percent free PSA cutoff of 18% to 20% detected about 50% of cancers while sparing up to 73% of unnecessary biopsies with a biopsy-to-cancer ratio of 3 to 4:1. Percent free PSA can be applied to the PSA 2 to 4 ng./ml. range to detect prostate cancer and only moderately increases the number of biopsies needed to detect 1 significant cancer compared to the greater than 4 to 10 ng./ml. range.

Aged↗

PubMed1991

Serum prostatic acid phosphatase activity and prostate specific antigen when the prostate gland is enlarged.

Serum prostatic acid phosphatase activity and prostate specific antigen levels were measured in the serum of 113 patients undergoing transurethral resection of an enlarged prostate gland, and the results compared with the histological diagnosis. Prostate-specific antigen was found to be the more sensitive indicator of malignancy, but prostatic acid phosphatase was more specific.

Acid Phosphatase↗

PubMed1982

Studies on carcinogenesis of human prostate. III. Long-term explant culture of normal prostate and benign prostatic hyperplasia: transmission and scanning electron microscopy.

Ultrastructural changes in normal human prostate and benign prostatic hyperplasia (BPH) during long-term explant culture were compared. Explants of normal prostate obtained at immediate autopsy of young adults of BPH obtained at the time of surgery were maintained as long as 24 weeks in vitro. Ultrastructural changes occurring in epithelial cells during culture were monitored by transmission and scanning electron microscopy. Essentially identical results were found for normal prostate and BPH. During the first week of culture, secretory epithelial cells degenerated and sloughed into the acinar lumen, resulting in an accumulation of necrotic debris. During this period, however, epithelial cells with ultrastructural characteristics of basal cells remained viable, repopulated glandular structures, migrated from glands and ducts, and epithelialized adjacent cut surfaces, eventually covering the explant. On explant surfaces, these basal cells initially were squamous-like, but they later became typically cuboidal, polygonal, or sometimes columnar and formed an epithelium, two cells or more thick. Epithelium with similar features lined acini within explants. Epithelial cells at the surface or within explants were distinguished by the presence of microvilli, junctional complexes, multiple Golgi complexes, well-developed rough endoplasmic reticulum, polyribosomes, nuclei with prominent nucleoli, orthodox mitochondria, scattered tonofilaments, and a basal lamina. Some epithelial cells extended from the lumen to the basal lamina; others were oriented along the basal lamina and did not extend to the lumen. By 1--2 weeks in vitro, these epithelial cells began synthesis of mucus-like material. At later intervals of culture, microvilli were shortened and mucosubstances were reduced. During culture, the stroma became progressively hypocellular and necrotic. In summary, explant-cultured epithelial cells of normal human prostate or BPH were similar ultrastructurally and were found to originate from basal cells, which alone survive culture conditions.

Adolescent↗

PubMed1997

Prostate attenuated replication competent adenovirus (ARCA) CN706: a selective cytotoxic for prostate-specific antigen-positive prostate cancer cells.

Prostate-specific antigen (PSA) is a widely used marker for the diagnosis and management of prostate cancer. Minimal enhancer/promoter constructs derived from the 5' flank of the human PSA gene (prostate-specific enhancer) were inserted into adenovirus type 5 DNA so as to drive the E1A gene, thereby creating a prostate-specific enhancer-containing virus, CN706. E1A was expressed at high levels in CN706-infected human PSA-producing LNCaP cells but not in CN706-infected DU145 cells, which are human prostate cells that do not express PSA. The titer of CN706 was significantly higher in LNCaP cells compared to several human cell lines that do not produce PSA (HBL100, PANC-1, MCF-7, DU145, and OVCAR3). Furthermore, in LNCaP cells, the yield of CN706 was dependent on exogenous androgen (R1881). CN706 destroyed large LNCaP tumors (1 x 10(9) cells) and abolished PSA production in nu/nu mouse xenograft models with a single intratumoral injection.

Adenovirus E1A Proteins↗

PubMed2000

Diagnosis of prostate adenocarcinoma using transurethral resection of the prostate after multiple negative transrectal biopsies and persistently elevated prostate-specific antigen level.

We report a case of prostate cancer diagnosis by transurethral resection of the prostate in a man who underwent more than 50 needle biopsies by three different physicians for an increasing prostate-specific antigen level. Radical prostatectomy resulted in removal of an organ-confined tumor (T2aN0M0), and a short follow-up revealed an undetectable prostate-specific antigen level.

Adenocarcinoma↗

PubMed2003

Distribution and secretory pathways of prostate specific antigen, alpha1-antichymotrypsin and prostate secretory granules in prostate cancers.

Using 19 radical prostatectomy specimens, we studied the histological distribution of free prostate specific antigen (PSA), total PSA, alpha1-antichymotrypsin (ACT) and prostate secretory granules (PSG) in both normal and cancerous cells of the prostate. After glutaraldehyde fixation, numerous fine eosinophilic droplets of PSG could be found mainly in the apical portions of normal acinous epithelial cells, but was markedly decreased in cancer cells. With antibodies against free PSA, normal acinous cells were granularly positive in the apical portion of the epithelium, which corresponded to the PSG, whereas cancer cells were diffusely positive. With antibodies against ACT, normal duct cells and cancer cells were often positive, but few normal acinous cells were positive. Presumably, these findings indicate that free PSA is secreted into the lumen as PSG in normal glands, but not by the same pathway in cancers where free PSA appears to accumulate due to a decrease of PSG, then leak into the blood producing complexed PSA to some extent in the cytoplasm. One factor analysis of variance (ANOVA) on the correlation of tumor differentiation or Gleason score with serum values of total PSA, free PSA and a free/total PSA ratio demonstrated no significant links. Elucidation of secretory mechanisms should provide better comprehension of various PSA indices for prostate cancer screening.

Adenocarcinoma↗

PubMed2003

Prostate-specific antigen levels and density in the internal and external glands of the prostate in benign prostatic hyperplasia patients with normal or gray-zone PSA levels.

OBJECTIVE: In patients with benign prostatic hyperplasia (BPH) showing normal prostate-specific antigen (PSA) levels (normal PSA group) and those with BPH showing gray-zone PSA levels (gray-zone PSA group), we assessed PSA levels secreted from the internal and external glands. MATERIALS AND METHODS: We performed transurethral enucleation of the prostate (TUE) in 102 BPH patients with normal PSA and 59 BPH patients with gray-zone PSA at our department from 1999 to 2001. Preoperatively and approximately 6 months postoperatively, we measured serum PSA levels and determined prostatic volumes via transrectal ultrasonography (TRUS) to calculate PSA levels secreted from the internal and external glands as well as various PSA density (PSAD) values. RESULTS: The total PSA level was 1.8 and 6.1 ng/ml in the normal and gray-zone PSA groups, respectively. The PSA level of the external gland was 0.6 and 0.8 ng/ml and the PSAD of the external gland was 0.07 and 0.08 ng/ml/cm(3) in the normal and gray-zone PSA groups, respectively. The internal gland PSA was 1.3 and 5.4 ng/ml and the internal gland PSAD value was 0.11 and 0.30 ng/ml/cm(3) in the normal and gray-zone PSA groups, respectively. CONCLUSIONS: Our results demonstrated that increased PSA levels in BPH cases with gray-zone PSA were attributable to increased PSA secreted from the internal gland rather than from the external gland. In our opinion, the determination of PSA and PSAD of the internal and external gland may be clinically significant in the future.

Aged↗

PubMed1994

Differentiation of benign prostatic hyperplasia and prostate cancer employing prostatic-specific antigen density.

To enhance the ability of prostate-specific antigen (PSA) to distinguish benign prostatic hyperplasia (BPH) from cancer of the prostate (CaP) Benson et al. defined a new parameter, PSA density (PSAD), which is the ratio of the serum PSA concentration to the volume of the prostate. We have employed this parameter in a prospective study of 28 patients with clinically localised CaP and 57 patients with BPH. Mean PSAD was 0.116 for the BPH patients and 0.46 for the CaP patients (p < 0.005). The authors conclude that the information provided by PSAD is superior to absolute PSA values in the differentiation between BPH and CaP.

Biomarkers, Tumor↗

PubMed1990

[Clinical studies on tumor markers for monitoring prostate cancer patients; the evaluation of prostate-specific antigen and comparison with prostatic acid phosphatase and gamma-seminoprotein].

To evaluate the usefulness of tumor markers in monitoring the patients with prostate cancer, serial measurements of serum prostate-specific antigen (PA), prostatic acid phosphatase (PAP) and gamma-seminoprotein (gamma-Sm) were performed in 78 stage C or D patients. Positive rates of each marker prior to the treatment were as follows; PA; 75%, PAP; 56% and gamma-Sm; 62% in stage C, and PA; 95%, PAP; 79% and gamma-Sm; 91% in stage D. In most cases showing PR (partial response) and S (stable) in clinical responses, these three markers decreased their serum titers corresponding to clinical course if the markers were elevated at the start of the treatment. But the usefulness of PAP was lessened because of its lower positive rate than those of PA and gamma-Sm. In 33 PD (progressive disease) cases, positive rates of each marker at time of clinical diagnosis as PD were found to be 85% in PA, 55% in PAP and 76% in gamma-Sm. And with the combination assays of these three tumor markers, positive rate was elevated to 88%. Moreover, elevation of serum values of these three markers at 3 months before the progression event were observed in 50% of PA, 39% of PAP and 46% of gamma-Sm. Then the prognostic significance of each marker was examined. In PA and PAP, there were statistical differences in non-relapsing rates between patients whose reduction rates from the pretreatment value on 7th day were more than and less than 50%. But in gamma-Sm, a statistical difference between each group was firstly observed on 14th day. As a result, in monitoring patients with prostate cancer, PA and gamma-Sm are more useful than PAP and, in prediction of patients' prognosis, PA is more useful than gamma-Sm.

Acid Phosphatase↗

PubMed2006

[Expression of nucleosomal binding protein 1 in normal prostate benign prostate hyperplasia, and prostate cancer and significance thereof].

OBJECTIVE: To investigate the expression of nucleosomal binding protein 1 (NSBP1) in normal prostate (NP), benign prostate hyperplasia (BPH), and prostate cancer (PCa) and significance thereof. METHODS: Western blotting was used to detect the expression of NSBP1 in 10 specimens of NP from voluntary donors who died of accidents, and 15 specimens of PCa resected during operation. Immunohistochemistry was used to detect the NSBP1 expression in 19 specimens of NP resected during complete cystectomy from patients with bladder carcinoma, and 26 specimens of BPH and 40 specimens of PCa, all resected during operation. RESULTS: Western blotting showed that the relative optical density (OD) of NSBP1 in the PCa tissue was 0.66 +/- 0.02, significantly higher than that of the NP tissue (0.26 +/- 0.03, t = 37.308, P < 0.01). Immunohistochemistry showed that the positive and weak positive rates of protein expression of NSBP1 in the PCa tissue was 80.0% (32/40), significantly higher than those of the NP tissue (36.8%, 7/19) and BPH (34.6%, 9/26) (t = -3.569 and t = -4.152, both P < 0.01). The NSBP1 expression level in the PCa tissue was not correlated with the pathological staging, grade, and serum prostate-specific antigen (P = 0.911, 0.666, and 0.779). CONCLUSION: Highly expressed in the PCa tissue, NSBP1 protein is may be involved in the carcinogenesis of PCa.

Adult↗

PubMed1992

Radiation therapy in prostate cancer: whole pelvis with prostate boost or small field to prostate?

The purpose of this retrospective study is to identify prostate cancer patients who would benefit from pelvic nodes irradiation (whole pelvis) as opposed to the small-field irradiation to the prostate only. Between 1975 and 1983, 126 patients were treated by whole pelvis (4,600-5,000 cGY) with prostate boost (2,000 cGY) radiation (WP + P). Median follow-up was six years and six months. Comparison was made with historic control of 116 patients irradiated at the same institutions between 1971 and 1977 by small field to the prostate (P) to a dose of 7,000-7,500 cGY. There was a significant five-year survival improvement in the current WP + P radiation in Stage C (72% vs 40%, p = 0.0004) and Stage B (92% vs 70%, p = 0.025) but not in Stage A2 patients. However, WP + P radiation significantly improved disease-free survival (DFS) in only well and moderately but not in poorly differentiated carcinoma with a combined well and moderately differentiated five-year DFS of 63 percent compared with the 45 percent in P radiation (p = 0.0228). Local tumor control was significantly improved in WP + P radiation in only Stage C cancers with their local recurrence rate 16 percent as compared with the 34 percent in P radiation (p = 0.0172). Although acute radiation reactions were more frequent in WP + P than P radiation (61% vs 41%, p = 0.0022), chronic radiation morbidity in both series were similar. Thus, whole pelvis with prostate boost radiation should be utilized in Stage B and Stage C cancers as this has shown to increase the survival of the patient without increasing chronic radiation morbidity.

Actuarial Analysis↗

PubMed1997

No germline mutations in the dimerization domain of MXI1 in prostate cancer clusters. The CRC/BPG UK Familial Prostate Cancer Study Collaborators. Cancer Research Campaign/British Prostate Group.

There is evidence that predisposition to cancer has a genetic component. Genetic models have suggested that there is at least one highly penetrant gene predisposing to this disease. The oncogene MXI1 on chromosome band 10q24-25 is mutated in a proportion of prostate tumours and loss of heterozygosity occurs at this site, suggesting the location of a tumour suppressor in this region. To investigate the possibility that MXI1 may be involved in inherited susceptibility to prostate cancer, we have sequenced the HLH and ZIP regions of the gene in 38 families with either three cases of prostate cancer or two affected siblings both diagnosed below the age of 67 years. These are the areas within which mutations have been described in some sporadic prostate cancers. No mutations were found in these two important coding regions and we therefore conclude that MXI1 does not make a major contribution to prostate cancer susceptibility.

Adult↗

PubMed1999

Cancer patient T cells genetically targeted to prostate-specific membrane antigen specifically lyse prostate cancer cells and release cytokines in response to prostate-specific membrane antigen.

The expression of immunoglobulin-based artificial receptors in normal T lymphocytes provides a means to target lymphocytes to cell surface antigens independently of major histocompatibility complex restriction. Such artificial receptors have been previously shown to confer antigen-specific tumoricidal properties in murine T cells. We constructed a novel zeta chain fusion receptor specific for prostate-specific membrane antigen (PSMA) termed Pz-1. PSMA is a cell-surface glycoprotein expressed on prostate cancer cells and the neovascular endothelium of multiple carcinomas. We show that primary T cells harvested from five of five patients with different stages of prostate cancer and transduced with the Pz-1 receptor readily lyse prostate cancer cells. Having established a culture system using fibroblasts that express PSMA, we next show that T cells expressing the Pz-1 receptor release cytokines in response to cell-bound PSMA. Furthermore, we show that the cytokine release is greatly augmented by B7.1-mediated costimulation. Thus, our findings support the feasibility of adoptive cell therapy by using genetically engineered T cells in prostate cancer patients and suggest that both CD4+ and CD8+ T lymphocyte functions can be synergistically targeted against tumor cells.

3T3 Cells↗

PubMed1998

Linkage analysis of chromosome 1q markers in 136 prostate cancer families. The Cancer Research Campaign/British Prostate Group U.K. Familial Prostate Cancer Study Collaborators.

Prostate cancer shows evidence of familial aggregation, particularly at young ages at diagnosis, but the inherited basis of familial prostate cancer is poorly understood. Smith et al. recently found evidence of linkage to markers on 1q, at a locus designated "HPC1," in 91 families with multiple cases of early-onset prostate cancer. Using both parametric and nonparametric methods, we attempted to confirm this finding, in 60 affected related pairs and in 76 families with three or more cases of prostate cancer, but we found no significant evidence of linkage. The estimated proportion of linked families, under a standard autosomal dominant model, was 4%, with an upper 95% confidence limit of 31%. We conclude that the HPC1 locus is responsible for only a minority of familial prostate cancer cases and that it is likely to be most important in families with at least four cases of the disease.

Chromosomes, Human, Pair 1↗