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At least 613 records · Page 34Linked to original sources

PubMed2002

High prevalence of screening-detected prostate cancer among Afro-Caribbeans: the Tobago Prostate Cancer Survey.

Risk for prostate cancer is high among African Americans. We hypothesized that risk for prostate cancer is also high in other populations of African descent. Our objective was to determine the screening-detected prevalence of prostate cancer in the predominantly Afro-Caribbean population on the island of Tobago. Male residents, ages 40-79 years, were invited to participate in a population-based screening for prostate cancer using serum prostate-specific antigen (PSA) and digital rectal exam (DRE). Men with elevated PSA (>or=4 ng/ml) or abnormal DRE were offered an ultrasound-guided sextant biopsy of the prostate gland. Men (2484), ages 40-79 years, underwent prostate cancer screening between September 1997 and June 2001. Mean age was 55.9, SD was 10.6 years, and median was 54 years. Mean serum PSA was 14.8 ng/ml, SD was 376 [excluding 4 values >or= 2 SD above the mean (1,112, 1,317, 1,818, and 18,330 ng/ml) mean PSA was 5.5 ng/ml and SD was 29.6], and median PSA was 1.2 ng/ml. Elevated PSA and/or abnormal DRE were observed in 31% (759 of 2484) overall, and in age groups 40-49 (87 of 843, 10%), 50-59 (201 of 729, 28%), 60-69 (262 of 584, 45%), and 70-79 (209 of 328, 64%). Of 681 men biopsied, 259 (38%, or 10% of the 2484 screened) were diagnosed with prostate cancer. Age-specific rates of screening detected prostate cancer were: 1%, ages 40-79 years; 7%, ages 50-59 years; 18%, ages 60-69 years; and 28%, ages 70-79 years. These screening results indicate a very high screening-detected prevalence of prostate cancer in this population of West African descent. These data support the hypothesis that populations of African descent share genetic and/or lifestyle factors that contribute to their elevated risk for prostate cancer.

Adult↗

PubMed2004

Plasma levels of heat shock protein 70 in patients with prostate cancer: a potential biomarker for prostate cancer.

Heat shock protein 70 (Hsp70) is a stress-inducible protein that is also known for its inhibitory effects on apoptosis. Increased Hsp70 expression is reported in a variety of tumor tissues. Heat shock protein 70 is detectable in plasma and could potentially be used as a biomarker for diagnosis or disease stratification. The relationship between plasma levels of Hsp70 and prostate cancer status has not been well studied. Our study was designed to test this relationship. One hundred twenty-five patients with localized/untreated or hormone-refractory prostate cancer were identified. Forty-five healthy male blood donors between 50 and 73 years of age served as controls. EDTA plasma was subjected to quantitative sandwich immunoassays for both Hsp70 and prostate-specific antigen (PSA). Wilcoxon rank-sum tests were used to examine differences by category. Maximally selected c2 statistics were used to identify cutoff points to best distinguish between categories. Plasma Hsp70 levels in the patients with localized untreated disease (n = 68; median, 0.8 ng/mL; interquartile range, 0.5-2.0) were significantly higher than those in the control group (n = 45; median, 0.5 ng/mL; interquartile range, 0.3-0.8; P = 0.0037). Although the primary cutoff point (1.15 ng/mL) significantly distinguished the localized untreated patients from the control group, plasma Hsp70 levels did not prove more effective than PSA as a predictor for diagnosis or stratification of patients with prostate cancer in the context of group comparisons. Nonetheless, several patients in the localized untreated group showed higher plasma levels of Hsp70 than the primary cutoff point even though their PSA levels were within normal range (< 4 ng/mL). Heat shock protein 70 is a marker of prostate cancer, although its clinical utility is uncertain. It is possible that when used in conjunction with PSA it might prove useful in identifying patients with early-stage prostate cancer who might otherwise be missed by PSA screening alone.

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PubMed2004

Validation of increasing prostate specific antigen as a predictor of prostate cancer death after treatment of localized prostate cancer with surgery or radiation.

PURPOSE: Many patients who undergo surgery or radiation therapy to treat localized prostate cancer experience an increase in serum prostate specific antigen (PSA) after treatment. This study documents patterns of PSA recurrence after surgery or radiation to treat localized prostate cancer and quantifies the extent to which an increasing PSA predicts death from prostate cancer. MATERIALS AND METHODS: Posttreatment PSA levels were measured on a population based cohort of 1136 men diagnosed with localized prostate cancer in community practice in Connecticut between 1990 and 1992, and treated within 6 months of diagnosis with surgery or radiation with or without androgen withdrawal therapy. The major outcome measure was death from prostate cancer. RESULTS: PSA recurrence followed a log-linear pattern over time. Patients who died of prostate cancer had a median PSA doubling time of 0.8 years (25th and 75th percentiles 0.5 to 1.4 years). Patients who did not die of prostate cancer within 10 years of diagnosis had either no posttreatment increase in serum PSA (40%) or had a PSA doubling time longer than 1 year (44%). CONCLUSIONS: Patients whose posttreatment PSA doubling times before the initiation of androgen withdrawal therapy are less than 1 year are at high risk of dying of prostate cancer within 10 years of diagnosis. Men with PSA recurrences that are doubling at rates greater than 1 year are at low risk of death from prostate cancer within 10 years of diagnosis.

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PubMed2005

Prostate cancer and prostate-specific antigen (PSA) screening in Austria.

The possible effect of prostate-specific antigen (PSA) testing on prostate cancer mortality has remained controversial, despite the test's widespread application. We examined age-specific mortality trends for prostate cancer in Austria before and after the introduction of (opportunistic) PSA testing, to ask whether PSA screening reduces prostate cancer mortality in a uniform cohort of men with equal access to health care. Prostate cancer mortality data covering all 9 federal states of Austria were analysed from 1970 to 2002. PSA testing became widely available in Austria not before 1989. Tyrol, one of the nine federal states of Austria, independently launched a mass prostate cancer prevention project in 1993. We applied join-point regression models to identify changes in the slope of age-specific mortality trends in selected age groups (50-59, 60-69, 70-79, and 80-89 years) and calculated the annual percent change (APC) in mortality between 1970 and 2002 for Tyrol and the rest of Austria separately. After 12 years of follow-up, we were not able to observe a significant reduction in prostate cancer mortality since the introduction of the PSA test in the age groups of 50-59, 60-69, and 80-89 years. A significant decrease was found in the age group of 70-79 (Austria without Tyrol 1989 through 2002: APC, -2.36; 95% CI, -3.38 to -1.34; Tyrol 1991 through 2002: APC, -6.42; 95% CI, -8.92 to -3.86). In this age group the join points 1989 and 1991 cannot be related to PSA testing. PSA screening does not appear to reduce prostate cancer mortality in a uniform cohort of men with equal access to health care. However, given the long lead-time for prostate cancer, even longer follow-up may still be needed to detect any important trends.

Age Distribution↗

PubMed2004

Survival of patients with hormone refractory prostate cancer in the prostate specific antigen era.

PURPOSE: The historically reported 12 to 18-month duration of survival of patients with hormone refractory prostate cancer is not consistent with current clinical experience. Furthermore, to our knowledge patient survival after serum prostate specific antigen (PSA) progressively increases from a nadir despite castrate testosterone has not been previously reported. For this reason we studied overall survival and the clinical variables that influence survival in patients with hormone refractory prostate cancer. MATERIALS AND METHODS: The study focused on 254 patients with prostate cancer on androgen deprivation therapy. Hormone refractory prostate cancer was defined as the first in a series of PSA elevations despite castrate levels of testosterone. The duration of survival in the hormone refractory phase was calculated from the date of the first PSA elevation to the date of death. RESULTS: Median survival after hormone refractory prostate cancer developed in patients initially staged with and without skeletal metastasis was 40 and 68 months, respectively. Six of more than 25 input variables were retained as significant in the final Cox model. Variables associated with longer survival were lower nadir PSA, younger age, higher pretreatment testosterone, no history of obstructive uropathy, no history of tobacco use (past or current) and lower alkaline phosphatase. CONCLUSIONS: Historical reports of survival in hormone refractory prostate cancer underestimate current survival observations. The likely explanations of this observation include delayed enrollment in clinical trials from which most survival data are derived, PSA lead time in staging and improved supportive care. Models predicting survival in patients with hormone refractory prostate cancer should consider multiple variables.

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PubMed2001

The use of telomerase activity for the detection of prostatic cancer cells after prostatic massage.

PURPOSE: Prostate cancer is the most commonly diagnosed cancer in the United States. The diagnosis or followup of prostate cancer in men older than 50 years is based on digital rectal examination, measurement of the free-to-total prostatic specific antigen ratio and transrectal ultrasound assisted needle biopsy of the prostate. We developed and evaluated a noninvasive method for diagnosing prostate cancer based on the measurement of telomerase activity after prostatic massage in fresh voided urine or after urethral washing. MATERIALS AND METHODS: We obtained 36 specimens of cells after prostatic massage in the fresh voided urine of 16 patients who subsequently underwent radical prostatectomy and after urethral washing in 20 who underwent prostate needle biopsies. Ethylenediaminetetraacetic acid was immediately added to the collected urine or washing to a final concentration of 20 mM. After protein extraction by CHAPS buffer each specimen was tested for telomerase activity in a 2-step modified telomeric repeat amplification protocol assay. The 2 prostate cancer cell lines PC-3 and LNCaP with high telomerase activity were used as a positive control. RESULTS: Telomerase activity was detected in 14 of 24 samples with known prostate cancer (sensitivity 58%). In contrast, no telomerase activity was found in the 12 cases without histological evidence of prostate tumor (specificity 100%). Eight of 9 poorly differentiated cancers expressed telomerase activity (89%), while only 6 of 15 well and moderately differentiated cancers showed telomerase activity (40%). CONCLUSIONS: Our data illustrate that telomerase activity may be detected in voided urine or washing after prostatic massage in patients with prostate cancer. Sensitivity was higher for poorly differentiated tumors. This approach is not currently available for detecting prostate cancer in clinical practice. However, these results are promising and further studies are ongoing.

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PubMed2003

Mutations in ribonuclease L gene do not occur at a greater frequency in patients with familial prostate cancer compared with patients with sporadic prostate cancer.

Several genetic loci are suspected to be involved in hereditary prostate cancer, including the hereditary prostate cancer 1 (HPC1) locus at chromosome 1q24-25. The ribonuclease L (RNase L) gene has been reported as the putative hereditary prostate cancer gene located at HPC1. If this is the case, mutations of RNase L should be found at a greater frequency in familial cancers than in sporadic prostate cancers. Examination of familial and sporadic cases of prostate cancer by polymerase chain reaction and DNA sequencing resulted in a mutational frequency rate that was not statistically different between the 2 forms of the disease. These results suggest that the mutations examined within this study are rare and may contribute to very few familial prostate cancers.

DNA Mutational Analysis↗

PubMed2005

Decreasing age at prostate cancer diagnosis over successive generations in prostate cancer families.

BACKGROUND: The decline in age at prostate cancer diagnosis over the past decade is partially attributable to prostate specific antigen (PSA) screening. We examined age at diagnosis over successive generations within prostate cancer families. METHODS: Families with at least two affected men were selected from the University of Michigan Prostate Cancer Genetics Project. The 1,345 individuals from 489 families were grouped into three generations. RESULTS: Risk of prostate cancer diagnosis at a given age was estimated to increase 1.31 (95% CI: 1.13-1.51) times from one generation to the next. Among men diagnosed prior to the PSA era, inferences were similar (hazard ratio = 1.28, 95% CI: 0.97-1.68). No maternal versus paternal disease transmission effect was observed. CONCLUSIONS: Age at prostate cancer diagnosis was observed to decrease over successive generations in families from an ongoing familial prostate cancer study. This finding, if confirmed, may have important implications for familial prostate cancer risk assessment.

Age Distribution↗

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.

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PubMed1992

Prostate cancer.

Clinically, prostate cancer (prostatic adenocarcinoma) is now the most frequently diagnosed cancer in males and the second leading cause of mortality due to cancer in the United States. However, because 75% of histologic prostate cancers remain functionally benign (will not metastasize and kill the patient), mass screening of the male population for the disease has become a hotly debated issue among urologists. The real challenge in the upcoming decade for geriatricians, though, will be to diagnose earlier in their course the prostate cancers which, if not treated, will metastasize and kill the patient and thus allow this subgroup of patients the opportunity to be treated more effectively. This review briefly discusses the etiology of prostate cancer, ways the disease may present, current treatments, depending on disease stage, screening in the diagnosis of prostate cancer, and quality of life issues important to patients confronted with the disease.

Adenocarcinoma↗

PubMed2002

Detection of human kallikrein 4 in healthy and cancerous prostatic tissues by immunofluorometry and immunohistochemistry.

BACKGROUND: Human kallikrein 4 (gene, KLK4; protein, hK4), a recently discovered member of the kallikrein gene family, shares many characteristics with prostate-specific antigen, the best available marker for prostate cancer. Because the protein has not been detected in any human tissue, we attempted to develop immunologic methods for hK4 analysis and use them to detect hK4 in healthy and cancerous tissue extracts and biological fluids. METHODS: We extracted total RNA from 20 pairs of matched (healthy-cancer) prostate tissue samples. KLK4 cDNA was amplified by reverse transcription-PCR (RT-PCR) and cloned in a pPICZalphaA expression vector. We then transformed the construct product into Pichia pastoris yeast strains and induced secreted recombinant protein production by addition of methanol. We purified the recombinant protein by nickel ion-affinity chromatography and used it as an immunogen in rabbits and mice to generate polyclonal anti-hK4 antibodies. These antibodies were used to develop a sandwich-type immunoassay suitable for hK4 quantification in biological fluids and tissue extracts. RESULTS: The immunoassay had a detection limit of 0.1 microg/L. We detected hK4 in 10 of 21 matched (healthy-cancer) prostate tissues, and hK4 was frequently higher in healthy tissues. In one matched-sample pair, the hK4 content was relatively high in both the healthy [4.62 microg/g of total protein (TP)] and the cancerous (1.22 microg/g of TP) prostate tissue. Among tissue extracts, we found the highest concentrations of hK4 in healthy (0.0-4.62 microg/g of TP) and cancerous (0.0-1.72 microg/g of TP) prostatic extracts and in placental extracts (0.0-0.05 microg/g of TP). We also detected traces of hK4 protein immunoreactivity in amniotic fluid (<0.1-0.6 microg/L), human breast milk (<0.1-0.75 microg/L), and seminal plasma (0.2-0.9 microg/L). Immunohistochemical studies showed cytoplasmic staining for hK4 protein in both malignant and benign epithelial cells of the prostate. However, we did not detect hK4 in cerebrospinal fluid, healthy and cancerous ovarian tissue extracts, and many other human tissue extracts. CONCLUSIONS: hK4 protein is present in some prostatic tissue extracts but at relatively low concentrations, although KLK4 mRNA is readily detectable by RT-PCR. We propose that the protein either is not synthesized efficiently or is degraded very quickly.

Animals↗

PubMed2003

Cyp17 genetic polymorphism in prostate cancer and benign prostatic hyperplasia.

Steroid hormones, especially androgens, are believed to play a key role in the etiology of prostate cancer. Therefore, polymorphisms in genes involved in the androgen metabolism may affect the risk of prostate cancer. One such gene is CYP17, which encodes the cytochrome P450c17alpha enzyme that mediates both 17alpha-hydroxylase and 17,20-lyase in the steroid biosynthesis pathway. A polymorphism in the 5'-promoter region of the CYP17 gene has been associated with increased risk for prostate cancer. The T to C transition in the risk allele creates a new recognition site for the restriction enzyme MspA1. In this study we investigated the distribution of this polymorphism in the Turkish population and its association with prostate cancer and benign prostatic hyperplasia. Genotype frequencies in the patients with prostate cancer or prostatic hyperplasia and the control group were not significantly different. Our data provide no evidence for an association between prostate cancer risk and the CYP17 gene polymorphism.

Adult↗

PubMed2026

Subclonal Complete Loss of CDKN1B as a Common Genomic Alteration in Prostate Cancer: Associations with Race and Prostate Cancer Outcomes.

BACKGROUND: Homozygous biallelic inactivation of CDKN1B is thought to be rare in cancer. Herein we evaluate the prevalence of intratumoral (subclonal) complete p27 protein loss (IPPL) in primary prostate cancer. EXPERIMENTAL DESIGN: We used immunohistochemistry (IHC) for p27 in a large cohort of whole tissue sections from radical prostatectomy (n=412) and metastases from self-identified African American (AA) and European American (EA) individuals. IPPL was evaluated alongside CDKN1B mRNA in-situ hybridization and next generation sequencing of laser captured cancer regions. Cox proportional hazards analyses assessed the association of IPPL with biochemical recurrence and development of metastases after radical prostatectomy. RESULTS: IPPL was detected in 18.1% of AA versus 12.2% of EA cases and was tightly correlated with CDKN1B mRNA loss and biallelic genomic loss. IPPL was associated with ≥pT3 pathologic stage and pN1 disease, however these associations were only significant among AA participants. IPPL was further associated in both univariate and multivariate analyses with the development of biochemical recurrence and metastasis after primary treatment, specifically in AA individuals. The prevalence of p27 genomic alterations in metastatic disease is higher than that of primary prostate cancer in publicly available datasets as well as our analysis of autopsy cases via IHC, indicating that complete p27 loss may be selected for in metastatic disease. CONCLUSIONS: Subclonal biallelic loss of CDKN1B resulting in complete p27 protein loss is one of the most commonly occurring biallelic tumor suppressor genomic alterations in primary prostate cancer, and could contribute to worse prostate cancer outcomes, specifically in AA males.

Journal Article↗

PubMed2001

Evidence for a prostate cancer linkage to chromosome 20 in 159 hereditary prostate cancer families.

Prostate cancer is the most common malignancy diagnosed in men in the US. Genetic susceptibility to prostate cancer has been well documented. A region at chromosome 20q13 (HPC20) has been reported to be linked to a prostate cancer susceptibility gene. To confirm this finding, we genotyped 16 markers spanning approximately 95 cM on chromosome 20 in 159 hereditary prostate cancer (HPC) families. Positive (but not statistically significant) linkage scores were observed from 20pter to 20q11, with the highest non-parametric linkage (NPL) score for the complete dataset of 1.02 (P=0.15) being observed at D20S195 at 20q11. Evidence for linkage from parametric analyses with a dominant or a recessive model was weak. Interestingly, consistent with the original findings of linkage to 20 g higher linkage scores were observed in the subsets of families with a later age at diagnosis (> or =65 years; n=80, NPL=1.94, P=0.029 at D20S186), fewer than five affected family members (n=69, NPL=1.74, P=0.037 at D20S889), or without male-to-male disease transmission (n=60, NPL=1.01, P=0.15 at D20S117). The region with positive linkage scores spanned approximately 60 cM from 20pter to 20q11 in these subsets of families. Our results are consistent with a prostate cancer susceptibility locus on chromosome 20.

Aged↗

PubMed2005

Prostate cancer in patients with screening serum prostate specific antigen values less than 4.0 ng/dl: results from the cooperative prostate cancer tissue resource.

PURPOSE: Prostate cancer can occur in patients with low screening serum prostate specific antigen (PSA) values (less than 4.0 ng/ml). It is currently unclear whether these tumors are different from prostate cancer in patients with high PSA levels (greater than 4.0 ng/ml). MATERIALS AND METHODS: From the Cooperative Prostate Cancer Tissue Resource database through March 2004, 3,416 patients with screening PSA less than 16.0 ng/ml diagnosed with prostate cancer between 1993 and 2004 were stratified in groups based on screening serum PSA. These subsets were compared for race, age at diagnosis, clinical and pathological stage, Gleason score, positive surgical margins, posttreatment recurrent disease, and vital status. RESULTS: We identified 468 (14%) patients with screening PSA less than 4.0 ng/ml, 142 (4.2%) of whom had a PSA of less than 2.0 ng/ml. This group included 40 black and 376 white patients. Men with low screening PSA treated with radical prostatectomy had smaller cancers, lower Gleason scores, lower pathological tumor (T) stage and lower PSA recurrence rates than men with high PSA levels (4 ng/ml or greater). These differences held true for men who were younger than 62 years or were white, whereas older or black men had tumor characteristics and outcomes similar to those with higher PSA levels. CONCLUSIONS: Young (younger than 62 years) or white patients with screening serum PSA less than 4.0 ng/ml had smaller, lower grade tumors and lower recurrence rates than patients with PSA 4.0 ng/ml or greater. This was not true for those older than 62 years and for black men.

Humans↗

PubMed2003

Radical cystectomy for bladder cancer after definitive prostate cancer treatment.

OBJECTIVES: To review our perioperative experience with patients presenting with high-risk bladder cancer who had undergone prior therapy for prostate cancer. With the increase in diagnosis and subsequent treatment of prostate cancer, more patients presenting with high-risk bladder cancer have undergone prior therapy for prostate cancer. Radical cystectomy in these patients can be technically challenging and may be associated with added morbidity. METHODS: A retrospective review of 458 patients treated with radical cystectomy between January 1993 and January 2002 revealed 29 patients (mean age 72 years) who had received definitive treatment for prostate cancer prior to cystectomy for bladder carcinoma. The initial treatment in this cohort was radical prostatectomy or external beam radiotherapy in 12 (41%) and 17 (59%) men, respectively. Cystectomy was performed for transitional cell carcinoma in 25 (86%), small cell carcinoma in 2 (6%), and sarcoma in 2 (6%) patients. RESULTS: At the time of cystectomy, the mean blood loss was 1175 mL (range 275 to 3500), and the median length of hospitalization was 8 days (range 4 to 23). No intraoperative or perioperative deaths occurred in this cohort. Twenty-seven early complications were identified in 16 (55%) of 29 patients; no rectal injuries occurred. Patients with prior radiotherapy had a higher rate of extravesical bladder carcinoma (60%) than those patients treated with prior prostatectomy (33%). An orthotopic neobladder diversion was created in 5 patients (17%). CONCLUSIONS: Patients with bladder cancer previously treated for prostate cancer with external beam radiotherapy or radical prostatectomy have an increased risk of perioperative complications compared with patients undergoing cystectomy without prior therapy. This risk is not prohibitive, and radical cystectomy should remain the treatment of choice for high-risk bladder cancer in this population. Furthermore, orthotopic urinary diversion may be a reasonable option and should be considered in select patients.

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PubMed1998

The University of California, Los Angeles/Jennifer Jones Simon Foundation symposium on prostate cancer and epithelial cell biology: bringing together basic scientists and clinicians in the fight against advanced prostate cancer.

Prostate cancer is the most common solid tumor in American men and is the second most common cause of cancer deaths. Although surgery and radiation therapy are effective for the treatment of organ-confined cancer, there is no effective treatment that is currently available for patients who have metastatic disease. Antiandrogen therapy is only palliative, and chemotherapy has largely been ineffective. However, recent advances in the understanding of the molecular biology of prostate cancer have lead to the development of new treatment strategies for metastatic cancer, including gene-based therapies, immunotherapies, and antiangiogenesis-based therapy. In association with the Jonsson Comprehensive Cancer Center and the University of California, Los Angeles Department of Urology, the Jennifer Jones Simon Foundation assembled 30 of the world's experts in prostate cancer research to review the most recent advances in the study of prostate cancer, with the hope that the resulting discussions would facilitate the rapid translation of new discoveries from the laboratory bench to the clinic.

Antineoplastic Agents↗

PubMed2000

Patterns of treatment of patients with prostate cancer initially managed with surveillance: results from The CaPSURE database. Cancer of the Prostate Strategic Urological Research Endeavor.

PURPOSE: We determined the demographic and clinical profile of men who elect surveillance as the initial management of prostate cancer as well as the incidence and predictors of secondary treatment of these patients. MATERIALS AND METHODS: The Cancer of the Prostate Strategic Urological Research Endeavor (CaPSURE) is a national disease registry of patients with various stages and treatments of prostate cancer. Using this database of 4,458 men we identified 329 (8.2%) who elected surveillance as the initial management of prostate cancer. Patients choosing watchful waiting were compared to other CaPSURE participants using the chi-square test. The likelihood of treatment initiation in the watchful waiting group was calculated using the Kaplan-Meier method. After adjusting for patient age, race, prostate specific antigen (PSA) at diagnosis, clinical T stage and total Gleason score the Cox proportional hazards regression model was used to determine significant predictors of treatment initiation. RESULTS: Compared with others in the database, patients on watchful waiting were more likely to be 75 years old or older (51% versus 16%, p <0.001), white (93% versus 85%, p <0.001), and have lower serum PSA (p <0.001), organ confined disease (97% versus 88%, p <0.001) and a total Gleason score of 7 or less (97% versus 88%, p <0.001). In the watchful waiting group there was a 52% likelihood of treatment initiation within 5 years of the diagnosis. Significant predictors of secondary treatment were age younger than 65 years and elevated serum PSA at diagnosis. Neither race, extraprostatic stage cT3 disease nor higher total Gleason score was a significant predictor of treatment. CONCLUSIONS: Men who elect initial watchful waiting for prostate cancer tend to be older, have lower serum PSA and more favorable disease characteristics than those who seek treatment. PSA at diagnosis is the dominant factor for predicting secondary treatment.

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