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Free-to-total prostate-specific antigen serum concentrations in patients with prostate cancer and benign prostatic hyperplasia.

OBJECTIVE: To determine whether the proportion of total serum prostate-specific antigen (tPSA) which is unbound or free (free PSA) offers a better discriminant for the detection of patients with prostate cancer (CaP) and those with benign prostatic hyperplasia (BPH) than does serum tPSA alone. PATIENTS AND METHODS: In a retrospective analysis, the proportion of free PSA was determined in the sera of 60 patients with histologically confirmed localized (n = 39; pT1-3NoMo) and metastatic (n = 21; T2-4NxM+) CaP and 45 patients with BPH. Forty patients with urolithiasis served as a control group. Serum levels of free and total PSA were determined using a chemiluminescent enzyme immunoassay. RESULTS: Patients with CaP had a lower percentage of free PSA (localized CaP median 8.8%; metastatic CaP median 7.1%) than patients with BPH (median 19.5%) and those with urolithiasis (median 18.8%: P < 0.001). The percentage of free PSA did not differ significantly between patients with clinically localized and metastatic disease. CONCLUSION: The determination of the proportion of free PSA enhanced the discrimination between BPH and CaP and may reduce the number of unnecessary biopsies in patients with an elevated PSA. The results warrant further investigations in a broader population to improve the clinical use of serum PSA as a tumour marker for discriminating patients with an early, potentially curable CaP from men with BPH.

Aged↗

Posttranslational truncation and inactivation of human E-cadherin distinguishes prostate cancer from matched normal prostate.

An essential event in the progression of adenocarcinoma is the loss of organized epithelial attachment (both to the basement membrane and to adjoining epithelial cells). The E-cadherin cell adhesion molecule has an established function in maintaining normal phenotype and tissue homeostasis, and loss of E-cadherin function has been implicated in tumorigenesis. Aberrations in E-cadherin are associated with prostate cancer progression; however, these aberrations are not simply a result of prodigious allelic loss. We have previously demonstrated a novel posttranslational truncation within the cytosolic domain of native Mr 120,000 E-cadherin to a membrane-bound Mr 97,000 species. We hypothesize that truncation of E-cadherin is an inactivating event that is significantly increased in localized prostate tumors and that it represents a novel molecular event that may distinguish prostate cancer from adjacent normal tissue. E-cadherin was characterized by Western blot analysis in matched normal and cancer tissue from 18 prostate cancer patients. Imaging and densitometry software were used to quantify the truncation of E-cadherin by measuring the ratio of Mr 97,000 E-cadherin to Mr 120,000 E-cadherin, which was significantly increased in the tumor aspect of the prostate gland. Herein, we report the first experiment comparing case-matched human normal and cancerous prostate tissue in the context of E-cadherin truncation.

Blotting, Western↗

Assessing anxiety in men with prostate cancer: further data on the reliability and validity of the Memorial Anxiety Scale for Prostate Cancer (MAX-PC).

Identifying which men with prostate cancer might benefit from mental health treatment has proven to be a challenging task. The authors developed the Memorial Anxiety Scale for Prostate Cancer (MAX-PC) in order to facilitate the identification of prostate cancer-related anxiety. A revised version of this scale was tested in a more clinically varied population. Ambulatory men with prostate cancer (N=367) completed a baseline assessment packet that included the MAX-PC and other psychosocial questionnaires. The MAX-PC showed high internal consistency and concurrent and discriminant validity. Factor analysis identified three distinct factors for the MAX-PC that corresponded to the intended subscales (General Prostate Cancer Anxiety, PSA (prostate-specific antigen) Anxiety, and Fear of Recurrence). PSA levels were not correlated with anxiety overall; however, anxiety was significantly higher among patients whose PSA levels were changing (i.e., rising, falling, and unstable), versus those with stable PSA levels. Also, in a multivariate analysis, the change in PSA levels was a significant predictor of MAX-PC scores, but not Hospital Anxiety and Depression Scale (HADS) scores. These results indicate that the MAX-PC is a valid and reliable measure of anxiety that assesses aspects of anxiety unique to men with prostate cancer, and it may provide a more sensitive measure of anxiety than the HADS for this population.

Adult↗

Risk of prostate cancer associated with a family history in an era of rapid increase in prostate cancer diagnosis (Australia).

OBJECTIVE: We conducted a case-control study of prostate cancer and familial risk of the disease in Australia between 1994 and 1998, a period during which the incidence of prostate cancer increased dramatically with widespread use of prostate-specific antigen (PSA) testing. METHODS: 1475 cases and 1405 controls were asked about prostate cancer in their first-degree relatives. Odds ratios (OR) were calculated using logistic regression. RESULTS: Cases were more likely to report a family history of prostate cancer than controls (OR 3.0; 95% confidence interval (CI) 2.3-3.9) and cases reporting an affected relative were younger (58.8 versus 60.9 years, p < 0.0001). The OR for an affected first-degree relative increased with increasing number of affected relatives and decreased with increasing age of the case. The OR for more than one affected first-degree relative was 6.9 (95% CI 2.7-18). The OR for an affected brother was 3.9 (95% CI 2.5-6.1) and for an affected father was 2.9 (95% CI 2.1-3.9) but these were not significantly different (p = 0.2). When analyses were repeated including only diagnoses made in relatives prior to 1992, the risks were generally similar except that the OR for an affected brother decreased to 3.1 (95% CI 1.2-3.9). When only relatives' diagnoses made after 1991 were included results were again similar to those for all relatives, although the effect for brothers was greater and the attenuation with age at diagnosis dissipated. CONCLUSIONS: The recent introduction of PSA testing that has resulted in a greater prevalence of apparent prostate cancer, does not appear to have substantially altered familial risks of disease, although effects associated with brothers may be inflated.

Adenocarcinoma↗

Prostate cancer in a large prostate is associated with a decreased prostate specific antigen failure rate after brachytherapy.

PURPOSE: A large prostate has been found to correlate with improved prostate cancer survival in men undergoing radical prostatectomy. In the current study we analyzed the relationship of prostate size and prostate specific antigen (PSA) failure in men undergoing brachytherapy for localized prostate cancer. MATERIALS AND METHODS: We studied data on 613 men who had undergone I radioactive seed implantation. Average patient age +/- SD was 65 +/- 7.2 years. Average prostate volume ultrasonically measured at seed insertion was 40 +/- 15 ml. All patients had a minimum of 2 years of followup. RESULTS: Men with a large prostate had increased freedom from failure compared to men with a small prostate. Failure time in men with an intermediate size prostate was between that for large and small prostates. This difference in failure rates was significant (log rank test p = 0.0002). We further analyzed our data with Cox regression. Large prostate size significantly correlated with increased time to PSA failure (p = 0.013) and it was independent of the significant effects of Gleason score, PSA, disease stage (p <0.001), minimal radiation dose covering 90% of prostate volume (p = 0.008) and hormone treatment, including androgen ablation (p = 0.001). CONCLUSIONS: Some investigators have postulated that paracrine signals acting to regulate epithelial proliferation in benign prostatic hypertrophy have beneficial influences on coexistent prostate cancer. Our finding that the effect of prostate size is independent of Gleason score, PSA and disease stage supports the paracrine signal mechanism. If a circulating substance, such as a cytokine, might be responsible for improved survival, this substance might be useful for treating prostate cancer. Moreover, since we found that prostate size is independent of PSA, Gleason score and tumor stage for predicting outcome, we hypothesize that patients with a small prostate treated with brachytherapy might benefit from hormone treatment and larger radiation doses. These measures are now generally reserved for men with more advanced tumors, higher PSA and increased Gleason scores.

Aged↗

[The significance of serum prostate-specific antigen, gamma-seminoprotein and prostatic acid phosphatase as prostate cancer markers].

Prostate-specific antigen (PA), gamma-seminoprotein (gamma-Sm) and prostatic acid phosphatase (PAP) have been evaluated in patients with prostate cancer, benign prostatic hyperplasia (BPH), chronic prostatitis and acute prostatitis. PA has proved to be diagnostically more sensitive than PAP and gamma-Sm for the detection of prostatic cancer. Although PA may be elevated more frequently than PAP and gamma-Sm in patients with BPH, there are possibilities that these patients with elevated PA and normal PAP and gamma-Sm may have prostatic cancer or precancerous conditions not detectable in our routine diagnostic procedures. We report two cases of prostatic cancer with persistently elevated PA and diagnosed after repeated biopsies. Our data suggest that PA is a sensitive and useful tumor marker for the diagnosis of prostatic cancer. PAP and gamma-Sm in combination with PA may serve as more useful for differential diagnosis and confirmation of prostatic cancer.

Acid Phosphatase↗

5alpha-reductase type 1 immunostaining is enhanced in some prostate cancers compared with benign prostatic hyperplasia epithelium.

PURPOSE: In the prostate testosterone is converted to the more potent androgen dihydrotestosterone by the enzymes 5alpha-reductase (5alphaR) types 1 (5alphaR1) and 2 (5alphaR2). Since 5alphaR2 is the dominant prostatic enzyme, the 5alphaR2 selective inhibitor finasteride has been widely used to treat benign prostatic hyperplasia (BPH). However, inhibition of both 5alphaR enzymes provides a greater decrease in serum dihydrotestosterone. We developed a specific antibody to 5alphaR1 and assessed expression in BPH and prostate cancer (pCa) tissue. The presence of this isoenzyme in localized prostate cancer would provide a rationale for assessing the efficacy of dual inhibition for prostate cancer prevention. MATERIALS AND METHODS: A polyclonal antibody to 5alphaR1 was developed and validated using 5alphaR1 and 5alphaR2 transfected COS-1 cells. A total of 26 BPH and 53 pCa specimens were assessed for 5alphaR1 protein expression using immunocytochemical methods. Also, 29 BPH and 37 pCa specimens were assayed for 5alphaR1 and 5alphaR2 enzyme activity. RESULTS: Specificity of the 5alphaR1 antibody was confirmed using transfected COS-1 cells. Cells transfected with 5alphaR1 showed specific staining in immunocytochemistry experiments and on Western blotting of cell lysates the expected 24 kDa band was observed. High intensity immunoreactivity for 5alphaR1 was observed in the tumor epithelium of 28% of pCa specimens. No high intensity epithelial staining was observed in BPH specimens. In 19% of pCa and 7% of BPH specimens 5alphaR1 enzyme activity was detected. CONCLUSIONS: The presence of increased 5alphaR1 in some prostatic malignancies suggests that it is worthwhile to investigate the use of a dual 5alphaR inhibitor to prevent or treat early stage prostate cancer.

3-Oxo-5-alpha-Steroid 4-Dehydrogenase↗

Therapeutic interactions between stathmin inhibition and chemotherapeutic agents in prostate cancer.

Limitations of prostate cancer therapy may be overcome by combinations of chemotherapeutic agents with gene therapy directed against specific proteins critical for disease progression. Stathmin is overexpressed in many types of human cancer, including prostate cancer. Stathmin is one of the key regulators of the microtubule network and the mitotic spindle and provides an attractive therapeutic target in cancer therapy. We recently showed that adenovirus-mediated gene transfer of anti-stathmin ribozyme could suppress the malignant phenotype of prostate cancer cells in vitro. In the current studies, we asked whether the therapeutic effects of stathmin inhibition could be further enhanced by exposure to different chemotherapeutic agents. Exposure of uninfected LNCaP human prostate cancer cells or cells infected with a control adenovirus to Taxol, etoposide, 5-fluorouracil (5-FU), or Adriamycin resulted in modest decrease in proliferation and clonogenicity. Interestingly, exposure of cells infected with an anti-stathmin adenovirus to Taxol or etoposide resulted in a complete loss of proliferation and clonogenicity, whereas exposure of the same cells to 5-FU or Adriamycin potentiated the growth-inhibitory effects of the anti-stathmin ribozyme, but the cells continued to proliferate. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling analysis of uninfected cells or cells infected with a control adenovirus showed modest induction of apoptosis in the presence of different drugs. In contrast, cells infected with the anti-stathmin adenovirus showed a marked increase in apoptosis on exposure to Taxol or etoposide and a modest increase on exposure to 5-FU or Adriamycin. Overall, the effects of combinations of anti-stathmin ribozyme with Taxol or etoposide were synergistic, whereas the effects of combinations of anti-stathmin ribozyme with 5-FU or Adriamycin were additive. Moreover, triple combination of anti-stathmin ribozyme with low noninhibitory concentrations of Taxol and etoposide resulted in a profound synergistic inhibition of proliferation, clonogenicity, and marked induction of apoptosis. This synergy might be very relevant for the treatment of prostate cancer because Taxol and etoposide are two of the most effective agents in this disease. Thus, this combination may provide a novel form of prostate cancer therapy that would avoid toxicities associated with the use of multiple chemotherapeutic agents at full therapeutic doses.

Adenoviridae↗

Cell death mechanisms associated with G2 radiosensitivity in patients with prostate cancer and benign prostatic hyperplasia.

Cells respond to genotoxic insults such as ionizing radiation by halting in the G2 phase of the cell cycle. Delayed cell death (mitotic death) can occur when the cell is released from G2, and specific spindle defects form endopolyploid cells (endoreduplication/tetraploidy). Enhanced G2 chromosomal radiosensitivity has been observed in many cancers and genomic instability syndromes, and it is manifested by radiation-induced chromatid aberrations observed in lymphocytes of patients. Here we compare the G2 chromosomal radiosensitivity in prostate patients with benign prostatic hyperplasia (BPH) or prostate cancer with disease-free controls. We also investigated whether there is a correlation between G2 chromosomal radiosensitivity and aneuploidy (tetraploidy and endoreduplication), which are indicative of mitotic cell death. The G2 assay was carried out on all human blood samples. Metaphase analysis was conducted on the harvested chromosomes by counting the number of aberrations and the mitotic errors (endoreduplication/tetraploidy) separately per 100 metaphases. A total of 1/14 of the controls were radiosensitive in G2 compared to 6/15 of the BPH patients and 15/17 of the prostate cancer patients. Radiation-induced mitotic inhibition was assessed to determine the efficacy of G2 checkpoint control in the prostate patients. There was no significant correlation of G2 radiosensitivity scores and mitotic inhibition in BPH patients (P = 0.057), in contrast to prostate cancer patients, who showed a small but significant positive correlation (P = 0.029). Furthermore, there was no significant correlation between G2 radiosensitivity scores of BPH patients and endoreduplication/ tetraploidy (P = 0.136), which contrasted with an extremely significant correlation observed in prostate cancer patients (P < 0.0001). In conclusion, cells from prostate cancer patients show increased sensitivity to the induction of G2 aberrations from ionizing radiation exposure but paradoxically show reduced mitotic indices and aneuploidy as a function of aberration frequency.

Aged↗

National Cancer Institute roundtable on prostate cancer: future research directions.

It is anticipated that this report will serve as a nucleus for stimulating meaningful studies of the biology of prostate cancer. Such studies will be essential for the control and ultimately the prevention of prostate cancer. The present focus was arrived at by consensus of an expert panel on prostate cancer. It is not the only focus and other developing areas will surely be opportune for new and creative research approaches. New concepts and novel treatments are urgently required to stem the increasing impact of prostate cancer.

Forecasting↗

[Vascular endothelial growth factor in patients with prostate cancer and benign prostatic hyperplasia].

The authors examined 25 patients with prostate cancer (PC) and 36 patients with benign prostatic hyperplasia (BPH). In the group of patients with morphologically verified PC mean serum level of vascular endothelial growth factor (VEGF) was significantly higher than in patients with BPH (p < 0.05). The study demonstrated strong negative association between VEGF and prostate specific antigen (PSA) levels (r = 0.72, p < 0.05) in PC patients. There was no association between VEGF serum level and the stage or malignancy of PC (Gleason score). In benign prostatic glands moderate VEGF expression was observed only in basal cells, whereas in cases of PC all tumor cells displayed active VEGF expression; the difference was significant (p < 0.05). High serum VEGF levels and its active expression in patients with PC suggest an important role of angiogenic factors in the pathogenesis of this disease. The negative association between VEGF and PSA serum levels in PC indirectly confirms antiangiogenic activity of PSA, shown before.

Aged↗

Measurement of complexed PSA in the differential diagnosis between prostate cancer and benign prostate hyperplasia .

BACKGROUND: To enhance the specificity of PSA in diagnosis of cancer, several approaches have been evaluated, having in common the study of fractions of PSA. The aim of this study was to evaluate the usefulness of complexed PSA in the differential diagnosis between benign prostate hyperplasia (BPH) and prostate cancer. METHODS: We determined the concentrations of complexed PSA (Bayer, Tarrytown, NY) and total PSA (Tandem-R Assay, Hybritech Incorporated, San Diego, CA) in 196 patients with BPH and in 55 patients with prostate cancer. Likewise, the percentage of free PSA (Wallac, Turku, Finland) was determined for 124 of these patients. RESULTS: The specificity of complexed PSA was found to be greater than that of total PSA for the cutoff values corresponding to sensitivities of 80%, 85%, and 90%. Similarly, the area under the curve obtained by receiver-operating curve analysis was greater for complexed PSA than for total PSA, although significant differences were not observed. The diagnostic usefulness of complexed PSA in the differential diagnosis between BPH and prostate cancer was found to be lower than the percentage of free PSA. CONCLUSIONS: We believe that differential diagnosis with complexed PSA between BPH and prostate cancer is of little use, due to low efficacy when PSA results are extreme.

Diagnosis, Differential↗

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↗

The National Cancer Data Base report on prostate cancer. American College of Surgeons Commission on Cancer and the American Cancer Society.

BACKGROUND: Previous Commission on Cancer data from the National Cancer Data Base (NCDB) examined time trends in disease stage, treatment patterns, and survival for patients with selected cancers. The most current (1992) data for prostate cancer are described in this Communication. METHODS: Calls for data yielded a total of 52,597 prostate cancer reports for 1986/1987 and 101,903 for 1992 from hospital cancer registries across the United States. RESULTS: Data were received for 154,500 patients with prostate cancer. Prostate cancer is detected increasingly at localized stages and among younger men. African American men have a continuing pattern of more advanced disease at diagnosis. Selection of prostatectomy as the primary treatment has increased, and its use varies by region and several patient and hospital characteristics. Selection of radiation treatment has increased to a lesser degree. The 5-year survival for patients diagnosed in 1986/1987 was 60%. Outcomes varied by stage, age, and race. CONCLUSION: The NCDB provides valuable information concerning patterns and trends in prostate cancer care in the United States. The data show that prostate cancer detection and treatment have changed markedly in recent years. These changes appear to be related to the increased use of early detection measures. The improvements in prostate cancer detection and trends in treatment have not affected the population evenly, with African American men having more advanced disease and lower survival. Continued monitoring of these important trends is needed.

Aged↗

Changing trends in national practice for external beam radiotherapy for clinically localized prostate cancer: 1999 Patterns of Care survey for prostate cancer.

PURPOSE: To report changing trends in external beam radiotherapy (EBRT) delivery practice for clinically localized prostate cancer as determined from the 1999 survey from the American College of Radiology National Patterns of Care Study. METHODS AND MATERIALS: The 1999 survey included a weighted sample of 36,496 patient records obtained from a stratified two-stage sample of 554 patient records. Patients were surveyed from 58 institutions and were treated between January 1999 and December 1999. Of these, 36% (weighted sample size, 13,293; unweighted sample size, 162) were treated with brachytherapy with or without EBRT and 64% (weighted sample size, 23,203; unweighted sample size, 392) were treated with EBRT only. The latter group is the subject of this report. The following trends in clinical practice were analyzed according to prognostic risk groups and other variables and compared with the results of the prior surveys: use of androgen deprivation therapy (ADT) in combination with EBRT, higher prescription dose levels, and administration of elective whole pelvic RT (WPRT). RESULTS: The incidence of ADT use for favorable, intermediate, and unfavorable-risk groups was 31%, 54%, and 79%, respectively. A multivariate logistic regression analysis revealed a statistically significantly increased likelihood of intermediate (p = 0.001) and unfavorable (p <0.0001) risk groups treated with ADT in conjunction with EBRT compared with favorable-risk patients. ADT use was more prevalent among treated patients in the 1999 survey than in the 1994 survey (51% vs. 8%, p <0.0001). Compared with the prior survey, a greater percentage of patients were treated with higher radiation doses in the 1999 survey (> or =72 Gy, 45% in 1999 vs. 3% in 1994, p <0.0001). In the 1999 survey, the proportion of patients with favorable, intermediate, and unfavorable tumors treated to doses > or =72 Gy was 43%, 38%, and 60%, respectively, compared with 4%, 3%, and 1%, respectively, in the 1994 survey. Compared with the 1994 survey, a large increase in the number of patients treated with brachytherapy (36% vs. 3%, p <0.0001). The frequency of WPRT use decreased from 92% in 1989 to 52% in 1994 to 23% in 1999. For the 1999 survey, a multivariate analysis indicated that unfavorable-risk patients (p = 0.016) and intermediate-risk patients (p = 0.018) were more likely to be treated with WPRT compared with favorable-risk patients. Nevertheless, even among unfavorable-risk patients, a substantial decline had occurred in the use of WPRT for the 1999 survey (70% for the 1994 survey compared with the 31% for the current survey; p = 0.003). CONCLUSION: The significantly increased use of ADT for high-risk patients and higher radiation doses, especially for intermediate- and high-risk patients, reflects the penetration and growing acceptance of clinical trial results that have demonstrated the efficacy of these treatment approaches. The relatively high proportion of favorable-risk patients treated with high radiation dose levels was greater than expected. A large increase in brachytherapy was observed compared with prior surveys. Most treated patients with high-risk disease did not undergo elective WPRT, which likely reflects the influences of prior trials, stage migration, and the commonly held belief that WPRT provides minimal benefit in the setting of higher radiation doses.

Aged↗

Ability of the 1992 and 1997 American Joint Committee on Cancer staging systems for prostate cancer to predict progression-free survival after radical prostatectomy for stage T2 disease.

PURPOSE: In a revised 1997 edition the American Joint Committee on Cancer (AJCC) staging for prostate cancer reduced the subdivision of T2 disease from 3 (T2a, T2b and T2c) to 2 substages by combining single lobe disease (T2a and T2b) into a single stage, now termed T2a. We retrospectively reviewed a large series of men with clinically organ confined prostate cancer who underwent surgery by a single surgeon to determine how this change affected the ability of the staging system to predict outcome. MATERIALS AND METHODS: Of 2, 293 cases treated with radical prostatectomy from 1982 to 1998, 1, 314 were clinically staged to have T2 disease. We analyzed the freedom from biochemical prostate specific antigen (PSA) progression after radical prostatectomy according to the 1992 and 1997 AJCC staging criteria. RESULTS: Overall the actuarial 5 and 10-year biochemical progression-free survival rates for the whole group were 82% and 71%, respectively. The actuarial recurrence-free rate was significantly different for patients with 1992 AJCC T2a (T2a92) versus T2b (T2b92) disease (p <0.0001) but similar for those with 1992 T2b versus T2c (T2c92) disease (p = 0.1165). The actuarial recurrence-free rate was significantly different for patients with 1997 AJCC T2a (T2a97) versus T2b (T2b97) disease (p = 0.0001). However, the overall recurrence-free rate was lower in the T2a97 group compared with the T2a92 group. CONCLUSIONS: The 1992 AJCC staging of T2 prostate cancer yielded a significant difference in the outcome of patients with single lobe disease (T2a92 and T2b92), which is obscured by the 1997 staging criteria. Therefore, we believe that the next revision of the AJCC staging system should revert back to the 1992 AJCC system of subdividing a single lobe disease category into T2a and T2b. Alternatively the committee may want to merge T2b92 and T2c92 stages into a new staging entity, since there was no statistical difference in the outcome of these 2 groups.

Adult↗

Today men with prostate cancer have larger prostates.

OBJECTIVES: To examine the relationship between prostate size and the method of cancer detection in men with organ-confined prostate cancer, and compare prostate size in men with and without cancer. METHODS: Prostate volume was evaluated in 720 men who had undergone radical prostatectomy for Stage T1c or Stage T2 cancer. Men with Stage T2 cancer were divided into those treated before 1989 (when widespread prostate-specific antigen [PSA] testing began), or not. Gland volume was also examined in 265 men participating in the Baltimore Longitudinal Study of Aging who had no clinical evidence of cancer. Volumes were compared using linear regression to allow for age. RESULTS: Prostate volume in men with Stage T1c cancer was statistically significantly larger than in men with Stage T2 cancer diagnosed in the pre-PSA era after adjusting for age (P = 0.0001), and statistically significantly larger than in men without cancer above age 47 years based on 95% confidence intervals. Prostate volumes in men with Stage T2 cancer diagnosed in the pre-PSA era and in men without cancer were not statistically significantly different. CONCLUSIONS: Prostate volume in men with PSA-detected, organ-confined cancer is larger than in men with palpable organ-confined cancer diagnosed in either the pre-PSA era or PSA era. These discrepancies may reflect a diagnostic bias due to the effect of benign prostatic hyperplasia on serum PSA that results in the selection of men with larger prostates for biopsy.

Adult↗