The Influence of Finasteride on the Development of Prostate Cancer
Ian M. Thompson, M.D., Phyllis J. Goodman, M.S., Catherine M. Tangen, Dr.P.H., M. Scott Lucia, M.D., Gary J. Miller, M.D., Ph.D., Leslie G. Ford, M.D., Michael M. Lieber, M.D., R. Duane Cespedes, M.D., James N. Atkins, M.D., Scott M. Lippman, M.D., Susie M. Carlin, B.A., Anne Ryan, R.N., Connie M. Szczepanek, R.N., B.S.N., John J. Crowley, Ph.D., and Charles A. Coltman, Jr., M.D.
Background Androgens are involved in the development of prostatecancer. Finasteride, an inhibitor of 5-reductase, inhibits theconversion of testosterone to dihydrotestosterone, the primaryandrogen in the prostate, and may reduce the risk of prostatecancer.
Methods In the Prostate Cancer Prevention Trial, we randomlyassigned 18,882 men 55 years of age or older with a normal digitalrectal examination and a prostate-specific antigen (PSA) levelof 3.0 ng per milliliter or lower to treatment with finasteride(5 mg per day) or placebo for seven years. Prostate biopsy wasrecommended if the annual PSA level, adjusted for the effectof finasteride, exceeded 4.0 ng per milliliter or if the digitalrectal examination was abnormal. It was anticipated that 60percent of participants would have prostate cancer diagnosedduring the study or would undergo biopsy at the end of the study.The primary end point was the prevalence of prostate cancerduring the seven years of the study.
Results Prostate cancer was detected in 803 of the 4368 menin the finasteride group who had data for the final analysis(18.4 percent) and 1147 of the 4692 men in the placebo groupwho had such data (24.4 percent), for a 24.8 percent reductionin prevalence over the seven-year period (95 percent confidenceinterval, 18.6 to 30.6 percent; P<0.001). Tumors of Gleasongrade 7, 8, 9, or 10 were more common in the finasteride group(280 of 757 tumors [37.0 percent], or 6.4 percent of the 4368men included in the final analysis) than in the placebo group(237 of 1068 tumors [22.2 percent], P<0.001 for the comparisonbetween groups; or 5.1 percent of the 4692 men included in thefinal analysis, P=0.005 for the comparison between groups).Sexual side effects were more common in finasteride-treatedmen, whereas urinary symptoms were more common in men receivingplacebo.
Conclusions Finasteride prevents or delays the appearance ofprostate cancer, but this possible benefit and a reduced riskof urinary problems must be weighed against sexual side effectsand the increased risk of high-grade prostate cancer.
To date, the management of prostate cancer, the most commonnondermatologic neoplasm in men in the United States, has focusedon early diagnosis and treatment. Given that the developmentof prostate cancer is a long-term process involving multiplesteps, however, prevention may be a more effective approach.
There is abundant evidence that androgens influence the developmentof prostate cancer.1,2,3 The development of finasteride, aninhibitor of steroid 5-reductase, the enzyme that converts testosteroneto the more potent androgen dihydrotestosterone, created anopportunity to test the possibility that lowering the androgenlevels in the prostate would reduce the risk of prostate cancer.We undertook a study to determine whether finasteride can reducethe prevalence of prostate cancer among initially healthy menduring a seven-year study period.
Methods
Study Design
Men 55 years of age or older with a normal digital rectal examination,no clinically significant coexisting conditions, and an AmericanUrological Association symptom score4 of less than 20 were recruited.The study was approved by institutional review boards at allsites. After the men had given written informed consent, bloodwas drawn to determine the level of prostate-specific antigen(PSA), and the men were issued a three-month supply of placebotablets for the run-in phase of the trial. If, after this three-monthperiod, the PSA level was 3.0 ng per milliliter or lower, adherencewas within 20 percent of the expected rate of placebo use, andthere were no clinically significant toxic effects, the menwere randomly assigned to finasteride (5 mg per day) or placebo.The planned duration of treatment was seven years. A dynamicallocation scheme was used for randomization to ensure thatthe treatment groups were balanced within each of the 221 studysites.
The men underwent annual digital rectal examinations and measurementsof PSA. Biannually, they were seen for reissuing of medication,counts of pills, and recording of clinically significant medicalconditions and side effects. Every three months, the men werecontacted by telephone for the collection of data on interimmedical events.
Because of the effect of finasteride on the PSA level, the measureof which is the primary method of detection of prostate cancer,an end-of-study biopsy was planned. At the end of seven years,all men who had not been given a diagnosis of prostate cancerwere offered an end-of-study prostate biopsy. This biopsy wasto be performed within 7 years ±90 days after the dateof randomization.
Prostate Biopsy
Measurements of PSA were performed in a central laboratory (withthe use of the Tandem E assay [Hybritech] until 2000 and theAccess assay [Beckman Coulter] thereafter). After the measurementof PSA at enrollment, all PSA measurements for men in the finasteridegroup were adjusted before being reported, because finasteridecauses a decrease in the PSA level.5 A centralized adjustment,overseen by an independent data and safety monitoring committee,ensured that the men in the finasteride group had a rate ofrecommendation for prostate biopsy approximately equal to thatamong men in the placebo group. Initially, the adjustment consistedof a doubling of the PSA values for finasteride-treated men,but on the basis of the goal of an equal percentage of biopsiesin each group, the factor was changed to 2.3 at the beginningof the man's fourth year in the study. PSA levels were initiallyreported as elevated or not elevated, but in October 1995, asclinical practice changed, adjusted values began to be reportedfor men with elevated PSA levels. The PSA values reported tothe men were thus the adjusted values for men in the finasteridegroup and the unadjusted values for men in the placebo group.If the digital rectal examination was abnormal or if the reportedPSA level was higher than 4.0 ng per milliliter at the annualexamination, prostate biopsy was recommended.
Biopsy was performed with the use of transrectal ultrasonographicguidance, and a minimum of six specimens was obtained. If thebiopsy was positive, the subject was removed from the study;if it was negative, he remained in the study. If prostatic intraepithelialneoplasia was found, a second biopsy was recommended.
All prostate biopsies were reviewed by a central pathology laboratoryand by pathologists at the study site, all of whom were unawareof the treatment-group assignment. Prostate tissue from anyother procedures performed (e.g., transurethral resection ofthe prostate) was sent to the central pathology laboratory forevaluation. Discordant interpretations were arbitrated by areferee pathologist, and concordance was achieved in all cases.
Statistical Analysis
The primary objective of the study was to determine whetherthe administration of finasteride for seven years could reducethe prevalence of prostate cancer during that period. We assumedthat the prevalence of prostate cancer during the seven yearsof the study would be 6 percent in the placebo group and thata 25 percent reduction in the prevalence in the finasteridegroup at seven years would be of clinical significance. We calculatedthat with a two-sided alpha of 0.05, a power of 0.92, and athree-year accrual period, we needed a sample size of 18,000.We also assumed that 60 percent of the men either would havean interim diagnosis of prostate cancer or would undergo anend-of-study biopsy. It was estimated that 20 percent of theparticipants would die during the study, that 5 percent woulddecline to undergo a prostate biopsy, and that 15 percent wouldbe lost to follow-up.
Another assumption was that the rate of nonadherence to thestudy treatment would be 14 percent and that 5 percent of themen in the placebo group would end up taking finasteride (thedrop-in rate). Serum dihydrotestosterone was measured in a randomlyselected 5 percent sample of men as a marker of adherence tostudy medication in the finasteride group and as a measure ofthe drop-in rate in the placebo group.6,7
The primary intention-to-treat analysis included men who receiveda diagnosis of prostate cancer during the study or who underwentan end-of-study biopsy. Medical events, side effects, and therates of temporary discontinuation of treatment are reportedfor all eligible men. All reported P values are two-sided.
An independent data and safety monitoring committee met everysix months and reviewed data on safety, adherence, and diagnosesof prostate cancer, as well as other data related to the monitoringof the study assumptions. This committee reported to the chairof the steering committee and made recommendations regardingrevisions to the protocol or adjustments for possible differencesin prostate-cancer–detection rates due to the effect offinasteride on the PSA level and prostate size. Because of theknown PSA-related bias and other potential detection biasesthat were anticipated, no formal interim stopping rules werespecified.
Results
Study Participants and Termination of the Study
Over a period of three years, 24,482 men were enrolled in thestudy, and of these men, 18,882 underwent randomization betweenJanuary 1994 and May 1997 — 12,016 of them during thefirst year of the trial. Most of the men who did not undergorandomization (3997) had a PSA level of more than 3.0 ng permilliliter. On February 21, 2003, 15 months before the anticipatedcompletion of the study, the data and safety monitoring committeemet and, on the basis of sensitivity analyses, recommended earlytermination of the study, since the study objective had beenmet and the conclusions were extremely unlikely to change withadditional diagnoses of prostate cancer and end-of-study biopsyresults. Because of the rapid initial accrual of participants,at the time of the analysis of the data and safety monitoringcommittee, 81.3 percent of the men had completed the seven yearsof the study. The current analysis is based on the 86.3 percentof the men who have now completed the seven years of the study.
Rates of Prostate Cancer and End-of-Study Biopsy
The rate of diagnosis of prostate cancer or end-of-study biopsywas 59.6 percent in the finasteride group and 63.0 percent inthe placebo group (P<0.001). Men with such a diagnosis mademore than 7 years plus 90 days after randomization or with anend-of-study biopsy performed after that time were excludedfrom the primary analysis (Table 1). Men were considered tohave refused a biopsy if the biopsy was not performed becauseof a coexisting condition or because the personal physicianrecommended against the procedure, as well as if the men themselvesrefused the biopsy. The rate of refusal of biopsy was higherthan had originally been estimated, but because the death rateand the rate of loss to follow-up were lower than had been anticipated,the overall ascertainment goal was achieved.
Table 1. Status of Men at the Time of the Analysis.
Of the 9060 men who were included in the final analysis, prostatecancer was detected in 803 of the 4368 in the finasteride group(18.4 percent) and 1147 of the 4692 in the placebo group (24.4percent), a relative risk reduction of 24.8 percent (95 percentconfidence interval, 18.6 to 30.6 percent; P<0.001). Thenumber of cases of prostate cancer detected either during thecourse of the study in a biopsy performed for cause (an elevatedPSA level or an abnormal digital rectal examination) or in abiopsy performed at the end of the study was higher in the placebogroup than in the finasteride group. Of the cases of prostatecancer that were diagnosed in a biopsy performed for cause,96.0 percent were found on biopsy and 4.0 percent were foundafter other procedures such as transurethral resection of theprostate. Figure 1 shows the incidence of prostate cancer inthe two treatment groups among all surviving men who underwentrandomization, excluding cases diagnosed on end-of-study biopsy.Finasteride was associated with a reduced prevalence of prostatecancer in all subgroups we examined (Table 2).
Figure 1. Cumulative Incidence of Prostate Cancer Diagnosed in a Biopsy Performed for Cause or after an Interim Procedure.
The number at risk is the number of surviving men still being followed who were free of prostate cancer, and the number of events includes all cases of prostate cancer detected on a biopsy performed for cause or after an interim procedure such as transurethral resection of the prostate.
Table 2. Prevalence of Prostate Cancer during the Seven Years of the Study, Overall and in Subgroups.
Rates of Recommended Biopsy
Biopsies were recommended during the trial if there was an elevatedPSA level, an abnormal digital rectal examination, or both.Such recommendations for biopsy during the trial were givento 2122 of the 9423 men who were randomly assigned to the finasteridegroup (22.5 percent) and 2348 of the 9457 eligible men who wererandomly assigned to the placebo group (24.8 percent, P<0.001)(Table 3).
Table 3. Reasons for Recommendations for Biopsy and Characteristics of Men Who Underwent the Recommended Biopsy and Men Who Did Not.
Although the rates of the prompts of biopsy among men in whoma biopsy was recommended and among men in whom a biopsy wasperformed differed according to treatment group, there was nosignificant difference between the proportions of recommendedbiopsies that were performed in the two groups either accordingto the number of recommendations for biopsy (P=0.10) or accordingto the number of men who had such a recommendation during thecourse of the trial (P=0.29). In the placebo group but not inthe finasteride group, the degree of elevation of the PSA levelwas related to whether or not a recommended prostate biopsywas performed. The annual rate at which biopsies were performedfor cause is shown in Figure 1. Of the 246 cancers found onbiopsies performed for cause at seven years, 57 were in menin whom biopsies had previously been recommended but had notbeen performed. If a PSA-adjustment factor of 2.0 had been usedfor the finasteride group throughout the study, 222 men in thefinasteride group who received a recommendation to undergo abiopsy during the course of the study because of an elevatedPSA level would not have had such a recommendation. A totalof 69 of these men underwent biopsy at the time of the recommendation,and 17 cases of prostate cancer were detected.
Rates of Nonadherence
The rate of nonadherence, estimated as the percentage of daysof treatment missed in men who had a diagnosis of prostate canceror an end-of-study biopsy, was 14.7 percent in the finasteridegroup and 10.8 percent in the placebo group. The rate of nonadherencein the finasteride group, as indicated by a dihydrotestosteronelevel of more than 16 ng per milliliter, was 14.5 percent, andthe drop-in rate in the placebo group, as indicated by a dihydrotestosteronelevel of 16 ng per milliliter or lower, was 6.5 percent.
A total of 36.8 percent of men in the finasteride group and28.9 percent in the placebo group temporarily discontinued treatmentat some time during the study for reasons other than death oran interim diagnosis of prostate cancer (P<0.001 for thecomparison between groups). The yearly rate of temporary discontinuationof treatment was highest during the men's first year in thestudy (10.0 percent in the finasteride group and 6.3 percentin the placebo group) and decreased steadily, so that by year5, the rate was 3.6 percent in the finasteride group and 3.4percent in the placebo group. Side effects of finasteride representedthe primary reason for the difference in the proportion of menwho temporarily discontinued treatment (1722 of 9423 men inthe finasteride group [18.3 percent] vs. 931 of 9457 men inthe placebo group [9.8 percent]).
Medical Events and Side Effects
Medical events and side effects (Table 4) were graded accordingto the toxicity criteria of the Southwest Oncology Group.8 Theseevents and side effects were reported by the men during directedinterviews over the course of their treatment. Reduced volumeof ejaculate, erectile dysfunction, loss of libido, and gynecomastiawere more common in the finasteride group than in the placebogroup (P<0.001 for all comparisons), whereas urinary urgency,urinary frequency, or both; prostatitis; urinary tract infection;and urinary retention were more common among men in the placebogroup (P<0.001 for all comparisons). There was no significantdifference in the number of deaths between the two groups: fivemen in each group died from prostate cancer.
Table 5 shows Gleason scores assigned by the central pathologylaboratory for all biopsies. There was a higher proportion oftumors with Gleason scores of 7, 8, 9, or 10 in the finasteridegroup (280 of 757 graded tumors [37.0 percent], or 6.4 percentof the 4368 men included in the analysis) than in the placebogroup (237 of 1068 graded tumors [22.2 percent], or 5.1 percentof the 4692 men included in the analysis; P<0.001 for thecomparison between groups in terms of the percentage of gradedtumors; relative risk of a high-grade tumor, 1.67 [95 percentconfidence interval, 1.44 to 1.93]; P=0.005 for the comparisonbetween groups in terms of the percentage of all men; relativerisk, 1.27 [95 percent confidence interval, 1.07 to 1.50]).To understand the risk of high-grade disease from the perspectivesof a man considering taking finasteride and of a man who isfound to have prostate cancer, we report these data in two ways.The rate of high-grade disease among men in whom prostate cancerwas diagnosed on a biopsy performed for cause was 188 of 393men in the finasteride group (47.8 percent) and 148 of 504 menin the placebo group (29.4 percent; P<0.001; relative risk,1.62 [95 percent confidence interval, 1.37 to 1.93]); the rateamong all men who underwent biopsy for cause was 188 of 1639men in the finasteride group (11.5 percent) and 148 of 1934men in the placebo group (7.7 percent; P<0.001; relativerisk, 1.50 [95 percent confidence interval, 1.22 to 1.84]).
Table 5. Gleason Scores for Prostate Cancers Detected.
Prostate volume was determined at the time of biopsy. The medianvolume among men in the finasteride group was 25.5 cm3, as comparedwith 33.6 cm3 among men in the placebo group (a 24.1 percentrelative difference). There was no significant difference betweenthe two groups in the number of biopsy specimens obtained: sextantbiopsy was performed in 81.5 percent of men in the finasteridegroup and 81.0 percent of men in the placebo group. Most prostatecancers detected during the trial were clinically localized.A total of 97.7 percent of cancers in men in the finasteridegroup were classified as T1 or T2, as were 98.4 percent of thosein men in the placebo group. Of the tumors found on end-of-studybiopsies that were not performed for cause, 21.1 percent werein men who had a concurrent PSA level between 2.6 and 3.9 ngper milliliter. Of the remaining tumors found on end-of-studybiopsies that were not performed for cause in men with a concurrentPSA level of 2.5 ng per milliliter or less, 15.4 percent hada Gleason grade of 7, 8, 9, or 10.
Discussion
The lifetime risk of prostate cancer in the United States is16.7 percent, and 28,900 men are expected to die of this diseasein 2003.9 This high rate and the unpredictable biology of prostatecancer make prevention of the disease an appealing strategy.Finasteride is an attractive chemopreventive agent, becauseit inhibits the conversion of testosterone to the more potentandrogen dihydrotestosterone within the prostate and has lowtoxicity. At the inception of our study, finasteride becameavailable for the treatment of benign prostatic hyperplasia(as Proscar [Merck]), and since then, it has been approved forthe treatment of male pattern baldness (Propecia [Merck]). Althoughit is used by millions of men for these indications, littleis known about its long-term effects on the prostate.
We faced a challenge in designing our study, because of theeffect of finasteride on the PSA level, measurement of whichis the primary method of screening for prostate cancer. Forthis reason, we planned to perform a prostate biopsy at theend of the study.6 We recognized the possibility that therewould be an increased number of positive biopsies among menwho received finasteride, because a proportionately greatervolume of gland would be sampled from smaller glands.10,11 Thiseffect could introduce a bias against any evidence of benefitfrom finasteride.
Every attempt was made to ensure that an equal proportion ofmen in each group was evaluated for prostate cancer; this wasthe logic behind the initial doubling of PSA values for menin the finasteride group and the later increase by a factorof 2.3 at the beginning of each participant's fourth year inthe study.5 An additional difference in the rate of evaluationfor prostate cancer between the two groups was a different numberof abnormal digital rectal examinations (1845 in the finasteridegroup vs. 2090 in the placebo group) (Table 3) and transurethralresections of the prostate. In addition, more men in the finasteridegroup than in the placebo group were categorized as having refusedthe end-of-study biopsy (25.4 percent vs. 22.8 percent, P<0.001),most likely because of the higher rate of temporary discontinuationof treatment in a group of men less committed to the study requirements.Although the difference between the groups in the overall rateof ascertainment of prostate-cancer status of 3.4 percentagepoints (59.6 in the finasteride group vs. 63.0 percent in theplacebo group) was statistically significant, we believe thatthis difference by itself is unlikely to have contributed substantiallyto the difference in the rate of detection of prostate cancer.
Seven years of finasteride treatment resulted in a 24.8 percentreduction in the prevalence of prostate cancer during that period.There was a reduction in relative risk among men who underwenta prostate biopsy before seven years and among men who underwentbiopsy at the end of the study. The risk reductions were similarin subgroups defined according to age, race or ethnic group,family history of prostate cancer, and stratum of PSA levelat randomization.
Decreases in sexual potency, libido, and ejaculate volume werefrequently reported over the course of the trial, as would beexpected in men in this age group who were followed for sevenyears with repeated queries regarding these symptoms.12 Theseside effects were more common in the finasteride group. Urinarysymptoms or events related to benign prostatic hyperplasia wereless common among men receiving finasteride — a findingthat is consistent with a previous report.13
High-grade disease was noted in 6.4 percent of the men in thefinasteride group, as compared with 5.1 percent of those inthe placebo group. A difference in the rate of high-grade diseasewas seen within the first year of the study. One possible explanationfor this difference is a grading bias: histologic changes thatmimic those of high-grade disease are caused by androgen-deprivationtherapy.14,15,16,17,18 There are, however, differences of opinionas to whether this effect occurs with finasteride. It is possiblethat finasteride induces high-grade tumors by reducing the levelof intracellular dihydrotestosterone within the prostate. Thereis evidence that the prostate tumors that develop in men withlow testosterone levels have higher Gleason grades and worseoutcomes than the prostate cancers that develop in men withnormal testosterone levels.19,20,21 It is also possible thatfinasteride selects for high-grade tumors by selectively inhibitinglow-grade tumors. Long-term follow-up in these men and furtherlaboratory research will be required to determine the reasonfor the association between finasteride and high-grade prostatecancer.
The tumors that were detected on biopsies performed for causewere clinically similar to those that are detected in clinicalpractice by screening of the PSA level and digital rectal examination.The clinical significance of cancers found in the end-of-studybiopsies (those not performed for cause) is unknown. Of themen with such diagnoses, 21.1 percent had PSA levels between2.6 and 3.9 ng per milliliter. Clinically significant tumorsare as common among men with PSA levels in this range as theyare among men with PSA levels between 4.0 and 10.0 ng per milliliter.22Of the remaining tumors found in men with PSA levels of 2.5ng per milliliter or less, 15.4 percent had high-grade cancer.
The overall cancer detection rate of 24.4 percent in the placebogroup is a matter of concern, because the eligibility criteriafor enrollment in the study selected for low-risk men with anexpected lifetime incidence of prostate cancer of 16.7 percentand a rate of death from prostate cancer of 3 to 4 percent.The rate of 24.4 percent suggests the possibility of overdiagnosisof disease.
The study raises two interrelated questions: did finasterideprevent or treat prostate cancer,23 and did finasteride preventor delay24,25 the appearance of prostate cancer? These issuesare important for the field of cancer prevention. The earlydifference in the incidence of prostate cancer between the twogroups suggests that finasteride may have treated subclinical,microscopical cancer early in the study, and the fact that thedifference continued to increase suggests that it preventedor delayed the onset of cancer. In either case, the effect isbeneficial.23,24,25
Physicians can use these results to counsel men regarding theuse of finasteride. It is important to stress that finasteridereduced the risk of prostate cancer in a clinical trial markedby frequent monitoring for disease and was associated with anincreased risk of diagnosis of high-grade prostate cancer. Fora man considering using this medication, the greater absolutereduction in the risk of prostate cancer must be weighed againstthe smaller absolute increase in the risk of high-grade disease.
There is also the matter of side effects: the incidence of adverseeffects on sexual function was higher with finasteride, butthe finasteride group had a lower incidence of urinary symptomsand complications than the placebo group. Using published informationon the outcomes of prostate-cancer treatment, men can weighthese trade-offs in the context of their own priorities regardingthe avoidance of prostate cancer as well as their urinary andsexual function to reach a personal decision regarding finasterideuse.26,27,28 As more is learned from the molecular biology ofprostate cancer about the risk of aggressive disease, data fromthis and other studies will help to refine the appropriate useof interventions such as finasteride.
Supported in part by Public Health Service grants (CA37429,CA35178, and CA45808) from the National Cancer Institute.
We are indebted to the 18,882 men who participated in this study;to the members of the data and safety monitoring committee;to the steering committee; to the study-site principal investigatorsand clinical research associates; to collaborators from theSouthwest Oncology Group, the Eastern Cooperative Oncology Group,and the Cancer and Leukemia Group B; and to Merck for providingthe finasteride and the placebo.
This article is dedicated to the memory of Gary Miller, M.D.,Ph.D.
Source Information
From the University of Texas Health Science Center, San Antonio (I.M.T.); the Southwest Oncology Group Statistical Center, Seattle (P.J.G., C.M.T., S.M.C., J.J.C.); the University of Colorado, Denver (M.S.L., G.J.M.); the National Cancer Institute, Bethesda, Md. (L.G.F., A.R.); the Mayo Clinic, Rochester, Minn. (M.M.L.); the Wilford Hall U.S. Air Force Medical Center, San Antonio, Tex. (R.D.C.); the Southeastern Medical Oncology Center, Goldsboro, N.C. (J.N.A.); the M.D. Anderson Cancer Center, Houston (S.M.L.); the Grand Rapids Community Clinical Oncology Program, Grand Rapids, Mich. (C.M.S.); and the Southwest Oncology Group Operations Office, San Antonio, Tex. (C.A.C.). This article was published at www.nejm.org on June 24, 2003.
Address reprint requests to the Southwest Oncology Group (SWOG-9217), Operations Office, 14980 Omicron Dr., San Antonio, TX 78245-3217.
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Prevention of Prostate Cancer with Finasteride
Rubin M. A., Kantoff P. W., Roehrborn C. G., Burke H. B., Schwartz D. T., Ross R. K., Skinner E., Cote R. J., Lee S. C., Ellis R. J., Barzell W. E., Thompson I. M. Jr., Goodman P. J., Coltman C. A. Jr.
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N Engl J Med 2003;
349:1569-1572, Oct 16, 2003.
Correspondence
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1: 182-186
[Abstract][Full Text]
Lucia, M. S., Darke, A. K., Goodman, P. J., La Rosa, F. G., Parnes, H. L., Ford, L. G., Coltman, C. A. Jr., Thompson, I. M.
(2008). Pathologic Characteristics of Cancers Detected in the Prostate Cancer Prevention Trial: Implications for Prostate Cancer Detection and Chemoprevention. Cancer Prevention Research
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Logothetis, C. J., Schellhammer, P. F.
(2008). High-Grade Prostate Cancer and the Prostate Cancer Prevention Trial. Cancer Prevention Research
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Redman, M. W., Tangen, C. M., Goodman, P. J., Lucia, M. S., Coltman, C. A. Jr., Thompson, I. M.
(2008). Finasteride Does Not Increase the Risk of High-Grade Prostate Cancer: A Bias-Adjusted Modeling Approach. Cancer Prevention Research
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Jayachandran, J., Freedland, S. J.
(2008). Prevention of Prostate Cancer: What We Know and Where We Are Going. American Journal of Men's Health
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Page, S. T., Amory, J. K., Bremner, W. J.
(2008). Advances in Male Contraception. Endocr. Rev.
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Kelly, K., Brader, P., Rein, A., Shah, J. P., Wong, R. J., Fong, Y., Gil, Z.
(2008). Attenuated multimutated herpes simplex virus-1 effectively treats prostate carcinomas with neural invasion while preserving nerve function. FASEB J.
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Barry, M. J., Kaufman, D. S., Wu, C.-L.
(2008). Case 15-2008 -- A 55-Year-Old Man with an Elevated Prostate-Specific Antigen Level and Early-Stage Prostate Cancer. NEJM
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Torkko, K. C., van Bokhoven, A., Mai, P., Beuten, J., Balic, I., Byers, T. E., Hokanson, J. E., Norris, J. M., Baron, A. E., Lucia, M. S., Thompson, I. M., Leach, R. J.
(2008). VDR and SRD5A2 Polymorphisms Combine to Increase Risk for Prostate Cancer in Both Non-Hispanic White and Hispanic White Men. Clin. Cancer Res.
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Choi, J.-Y., Neuhouser, M. L., Barnett, M. J., Hong, C.-C., Kristal, A. R., Thornquist, M. D., King, I. B., Goodman, G. E., Ambrosone, C. B.
(2008). Iron intake, oxidative stress-related genes (MnSOD and MPO) and prostate cancer risk in CARET cohort. Carcinogenesis
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Amory, J. K., Kalhorn, T. F., Page, S. T.
(2008). Pharmacokinetics and Pharmacodynamics of Oral Testosterone Enanthate Plus Dutasteride for 4 Weeks in Normal Men: Implications for Male Hormonal Contraception. J Androl
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Kristal, A. R., Arnold, K. B., Schenk, J. M., Neuhouser, M. L., Goodman, P., Penson, D. F., Thompson, I. M.
(2008). Dietary Patterns, Supplement Use, and the Risk of Symptomatic Benign Prostatic Hyperplasia: Results from the Prostate Cancer Prevention Trial. Am J Epidemiol
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Wako, K, Kawasaki, T, Yamana, K, Suzuki, K, Jiang, S, Umezu, H, Nishiyama, T, Takahashi, K, Hamakubo, T, Kodama, T, Naito, M
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Rondanina, G., Puntoni, M., Severi, G., Varricchio, C., Zunino, A., Feroce, I., Bonanni, B., Decensi, A.
(2008). Psychological and Clinical Factors Implicated in Decision Making About a Trial of Low-Dose Tamoxifen in Hormone Replacement Therapy Users. JCO
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Page, S. T., Bremner, W. J., Clark, R. V., Bush, M. A., Zhi, H., Caricofe, R. B., Smith, P. M., Amory, J. K.
(2008). Nanomilled Oral Testosterone Plus Dutasteride Effectively Normalizes Serum Testosterone in Normal Men With Induced Hypogonadism. J Androl
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Barry, M. J.
(2008). Commentary: How Serious Is Getting a Diagnosis of Prostate Cancer?. The Oncologist
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Gelmann, E. P.
(2008). Complexities of Prostate-Cancer Risk. NEJM
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Hormones, E., Prostate Cancer Collaborative Group,
(2008). Endogenous Sex Hormones and Prostate Cancer: A Collaborative Analysis of 18 Prospective Studies. JNCI J Natl Cancer Inst
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Carpenter, W. R., Robinson, W. R., Godley, P. A.
(2008). Getting Over Testosterone: Postulating a Fresh Start for Etiologic Studies of Prostate Cancer. JNCI J Natl Cancer Inst
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Simoneau, A. R., Gerner, E. W., Nagle, R., Ziogas, A., Fujikawa-Brooks, S., Yerushalmi, H., Ahlering, T. E., Lieberman, R., McLaren, C. E., Anton-Culver, H., Meyskens, F. L. Jr.
(2008). The Effect of Difluoromethylornithine on Decreasing Prostate Size and Polyamines in Men: Results of a Year-Long Phase IIb Randomized Placebo-Controlled Chemoprevention Trial. Cancer Epidemiol. Biomarkers Prev.
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Wilt, T. J, N'Dow, J.
(2008). Benign prostatic hyperplasia. Part 2--Management. BMJ
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Albertelli, M. A., O'Mahony, O. A., Brogley, M., Tosoian, J., Steinkamp, M., Daignault, S., Wojno, K., Robins, D. M.
(2008). Glutamine tract length of human androgen receptors affects hormone-dependent and -independent prostate cancer in mice. Hum Mol Genet
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Sedjo, R. L., Byers, T., Barrera, E. Jr., Cohen, C., Fontham, E. T. H., Newman, L. A., Runowicz, C. D., Thorson, A. G., Thun, M. J., Ward, E., Wender, R. C., Eyre, H. J., for the ACS Cancer Incidence & Mortality Ends Comm,
(2007). A Midpoint Assessment of the American Cancer Society Challenge Goal to Decrease Cancer Incidence by 25% Between 1992 and 2015. CA Cancer J Clin
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Platz, E. A.
(2007). Epidemiologic Musing on Statin Drugs in the Prevention of Advanced Prostate Cancer. Cancer Epidemiol. Biomarkers Prev.
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Haas, G. P., Delongchamps, N. B., Jones, R. F., Chandan, V., Serio, A. M., Vickers, A. J., Jumbelic, M., Threatte, G., Korets, R., Lilja, H., de la Roza, G.
(2007). Needle Biopsies on Autopsy Prostates: Sensitivity of Cancer Detection Based on True Prevalence. JNCI J Natl Cancer Inst
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Banach-Petrosky, W., Jessen, W. J., Ouyang, X., Gao, H., Rao, J., Quinn, J., Aronow, B. J., Abate-Shen, C.
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Hoque, A., Parnes, H. L., Stefanek, M. E., Heymach, J. V., Brown, P. H., Lippman, S. M.
(2007). Meeting Report: Fifth Annual AACR Frontiers in Cancer Prevention Research. Cancer Res.
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Lucia, M. S., Epstein, J. I., Goodman, P. J., Darke, A. K., Reuter, V. E., Civantos, F., Tangen, C. M., Parnes, H. L., Lippman, S. M., La Rosa, F. G., Kattan, M. W., Crawford, E. D., Ford, L. G., Coltman, C. A. Jr, Thompson, I. M.
(2007). Finasteride and High-Grade Prostate Cancer in the Prostate Cancer Prevention Trial. JNCI J Natl Cancer Inst
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Cohen, Y. C., Liu, K. S., Heyden, N. L., Carides, A. D., Anderson, K. M., Daifotis, A. G., Gann, P. H.
(2007). Detection Bias Due to the Effect of Finasteride on Prostate Volume: A Modeling Approach for Analysis of the Prostate Cancer Prevention Trial. JNCI J Natl Cancer Inst
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(2007). High-Grade Prostate Cancer in the Prostate Cancer Prevention Trial: Fact or Artifact?. JNCI J Natl Cancer Inst
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Crawford, E. D.
(2007). Is a Screening Interval of Every 4 Years for Prostate Cancer Acceptable?. JNCI J Natl Cancer Inst
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Key, T. J, Appleby, P. N, Allen, N. E, Travis, R. C, Roddam, A. W, Jenab, M., Egevad, L., Tjonneland, A., Johnsen, N. F, Overvad, K., Linseisen, J., Rohrmann, S., Boeing, H., Pischon, T., Psaltopoulou, T., Trichopoulou, A., Trichopoulos, D., Palli, D., Vineis, P., Tumino, R., Berrino, F., Kiemeney, L., Bueno-de-Mesquita, H B., Quiros, J R., Gonzalez, C. A, Martinez, C., Larranaga, N., Chirlaque, M. D., Ardanaz, E., Stattin, P., Hallmans, G., Khaw, K.-T., Bingham, S., Slimani, N., Ferrari, P., Rinaldi, S., Riboli, E.
(2007). Plasma carotenoids, retinol, and tocopherols and the risk of prostate cancer in the European Prospective Investigation into Cancer and Nutrition study. Am. J. Clin. Nutr.
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Nam, R. K., Toi, A., Klotz, L. H., Trachtenberg, J., Jewett, M. A.S., Appu, S., Loblaw, D. A., Sugar, L., Narod, S. A., Kattan, M. W.
(2007). Assessing Individual Risk for Prostate Cancer. JCO
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Kauh, J., Khuri, F. R.
(2007). Can Statins Pass the Aspirin Litmus Test in Cancer?. JCO
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Brown, P. H.
(2007). Chemoprevention Clinical Trials: It Is Time to Turn Success into Progress. Cancer Epidemiol. Biomarkers Prev.
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de Vere White, R. W.
(2007). Finasteride for Chemoprevention of Prostate Cancer: Why Has It Not Been Embraced?. JCO
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Thompson, I. M., Pauler Ankerst, D., Chi, C., Goodman, P. J., Tangen, C. M., Lippman, S. M., Lucia, M. S., Parnes, H. L., Coltman, C. A. Jr
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Giovannucci, E.
(2007). Does Prostate-Specific Antigen Screening Influence the Results of Studies of Tomatoes, Lycopene, and Prostate Cancer Risk?. JNCI J Natl Cancer Inst
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Moinpour, C. M., Darke, A. K., Donaldson, G. W., Thompson, I. M. Jr, Langley, C., Ankerst, D. P., Patrick, D. L., Ware, J. E. Jr, Ganz, P. A., Shumaker, S. A., Lippman, S. M., Coltman, C. A. Jr
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(2007). Sex Steroids and All-Cause and Cause-Specific Mortality in Men. Arch Intern Med
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(2007). Prostate-specific antigen in the early detection of prostate cancer. CMAJ
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(2007). Anthropometrics and Prostate Cancer Risk. Am J Epidemiol
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(2007). Obesity and Prostate Cancer: Making Sense out of Apparently Conflicting Data. Epidemiol Rev
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Ji, Q., Chang, L., Stanczyk, F. Z., Ookhtens, M., Sherrod, A., Stolz, A.
(2007). Impaired Dihydrotestosterone Catabolism in Human Prostate Cancer: Critical Role of AKR1C2 as a Pre-Receptor Regulator of Androgen Receptor Signaling. Cancer Res.
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(2007). Body Mass Index, Weight Change, and Risk of Prostate Cancer in the Cancer Prevention Study II Nutrition Cohort. Cancer Epidemiol. Biomarkers Prev.
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Manassero, F., Erba, P., Mariani, G., Mogorovich, A., Giannarini, G., Selli, C.
(2007). Metastatic Prostate Cancer After Orchiectomy, Radiotherapy, and Testosterone Replacement in a Patient With Bilateral Seminoma. J Androl
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Srinivasan, S., Ranga, R. S., Burikhanov, R., Han, S.-S., Chendil, D.
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Bauman, D. R., Steckelbroeck, S., Peehl, D. M., Penning, T. M.
(2006). Transcript Profiling of the Androgen Signal in Normal Prostate, Benign Prostatic Hyperplasia, and Prostate Cancer. Endocrinology
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(2006). Androgen Induction of Prostate Cancer Cell Invasion Is Mediated by Ezrin. J. Biol. Chem.
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Gong, Z., Neuhouser, M. L., Goodman, P. J., Albanes, D., Chi, C., Hsing, A. W., Lippman, S. M., Platz, E. A., Pollak, M. N., Thompson, I. M., Kristal, A. R.
(2006). Obesity, diabetes, and risk of prostate cancer: results from the prostate cancer prevention trial.. Cancer Epidemiol. Biomarkers Prev.
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Ammar, H., Malani, A. K, Gupta, C.
(2006). Benign prostatic hyperplasia: Caveat for finasteride should be discussed before prescribing. BMJ
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Patel, A. K, Chapple, C. R
(2006). Benign prostatic hyperplasia: Authors' reply. BMJ
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Thompson, I. M., Chi, C., Ankerst, D. P., Goodman, P. J., Tangen, C. M., Lippman, S. M., Lucia, M. S., Parnes, H. L., Coltman, C. A. Jr.
(2006). Effect of Finasteride on the Sensitivity of PSA for Detecting Prostate Cancer.. JNCI J Natl Cancer Inst
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Gao, H., Ouyang, X., Banach-Petrosky, W. A., Shen, M. M., Abate-Shen, C.
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Svatek, R. S., Lee, J. J., Roehrborn, C. G., Lippman, S. M., Lotan, Y.
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Matthiesson, K. L., McLachlan, R. I.
(2006). Male hormonal contraception: concept proven, product in sight?. Hum Reprod Update
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Kelloff, G. J., Lippman, S. M., Dannenberg, A. J., Sigman, C. C., Pearce, H. L., Reid, B. J., Szabo, E., Jordan, V. C., Spitz, M. R., Mills, G. B., Papadimitrakopoulou, V. A., Lotan, R., Aggarwal, B. B., Bresalier, R. S., Kim, J., Arun, B., Lu, K. H., Thomas, M. E., Rhodes, H. E., Brewer, M. A., Follen, M., Shin, D. M., Parnes, H. L., Siegfried, J. M., Evans, A. A., Blot, W. J., Chow, W.-H., Blount, P. L., Maley, C. C., Wang, K. K., Lam, S., Lee, J. J., Dubinett, S. M., Engstrom, P. F., Meyskens, F. L. Jr., O'Shaughnessy, J., Hawk, E. T., Levin, B., Nelson, W. G., Hong, W. K., for the AACR Task Force on Cancer Prevention,
(2006). Progress in Chemoprevention Drug Development: The Promise of Molecular Biomarkers for Prevention of Intraepithelial Neoplasia and Cancer--A Plan to Move Forward. Clin. Cancer Res.
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(2006). Clinical Trials in the Wake of Vioxx: Requiring Statistically Extreme Evidence of Benefit to Ensure the Safety of New Drugs. Circulation
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Thompson, I. M., Ankerst, D. P., Chi, C., Goodman, P. J., Tangen, C. M., Lucia, M. S., Feng, Z., Parnes, H. L., Coltman, C. A. Jr.
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Dolder, C. R
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Hayes, F.
(2006). Relationship Between Testosterone Levels, Insulin Sensitivity, and Mitochondrial Function in Men: Response to Kaplan and Crawford. Diabetes Care
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Fontanarosa, P. B., Cole, H. M.
(2006). Theme Issue on Men's Health: Call for Papers. JAMA
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Bettuzzi, S., Brausi, M., Rizzi, F., Castagnetti, G., Peracchia, G., Corti, A.
(2006). Chemoprevention of Human Prostate Cancer by Oral Administration of Green Tea Catechins in Volunteers with High-Grade Prostate Intraepithelial Neoplasia: A Preliminary Report from a One-Year Proof-of-Principle Study. Cancer Res.
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(2006). Circulating Steroid Hormones and the Risk of Prostate Cancer. Cancer Epidemiol. Biomarkers Prev.
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(2005). Erectile Dysfunction and Subsequent Cardiovascular Disease. JAMA
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[Abstract][Full Text]
-reductase, inhibits the conversion of testosterone to dihydrotestosterone, the primary androgen in the prostate, and may reduce the risk of prostate cancer. 
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