role of repeated biopsy of the prostate in predicting disease progression in patients with prostate...
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Role of Repeated Biopsy of the Prostate inPredicting Disease Progression in PatientsWith Prostate Cancer on Active Surveillance
Mohammed Al Otaibi, MD1
Philip Ross, MD1
Nader Fahmy, MD1
Suganthiny Jeyaganth, MsC1
Helen Trottier, PhD2
Kanishka Sircar, MD3
Louis R. B�egin, MD3
Luis Souhami, MD4
Wassim Kassouf, MD1
Armen Aprikian, MD1
Simon Tanguay, MD1
1 Division of Urology, Department of Surgery,McGill University Health Center, Montreal, Que-bec, Canada.
2 Division of Cancer Epidemiology, McGill Univer-sity Health Center, Montreal, Quebec, Canada.
3 Department of Pathology, McGill UniversityHealth Center, Montreal, Quebec, Canada.
4 Department of Radiation Oncology, McGill Uni-versity Health Center, Montreal, Quebec, Canada.
BACKGROUND. Active surveillance (AS) with deferred treatment is an established
management option for patients with prostate cancer and favorable clinical pa-
rameters. The impact of repeat biopsy after diagnosis was examined in a cohort
of men with prostate cancer on AS.
METHODS. In all, 186 men with prostate cancer with favorable parameters or who
refused treatment were conservatively managed by AS. Of these, 92 patients had
at least 1 biopsy after diagnosis. Patients were followed every 3 to 6 months with
prostate-specific antigen (PSA) and physical examination and were offered
rebiopsy annually or if there were any changes on physical examination or in the
PSA value. Disease progression while on AS was defined as having �1 of the
following: �cT2b disease, �3 positive cores, >50% of cancer in at least 1 core, or
a predominant Gleason pattern of 4 in rebiopsies.
RESULTS. The median age of the patients at the time of diagnosis was 67 years
(range, 49–78 years). The median follow-up was 76 months (range, 20–169
months). Of the 92 patients who underwent repeat biopsies, 42 patients, 25
patients, 13 patients, 10 patients, and 2 patients had 1, 2, 3, 4, and 5 rebiop-
sies, respectively. A total of 34 patients (36%) demonstrated disease progres-
sion on rebiopsy. The first rebiopsy was positive for cancer in 48 patients
(52.2%) and negative in 44 patients (47.8%). The 5-year actuarial progression-
free probability was 82% for patients with a negative first repeat biopsy com-
pared with 50% for patients with a positive first rebiopsy (P 5 .02). A PSA dou-
bling time <67 months was associated an increased risk of disease progression
on biopsy.
CONCLUSIONS. Negative rebiopsy in patients with prostate cancer on AS is asso-
ciated with low-volume disease. The result of first repeated biopsy appears to
have a strong impact on disease progression. Patients with a positive first
repeated biopsy should be considered for treatment. An intensive biopsy protocol
within the first 2 years is required to identify and treat those patients. Cancer
2008;113:286–92. � 2008 American Cancer Society.
KEYWORDS: prostate cancer, active surveillance, prostatic biopsy, disease pro-gression.
P rostate cancer remains the most common cancer in men. With
a progressive decrease in the prostate-specific antigen (PSA)
threshold leading to prostate biopsy, there exists significant stage
migration with an earlier prostate cancer diagnosis.1–3 This new rea-
lity leads to the more frequent diagnosis of cancer judged to be
potentially insignificant. The prevalence of prostate cancer in men
aged >50 years has been estimated to be as high as 40%.4–7 A large
proportion of these cancers are potentially insignificant and if left
Address for reprints: Simon Tanguay, MD, Divisionof Urology, Department of Surgery, McGill Univer-sity Health Center, 1650 Cedar Avenue, L8-318,Montreal, QC H3G 1A4, Canada; Fax: (514) 934-8297; E-mail: [email protected]
Received December 11, 2007; revision receivedFebruary 25, 2008; accepted March 6, 2008.
ª 2008 American Cancer SocietyDOI 10.1002/cncr.23575Published online 16 May 2008 in Wiley InterScience (www.interscience.wiley.com).
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untreated may not necessarily impact an individual
patient’s survival or quality of life.8–10
During the PSA era, a man’s lifetime risk of being
diagnosed with prostate cancer has risen from 9% to
17%.11,12 In addition, the Prostate Cancer Prevention
Trial demonstrated that 24.4% of normal men in a
placebo group were eventually diagnosed with pros-
tate cancer.13
Observation until evidence that the cancer is
aggressive enough to warrant therapy may be appro-
priate for some patients but is potentially associated
with a lower cure rate once treatment is initiated.
Many patients with potentially insignificant tumors
are interested in the concept of active surveillance
with delayed intervention. Although attractive, this
approach is only feasible if we are able to clearly
identify patients when their disease is changing. The
challenge remains to accurately identify those men
with an aggressive, localized prostate cancer, which
has the potential to impact survival if left untreated,
while sparing or delaying treatment to avoid the
morbidity of a treatment that may not change the
natural history of the disease.
Active surveillance (AS) studies suggest that the
risk of disease progression increases over time, a pat-
tern that is different from the risk of disease progres-
sion or recurrence after definitive therapy, which
diminishes over time.14,15 Therefore, patients on AS
must accept frequent and regular evaluations of the
status of their cancer for as long as they remain
potential candidates for definitive therapy. Of the
various parameters monitored in these men, patho-
logic findings on prostate biopsy remain the most
objective measures of the evolution of their cancer.
Pathologic features such as grade and tumor volume
are important to monitor because they play a major
role in treatment decision-making of patients en-
rolled in AS. We reviewed the experience of our AS
cohort focusing on men with at least 1 prostatic
rebiopsy to better understand the prognostic signifi-
cance of the various clinical and pathologic diagnos-
tic characteristics and how they can help predict
patient outcome.
MATERIALS AND METHODSA cohort of 186 patients diagnosed between 1987
and 2006 with an adenocarcinoma of the prostate
with favorable pathologic and biochemical parame-
ters or those refusing definitive treatment were man-
aged with AS. The reasons for AS included patient
choice, limited life expectancy because of advanced
age or poor medical condition, and presumed insig-
nificant prostate cancer. Patients were followed at
3-month to 6-month intervals with serial serum PSA
levels and digital rectal examinations (DRE). PSAs
were performed with different assays during the ob-
servation period. Patients were offered transrectal
ultrasound (TRUS)-guided biopsy annually or if there
was a change on DRE or in the PSA value. Patients
were tracked prospectively in a disease management
database. All data were reviewed and analyzed retro-
spectively. Of the 186 patients under AS, 92 had at
least 1 repeat prostatic biopsy and constitute the
cohort of patients studied.
Clinical disease progression was defined as
increased T classification to �cT2b. Pathologic pro-
gression was defined by finding any of 1 of the follow-
ing pathologic features on repeat biopsy (provided
such findings were not present at the time of diagnos-
tic biopsy): 1) �3 positive cores, 2) >50% cancer in at
least 1 core, and 3) a predominant Gleason pattern of
4 noted on repeat biopsy.
All biopsies were retrospectively reviewed by 1 of
2 genitourinary pathologists (K.S. and L.R.B.). The
decision to initiate treatment was based on evidence
of pathologic disease progression on repeat biopsy,
biochemical disease progression, or patient prefer-
ence.
A PSA doubling time (PSADT) was calculated by
linear regression analysis.16 Progression-free survival
estimates were calculated using the Kaplan-Meier
method and comparative evaluations were performed
using the log-rank test. Univariate and multivariate
analysis for multiple variables were performed using
Cox regression analysis. The median value of each
variable was used as a cutoff except PSADT, in which
we used the tertile as a cutoff. All statistical analysis
were performed using Stata software (version 9.2;
StataCorp, College Station, Tex)
RESULTSThe median age at diagnosis was 67 years (range,
49–78 years). Of the 92 patients who were rebiopsied,
81 (88%) had a PSA � 10 ng/mL and 90 (98%) had
clinical �cT2a disease at the time of diagnosis. The
clinical and pathologic characteristics at diagnosis
are summarized in Table 1. The mean and median
follow-up was 79 months and 76 months, respec-
tively (range, 20–169 months). In our cohort, 42
patients, 25 patients, 13 patients, 10 patients, and 2
patients had 1, 2, 3, 4, and 5 repeat TRUS-guided
biopsies, respectively. Prostatic biopsies were per-
formed by different urologists within our division.
The mean and median numbers of biopsy cores were
7 and 8, respectively (range, 6-16 cores). Given our
long follow-up, several patients underwent an initial
Repeated Prostatic Biopsy/Al Otaibi et al. 287
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sextant biopsy because it was the standard at the
time. Repeat biopsies were performed using a stand-
ard biopsy template.
At the time of this analysis, 34 patients (36%)
had either pathologic or clinical disease progression
(Fig. 1A) (Table 2). The first repeat biopsy was posi-
tive for cancer in 48 patients (52%) and negative in
44 patients (48%). Of the 48 patients with a positive
first repeat biopsy, 23 (48%) eventually demonstrated
either clinical or pathologic disease progression with
a mean and median time to disease progression of
16 months and 19 months, respectively. Only 11 of
the 44 patients (25%) with a negative first repeat
biopsy eventually demonstrated disease progression,
with a mean and median time to disease progression
of 19 months and 40 months, respectively. Of the 44
patients with negative first repeat biopsy, 13 patients
went on to have a second negative repeat prostatic
biopsy and 5 patients had �3 consecutive negative
repeat prostatic biopsies, and 4 patients and 0
patients, respectively, demonstrated clinical or patho-
logic disease progression.
The 5-year actuarial progression-free survival
probability was 82% for patients with a negative first
rebiopsy compared with 50% for those with a posi-
tive first rebiopsy (P 5 .02) (Fig. 1B).
In our cohort, 42 patients had a persistent posi-
tive repeated biopsy and 32 patients had a persistent
negative repeated biopsy. Clinical and pathologic
characteristics of the 2 groups at the time of diagno-
sis are illustrated in Table 3. The median PSADT in
patients with a persistently negative repeat prostatic
biopsy was 154 months and was 64 months in
patients with a positive repeat biopsy (P 5 .02).
Table 4 illustrates the multiple clinical and path-
ologic variables evaluated in a logistic regression
model to assess their ability to predict disease pro-
gression. The first repeated biopsy, the highest
percentage of cancer in any core at the time of diag-
nosis, Gleason score at diagnosis, PSA at diagnosis,
and the number of positive cores at diagnosis were
found to be predictive of disease progression on uni-
variate analysis (P � .02). On multivariate analysis, a
TABLE 1Clinical and Pathologic Features of the 92 Patients atthe Time of Diagnosis
Age, y
Mean 66 � 6
Median (range) 67 (49–78)
PSA, ng/mL
<4 21 (23%)
4.1-10 60 (65%)
10.1-20 9 (10%)
>20 2 (2%)
c-Stage
T1a 2 (2%)
T1c 64 (70%)
T2a 24 (26%)
T2b 2 (2%)
Gleason score
�6 71 (77%)
314 16 (18%)
413 3 (3%)
�8 2 (2%)
PSA indicates prostate-specific antigen.
FIGURE 1. (A) Overall probability of remaining free of disease progressionin all 92 patients. (B) Probability of remaining free of disease progression
stratified by the result of the first rebiopsy.
TABLE 2Number of Patients Who Developed Disease Progression in EachProgression Criterion
Progression criterion No. %
�cT2b 9 26
>50% cancer 13 38
Predominant grade 4 5 15
�3 positive cores 22 65
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PSADT � 67 months remained the only significant
predictor of disease progression.
Of the 92 men who were rebiopsied, 29 (31%)
ultimately received definitive treatment. The median
time to treatment was 44 months. Of these 29
patients, 10 patients (34.5%) were treated by radical
prostatectomy (RP), 9 patients (31%) were treated
with radiotherapy alone, 6 patients (21%) were trea-
ted with androgen ablation alone, and 4 patients
(14%) were treated with a combination of radiother-
apy and androgen ablation. The decision to treat was
attributed to local pathologic disease progression in
27 patients (93%) and patient preference in 2
patients (7%).
Of the 10 patients who underwent RP, all but 1
had organ-confined disease. Table 5 shows the clini-
cal and pathologic features of these patients.
Of the 13 patients who were treated by radiother-
apy, 11 were treated with external beam radiotherapy
and 2 were treated with brachytherapy (1 with per-
manent seed implant and the other with high-dose-
rate brachytherapy).
Of the 29 patients treated, 4 (13%) failed their
first-line treatment at a median post-treatment
follow-up of 48 months (Table 6). Of the 92 patients,
2 (2.2%) developed bone metastasis. No patients died
of prostate cancer; 2 patients died of other causes.
DISCUSSIONBetween 30% and 50% of patients with favorable,
localized prostate cancer remain free of progression
at 10 years on AS. Therefore, AS with definitive treat-
ment in those patients with disease progression may
be an attractive alternative to initial curative treat-
ment. Because the PSADT has been estimated to be
2 to 4 years, the median follow-up of 76 months,
which to our knowledge is the longest follow-up of
an AS series reported in the literature, represents 1 of
the strengths of the current study. For men on AS,
several factors have been investigated in an effort to
improve our ability to predict disease progression.
Diagnostic PSA values, including free and total levels,
were examined by several investigators including
ourselves and were not found to be helpful in the
identification of men who require therapy.16–23 Con-
versely, PSADT has been shown to be a predictor of
disease progression. Choo et al.18 suggested that the
definition of disease progression for men on AS
include a PSADT of <2 years on the basis of at least
3 separate PSA measurements during a minimum of
6 months. However, in their series using these crite-
ria, 6 of 9 men who underwent RP had extraprostatic
disease, suggesting that this PSADT threshold may
be too short to effectively identify patients at risk of
disease progression. In our cohort, only 5 patients
had a PSADT of <2 years and 3 of these patients
demonstrated pathologic disease progression. The
results of the current study demonstrated that a
PSADT of <67 months was associated with an
increased risk of pathologic disease progression.
Patel et al.24 did not find a correlation between
PSADT and disease progression in their series.
Our definition of pathologic disease progression
was based on criteria defining significant versus in-
significant prostate cancer. These criteria are being
used in ongoing clinical trials evaluating AS in
patients with prostate cancer. Pathologic disease pro-
gression was most often defined by an increase in tu-
mor volume, whereas only 5 patients (15%) were
considered to have disease progression as a result of
Gleason pattern upgrading to 4. Pathologic findings
of any cores involved with >20% of cancer at the
time of diagnosis or �2 cores positive for cancer at
the time of diagnosis were associated with an
increased risk of disease progression. The results of
the current study demonstrated that the absence of
cancer on repeated core needle biopsy early after
initial diagnosis identified those patients who were
TABLE 3Clinical and Pathologic Features at the Time of Diagnosis of thePatients With Persistently Positive and Patients With PersistentlyNegative Repeated Biopsy Results
Persistently Crude
Negative
(N532)
Positive
(N542) OR (95%CI) [P]*
Clinical stage
�T1c 20 (63%) 30 (71%)
T2a 12 (37%) 10 (24%) 0.6 (0.2–1.5) [03]
�T2b 2 (5%)
PSA, ng/mL
�4 11 (35%) 5 (12%)
>4 to �10 19 (59%) 30 (71%) 3.5 (1.04–11.6) [.043]
>10 to �20 2 (7%) 4 (10%) 4.4 (0.6–32.5) [.15]
>20 3 (7%)
Positive cores
1 28 (87%) 19 (45%)
�2 4 (13%) 23 (55%) 8.5 (2.5–28.4) [.001]
Median % of cancer y 6% 20%
Gleason score
�6 28 (88%) 28 (67%)
314 3 (9%) 12 (26%) 4.0 (1.0–15.7) [.04]
413 1 (3%) 2 (7%) 2.0 (0.2–23.3) [.58]
�8
OR indicates odds ratios; 95% CI, 95% confidence interval; PSA, prostate-specific antigen.
* Odd ratios were derived from logistic regression analysis.y The median of the core with the highest percentage of cancer.
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less likely to develop disease progression. Patel
et al.24 and Carter et al.25 reported a similar associa-
tion between the results of first repeated biopsy and
the risk of disease progression. However, these stu-
dies were limited by their limited follow-up periods
of 44 months and 25 months, respectively. Surpris-
ingly, 4 (30%) of the 13 patients who had 2 consecu-
tive negative repeated biopsies after diagnosis
ultimately demonstrated disease progression on sub-
sequent biopsies and their median time to progres-
sion was 60 months. This reinforces the need to
maintain close follow-up and to continue to repeat
biopsy in patients on AS as long as they remain can-
didates for definitive therapy. In our cohort, men
who continued to have negative biopsies were unli-
kely to develop disease progress. Meanwhile, >50%
of the patients with cancer on repeat biopsy will de-
velop disease progression within 5 years. Therefore,
TABLE 4Incidence Rate and 95% CIs of Disease Progression Stratified by Covariate Variables as Well as Cox Regression Model to Assess WhetherThose Variables Can Predict Disease Progression With the Probability of Disease Progression Over Time
No.No. ofevent
Incident rate*(95% CI)
Cox regression model to predictdisease progression
Probability of disease progressionyCrude model Adjusted model
HR (95%CI) [P] HR (95%CI) [P] 12 months 24 months 60 months
Total 92 34 6.6 (4.7–9.2) 8.7 (4.5–16.6) 23.4 (15.9–33.6) 35.8 (26.3–47.3)
Median age at diagnosis, y
<67 37 15 5.9 (3.6–9.8) 8.1 (2.7–23.1) 31.0 (18.4–48.9) 33.9 (20.8–52.0)
�67 55 19 7.3 (4.6–11.4) 1 (0.5–2.0) [1.0] 9.1 (3.9–20.5) 18.5 (10.4–31.7) 38.5 (25.5–54.7)
First rebiopsy
Negative 44 11 3.9 (2.1–7.0) 9.1 (3.5–22.4) 13.8 (6.4–28.1) 19.3 (10.1–35.0)
Positive 48 23 10.0 (6.6–15) 2.5 (1.2–5.3) [.02] 2.0 (0.7–5.0) [.3] 8.3 (3.2–20.7) 32.16 (20.8–47.6) 50.7 (36.6–66.6)
T classification at diagnosis
�T1c 64 23 6.6 (4.4–9.9) 10.9 (5.4–21.6) 27.3 (17.9–40.2 35.7 (24.7–49.7)
>T1c 26 11 7.6 (4.2–13.7) 1.2 (0.6–2.4) [.7] 3.9 (0.5–24.3) 15.9 (6.3–37.0) 38.0 (21.7–60.7)
PSA doubling time, mo{
�67 29 17 14.9 (9.3–24.0) 3.4 (1.4–8.4) [.007] 3.0 (1.2–7.8) [.02] 10.3 (3.5–28.7) 35.7 (21.0–56.2) 58.7 (39.8–78.5)
>67 to �196 29 7 3.4 (1.6–7.2) 10.3 (3.5–28.7) 10.3 (3.5–28.7) 19.3 (8.4–40.7)
>196 30 8 4.3 (2.1–8.6) 1.2 (0.4–3.4) [.7] 6.7 (1.7–24.1) 20.4 (9.7–39.9) 28.4 (15.2–49.1)
Total core at diagnosis
�6 61 25 7.1 (4.8–10.5) 9.8 (4.54–20.6) 23.5 (14.7–36.5) 39.0 (27.6–53.2)
>6 31 9 5.5 (2.8–10.5) 0.7 (0.3–1.5) [.4] 6.5 (1.7–23.4) 23.2 (11.8–42.7) 27.8 (14.8–48.3)
% of core at diagnosis{
�20 49 12 3.9 (2.2–6.8) 4.1 (1.0–15.3) 16.8 (12.3–37.0) 21.8 (12.3–37.0)
>20 23 12 13.6 (7.7–23.9) 3.2 (1.4–7.2) [.006] 2.3 (0.8–6.2) [.10] 13.0 (4.4–35.2) 35.9 (19.8–81.6) 59.3 (38.0–82.0)
Prostate volume at diagnosis{
�40 34 13 6.3 (3.7–10.9) 11.8 (4.6–28.4) 20.8 (10.5–38.8) 32.0 (18.4–51.5)
>40 45 15 6 (3.6–9.9) 0.9 (0.4–1.9) [.8] 6.7 (2.2–19.3) 22.9 (13.0–38.4) 34.2 (21.6–51.1)
Gleason score at diagnosis
�6 69 20 4.8 (3.1–7.4) 7.3 (3.1–16.5) 22.1 (14.0–34.0) 25.6 (16.7–38.0)
>6 23 14 14.3 (8.5–24.2) 2.7 (1.4–5.5) [.04] 1.8 (0.8–4.0) [.15] 13.0 (4.4–35.2) 27.5 (13.4–51.4) 66.0 (45.0–85.6)
PSA at diagnosis, ng/mL
�10 77 24 5.3 (3.6–7.9) 5.2 (2.0–13.3) 21.6 (13.8–32.8) 30.2 (20.7–43.0)
>10 15 10 16.1 (8.7–30.0) 2.7 (1.4–5.8) [.008] 1.9 (0.8–4.8) [.16] 26.7 (11.0–56.4) 33.3 (15.4–62.5) 63.0 (39.2–86.2)
No. of rebiopsies performed
1 45 16 7.6 (4.7–12.5) 4.4 (1.1–16.6) 23.8 (13.5–39.7) 38.4 (25.0–56.0)
�2 47 18 5.9 (3.7–9.3) 0.9 (0.4–1.7) [.7] 12.8 (6.0–26.2) 23.4 (13.7–38.3) 33.1 (21.4–49.0)
Core at diagnosis
�1 62 18 4.7 (3.0–7.5) 8.1 (3.4–18.3) 18.1 (10.5–30.4) 26.5 (16.8–40.3)
>1 30 16 12.0 (7.3–19.5) 2.3 (1.2–4.7) [.02] 1.4 (0.5–3.9) [.48] 10.0 (3.3–27.9) 34.2 (20.1–54.3) 54.6 (37.1–74.0)
95% CI indicates 95% confidence interval; HR, hazards ratio; PSA, prostate-specific antigen.
* The progression incident rate is equal to the number of events per 1000 man-months.y The percentage probability of subjects developing disease progression at the end of the interval period (12 months, 24 months, and 60 months) derived by life table analysis (probability multiplied by 100).{ Does not sum to total because of missing values.
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we strongly recommend considering treatment in
men on AS who demonstrate cancer on repeat bi-
opsy. When pathologic disease progression was
observed on follow-up rebiopsy, it tended to occur
within the first 2 years after diagnosis in the majority
of cases. This occurred regardless of the result of the
first rebiopsy. An intensive biopsy protocol should be
pursued for men on AS during the first 2 years after
diagnosis. Of the patients treated with RP, only 1
(10%) had extracapsular extension, suggesting that a
strict surveillance protocol with serial DRE and
repeat prostatic biopsy allows for prompt and effec-
tive intervention in AS patients, whereas little or no
impact on curability of the disease is observed. De-
spite previous reports, we did not observe a signifi-
cant discrepancy between the TRUS biopsy and the
RP Gleason score. This may be a result of less sam-
pling error given the multiple TRUS biopsies before
surgery (median, 3 TRUS biopsies).
ConclusionsA strict annual rebiopsy strategy for the first 2 years
after diagnosis helps to identify those patients with
prostate cancer who are more likely to developed
disease progression on AS and appears to allow clini-
cians the opportunity to offer appropriate definitive
treatment without compromising cancer cure.
Patients with 2 consecutive negative repeated biop-
sies should continue to undergo repeat biopsy every
2 to 3 years. We encourage further study of rebiopsy
strategies and the continued follow-up of men on AS
to validate these findings.
REFERENCES1. McGregor M, Hanley JA, Boivin JF, McLean RG. Screening
for prostate cancer: estimating the magnitude of overdetec-
tion. CMAJ. 1998;159:1368–1372.
2. Etzioni R, Penson DF, Legler JM, et al. Overdiagnosis due
to prostate-specific antigen screening: lessons from U.S.
prostate cancer incidence trends. J Natl Cancer Inst. 2002;
94:981–990.
3. Singh H, Canto EI, Shariat SF, et al. Improved detection of
clinically significant, curable prostate cancer with system-
atic 12-core biopsy. J Urol. 2004;171:1089–1092.
4. Breslow N, Chan CW, Dhom G, et al. Latent carcinoma of
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TABLE 5Clinical and Pathologic Features and Follow-up of Patients Treated by Radical Prostatectomy
Time totreatment, mo PSA at RP
Stage Gleason score
Surgical marginsPostoperativefollow-up, mo StatusClinical Pathologic Biopsy RP
1 17 7.3 T1c T2b 313 314 Negative 11 NED
2 27 7.1 T1c T2c 314 314 Negative 9 NED
3 16 5.0 T2a T2c 314 314 Negative 72 NED
4 84 6.1 T1c T2a 313 313 Negative 71 AWD
5 16 8.9 T1c T0* 414 Negative 108 NED
6 17 8.0 T1c T2a 314 313 Negative 72 NED
7 78 7.2 T2a T2a 313 313 Negative 48 NED
8 59 6.1 T1c T2a 313 313 Negative 18 NED
9 12 10.3 T2a T2b 312 314 Negative 47 NED
10 76 6.7 T1c T3a 314 314 Positive 44 AWD
PSA indicates prostate-specific antigen; RP, radical prostatectomy; NED, no evidence of disease; AWD, alive with disease.
* This patient received a luteinizing hormone-releasing hormone agonist 3 months prior to surgery.
TABLE 6Patients Who Underwent Treatment Stratified by Treatment Modality
Therapy
Median time to treatment
(range), mo
Median post-therapy
follow-up (range), mo
Treatment
failure
RP (n 5 10) 21 (17–84) 47 (9–108) 2
Radiotherapy (n 5 9) 34 (9–39) 57 (7–102) 1
Radiotherapy plus hormonal therapy (n 5 4) 48 (36–76) 44 (12–48) 1
Hormonal therapy (n 5 6) 52 (18–84) 45 (9–89) 0
RP indicates radical prostatectomy.
Repeated Prostatic Biopsy/Al Otaibi et al. 291
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