Annals of Internal Medicine䊛

In the Clinic®
Prostate Cancer
Prevention

P
rostate cancer is the second most com-
monly diagnosed type of cancer in the
United States and the fifth most common Screening
cause of death from cancer (1). However, most
cases are clinically insignificant, and prevalence
increases rapidly with age. Prostate cancer is
found at autopsy in over half of U.S. men older
Diagnosis and Staging
than 50 years but is the cause of death in only
3%. It generally does not become symptomatic
until it metastasizes, usually to bones. Primary Shared Decision Making
treatment methods often cause sexual, urinary,
and bowel dysfunction. Deferring treatment un-
til palliation of symptomatic metastatic cancer Treatment
(watchful waiting) or active treatment for evi-
dence of progression that warrants curative
therapy (active surveillance) is an important op- Tool Kit
tion for many men. Therefore, shared decision
making is required for screening and, for treat-
ment choices, consultation with multidisci- Patient Information
plinary providers.

The CME quiz is available at www.annals.org/intheclinic.aspx. Complete the quiz to earn up to 1.5 CME credits.

Physician Writer
James A. Talcott, MD, SM
CME Objective: To review current evidence for prevention, screening, diagnosis and staging,
shared decision making, and treatment of prostate cancer.
Funding Source: American College of Physicians.
Disclosures: Dr. Talcott, ACP Contributing Author, has disclosed no conflicts of interest. Forms
can be viewed at www.acponline.org/authors/icmje/ConflictOfInterestForms
.do?msNum=M15-1986.
With the assistance of additional physician writers, the editors of Annals of Internal Medi-
cine develop In the Clinic using MKSAP and other resources of the American College of
Physicians.
In the Clinic does not necessarily represent official ACP clinical policy. For ACP clinical
guidelines, please go to https://www.acponline.org/clinical_information/guidelines/.
© 2015 American College of Physicians

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Prevention
1. Siegel RL, Miller KD,
Jemal A. Cancer statistics,
2015. CA Cancer J Clin.
2015;65:5-29. [PMID:
25559415]
2. Lippman SM, Klein EA,
Goodman PJ, Lucia MS,
Thompson IM, Ford LG,
et al. Effect of selenium
and vitamin E on risk of
prostate cancer and other
cancers: the Selenium and
Vitamin E Cancer Preven-
tion Trial (SELECT). JAMA.
2009;301:39-51. [PMID:
19066370]
3. Clark LC, Combs GF Jr,
Turnbull BW, Slate EH,
Chalker DK, Chow J, et al.
Effects of selenium sup-
plementation for cancer
prevention in patients
with carcinoma of the
skin. A randomized con-
trolled trial. Nutritional
Prevention of Cancer
Study Group. JAMA.
1996;276:1957-63.
[PMID: 8971064]
4. The effect of vitamin E and
beta carotene on the inci-
dence of lung cancer and
other cancers in male
smokers. The Alpha-
Tocopherol, Beta Carotene
Cancer Prevention Study
Group. N Engl J Med.
1994;330:1029-35.
[PMID: 8127329]
5. Klein EA, Thompson IM Jr,
Tangen CM, Crowley JJ,
Lucia MS, Goodman PJ,
et al. Vitamin E and the
risk of prostate cancer: the
Selenium and Vitamin E
Cancer Prevention Trial
(SELECT). JAMA. 2011;
306:1549-56. [PMID:
21990298]
6. Thompson IM, Goodman
PJ, Tangen CM, Lucia MS,
Miller GJ, Ford LG, et al.
The influence of finas-
teride on the develop-
ment of prostate cancer.
N Engl J Med. 2003;349:
215-24. [PMID:
12824459]
7. Andriole GL, Bostwick DG,
Brawley OW, Gomella LG,
Marberger M, Montorsi F,
et al; REDUCE Study
Group. Effect of dutas-
teride on the risk of pros-
tate cancer. N Engl J Med.
2010;362:1192-202.
[PMID: 20357281]
8. Thompson IM Jr, Good-
man PJ, Tangen CM,
Parnes HL, Minasian LM,
Godley PA, et al. Long-
term survival of partici-
pants in the prostate can-
cer prevention trial. N Engl
J Med. 2013;369:603-10.
[PMID: 23944298]
姝 2015 American College of Physicians
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Androgen-deprivation therapy
(ADT) is the mainstay of treatment
for patients with recurrent or meta-
static prostate cancer. Several new
No dietary interventions are
proven to prevent prostate can-
cer. Although most case– control
studies have shown a correlation
between animal fat and pros-
tate cancer, most prospective
studies have not. Thus, evi-
dence about the benefits of
reducing animal fat intake
conflicts. Despite inverse asso-
ciations seen in observational
studies between selenium lev-
els/vitamin E intake and pros-
tate cancer incidence, a large
randomized prevention trial
that studied these agents found
no benefit (2). Although other
nutritional components, such as
other antioxidants and lycopene,
have been associated with de-
creased risk in observational di-
etary studies and randomized pre-
vention trials that were focused on
other types of cancer (3, 4), their
use has not been shown to reduce
the risk for prostate cancer in clini-
cal trials.
SELECT (Selenium and Vitamin E Cancer Pre-
vention Trial) was a randomized, placebo-
controlled study of the effects of selenium, vi-
tamin E, or both on prostate cancer incidence
in 35 533 healthy men. It was stopped early
after 5 years of follow-up and found no reduc-
tion in prostate cancer risk in any treatment
group. It did find a nonsignificant increase
(P = 0.06) in prostate cancer risk with vitamin
E alone (2); at 7-year follow-up, a significant
increase was found (hazard ratio [HR], 1.17
[95% CI, 1.004 to 1.36]) (5).
Because of the central role of an-
drogens in prostate cancer carci-
nogenesis and progression, 5␣-
reductase inhibitors, which block
the conversion of testosterone to
more potent androgens, have
been tested as chemoprevention
agents. In large randomized tri-
als, finasteride (6) and dutas-
ITC2 In the Clinic Annals of Internal Medicine
treatments for castrate-resistant
prostate cancer have become
available, but most produce brief
survival benefits at high cost.
teride (7) reduced the incidence
of low-risk prostate cancer by
one fourth, but more higher-
grade cancers (Gleason score 8
to 10) were found. Use of 5␣-
reductase inhibitors reduces the
incidence of low-grade prostate
cancer, which may decrease over-
diagnosis and overtreatment.
However, they do not prolong life
and increase sexual dysfunction.
Therefore, these agents should not
be prescribed for most men.
The PCPT (Prostate Cancer Prevention Trial),
a large 7-year study, randomly assigned
men at low risk for prostate cancer to pla-
cebo or finasteride and monitored them
with annual digital rectal examination (DRE)
and prostate-specific antigen (PSA) mea-
surements. Men with suspicious or abnor-
mal findings had biopsy, as did those who
had not had a biopsy by the end of the
study. Of the 9060 men included in the final
analysis, prostate cancer was detected in
18.4% of the finasteride group compared
with 24.4% of the control group. However,
more men in the finasteride group had tu-
mors with a Gleason score of 7 or higher
(6.4% vs. 5.1%; P<0.001). Men receiving fi-
nasteride were 6% more likely to report
erectile dysfunction and loss of libido (6). In
15-year follow-up, overall mortality did not
differ between groups (8).
The REDUCE (Reduction by Dutasteride of Pros-
tate Cancer Events) study examined the effect
of dutasteride on prostate cancer in men at in-
creased risk. More than 8000 men aged 50 to
75 years with a recent elevated PSA level and
negative results on biopsy were randomly as-
signed to daily dutasteride or placebo for 4
years. Prostate cancer was diagnosed in 19.9%
of men in the dutasteride group compared
with 25.1% in the control group, but the 5.1%
risk reduction was primarily confined to low-
risk cancer (Gleason score 5 or 6). During years
3 and 4, there were 12 tumors with a Gleason
score of 8 to 10 in the dutasteride group com-
pared with 1 in the control group (P = 0.003).
Cardiac events were more common in the du-
tasteride group (30 events [0.7%] vs. 16
events [0.4%]; P = 0.03%) (7).
1 December 2015
 Prevention... Despite observed correlations between dietary nutrients
and prostate cancer incidence and mortality rates, trials do not support
dietary alterations or supplements to prevent prostate cancer. Use of
5␣-reductase inhibitors, which block conversion of testosterone to more
potent androgens, reduces the incidence of low-grade prostate cancer,
which may lower overdiagnosis and overtreatment. However, they do
not decrease the incidence of high-grade cancer or mortality and may
have adverse side effects.

CLINICAL BOTTOM LINE

Screening for prostate cancer is
controversial. Because most men
diagnosed with prostate cancer
die of another cause, and cura-
tive treatment with surgery or
radiation commonly causes sex-
ual, urinary, or bowel dysfunc-
tion, there is moderate evidence
that harms outweigh benefits in
the prime age group for screen-
ing, 50 to 69 years. PSA testing
produces false-positive and false-
negative results, leading to over-
diagnosis and false reassurance.
In addition, sampling error in the
biopsy process adds uncertainty
to the interpretation of negative
results. The U.S. Preventive Ser-
vices Task Force has recom-
mended against screening be-
cause of the substantial risk for
harm. However, since patients
may place different weights on
the harms of screening com-
pared with the benefit of possibly
reducing prostate cancer mortal-
ity, shared decision making is
essential. Data are inadequate to
make recommendations for pa-
tients with significant risk factors—
African American race or a first-
degree family history of prostate
cancer. Physicians should discuss
the benefits and harms of PSA
testing in standard-risk men aged
50 to 69 years, and for those with
risk factors, beginning at age 40
or 45 years. PSA testing should
not be offered to men younger
than 50 years who have no risk
factors. Because of the lead time
Screening
between screen detection and
symptoms and the slow growth
of most prostate cancers, screen-
ing and treatment of most men
older than 69 years or who have
comorbid conditions that limit
their life expectancy to less than
10 to 15 years are unlikely to re-
sult in benefit.
PSA testing is the most useful
screening test. DRE and imaging
methods, such as ultrasonogra-
phy or magnetic resonance im-
aging, are less sensitive and have
not been shown to be effective.
Prostatitis, prostate biopsies, uri-
nary tract infection, and prostate
massage can elevate serum PSA
levels, and ejaculation can cause
9. Schröder FH, Hugosson J,
minor PSA increases. The sensi- Roobol MJ, Tammela TL,
Zappa M, Nelen V, et al;
tivity of PSA testing, using a ERSPC Investigators.
threshold of 4.0 ng/mL, is 21% Screening and prostate
cancer mortality: results of
for all cancer and 51% for high- the European Randomised
grade cancer; specificity is 91%. Study of Screening for
Prostate Cancer (ERSPC) at
13 years of follow-up.
The findings of 2 large randomized trials that Lancet. 2014;384:2027-
evaluated screening with serum PSA testing, 35. [PMID: 25108889]
10. Andriole GL, Crawford
the ERSPC (European Randomized Study of ED, Grubb RL 3rd, Buys
SS, Chia D, Church TR,
Screening for Prostate Cancer) (9) and the U.S. et al; PLCO Project Team.
PLCO (Prostate, Lung, Colorectal and Ovarian) Prostate cancer screening
in the randomized Pros-
cancer screening trial (10, 11), conflict. The tate, Lung, Colorectal,
ERSPC study protocol varied by nation, but and Ovarian Cancer
Screening Trial: mortality
most participants were aged 50 to 69 years results after 13 years of
and randomly assigned to be invited or not to follow-up. J Natl Cancer
Inst. 2012;104:125-32.
have PSA screening every 4 years. Patients as-
[PMID: 22228146]
signed to screening were more likely to be 11. Andriole GL, Crawford
seen and receive cancer treatment at academic ED, Grubb RL 3rd, Buys
SS, Chia D, Church TR,
centers, whereas control patients were usually et al; PLCO Project Team.
treated locally. Screened patients were slightly Mortality results from a
randomized prostate-
more likely to receive prostatectomy for high- cancer screening trial.
N Engl J Med. 2009;
risk cancer than control patients. At 13-year 360:1310-9. [PMID:
follow-up, prostate cancer deaths were re- 19297565]

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 duced by 31%, or 1.28 per 1000 men ran-
domly assigned, but all-cause mortality did
not differ. Prostate cancer incidence was 57%
higher in the screening group (relative risk
[RR], 1.57 [CI, 1.51 to 1.62]). The RR of death
was 0.79 (0.69 to 0.91). To prevent 1 death
required 781 men to be invited for screening
and 27 cancers to be detected. Most of the
benefit of screening was found in the Gote-
berg, Sweden, site, which randomly assigned
20 000 000 men to be offered PSA testing ev-
ery 2 years and had a lower threshold for bi-
opsy (3.0 ng/dL initially, later reduced to 2.5
ng/dL) (12). However, after 13 years of
follow-up in the PLCO study, no reduction in
prostate cancer mortality was found, with 3.7
and 3.4 deaths per 10 000 patient-years in the
screening and control groups, respectively (RR,
1.09 [CI, 0.87 to 1.36]) (10, 11). This trial as-
signed 76 693 men to either annual PSA test-
ing for 6 years and DRE for 4 years or to usual
care. Compliance with PSA testing was 85% in
the screening group; in the usual care group,
52% of men had had PSA screening by the
sixth year, which was less than anticipated in
the study design.

Screening... Screening for prostate cancer and active treatment may

prevent some prostate cancer deaths, mostly a decade or more later.
However, screening also produces false-negative and false-positive re-
sults and overdiagnosis. Cancer treatments cause sexual dysfunction in
most men and distinct patterns of urinary and bowel symptoms. There-
fore, harm is much more likely than benefit. Because men differ in how
they weigh these outcomes, a shared decision-making process that re-
views benefits and harms is essential to any informed decision to
screen. However, providers should recommend against screening for
men who have no risk factors and are younger than 50 years, most men
older than 69 years, and those with a life expectancy less than 10 years.

CLINICAL BOTTOM LINE

Diagnosis and Staging

12. Hugosson J, Carlsson S,
Aus G, Bergdahl S,
Khatami A, Lodding P,
et al. Mortality results
from the Göteborg ran-
domised population-
based prostate-cancer
screening trial. Lancet
Oncol. 2010;11:725-32.
[PMID: 20598634]
The work-up of patients sus-
pected of having prostate cancer
requires an awareness that the
diagnosis can be harmful. Be-
cause of the high prevalence of
clinically insignificant prostate
cancer found in older men at au-
topsy and the slow progression
of low-risk cancer, the potential
for overdiagnosis of harmless
prostate cancer is substantial.
Further, any cancer diagnosis
causes unwelcome conse-
quences, from social, economic,
and psychological consequences
of the cancer “label” to anxiety
related to choosing a treatment.
Testing to diagnose prostate can-
cer should focus on patients with
a life expectancy of at least 10 to
15 years who would have cura-
tive treatment if diagnosed.
Symptoms are of limited value in
identifying patients likely to have
prostate cancer. Lower urinary
tract obstructive symptoms
(LUTS) are prevalent in older men
and have a low positive predic-
tive value. However, it is prudent
to measure serum PSA levels and
perform DRE in men with hema-
tospermia; pelvic pain; or symp-
toms of metastatic prostate can-
cer, such as bone pain; and to
discuss similar investigation of
rapidly progressing LUTS or
erectile dysfunction. PSA levels
should be measured before DRE
because it can cause slight
increases.
Patients with confirmed eleva-
tions in serum PSA levels (>4.0
ng/mL) or a prostate nodule or
suspicious induration on DRE
should be referred to a urologist
for transrectal ultrasound– guided
biopsy. Because PSA levels may
vary, elevations should be con-
firmed, particularly if the initial
elevation occurred after urinary

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 Table. Anatomical Stage and Prognosis Groups*
Group Tumor Node Metastasis PSA Gleason Score
I T1a-c N0 M0 PSA <10 ≤6
T2a N0 M0 PSA <10 ≤6
T1-2A N0 M0 PSA X X
IIA T1a-c N0 M0 PSA <20 7
T1a-c N0 M0 PSA ≥10–<20 ≤6
T2a N0 M0 PSA ≥10–<20 ≤6
T2a N0 M0 PSA <20 7
T2b N0 M0 PSA <20 ≤7
T2b N0 M0 PSA X X
IIB T2c N0 M0 Any PSA Any
T1-2 N0 M0 PSA ≥20 Any
T1-2 N0 M0 Any PSA ≥8
III T3a-b N0 M0 Any PSA Any
IV T4 N0 M0 Any PSA Any
Any N1 M0 Any PSA Any
Any Any M1 Any PSA Any

AJCC = American Joint Committee on Cancer; PSA = prostate-specific antigen; X =

unknown.
* Once a diagnosis of prostate cancer is made, patients with high-risk disease (T3, T4,
high PSA levels, or Gleason score 8 to 10) usually have a bone scan. Computed
tomography should also be considered, especially in patients suspected of having
more advanced disease. Reprinted with permission from the AJCC, Chicago, IL. The
original source for this material is the AJCC Cancer Staging Manual, Seventh Edi-
tion (2010), published by Springer Science and Business Media LLC (www.spnnger.com).

tract infection, DRE, or recent “Early” or clinically localized pros-

pretest ejaculation. Alternative
PSA measures, including density,
velocity, the proportion of free to
protein-bound PSA, and age-
specific thresholds, as well as the
prostate cancer antigen 3 test,
alter test characteristics but do
not have proven benefit.
Because systematic biopsies are
subject to sampling error, re-
peated biopsy may discover can-
cer in men with previously nega-
tive results, especially if 6 or
fewer cores were initially sam-
pled. Therefore, biopsy is often
repeated in 6 to 12 months for
patients with sustained PSA ele-
vations. Strategies to enhance
the yield from repeated biopsies
include increasing the number of
samples and using imaging
methods, including transrectal
magnetic resonance imaging, to
direct sampling to suspicious ar-
eas. However, these approaches
are investigative and have no
proven benefit.
tate cancer is confined within the
prostate capsule, and local treat-
ments are potentially curative.
Locally advanced cancer extends
beyond the prostate capsule,
including the seminal vesicles,
and can also be treated with po-
tentially curative methods that
often involve radiation and ADT.
Advanced prostate cancer—that
which has spread to retroperito-
neal lymph nodes or to bone—is
treated palliatively.
The most common symptom of
prostate cancer is bone pain; other
signs include weight loss, neuro-
logic dysfunction related to spinal
cord compression, normocytic
anemia, and cachexia. Computed
tomography and bone scans are
appropriate staging tests for pa-
tients at high risk for advanced
cancer and may be considered for
those at intermediate risk but not
for those at low risk. Positron emis-
sion tomography has no role in
staging prostate cancer.

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 Spinal cord compression can re-
sult in back pain, vertebral ten-
derness, lower-extremity weak-
ness, perineal numbness, urinary
retention or incontinence, and
fecal incontinence or constipa-
tion. It is a medical emergency,
requiring spinal magnetic reso-
nance imaging, high-dose corti-
costeroids, and either radiation
or surgery.
The staging of prostate cancer is
shown in the Table.

Diagnosis and Staging... The diagnosis of clinically localized prostate

cancer should focus on patients with at least a 10- to 15-year life expec-
tancy who would receive treatment if diagnosed. Although prostate
cancer may cause or worsen obstructive LUTS, these symptoms are very
prevalent in older men and nonspecific. However, rapidly worsening
LUTS and impotence, hematospermia, and pelvic pain may signify pros-
tate cancer, as may bone pain, the most common symptom of meta-
static prostate cancer. These symptoms, abnormal results on DRE, and
confirmed PSA elevations merit referral to a urologist. The prevalence
of metastasis in patients with low-risk prostate cancer is low, and such
patients should not have imaging. However, men with PSA concentra-
tions 20 ng/mL or greater, Gleason score higher than 7, or T3 cancer
should undergo a bone scan and abdominal–pelvic computed tomog-
raphy. Spinal metastasis may cause spinal cord compression, which is a
medical emergency.

CLINICAL BOTTOM LINE

Shared Decision Making

13. Fowler FJ Jr,
McNaughton Collins M,
Albertsen PC, Zietman A,
Elliott DB, Barry MJ.
Comparison of recom-
mendations by urologists
and radiation oncologists
for treatment of clinically
localized prostate cancer.
JAMA. 2000;283:3217-
22. [PMID: 10866869]
14. Aizer AA, Paly JJ, Mi-
chaelson MD, Rao SK,
Nguyen PL, Kaplan ID,
et al. Medical oncology
consultation and minimi-
zation of overtreatment
in men with low-risk
prostate cancer. J Oncol
Pract. 2014;10:107-12.
[PMID: 24399853]
What are the roles of shared
decision making, consultation,
and primary care providers?
Men with clinically localized pros-
tate cancer have several treat-
ment options. The first choice is
whether to defer treatment or
have curative treatment. Curative
treatment may prevent later me-
tastases and death but often
causes significant urinary, bowel,
and sexual side effects. Active
treatments have no proven differ-
ences in efficacy but vary in side
effects. For this reason, treatment
decisions are best made by
shared decision making with the
patient and cancer specialists.
Patients should strongly consider
soliciting input from radiation
and medical oncologists, in addi-
tion to the diagnosing urologist.
Reviewing a decision aid that
presents the important issues
and evidence in a balanced, clear
fashion prepares the patient for
effective consultation.
Surgery and radiation are alter-
native approaches for curative
local treatment in appropriate
candidates. Prostate cancer spe-
cialists are more confident in the
treatment they provide and more
often recommend it. (13). Con-
sultation with a medical oncolo-
gist is associated with increased
likelihood of choosing active sur-
veillance over immediate curative
therapy (14). Primary care provid-
ers are often insufficiently in-
formed about treatment options
to recommend or endorse spe-
cific approaches, but they can
play an important role by encour-
aging patients to take the time
for thorough consultation and to
make informed treatment deci-
sions. Prostate cancer does not
require the precipitous interven-
tions of some other rapidly pro-
gressing cancers, such as acute
leukemia. Although significantly
delaying acting on an informed
treatment decision is unwise, tak-

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 ing the time to absorb the diag-
nosis and consider competing
options with their divergent con-
sequences reduces the likeli-
hood of ill-informed decisions
that patients later regret.
Shared decision making is central
to providing patient-centered
care that improves outcomes
(15). It is a collaborative process
between patients and their pro-
viders informed by the best med-
ical evidence and reflects the pa-
tient's well-considered goals and
concerns (16). Essential informa-
tion includes the reason for the
interventions, benefits and
harms, alternative approaches,
and the clear statement that the
patient has a choice (which can
be found in decision aids [e.g.,
www.effectivehealthcare.ahrq
.gov/ehc/decisionaids/prostate
-cancer/]). Because prostate
cancer specialists have diverse
perspectives that affect their
recommendations, a balanced
viewpoint is best achieved from
multidisciplinary consultation.
Analyses using large databases
have confirmed that for complex
cancer procedures, outcomes
are, on average, better after
treatment at high-volume institu-
tions and from high-volume pro-
viders (17). Primary care provid-
ers should encourage their
patients to ask potential treating
oncologists how many patients
they treat annually.

Shared Decision Making... Men with clinically localized prostate cancer

face complex treatment choices that should be based on how they
value potential benefits and harms. Prostate cancer specialists usually
recommend the treatment they provide; for this reason, treatment deci-
sions should be shared between the patient and surgical, radiation, and
medical oncologists. Essential information for an informed decision in-
cludes the reason for the intervention, benefits and harms, alternative
approaches, and a clear statement that the patient has a choice.

CLINICAL BOTTOM LINE

Treatment
What options should be mary treatment for localized
considered for patients with prostate cancer.
clinically localized prostate 15. Stacey D, Bennett CL,
No high-quality studies have Barry MJ, Col NF, Eden
cancer?
compared the efficacy of surgical KB, Holmes-Rovner M,
Treatment options include watch- et al. Decision aids for
and radiation treatments for people facing health
ful waiting (deferred treatment), treatment or screening
prostate cancer. Observational decisions. Cochrane
active surveillance (monitoring
studies are strongly confounded Database Syst Rev. 2011:
for signs of progression that trig- CD001431. [PMID:
by indication: Patients who un- 21975733]
ger curative treatment), radical 16. Charles C, Gafni A,
dergo RP have a better prognosis Whelan T. Shared
prostatectomy (RP), external-
and less comorbidity, so they decision-making in the
beam radiation therapy (EBRT), medical encounter: what
would survive longer regardless does it mean? (or it takes
and brachytherapy (placement at least two to tango).
of radioactive sources, or of treatment. However, the Pro- Soc Sci Med. 1997;44:

“seeds”). Each of these ap- tecT (Prostate testing for cancer 681-92. [PMID:
9032835]
proaches is appropriate for pa- and Treatment) trial randomly 17. Begg CB, Cramer LD,
Hoskins WJ, Brennan
tients with low-risk prostate can- assigned more than 1600 men MF. Impact of hospital
volume on operative
cer. ADT is given in conjunction with PSA screening–detected mortality for major can-
with EBRT for high-risk cancer prostate cancer to active moni- cer surgery. JAMA. 1998;
280:1747-51. [PMID:
but it is inappropriate as pri- toring, EBRT, or RP. Publication of 9842949]

1 December 2015 Annals of Internal Medicine In the Clinic ITC7 姝 2015 American College of Physicians
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18. Lane JA, Donovan JL,
Davis M, Walsh E, Ded-
man D, Down L, et al;
ProtecT study group.
Active monitoring, radi-
cal prostatectomy, or
radiotherapy for localised
prostate cancer: study
design and diagnostic
and baseline results of
the ProtecT randomised
phase 3 trial. Lancet
Oncol. 2014;15:1109-
18. [PMID: 25163905]
19. Sanda MG, Dunn RL,
Michalski J, Sandler HM,
Northouse L, Hembroff L,
et al. Quality of life and
satisfaction with outcome
among prostate-cancer
survivors. N Engl J Med.
2008;358:1250-61.
[PMID: 18354103]
20. Resnick MJ, Koyama T,
Fan KH, Albertsen PC,
Goodman M, Hamilton
AS, et al. Long-term
functional outcomes after
treatment for localized
prostate cancer. N Engl J
Med. 2013;368:436-45.
[PMID: 23363497]
21. Talcott JA, Rossi C, Shi-
pley WU, Clark JA, Slater
JD, Niemierko A, et al.
Patient-reported long-
term outcomes after
conventional and high-
dose combined proton
and photon radiation for
early prostate cancer.
JAMA. 2010;303:1046-
53. [PMID: 20233822]
22. D’Amico AV, Chen MH,
Oh-Ung J, Renshaw AA,
Cote K, Loffredo M, et al.
Changing prostate-
specific antigen outcome
after surgery or radio-
therapy for localized
prostate cancer during
the prostate-specific
antigen era. Int J Radiat
Oncol Biol Phys. 2002;
54:436-41. [PMID:
12243819]
23. Klotz L, Vesprini D,
Sethukavalan P, Jethava
V, Zhang L, Jain S, et al.
Long-term follow-up of a
large active surveillance
cohort of patients with
prostate cancer. J Clin
Oncol. 2015;33:272-7.
[PMID: 25512465]
24. Tosoian JJ, Mamawala
M, Epstein JI, Landis P,
Wolf S, Trock BJ, et al.
Intermediate and longer-
term outcomes from a
prospective active-
surveillance program for
favorable-risk prostate
cancer. J Clin Oncol.
2015 Aug 31. [PMID:
26324359 [Epub ahead
of print]
25. Walsh PC, Mostwin JL.
Radical prostatectomy
and cystoprostatectomy
with preservation of
potency. Results using a
new nerve-sparing tech-
nique. Br J Urol. 1984;
56:694-7. [PMID:
6534493]
姝 2015 American College of Physicians
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10-year follow-up of the primary
end point, prostate cancer–
specific survival, is expected by
December 2015 (18).
Deferring curative therapy of
low-risk cancer, either until me-
tastases occur (watchful waiting)
or until evidence of more aggres-
sive cancer appears (active sur-
veillance), to delay or avoid
treatment-related toxicity entails
a small increased risk for mortal-
ity. Active treatments cause side
effects, particularly in the first 3 to
5 years after treatment (19). Most
men develop erectile dysfunction
after all active treatments, al-
though onset is delayed after ra-
diation treatments. RP more of-
ten causes erectile dysfunction
and urinary incontinence, al-
though brachytherapy may cause
late incontinence. Radiation
treatments produce radiation
proctitis, which causes transient
diarrhea, bowel urgency, and
tenesmus, which decrease over
time, and persistent rectal bleed-
ing. Brachytherapy increases
short-term urinary obstructive
symptoms that may progress to
complete obstruction. A 2011
systematic review of treatments
for localized prostate cancer from
the U.S. Preventive Services Task
Force concluded that there was
an additional patient with erectile
dysfunction for every 3 men
treated with RP and for every 7
men treated with radiation ther-
apy, and 1 additional patient with
urinary incontinence for every 5
men treated with prostatectomy.
However, patient-reported dys-
function attenuates in long-term
follow-up, which may indicate
the resolution of dysfunction or
the patient's adaptation to his
changed circumstances (20, 21).
Low-risk cancer is defined as
a serum PSA level <10 ng/dL,
Gleason score ≤6, and clinical
tumor stage ≤ T2a. Intermediate-
risk cancer has a serum PSA level
≥10 ng/dL but <20 ng/dL, Glea-
ITC8 In the Clinic
son score 6, or clinical tumor
stage T2b or T2c. High-risk can-
cer has a serum PSA level ≥20
ng/dL, Gleason score 8 to 10, or
clinical tumor stage T3 (22). A
higher serum PSA level or Glea-
son score increases the likeli-
hood that untreated cancer will
metastasize and that it will recur
after local treatment. Patients
with low-risk prostate cancer or
who have less favorable cancer
and a life expectancy of 10 years
or less should be offered active
surveillance or watchful waiting.
Active surveillance uses regular
PSA, DRE, and scheduled rebi-
opsy to identify clinical progres-
sion or a higher-grade cancer
than initially diagnosed, allowing
for escalation to active therapy if
assessed risk increases (23). Ac-
tive surveillance programs differ
in entry criteria and monitoring
protocols but report low prostate
cancer–specific long-term mortal-
ity rates (23, 24).
RP, which removes the prostate
and seminal vesicles, is an effec-
tive option for patients with clini-
cally localized prostate cancer.
However, it results in erectile dys-
function for most men (60% to
90%) and incontinence for many
(7% to 54%). Use of nerve-
sparing surgery, which depends
on the cancer's location and ex-
tent, may reduce erectile dys-
function (25). Minimally invasive
surgery, including robotic-
controlled approaches, slightly
shortens hospital stays and may
reduce recovery times but does
not improve cancer control or
quality-of-life outcomes.
The Scandinavian randomized
trial, which predated widespread
PSA screening, compared RP and
watchful waiting. At a median
10.8-year follow-up it found a
5.4% absolute reduction in pros-
tate cancer–specific survival after
prostatectomy but overall mortal-
ity did not differ (HR, 0.90 [CI,
0.56 to 1.43]) (26). However, after
Annals of Internal Medicine 1 December 2015
 an additional 3 years of follow- apy. Large randomized trials of
up, overall mortality was reduced adjuvant ADT for 4 months (31)
in the prostatectomy group, with or 2 years or longer (32, 33) have
an estimated absolute benefit of found improved cancer-specific
6.1% at 15 years (27). The first survival and, in most cases, over-
randomized trial during the PSA all survival (34). However, the op-
era, PIVOT (Prostate cancer Inter- timal duration of adjuvant hor-
vention Versus Observation monal therapy has not been
Trial), reported 47.0% mortality in determined. Combined radia- 26. Bill-Axelson A, Holmberg
L, Ruutu M, Garmo H,
the RP group and 49.9% in the tion therapy and ADT may be Stark JR, Busch C, et al;
observation group after 10 years considered for patients with SPCG-4 Investigators.
Radical prostatectomy
of follow-up (P = 0.22) (28). intermediate-risk cancer on the versus watchful waiting
in early prostate cancer.
basis of expert opinion. N Engl J Med. 2011;
Between 1989 and 1999, the Scandinavian 364:1708-17. [PMID:
Prostate Cancer Group (SPCG-4) randomly as- Brachytherapy is appropriate for 21542742]
27. Bill-Axelson A, Holmberg
signed 695 men with clinical localized pros- men with low-risk cancer, particu- L, Garmo H, Rider JR,
tate cancer to RP or watchful waiting. Most larly nonpalpable T1c tumors, Taari K, Busch C, et al.
Radical prostatectomy or
men had been diagnosed through clinical evi- and minimal or no urinary ob- watchful waiting in early
dence of cancer rather than screening. The pri- struction. EBRT is sometimes prostate cancer. N Engl J
mary outcome was prostate cancer–specific Med. 2014;370:932-42.
added to brachytherapy for pa- [PMID: 24597866]
survival. After a median of 10.8 years of follow- 28. Wilt TJ, Brawer MK,
up, the prostatectomy patients had a 35% re- tients with palpable nodules and Jones KM, Barry MJ,
intermediate-risk features. Aronson WJ, Fox S, et al;
duced risk for death from prostate cancer (RR, Prostate Cancer Interven-
0.65I [CI, 0.45 to 0.94]) and an estimated ab- tion versus Observation
What options should be Trial (PIVOT) Study
solute risk reduction at 12 years of 5.4% (CI, Group. Radical prostatec-
considered for men with an
0.2% to 11.1%). However, overall mortality tomy versus observation

was not significantly reduced, with 137 deaths increasing PSA level after for localized prostate
cancer. N Engl J Med.
in the prostatectomy group and 156 in the treatment for localized prostate 2012;367:203-13.
[PMID: 22808955]
watchful waiting group (P = 0.09) (29). At a cancer or for those at high risk 29. Bill-Axelson A, Holmberg
median 12.8 years of follow-up, overall sur- after prostatectomy? L, Filén F, Ruutu M,
Garmo H, Busch C, et al;
vival was improved in the surgery group—1 Serum PSA level is monitored Scandinavian Prostate
death was prevented for every 17 men ran- Cancer Group Study
regularly in men after local treat- Number 4. Radical pros-
domly assigned to prostatectomy (30). tatectomy versus watch-
ment for prostate cancer. A con- ful waiting in localized
PIVOT randomly assigned 731 men with local- firmed PSA increase from the prostate cancer: the
Scandinavian prostate
ized prostate cancer to RP or observation be- posttreatment nadir (“biochemi- cancer group-4 random-
tween 1994 and 2002. Three fourths of study cal relapse”) indicates persistent ized trial. J Natl Cancer
Inst. 2008;100:1144-54.
patients were diagnosed as a result of elevated cancer and high risk for metasta- [PMID: 18695132]
or increased PSA levels. The primary outcome sis. Because the goal of prosta- 30. Holmberg L, Bill-Axelson
A, Steineck G, Garmo H,
was overall mortality. After a median follow-up tectomy is to remove all tissue Palmgren J, Johansson
of 10.0 years, 47.0% of men assigned to pros- while benign prostate tissue may E, et al. Results from the
Scandinavian Prostate
tatectomy had died compared with 49.9% of
persist after successful radiation, Cancer Group Trial Num-
men in the observation group, an absolute dif- ber 4: a randomized
ference of 2.9% (HR, 0.88 [CI, 0.71 to 1.08]; the definitions of PSA recurrence controlled trial of radical
prostatectomy versus
P = 0.22). Prostate cancer–specific mortality after surgery and radiation differ. watchful waiting. J Natl
was 5.8% in the surgery patients compared Further, PSA levels may increase Cancer Inst Monogr.
2012;2012:230-3.
with 8.4% in the observation group, an abso- after radiation treatments that are [PMID: 23271778]
lute difference of 2.6% (HR, 0.63[CI, 0.36 not sustained (“PSA bounce”). 31. Jones CU, Hunt D,
McGowan DG, Amin MB,
to1.09]; P = 0.9]) (28). Administering ADT may be bene- Chetner MP, Bruner DW,
et al. Radiotherapy and
ficial, although the evidence is short-term androgen
EBRT, preferably with three- unclear in patients without metasta- deprivation for localized
dimensional conformal-beam or ses. Intermittent ADT in cases of in-
prostate cancer. N Engl J
Med. 2011;365:107-18.
intensity-modulated radiation, is creasing PSA level is as effective as [PMID: 21751904]
an effective option for patients continuous treatment (35).
32. Bolla M, Gonzalez D,
Warde P, Dubois JB,
with clinically localized or locally Mirimanoff RO, Storme
G, et al. Improved sur-
advanced prostate cancer. Pa- Patients with high-risk findings vival in patients with
tients with high-risk cancer after prostatectomy may benefit locally advanced prostate
cancer treated with radio-
should be given radiation ther- from radiation therapy or ADT. A therapy and goserelin.
apy and 2 years of ADT, begun randomized trial of 98 men with N Engl J Med. 1997;
337:295-300. [PMID:
2 months before radiation ther- node-positive prostate cancer 9233866]

1 December 2015 Annals of Internal Medicine In the Clinic ITC9 姝 2015 American College of Physicians
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 after prostatectomy found that What options should be
immediate compared with de- considered for patients with
ferred ADT improved overall and newly diagnosed metastatic
33. Widmark A, Klepp O, prostate-cancer mortality (36). prostate cancer?
Solberg A, Damber JE,
Angelsen A, Fransson P,
A randomized trial compared im- ADT should be offered to patients
et al; Scandinavian Pros-
tate Cancer Group Study mediate postoperative radiother- with metastatic prostate cancer.
7. Endocrine treatment, Approaches include GnRH ago-
with or without radio- apy (60 Gy delivered over 6
therapy, in locally ad-
weeks) to delaying radiation until a nists, such as goserelin and leu-
vanced prostate cancer
(SPCG-7/SFUO-3): an PSA rise in 1005 men with a posi- prolide; GnRH antagonists, such as
open randomised phase
tive surgical margin. After a me- degarelix; and bilateral orchiec-
III trial. Lancet. 2009;
373:301-8. [PMID: dian follow-up of 10.6 years, bio- tomy. A 4-week course of a non-
19091394]
34. Horwitz EM, Bae K, chemical progression-free survival steroidal antiandrogen, such as
Hanks GE, Porter A, Gri-
was improved in the immediate- flutamide or bicalutamide, should
gnon DJ, Brereton HD,
et al. Ten-year follow-up radiotherapy group (HR, 0.49 [CI, be started 1 to 2 weeks before the
of radiation therapy
0.41 to 0.59]; P <0.0001), but long- first GnRH agonist injection to pre-
oncology group protocol
92-02: a phase III trial of
term complications were more vent cancer flare from the surge in
the duration of elective
androgen deprivation in common (37). serum androgens.
locally advanced prostate
cancer. J Clin Oncol.
What are the potential adverse For patients with extensive me-
2008;26:2497-504.
[PMID: 18413638] effects of ADT? tastases, adding docetaxel to ini-
35. Crook JM, O’Callaghan tial ADT delays progression and
CJ, Duncan G, Dearnaley ADT uniformly causes erectile
DP, Higano CS, Horwitz
dysfunction and loss of libido. It prolongs life (40). For patients
EM, et al. Intermittent
androgen suppression also often causes hot flashes, fa- who progress on ADT and have
for rising PSA level after
tigue, gynecomastia, loss of mus- not achieved castrate levels of
radiotherapy. N Engl J
Med. 2012;367:895-
cle mass, gain of adipose tissue, serum testosterone (<50 ng/dL),
903. [PMID: 22931259]
36. Messing EM, Manola J, and osteoporosis. Because of the bilateral orchiectomy should be
Sarosdy M, Wilding G,
association between gonado- offered. Intermittent ADT re-
Crawford ED, Trump D.
Immediate hormonal trophin-releasing hormone duces some side effects but data
therapy compared with
(GnRH) agonists and diabetes/ conflict on whether it controls
observation after radical
prostatectomy and pelvic
cardiovascular disease, monitor- cancer equally well (41, 42).
lymphadenectomy in
men with node-positive ing modifiable disease markers, What options should be
prostate cancer. N Engl J
Med. 1999;341:1781-8. such as increased serum glucose considered for patients with
[PMID: 10588962] levels, osteoporosis, and hyper-
37. Bolla M, van Poppel H, castrate-resistant metastatic
Tombal B, Vekemans K, tension, may be helpful. In- prostate cancer?
Da Pozzo L, de Reijke
TM, et al; European creased exercise may prevent ADT is not curative, and metasta-
Organisation for Re- adverse body composition ses will progress despite treat-
search and Treatment of
Cancer, Radiation Oncol- changes and reduce fatigue. ment. Several efficacious palliative
ogy and Genito-Urinary
Groups. Postoperative
Bisphosphonates, particularly systemic treatment options have
radiotherapy after radical
prostatectomy for high- parenteral agents, mitigate the become available in the past de-
risk prostate cancer:
long-term results of a progression and symptoms of cade, although most prolong sur-
randomised controlled osteoporosis, but have adverse vival on average by a few months
trial (EORTC trial 22911).
Lancet. 2012;380:2018- side effects, including the un- and are very costly. The optimal
27. [PMID: 23084481]
common development of osteo- order for using these agents has
38. Yuen KK, Shelley M, Sze
WM, Wilt T, Mason MD. necrosis of the jaw (38). Reducing not been determined. Many pa-
Bisphosphonates for tients receive more than one
advanced prostate can- the frequency and number of
cer. Cochrane Database
bisphosphonate treatments may treatment.
Syst Rev. 2006:
CD006250. [PMID: reduce the incidence of osteone- Docetaxel is currently the first-
17054286]
39. Smith MR, Egerdie B, crosis. Denosumab, an antibody line systemic treatment for meta-
Hernández Toriz N, Feld- against the receptor activator of static or rapidly progressive pros-
man R, Tammela TL,
Saad F, et al; Deno- nuclear factor-␬B, RANKL, re- tate cancer, especially if the
sumab HALT Prostate
Cancer Study Group.
duced vertebral but not overall patient has extensive bone
Denosumab in men fracture rates and increased metastases (43).
receiving androgen-
deprivation therapy for bone density compared with
prostate cancer. N Engl J zoledronic acid, a parenteral Adding diethylstilbestrol or a
Med. 2009;361:745-55.
[PMID: 19671656] bisphosphonate (39). nonsteroidal antiandrogen to

姝 2015 American College of Physicians ITC10 In the Clinic Annals of Internal Medicine 1 December 2015
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 the GnRH agonist may achieve a poses the lymphocytes to an immu- 40. Sweeney CJ, Chen YH,
Carducci M, Liu G, Jar-
response in men with castrate- nostimulatory fusion protein ex vivo rard DF, Eisenberger M,
et al. Chemohormonal
resistant prostate cancer. Be- and infuses the stimulated cells with therapy in metastatic
cause adrenal steroids can be additional prostate antigens and hormone-sensitive pros-
tate cancer. N Engl J
peripherally converted to testos- granulocyte-macrophage colony- Med. 2015;373:737-46.
terone, additional agents that stimulating factor. It does not shrink [PMID: 26244877]
41. Hussain M, Tangen CM,
target testosterone production, the tumor or reduce PSA levels, but Berry DL, Higano CS,
Crawford ED, Liu G, et al.
such as the CYP17 inhibitor abi- it has prolonged survival in 2 ran- Intermittent versus con-
raterone acetate and the more domized trials. tinuous androgen depri-
vation in prostate cancer.
potent antiandrogen enzalut- N Engl J Med. 2013;
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42. Magnan S, Zarychanski
The autologous cellular immuno- prolong life in men with painful R, Pilote L, Bernier L,
Shemilt M, Vigneault E,
therapy treatment sipuleucel-T ex- bone metastases. et al. Intermittent vs
continuous androgen
deprivation therapy for
prostate cancer: a sys-
Treatment... Low-risk prostate cancer treatment approaches include tematic review and meta-
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2015:1-10. [PMID:
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therapy. ADT is given in conjunction with EBRT for high-risk cancer but 43. Tannock IF, de Wit R,
Berry WR, Horti J, Plu-
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pared prostatectomy with radiotherapy for prostate cancer. Patients with TAX 327 Investigators.
high-risk findings after prostatectomy may benefit from EBRT or ADT. Men Docetaxel plus predni-
sone or mitoxantrone
with metastatic prostate cancer in whom ADT has failed should be offered plus prednisone for
surgical castration, a GnRH agonist preceded by a nonsteroidal antiandro- advanced prostate can-
cer. N Engl J Med. 2004;
gen, or a GnRH antagonist. Adding docetaxel to ADT delays progression 351:1502-12. [PMID:
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castrate-resistant prostate cancer briefly prolong survival.

CLINICAL BOTTOM LINE

In the Clinic NIH MedLine Plus

https://www.nlm.nih.gov/medlineplus/prostatecancer

Tool Kit
.html#cat77
Guidelines

Prostate Cancer
https://www.auanet.org/education/guidelines/prostate
-cancer.cfm
www.esmo.org/Guidelines/Genitourinary-Cancers
/Cancer-of-the-Prostate
www.nccn.org/professionals/physician_gls/pdf
/prostate.pdf
Description and Information
IntheClinic
www.cancer.gov/types/prostate/hp/prostate-treatment
-pdq
www.mayoclinic.org/diseases-conditions/prostate
-cancer/basics/definition/CON-20029597?p=1
Patient Resources in English
www.ucsfhealth.org/education/patients_guide_to
_prostate_cancer/treatments/
www.cancer.org/acs/groups/content/@editorial
/documents/document/acspc-044303.pdf
www.cancer.org/cancer/prostatecancer/overviewguide
/prostate-cancer-overview-additional
Patient Resources in Spanish
https://www.nlm.nih.gov/medlineplus/spanish
/prostatecancer.html
www.cancer.org/espanol/servicios
/comocomprendersudiagnostico/fragmentado/despues
-del-diagnostico-una-guia-para-los-pacientes-y-sus
-familias-intro

1 December 2015 Annals of Internal Medicine In the Clinic ITC11 姝 2015 American College of Physicians
Downloaded From: http://annals.org/ by a Lake Erie Coll of Osteopathic Med User on 05/03/2016
 WHAT YOU SHOULD In the Clinic
Annals of Internal Medicine
KNOW PROSTATE CANCER
What Is Prostate Cancer?
Prostate cancer starts in a man's prostate gland, a
small gland below the bladder and is one of the
most common types of cancer in adult men. You
may be at higher risk for if you:
• Are an older man
• Have a family history of prostate cancer
• Are African American
Screening
Screening means looking for cancer before any symp-
toms arise. It can lead to early detection and treat-
ment of prostate cancer, which may reduce some
illnesses and deaths; however, screening tests can
also cause harms from unnecessary treatment. In
some cases, finding prostate cancer early through
screening may not help you live longer than if the
cancer was found later. If you decide to be screened,
the following tests may be used:
• A prostate-specific antigen (PSA) test. This is a
blood test. If your PSA levels are high, it may mean
you have prostate cancer.
• A digital rectal examination. This is when your
doctor inserts a gloved finger into your rectum to
check for lumps or tissue that feels abnormal. have serious risks. It's important to talk with your doc-
Since it can be difficult for your doctor to feel what tor about your options and weigh all your choices.
is abnormal, this test is usually not helpful. This will help you make the best decision possible.
Screening is not recommended for men younger than Treatment options can include:
50 years with no family history of prostate cancer or • Keeping a close watch on your symptoms and
men older than 69 years. It's important to speak with waiting to start treatment. This option can be
your doctor about screening so that you can make a useful for men with early-stage cancer that

decision that's right for you.
What Are the Warning Signs?
Symptoms of prostate cancer can be different for
everyone. Some men don't have any symptoms,
and many are the same as those of other condi-
tions. The most common symptoms are:
• Trouble urinating
• Weak or stopped flow of urine
• Frequent urination, especially at night
• Pain or burning during urination
• Blood in the urine or semen
• Pain in the back, hips, or pelvis that won't go away
• Painful ejaculation
How Is Prostate Cancer Diagnosed?
If screening suggests prostate cancer, more tests
can be done. This may include a biopsy. During
a biopsy, a small piece of tissue will be removed
from your prostate and looked at under a micro-
scope to check for cancer cells. Your doctor may
also use an ultrasound or an MRI to take a closer
look at your prostate.
How Is It Treated?
Your treatment will depend on how far along your can-
cer is. There are many options for treatment that can
Patient Information
may be slow-growing.
• Surgery to remove the cancer.
• Radiation to eliminate the cancer.
Questions For My Doctor
• Am I at risk?
• Are there ways to prevent prostate cancer?
• Should I be screened?
• What will happen if I don't get screened?
• Which treatment option is best for me?
• What are the risks of different treatments?
• What will happen if I don't get treatment?
Bottom Line
• Prostate cancer is cancer that starts in the
prostate gland. It is one of the most common
types of cancer in adult men.
• It may cause no symptoms. When symptoms are
present they may include problems urinating, pain
in the bones, and painful ejaculation.
• It's important to speak with your doctor about
your screening options.
• Diagnosis may include a biopsy to check for
cancer cells.
• Treatment depends on how far along your
cancer is and can include watching your
symptoms, surgery, and radiation.

For More Information

Centers for Disease Control and Prevention
www.cdc.gov/cancer/prostate/
Medline
https://www.nlm.nih.gov/medlineplus/prostatecancer.html
National Cancer Institute
www.cancer.gov/types/prostate

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