Despite widespread use of prostate specific
antigen (PSA) serologic testing to screen for prostate cancer
in men, authorities disagree on the benefit of this test and
its optimal use. The epidemiology of prostate cancer and the
characteristics of the PSA test provide compelling arguments
for its use, but no clear evidence shows that the test improves
outcomes as measured by cause-specific mortality--the only measure
without bias. Further, the cost-effectiveness of using PSA for
population screening and the policy issues related to prostate
cancer screening and treatment create an apparent conflict between
the public health perspective and the interests of individual
patients and practitioners.
Introduction
Prostate cancer screening offers a vivid contemporary example
of how the divergent perspectives of public health and clinical
practitioners can lead to a rancorous debate. The conflict originated
from a recent shift in medical practice toward prevention and
evidence-based practice. Preventive medical practice is becoming
standard practice because of its ability to improve health outcomes
and because of its presumed long-term potential to decrease
the cost of medical care.1,2 To minimize variation
in practice and to achieve the best health outcomes, preventive
care attempts to consistently follow practices that are based
on valid scientific evidence.3 To support these goals,
the US Public Health Service and the Canadian Task Force on
the Periodic Health Examination jointly developed an explicit
process for formulating evidence-based guidelines and used these
guidelines to review preventive practices.4 This
process did not produce adequate evidence to recommend routine
screening for prostate cancer; instead, routine screening was
given a "D" rating, indicating that the practice is
potentially harmful. Using different assumptions, methods, and
level of required evidence, other groups5 disagreed
with these recommendations for prostate cancer screening6-12
(Table 1). Recommendations from
the various Kaiser Permanente Regions mirror this spectrum of
opinion.13 While the medical community debates the
available evidence and most appropriate threshold for screening,
patients and community health groups remain confused; in this
scenario, health care agen
cies and health plans are caught in the middle, attempting to
diplomatically maintain their credibility with all sides.
This discussion elucidates the various expert
opinions in this controversy and explores the basis for their
divergence. Other references14-24 provide more extensive
and explicit reviews of the voluminous literature.
Prostate Cancer: Epidemiology
and Risk Factors
Few would dispute the serious personal consequences and substantial
public health impact of prostate cancer, which is the second
leading cause of death from cancer among men in the United States
and accounts for 14% of all cancer-related deaths in US males.
Prostate cancer will affect one in five American men during
their lifetimes, and about 3% of these men will die from it.
A total of 209,000 new cases of prostate cancer and 41,800 deaths
from the disease were predicted for 1997.23 The prevalence,
incidence, and mortality rate increase exponentially for men
aged 50 years and older, guaranteeing that the problem of prostate
cancer will grow as our population ages.24 The ageadjusted
incidence rate is 21 cases per 100,000 personyears for US white
men under age 65 years and is 819 per 100,000 personyears for
US white men aged 65 years and older.
One-third to one-fourth of men who have clinically
significant prostate cancer will die from it; however, due to
its association with older age, prostate cancer causes the least
loss of mean life-years of all cancers: eight years. In 1992,
61% of prostate cancer patients were aged 75 years or older;
median age at death was 77 years.25 Survival depends
on stage and histologic grade of tumor and whether or not it
is confined to the prostate. On average, only 58% of tumors
are discovered while still localized. Patients with localized
disease (stage A1) have a 12% chance of dying from it if they
remain untreated for 10 years. The 10-year survival rate for
patients with regional extension of prostate cancer is 55%;
for patients with distant metastases, 15%.
These survival statistics and the 3% lifetime
risk of death from prostate cancer must be reconciled with the
incidence of histologic cancer shown by autopsy studies: 22%
of men aged 50-59 years, 36% of men aged 60-69 years, 38% of
men aged 70-79 years, and 54% of men aged 80 years and older.
These rates imply that nine million cases of undiscovered prostate
cancer could currently exist in US men aged 50 years and older
and that only 1 of 380 men with prostate cancer will die from
it.26 The possibility of undiscovered prostate cancer
suggests a need for more early detection efforts.19
Clearly, tumor properties differ: some behave aggressively,
whereas others are indolent.
Marked ethnic differences in prostate cancer rates
have increased the pressure on public health agencies to support
screening efforts.24 In the United States, Hispanic
and Asian men have lower incidence rates than white men, whereas
African-American men have both a higher incidence of prostate
cancer (234 cases per 100,000 population in 1994) than white
men (135 cases per 100,000 population in 1994) and higher mortality
(56 cases per 100,000 population) than white men (24 cases per
100,000 population in 1994).27,28,29 African-American
men also have a higher stage of cancer at diagnosis: only 35%
are first seen with localized cancer compared with 62% of white
men. Data concerning racial differences in five-year survival
rates conflict when stratified for tumor grade and cancer stage.
Although the clinical incidence of prostate cancer is 30% to
50% higher among AfricanAmerican men, autopsy data show similar
prevalence of undiscov
ered disease. To date, no consistent data explain the observed
differences in incidence, mortality, or tumor stage; and these
differences are likely to be explained by multiple factors.28-31
In addition to age and race, family history among
first-degree relatives is the only other definitive risk factor
for prostate cancer. Currently, we have no good evidence that
primary prevention (ie, avoidance of risk factors) can decrease
incidence and mortality19,21; this lack of evidence
leaves secondary prevention efforts (ie, early screening to
detect treatable cases) as the best hope.
Use of Screening Tests
Screening refers to testing done to detect disease in persons
who are not yet symptomatic and who are apparently well. Although
appealing in principle, effectiveness of screening can be difficult
to prove.32 Screening tests are usually not intended
to be diagnostic; persons who screen positive must be further
evaluated to determine if they have the disease. We tend to
assume that earlier detection leads to intervention that decreases
morbidity or mortality from the disease, but this assumption
is not always true. A higher standard is needed to show the
effectiveness of screening a population of apparently healthy
persons. Several criteria should be used to determine whether
a test can be used effectively for mass screening33-35
(Table 2).
In addition to their ability to improve outcomes,
screening tests should be judged on their accuracy as measured
by sensitivity and specificity.36 Sensitivity
is the probability that a person affected with the disease will
test positive. High test sensitivity means that few people affected
with the disease test negative; low test sensitivity means that
many persons who actually have the disease will test negative.
These false negative results incorrectly reassure affected persons
that they do not have the disease. Specificity is the
probability that the test will yield a negative result when
the disease is not present. If conditions other than the disease
cause the test to be positive, these false positive results
will lead to more unnecessary testing. For diseases with low
prevalence (eg, cancer), screening tests generate many more
false positive results than true positive results. The discretionary
cutoff level that defines a positive test determines sensitivity
and specificity; gains in one are made at the expense of the
other.
The positive predictive value (PPV) of
a screening test measures yield of the test when applied to
a population and indicates the probability that a person who
tests positive actually has the disease. For a given sensitivity
and specificity, the PPV varies directly with prevalence of
the disease. Actual yield also depends on compliance with screening,
follow-up diagnosis, and treatment.
Screening Tests for Prostate
Cancer
Identifying prostate cancer early in the course of the disease
is compelling because the cancer generally causes no symptoms
until it reaches an advanced stage. Most men who have been diagnosed
with prostate cancer were initially thought to have the disease
on the basis of digital rectal examination (DRE) and serum prostate-specific
antigen (PSA).37,38
Screening with DRE seems a logical approach because
most prostate cancer begins in the peripheral zone adjacent
to the rectum. However, for several reasons, DRE is a poor routine
sequential screening test. DRE is not sufficiently sensitive,
having a PPV ranging from 15% to 30%, and has a detection rate
of 1% to 3% in screened populations.19,39 Because
most prostate cancer detected has already spread beyond the
gland, DRE fails to improve survival. The test is relatively
subjective, has poor reproducibility, and is highly dependent
on the examiner's level of experience. In addition, regular
DRE is unacceptable to many men.
The PSA test, which measures levels of an enzyme
produced by prostatic tissue, has some of the attributes of
an ideal screening test: it is reproducible, inexpensive, generates
results rapidly, is easy to perform, is accessible to clinicians,
and is well tolerated by patients. The availability of the PSA
test has resulted in a steep increase in its use40
and has been credited with "creating an epidemic"
of prostate cancer (because it revealed many existing cases
of cancer). Unfortunately, the PSA test has several disadvantages:
it lacks specificity; PSA levels can be elevated not only in
cancer but also in benign prostatic hypertrophy; and the test
cannot reliably predict prognosis or progression of disease.41
Results of PSA testing have varied widely between studies; however,
on average, the PSA test has a sensitivity of 70% to 80%, specificity
of 38% to 59%, and PPV of 20% to 30% in asymptomatic men, and
the detection rate among study volunteers is about 3% to 5%.39
Thus, at the common cutoff point of 4.0 mg/ml, the PSA test
may fail to detect 10% to 30% of clinically relevant cases of
cancer; and as many as three of four positive test results are
falsely positive.17
Nonetheless, many studies have documented the
validity of PSA testing as a method for assessing the risk of
prostate cancer.38,39,42,43 Moreover, most cancer
detected by PSA is considered clinically significant,4447
and by detecting localized cancer, annual screening can reduce
the frequency of metastatic cancer.48 Some of the
most convincing evidence for the usefulness of PSA testing comes
from prospective studies of other illnesses where serum was
frozen, tested for PSA level, and compared with serum of patients
subsequently diagnosed with prostate cancer.48 One
such study of 22,000 physicians49 found sensitivity
of 73% in the first four years and a mean lead time of 5.5 years
until diagnosis. A single test would have detected 80% of aggressive
cancers diagnosed within five years and 50% of aggressive cancers
appearing 9-10 years later. Few men in the study had a long
disease-free interval followed by diagnosis of nonaggressive
cancer.50 However, the authors40 did not
state the number of men who had potentially curable disease
when the blood sample was taken.
Several methods have been proposed for increasing
the sensitivity and specificity of the PSA test, including measurement
of age- and race-specific values, velocity (rate) of change
in PSA level, ratio of bound to unbound forms of PSA, and PSA
density; but none of these methods have gained widespread acceptance.50
Currently, the most effective method for early
detection of prostate cancer is combined use of DRE and PSA
testing to assess risk. PSA detects 33% of cases missed by DRE,
and DRE finds 20% of cases missed by PSA. A third technique,
transrectal ultrasound, has not been found to be an effective
screening test when used by itself, but the technique is commonly
used to guide biopsy of the prostate gland.42,51,52
The standard for confirming the diagnosis of prostate cancer
is transrectal biopsy using a spring-driven instrument, taking
six specimens in a systematic pattern.
Outcomes of Screening for Prostate
Cancer
To determine ultimate outcome, treatment must be considered
in combination with screening. Early diagnosis leads to other
invasive tests and treatments that may produce complications
without improving cause-specific mortality. Three main treatments
are used for prostate cancer--radical prostatectomy, external
or interstitial radiation therapy, and hormonal treatment--but
radical prostatectomy predominates because the prospect of surgically
curing localized cancer is so appealing. Driven by the increased
number of prostate cancer diagnoses resulting from PSA testing,
rates of prostatectomy have risen steadily. This increase cannot
be fully justified by results, because the rates remain high
in men aged 70 years
and older (who account for a third of the procedures done) despite
the suggestion that less aggressive treatment is indicated when
life expectancy is less than 10 years.53-56 Whether
and when early treatment effectively reduces mortality remains
to be proved.
One argument for aggressively treating prostate
cancer is the survival rate after such treatment: this rate
approximates the expected survival rate among men of similar
ages in the general population. Studies promoting nonintervention
are criticized for their technique and conclusions,57
yet studies of aggressive treatment are all uncontrolled.26
Pooled data of nonrandomized studies of conservative treatment
suggest that low-grade tumors could be treated conservatively
with delayed hormone therapy.56 At 15-year follow-up,
a nonrandomized group of patients with low-grade tumors had
4% to 7% cause-specific mortality.58 Although the
benefit of treatment is debated, the complications are well
known and may be higher than commonly reported59-62
(Table 3).
In the absence of experimental screening trials
with the end point being cause-specific mortality, decision
analyses have attempted to determine screening outcomes. A structured
literature review published in 199315 was unable
to determine treatment effectiveness for localized cancer because
of methodologic inadequacy in studies reported in the literature.
Other analyses17,41 show the potential for excess
deaths from treatment, even given conservative assumptions.
One decision analysis for localized prostate cancer screening
and treatment55 showed that in most cases, the potential
benefits of therapy are small enough that the choice is sensitive
to patient preference for various outcomes and discounting.55
When this analysis was redone with assumptions favoring screening
and treatment, a 50-year-old man could expect to gain, on average,
17 days of life as a result of screening. For clinically localized
cancer, surgery can add 3 years of life at age 55 years and
1.5 years at age 65 years.18
Barry22 analyzed a model for treating
Medicare-eligible men who had been screened once and treated
with radical prostatectomy; the net expected benefit shown was
1.52 additional years of life at age 65 years, 0.85 additional
years of life at age 70 years, and 0.43 additional years of
life at age 75 years. The study22 showed that if
aggressive treatment is ineffective, each cohort would lose
200 life-years, many biopsy procedures would be done, and a
small number of surgical deaths and many new complications would
result. Uncertainty about the benefit of aggressive intervention
and screening is created by the inability to predictively identify
aggressive cancers.54,63 The definition of clinically
significant cancer depends on tumor size, pathologic grade of
tumor, doubling time, and patient life expectancy as well as
host factors64; however, these factors cannot all
be known at initial detection. For indolent tumors detected
by PSA testing, less aggressive therapy would give the same
results as radical surgery or radiation therapy65;
clinical markers can be used to predict the need for intervention.44,45
However, using PSA density, PSA volume, and tumor grade noted
at biopsy, Catalona and colleagues39 found that only
11% of prostatic tumors were clinically insignificant. They
predicted clinically significant cancer with 95% accuracy but
had only 66% accuracy in predicting when to use watchful waiting
in identifying clinically significant cancer. They concluded
that an aggressive approach to diagnosis and treatment should
be used for men who have 10- to 15-year life expectancy and
apparently localized cancer.39
Arguments for and against routine prostate cancer
screening are summarized in Table
4.10,66-70
Analyzing the Cost of Screening
for Prostate Cancer
All routine health screening programs result in higher net costs
than when no screening is done. Therefore, the cost-effectiveness
of these interventions must be evaluated before monetary and
personnel resources are committed to a program of routine screening.
Prospective cost-effectiveness analyses of routine screening
for prostate cancer are necessarily imprecise, because questions
remain concerning the effects of various treatments.
Although screening may cost as little as $1500
per patient diagnosed with prostate cancer compared with $30,000
per patient diagnosed with breast cancer,52 the main
costs incurred from routine health screening are attributable
to follow-up diagnostic and treatment modalities and the complications
which result from use of these modalities.22 Cost
analyses of prostate cancer screening have yielded widely different
values, which range from a low of $12,000-$15,000 per year of
life saved (in 55-65 year-old men)18,22 to more commonly
accepted figures ($113,000-$214,000 per year of life saved)41,65
and to an extreme value of $729,000 per life-year saved.41
No reliable conclusions about precise costs can be made, but
screening can be cost-effective. Given the scope of population
screening, however, the cost may be staggeringly high. A clinical
decision analysis estimate that the cost of mass screening for
prostate cancer and treatment of cancers identified and complications
resulting would be $12-28 billion (depending on PSA cutoff)
and $3 billion per year thereafter--in other words, 5% of the
total annual US expenditures for health care. High costs could
continue to result if detection levels were high.71
Future Research on Prostate
Cancer
Currently, data on treatment outcome are derived from observational
cohort studies. The gold-standard study method used in medical
science is the randomized controlled trial, which eliminates
the biases found in uncontrolled, volunteer, early-detection
studies.72 Several large-scale trials currently in
progress could provide valid data to answer the question of
whether routine screening and treatment for prostate cancer
reduce cause-specific morbidity and mortality in this disease.
However, because these trials are prospective and because their
endpoint--prostate cancer outcome--remains unknown for as long
as 15 years after detection by screening, reliable results are
not likely for another decade. The trials include the International
Prostate Screening Trial Evaluation Group, recruiting 300,000
men from nine European countries73; the National
Cancer Institute's Prostate, Lung, Colon, Ovarian cancer (PLCO)
study,74 which has recruited nearly 50,000 men in
the United States; the Prostate Cancer Intervention versus Observation
Trial (PIVOT),75 launched by the National Cancer
Institute; the Scandinavian Prostatic Cancer Group (SPCG4),76
a randomized trial begun in the 1980s which compares results
of radical prostatectomy and results of deferred treatment;
and the United Kingdom Medical Research Council trial (PRO6).77
Critics claim these trials are unnecessary, because
sufficient data already exist to justify treatment. Others argue
that randomized studies are premature because the PSA test is
inadequate (ie, it fails to differentiate between clinically
significant and insignificant cancer).74 Social policies
that promote mass screening undermine the studies and make it
difficult to recruit volunteers to be randomized. Despite the
pressure for immediate screening and treatment, a more rational
approach is to devote resources and time to generating convincing
evidence for or against routine screening for prostate cancer;
such an approach will benefit patients and the health care system
in the long run.10
Policy Perspectives
Population Perspective vs Perspectives Focusing on Individual
Practitioners and Patients
The controversy over routine screening for prostate cancer can
be framed from several different perspectives, each contributing
to the vigor of the policy debate.
To justify widespread population screening for
any condition, planners must identify a benefit more precisely
defined than "ill people should be treated"; the benefit
must be based on more than the general belief that "it
is a good idea" or that it is "likely to be effective."
Clinicians tend to believe that patients benefit from diagnosis
itself and that after a diagnosis is made, the clinician must
necessarily treat the disease; in regard to cancer, the mission
is to find cancer as early as possible and to eradicate it.
Under pressure to treat, however, a clinician's judgment may
be impaired by presumption of benefit. Practitioner preference
has traditionally determined standards of medical practice,
but after new tests or treatments have gained acceptance among
practitioners, changing the expectations of the public and the
practice of the medical profession can be very difficult.10,70,78
The controversy over routine PSA testing is even more confusing
because it blurs the distinction between screening tests and
diagnostic tests.20
From the perspective of the urologist, adequate
tests and treatment for prostate cancer exist: because prostate
cancer cannot be prevented and because metastatic disease cannot
be cured, the best hope of decreasing mortality lies in detecting
and removing organconfined cancer in young men.79
The perspective of the individual patient is that
every man has a right to know if he has prostate cancer when
it is still at a curable stage.80,81 Survivors of
prostate cancer are convinced that PSA testing saved their lives
despite decrease in quality of life. Patients dying from prostate
cancer and friends and relatives of men who died from the disease
are convinced that early detection saves lives.
The Public as Informed Consumer
Until consensus develops over the data, patients should be educated
concerning the potential benefits and drawbacks of early detection
and treatment and should be allowed to make individual decisions
jointly with their medical provider.4,18 As much
as patients like to be involved in making medical decisions,
they prefer a clear choice and cannot understand how studies
can give conflicting information and create disagreement within
the medical community.82 Decisions require assessment
of patient preferences about health outcomes, and the patient's
willingness to trade current health (diagnosis of cancer and
potential treatment complications) for potential future benefit
(decreased cancer morbidity or mortality).14,83 The
profusion of Internet sites providing detailed medical information
reflects the need for information as well as patients' suspicion
that they cannot get adequate or accurate information from physicians.
The proliferation of cancer support groups attests to the complexity
of these decisions and the anxiety that they cause.
Group Health Cooperative of Puget Sound has trained
physicians to use a process of shared decision-making in addressing
patients' concerns about prostate cancer screening. In so doing,
they found that PSA test ordering decreased, especially among
50- to 74-year-old men who came for routine visits; this finding
suggests that patients who have been fully informed of the risks
and benefits of screening by PSA testing may choose not to receive
this screening.40
Ethical Issues
Ethical arguments can support either side of the prostate cancer
screening debate: delaying screening for prostate cancer until
randomized controlled trials are completed is unethical when
detecting localized cancer is of some benefit; conversely, until
better modes of treatment for prostate cancer are available
or current modes of treatment are found to have more obvious
benefits, randomized trials of screening are unethical because
they result in morbidity in patients with localized cancer.78
An opposing view is that a randomized trial is unethical only
if the answer is already known. After medical opinion has accepted
the value of treatment, no ethical alternative exists; at that
point, objection arises to planning randomized trials of intervention
and treatment.34 To represent an intervention as
effective when its efficacy is uncertain is itself unethical.10,14,84
Role in Medical Quality
Prostate cancer screening illustrates both the importance and
the limitations of evidencebased methods in medical practice.
In the past, many medical interventions based on reasonably
sound pathophysiologic principles (for example, chest x-ray
and sputum cytology for lung cancer screening) were championed
until clinical trials proved them worthless for the given purpose.85
The US Preventive Services Task Force based its conclusions
on strict methodology so that these conclusions would be consistent
and credible for a broad range of screening tests and therapeutic
interventions. Circumventing this methodology could be detrimental
to quality and value as evolving forces in medicine.86
The paradigm may be shifting so that the burden of proof rests
with the promoters of a particular treatment;21,65
however, in the current debate, those who cautiously advise
waiting for further proof appear to be on the defensive.85
The traditional approach of assembling a consensus conference
that includes experts and members of the public is unlikely
to resolve the disagreement among the experts and is unlikely
to explicitly weigh scientific and value decisions. This scenario
occurred in the case of a consensus conference on breast cancer
screening for 40- to 50-year-old women: the conference contributed
nothing to resolution of the dispute.87
Health Care Policy Issues: Complicating
the Debate
The question of routine prostate cancer screening is
becoming increasingly distorted by financial and political interests.
When federal health care agencies decided not to sponsor or
fund population screening for prostate cancer, the decision
was seen as discriminatory, "two-tiered" health care.
Governmental refusal to pay may also seem to conflict with physicians'
obligations to individual patients and may seem to ignore the
desires of individual patients.88,89
Resources are not unlimited, and the pursuit of
unproved interventions shifts resources from known effective
health services.2,10 We can no longer provide all
services to everyone without first identifying likely beneficiaries
of these services; however, it is difficult to withdraw or restrict
services--even to groups who receive these services inappropriately--after
these services have become expected.90
Public debate may be inappropriate for crafting
health policy. Disdainful of the slow process of scientific
trials and armed with painful stories of prostate cancer deaths,
an impatient public insists on routine screening. Eager to support
these members of the public, elected officials have proposed
numerous initiatives that mandate coverage for routine prostate
screening and treatment and that require physicians to provide
information on prostate cancer screening. The 105th
Congress proposed at least six different bills to provide coverage
for early detection of prostate cancer under part B of the Medicare
program despite a comprehensive, evidence-based analysis sponsored
by the Agency for Health Care Policy and Research that concluded
"it is premature to offer a Medicare benefit for PSA testing
for early detection of prostate cancer."22 In
California, the Grant H. Kenyon Prostate Cancer Act (SB 1) was
passed in 1997 because Congressman John Burton's friend (for
whom the act is named) died from prostate cancer, and Representative
Burton believed that PSA screening could have saved his friend's
life. The bill requires physicians to provide information about
diagnostic procedures, including PSA testing, to patients having
DRE of the prostate. This mandate is an ominous example of legislated
health care policy-by-anecdote that leads to microregulation
of medical practice. Moreover, the mandate shows the degree
to which the public distrusts the medical profession to determine
and provide the best care for patients. This microregulation
has continued under the guise of HMO reform and as such could
create two standards for medical practice: evidence-based guidelines
and legislation-based mandates. Further, this microregulation
threatens to deter the move toward a scientific, outcome-based
approach to medicine and undermines efforts to rationally budget
and control medical expenditures.
Conclusion
Despite growing use of PSA testing to screen for prostate cancer
in adult men, authorities disagree about the optimal use of
this test. Lack of knowledge concerning the relative effectiveness
of treatment options--and our inability to predict disease course
and prognosis in individual cases of cancer detected by screening--prevent
consensus over the widespread use of this screening. Physicians
are faced with conflicting recommendations, patient demand,
and the threat of legal mandates for PSA screening.16
Currently, the most rational response by individual physicians
is to make informed decisions jointly with the patient before
testing is done. Early detection may not change the outcome
for cancer patients, but in this emotionally and politically
charged climate, patients may benefit from knowing the diagnosis
and having the opportunity to participate in treatment decisions.
Even if pending randomized controlled trials show that routine
PSA testing has no benefit, we will have an uphill battle to
overcome patients' and physicians' desire for early diagnosis.
Ironically, widespread disagreement about the benefit of an
intervention is likely to indicate that the effectiveness is
minimal.83,87 We can only hope that future advances
will provide a screening test that can better predict prognosis
as well as diagnosis and will provide modes of treatment that
result in less morbidity than is seen currently. Meanwhile,
the pressure from medical practitioners, medical societies,
advocacy groups and legislators to adopt population screening
using PSA undermines attempts to scientifically evaluate new
health care interventions and rationally allocate scarce health
care resources.
Related material published as:
Backer H, Wallack L, Winett L. Prostate cancer screening controversies.
In: Wallack L, Winett L, editors. Media advocacy in cancer prevention
and control. ASPH/CDC Cooperative Agreement #S581-17/17. Berkeley,
CA: University of California School of Public Health; 1998.
P. 1-11, 1-5, 1-2.
References
1. Fries JF, Koop CE, Beadle CE, Cooper PP, England MJ, Greaves
RF, et al. Reducing health care costs by reducing the need and
demand for medical services. The Health Project Consortium.
N Engl J Med 1993;329:321-5.
2. Vogt TM, Hollis JF, Lichtenstein E, Stevens VJ, Glasgow R,
Whitlock E. The medical care system and prevention: the need
for a new paradigm. HMO Pract 1998 Mar;12(1):5-13.
3. Blumenthal D. Quality of health care. Part 4: The origins
of the quality-of-care debate. N Engl J Med 1996;335:1146-9.
4. US Preventive Services Task Force. Guide to clinical preventive
services: report of the US Preventive Services Task Force. 2nd
ed. Baltimore: Williams & Wilkins; 1996.
5. United States Office of Disease Prevention and Health Promotion.
Clinician's handbook of preventive services: put prevention
into practice. 2nd ed. Washington, DC: US Department of Health
and Human Services; 1998.
6. von Eschenbach A, Ho R, Murphy GP, Cunningham M, Lins N.
American Cancer Society guideline for the early detection of
prostate cancer: update, June 10, 1997. Cancer 1997;80:1805-7.
7. Liebel SA. ACR appropriateness criteria. Expert Panel on
Radiation Oncology. American College of Radiology. Int J Radiat
Oncol Biol Phys 1999;43:125-68.
8. Brawley OW. Prostate carcinoma incidence and patient mortality:
the effects of screening and early detection. Cancer 1997;80:1857-63.
9. Sherriff R, Best L, Roderick P. Population screening in the
NHS: a systematic pathway from evidence to policy formulation.
J Public Health Med 1998;20:58-62.
10. Feightner JW. The early detection and treatment of prostate
cancer: the perspective of the Canadian Task Force on the Periodic
Health Examination. J Urol 1994;152(5 Pt 2):1682-4.
11. Canadian workshop on screening for prostate cancer, proceedings.
Quebec City, Quebec, March 24-27, 1994. Can J Oncol 1994;4 Suppl
1:1-138.
12. Lefevre ML. Prostate cancer screening: more harm than good?
Am Fam Physician 1998;58:432-8.
13. National Prevention Partners. Survey of preventive practices.
Oakland, CA: Kaiser Permanente Medical Care Program; 1997.
14. Woolf SH. Screening for prostate cancer with prostate-specific
antigen: an examination of the evidence. N Engl J Med 1995;333:1401-5.
15. Wasson JH, Cushman CC, Bruskewitz RC, Littenberg B, Mulley
AG Jr, Wennberg JE. A structured literature review of treatment
for localized prostate cancer. Prostate disease Patient Outcome
Research Team. Arch Fam Med 1993;2:487-93. [published erratum
appears in Arch Fam Med 1993 Oct;2(10):1030]
16. Mandelson MT, Wagner EH, Thompson RS. PSA screening: a public
health dilemma. Annu Rev Public Health 1995;16:283-306.
17. Kramer BS, Brown ML, Prorok PC, Potosky Al, Gohagan JK.
Prostate cancer screening: what we know and what we need to
know. Ann Intern Med 1993;119:914-23.
18. Coley CM, Barry MJ, Fleming C, Fahs MC, Mulley AG. Early
detection of prostate cancer. Part II: Estimating the risks,
benefits and costs. American College of Physicians. Ann Intern
Med 1997;126:468-79.
19. Coley CM, Barry MJ, Fleming C, Mulley AG. Early detection
of prostate cancer. Part 1: Prior probability and effectiveness
of tests. The American College of Physicians. Ann Intern Med
1997;126:394-406.
20. Part III: Screening for prostate cancer. American College
of Physicians. Ann Intern Med 1997;126:480-4.
21. Barry MJ, Fleming C, Coley CM, Wasson JH, Fahs MC, Oesterling
JE. Should Medicare provide reimbursement for prostate-specific
antigen testing for early detection of prostate cancer? Part
I: Framing the debate. Urology 1995;46:2-13.
22. Barry MJ, Fleming C, Coley CM, Wasson JH, Fahs MC, Oesterling
JE. Should Medicare provide reimbursement for prostate-specific
antigen testing for early detection of prostate cancer? Part
IV: Estimating the risks and benefits of an early detection
program. Urology 1995;46:445-61.
23. National Cancer Institute. Cancer facts: prostate cancer.
Data from the Surveillance, Epidemiology and End Results Program
(SEER). Bethesda, MD: National Institutes of Health; 1996.
24. Boyle P, Maisonneuve P, Napalkov P. Incidence of prostate
cancer will double by the year 2030: the argument for. Eur Urol
1996;29 Suppl 2:3-9.
25. Horm JW, Sondik EJ. Person-years of life lost due to cancer
in the United States, 1970 and 1984. Am J Public Health 1989;79:1490-3.
26. Pollack HM, Resnick MI. Prostate-specific antigen and screening
for prostate cancer: much ado about something? Radiology 1993;189:353-6.
27. Landis SH, Murray T, Bolden S, Wingo PA. Cancer Statistics,
1998. CA Cancer J Clin 1998;48:6-29. [published errata appear
in CA Cancer J Clin 1998 May-Jun;48(3):192 and 1998 Nov-Dec;48(6):329]
28. Morton RA. Racial differences in adenocarcinoma of the prostate
in North American men. Urology 1994;44:637-45.
29. Merrill RM, Brawley OW. Prostate cancer incidence and mortality
rates among white and black men. Epidemiology 1997;8:126-31.
30. Smith DS, Bullock AD, Catalona WJ, Herschman JD. Racial
differences in a prostate cancer screening study. J Urol 1996;156:1366-9.
31. Powell IJ. Prostate cancer and African-American men. Oncology
(Huntingt) 1997;11:599-605; discussion 606-15 passim.
32. Cochrane AL, Holland WW. Validation of screening procedures.
Br Med Bull 1971;27:3-8.
33. Hulka BS. Cancer screening: degrees of proof and practical
application. Cancer 1988;62 (8 Suppl):1776-80.
34. Wilson J, Jungner G. Principles and practice or screening
for disease. Public Health Papers. Vol. 34. Geneva: World Health
Organization; 1968:1-77.
35. Mant D, Fowler G. Mass screening: theory and ethics. BMJ
1990;300:916-8.
36. Scherokman B. Selecting and interpreting diagnostic tests.
The Permanente Journal 1997 Spring;1(2):4-7.
37. Carter H, Partin A. Diagnosis and staging of prostate cancer.
In: Walsh P, Retik A, Vaughan E, Wein A, editors. Campbell's
Urology. 7th ed. Philadelphia: Saunders; 1998. p. 2519-37.
38. Mettlin C, Murphy GP, Babaian RJ, Chesley A, Kane RA, Littrup
PJ, et al. The results of a five-year early prostate cancer
detection intervention. Investigators of the American Cancer
Society National Prostate Cancer Detection Project. Cancer 1996;77:150-9.
39. Catalona WJ, Richie JP, Ahmann FR, Hudson MA, Scardino PT,
Flanigan RC, et al. Comparison of digital rectal examination
and serum prostate specific antigen in the early detection of
prostate cancer: results of a multicenter clinical trial of
6,630 men. J Urol 1994;151:1283-90.
40. Handley MR, Stuart ME. The use of prostate specific antigen
for prostate cancer screening: a managed care perspective. J
Urol 1994;152 (5 Pt 2):1689-92.
41. Krahn MD, Mahoney JE, Eckman MH, Trachtenberg J, Pauker
SG, Detsky AS. Screening for prostate cancer: a decision analytic
view. JAMA 1994;272:773-80.
42. Brawer MK, Chetner MP, Beatie J, Buchner DM, Vessella RL,
Lange PH. Screening for prostatic carcinoma with prostate specific
antigen. J Urol 1992;147(3 Pt 2):841-5.
43. Smith DS, Catalona WJ, Herschman JD. Longitudinal screening
for prostate cancer with prostate-specific antigen. JAMA 1996;276:1309-15.
44. Carter HB, Sauvageot J, Walsh PC, Epstein JI. Prospective
evaluation of men with stage T1C adenocarcinoma of the prostate.
J Urol 1997;157:2206-9.
45. Epstein JI, Walsh PC, Carmichael M, Brendler CB. Pathologic
and clinical findings to predict tumor extent of nonpalpable
(stage T1C) prostate cancer. JAMA 1994;271:368-74.
46. Oesterling JE, Suman VJ, Zincke H, Bostwick DG. PSA-detected
(clinical stage T1C or B0) prostate cancer: pathologically significant
tumors. Urol Clin North Am 1993;20:687-93.
47. Stormont TJ, Farrow GM, Myers RP, Blut ML, Zincke H, Wilson
TM, et al. Clinical stage B0 or T1C prostate cancer: nonpalpable
disease identified by elevated serum prostate-specific antigen
concentration. Urology 1993;41:3-8.
48. Labrie F, Candas B, Cusan L, Gomez JL, Diamond P, Suburu
R, et al. Diagnosis of advanced or non-curable prostate cancer
can be practically eliminated by prostate-specific antigen.
Urology 1996;47:212-7.
49. Gann PH, Hennekens CH, Stampfer MJ. A prospective evaluation
of plasma prostate-specific antigen for detection of prostatic
cancer. JAMA 1995;273:289-94.
50. Pienta K. Etiology, epidemiology, and prevention of carcinoma
of the prostate. In: Walsh P, Retik A, Vaughan A, Wein A, editors.
Campbell's Urology. 7th ed. Philadelphia: Saunders; 1998. p.
2489-96.
51. Stamey TA. Diagnosis of prostate cancer: a personal view
[editorial]. J Urol 1992;147(3 Pt 2):830-2.
52. Labrie F, Dupont A, Suburu R, Cusan L, Tremblay M, Gomez
JL, et al. Serum prostate specific antigen as pre-screening
test for prostate cancer. J Urol 1992;147:846-51; discussion
851-2.
53. Lu-Yao GL, McLerran D, Wasson J, Wennberg JE. An assessment
of radical prostatectomy: time trends, geographic variation,
and outcomes. The Prostate Patient Outcomes Research Team. JAMA
1993;269:2633-6.
54. Lu-Yao GL, Greenberg ER. Changes in prostate cancer incidence
and treatment in USA. Lancet 1994;343:251-4.
55. Fleming C, Wasson JH, Albertsen PC, Barry MJ, Wennberg JE.
A decision analysis of alternative treatment strategies for
clinically localized prostate cancer. Prostate Patient Outcomes
Research Team. JAMA 1993;269:2650-8.
56. Chodak GW, Thisted RA, Gerber GS, Johansson JE, Adolfsson
J, Jones GW, et al. Results of conservative management of clinically
localized prostate cancer. N Engl J Med 1994;330:242-8.
57. Steinberg GD, Bales GT, Brendler CB. An analysis of watchful
waiting for clinically localized prostate cancer. J Urol 1998;159:1431-6.
58. Albertsen PC, Hanley JA, Gleason DF, Barry MJ. Competing
risk analysis of men aged 55 to 74 years at diagnosis managed
conservatively for clinically localized prostate cancer. JAMA
1998;280:975-80.
59. D'Amico AV, Whittington R, Malkowicz SB, Schultz D, Blank
K, Broderick GA, et al. Biochemical outcome after radical prostatectomy,
external beam radiation therapy, or interstitial radiation therapy
for clinically localized prostate cancer. JAMA 1998;280:969-74.
60. Talcott JA, Rieker P, Propert KJ, Clark JA, Wishnow KI,
Loughlin KR, et al. Patient-reported impotence and incontinence
after nerve-sparing radical prostatectomy. J Natl Cancer Inst
1997;89:1117-23.
61. Talcott JA, Rieker P, Clark JA, Propert KJ, Weeks JC, Beard
CJ, et al. Patient-reported symptoms after primary therapy for
early prostate cancer: results of a prospective cohort study.
J Clin Oncol 1998;16:275-83.
62. Centers for Disease Control and Prevention. Prostate cancer:
Can we reduce deaths and preserve quality of life? Atlanta:
National Center for Chronic Disease Prevention and Health Promotion,
1998.
63. Lange PH. Prognostic factors and the clinical significance
of cancers detected by screening: growth rate and progression
of prostate cancer [editorial]. J Urol 1994;152(5 Pt 2):1707-8.
64. Dugan JA, Bostwick DG, Myers RP, Qian RMJ, Bergstralh EJ,
Oesterling JE. The definition and preoperative prediction of
clinically insignificant prostate cancer. JAMA 1996;275:288-94.
65. Albertsen PC. Screening for prostate cancer is neither appropriate
nor cost-effective. Urol Clin North Am 1996;23:521-30.
66. Mettlin CJ, Murphy G. The National Cancer Data Base report
on prostate cancer. Cancer 1994;74:1640-8.
67. Walsh PC. Why make an early diagnosis of prostate cancer.
[editorial] J Urol 1992;147 (3 Pt 2):853-4.
68. Collins MM, Ransohoff DF, Barry MJ. Early detection of prostate
cancer: serendipity strikes again. JAMA 1997;278:1516-9.
69. Chodak GW. Comparing treatments for localized prostate cancer--persisting
uncertainty [editorial]. JAMA 1998;280:1008-10.
70. Woolf SH. Public health perspective: the health policy implications
of screening for prostate cancer. J Urol 1994;152(5 Pt 2):1685-8.
71. Optenberg SA, Thompson IM. Economics of screening for carcinoma
of the prostate. Urol Clin North Am 1990;17:719-37.
72. Denis L, Norlen BJ, Holmberg L, Begg CB, Damber JE, Wilt
TJ. Planning controlled clinical trials: prostatic cancer. Urology
1997;49(4A Suppl):15-26.
73. Auvinen A, Rietbergen JB, Denis LJ, Schroder FH, Prorok
PC. Prospective evaluation plan for randomised trials of prostate
cancer screening. The International Prostate Cancer Screening
Trial Evaluation Group. J Med Screen 1996;3(2):97-104.
74. Vanchieri C. Prostate cancer screening trials: fending off
critics to recruit men [news]. J Natl Cancer Inst 1998;90:10-2.
75. Wilt TJ, Brawer MK. The Prostate Cancer Intervention Versus
Observation Trial (PIVOT). Oncology (Huntingt) 1997;11:1133-9;
discussion 1139-40, 1143.
76. Hoisaeter PA, Rasmussen F. The Scandinavian Prostatic Cancer
Group. Scand J Clin Lab Invest Suppl 1985;179:7-11
77. Waymont B, Lynch TH, Dunn J, Bathers S, Wallace DM. Treatment
preferences of urologists in Great Britain and Ireland in the
management of prostate cancer. Br J Urol 1993;71:577-82.
78. Adami H-O, Baron JA, Rothman KJ. Ethics of a prostate cancer
screening trial. Lancet 1994;343:958-60.
79. Olsson CA, Goluboff ET. Detection and treatment of prostate
cancer: perspective of the urologist. J Urol 1994;152(5 Pt 2):1695-9.
81. Howe RJ. Prostate cancer: a patient's perspective. J Urol
1994;152(5 Pt 2):1700-3.
78. Litwin MS, deKernion JB. Perspectives on the problem of
prostate cancer [editorial]. J Urol 1994;152(5 Pt 2):1680-1.
82. Panel discussion on prostate cancer screening. J Urol 1994;152(5
Pt 2):1704-6.
83. Pauker SG, Kassirer JP. Contentious screening decisions:
does the choice matter? [editorial]. N Engl J Med 1997;336:1243-4.
84. Wald N. Ethical issues in randomised prevention trials.
BMJ 1993;306:563-5.
85. Collins MM, Barry MJ. Controversies in prostate cancer screening:
analogies to the early lung cancer screening debate. JAMA 1996;276:1976-9.
86. Woolf SH. Screening for prostate cancer [letter]. Lancet
1997;349:1098-9.
87. Fletcher SW. Whither scientific deliberation in health policy
recommendations? Alice in the Wonderland of breast-cancer screening.
[editorial]. N Engl J Med 1997;336:1180-3.
88. Woolf SH. Should we screen for prostate cancer? [editorial].
BMJ 1997;314:989-90.
89. The prostate question, unanswered still [editorial]. Lancet
1997;349:443.
90. Polizzi CM. Issues in cancer screening: a prostate case
study. Jurimetrics 1995;36:33-58.