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Information from PDQ -- for Health Professionals
Screening for bladder cancer
208/10681
** SUMMARY OF EVIDENCE **
There is insufficient evidence to determine whether a decrease in mortality
from bladder cancer occurs with hematuria testing, urinary cytology testing, or
a variety of other tests on exfoliated urinary cells or other urinary
substances.
Level of Evidence for preceding statement: 5
Opinions of respected authorities based on clinical experience,
descriptive studies, or reports of expert committees.
** SIGNIFICANCE **
-- Incidence and Mortality --
Bladder cancer is the sixth most commonly diagnosed malignancy in the United
States. Approximately 56,500 new cases are expected to be diagnosed in
2002.[1] Bladder cancer is more than 2.5 times more likely to be diagnosed in
men than women, and occurs almost twice as often in whites as in blacks of
either gender. The incidence of bladder cancer among other ethnic and racial
groups within the United States falls between that of blacks and whites. The
incidence of bladder cancer increases with age. Approximately 80% of newly
diagnosed cases in both men and women occur in people aged 60 years and
older.[1]
It is estimated that 12,600 Americans will die of bladder cancer in 2002.[1]
Females are approximately twice as likely as males to die from the disease. A
greater percentage of females are diagnosed at more advanced stages than men,
which may contribute to the higher case mortality rate in women.[2,3] In
addition to relative delays in diagnoses among women,[4] other factors
contributing to the higher death rate may include the higher portion of
nontransitional cell cancer histologies that occur in women; the relative
thinness of the elderly adult female bladder (perhaps permitting more rapid
extravesical spread); possible differences in the relative proportion of higher
grade transitional cell carcinomas between men and women; and the older median
age at presentation in women than men.
Blacks who develop bladder cancer are approximately twice as likely as whites
to die from the disease. Blacks are also diagnosed at more advanced stages of
bladder cancer than whites.[2,5] They have poorer survivals than whites for
each stage.[2] While some of these statistics may reflect intragroup stage
migration, there may also be yet-to-be-elucidated host and disease biological
variables between the races that contribute to these survival differences.
More than twice as many blacks (10.9%) as whites (5.4%) diagnosed with bladder
cancer receive no treatment for their disease, which may also play a role.[2]
The age-adjusted mortality has decreased in both races and genders over the
past 30 years.[6] These changes may reflect earlier diagnosis, better therapy,
or both.
-- Risk Factors --
Several populations with a variety of exposures appear to be at higher risk for
developing bladder cancer. By far the greatest known environmental risk factor
in the general population is cigarette smoking, with individuals who smoke
having a fourfold to sevenfold increased risk of developing bladder cancer than
individuals who have never smoked.[7-9] Risk is reduced with cessation of
smoking, but a relatively small decrease in incidence is seen for the first 5
to 7 years after cessation. Even after 10 years, the risk of an individual
developing bladder cancer is still almost twice that of an individual who has
never smoked.
Among the chemicals implicated in smoking-induced bladder cancer are
aminobiphenyl and its metabolites.[10] It is possible that inherited and
inducible enzymes are important in the activation and detoxification of
aminobiphenyls and other putative bladder carcinogens. These enzymes include
N-acetyltransferase 2 (NAT2),[11] cytochrome P450 1A2 (CYT 1A2),[12] and
glutathione S-transferase M 1.[13] Several studies have indicated that
specific genotypes and phenotypes of these enzymes and their activities,
particularly in the liver and urothelium, are associated with susceptibility to
smoking-induced bladder cancer and bladder cancer induced by other aryl amines,
particularly in industrially exposed populations.[11-16] Not all of these
studies, however, have been well controlled for active or former smoking
histories.
A variety of industrial exposures have also been implicated as risk factors for
developing bladder cancer, primarily aromatic amines present in the production
of dyes, and benzidine and its derivatives,[17] combustion gases and soot from
coal, possibly chlorinated aliphatic hydrocarbons,[18] chlorination by-products
in heated water,[19] and certain aldehydes (e.g., acrolein used in chemical
dyes and in the rubber and textile industries).[20]
Occupations reported to be associated with an increased risk of bladder cancer
include those that involve organic chemicals such as dry cleaners, paper
manufacturers, rope and twine makers, and workers in apparel
manufacturing.[17-20]
Additional risk factors that predispose an individual to more aggressive forms
of bladder cancer include prolonged exposures to urinary foreign bodies and
infections;[21] Schistosoma hematobium (Bilharzial) bladder infections;[22]
exposure to cyclophosphamide [23-26] and perhaps other alkylating agents
such as ifosfamide (although the use of mesna in conjunction with these agents
has reduced the incidence);[27] and pelvic radiation therapy for other
malignancies.[28-30] Renal transplant recipients appear to have an increased
incidence of bladder cancer.[31] Individuals with chronic acetaminophen and
phenacetin exposure have a higher incidence of urothelial cancer, more often in
the upper urinary tract [32] than in the bladder.[33,34]
It is estimated that 5% to 15% of patients in the United States who eventually
die from bladder cancer will have strong exposure histories to the above-named
environmental factors (other than smoking).[35]
-- Inheritance --
Although occasional familial clusters have been anecdotally reported [36-38]
and bladder cancer (as well as upper tract transitional cell carcinoma) is part
of the Lynch family cancer syndrome II,[39] there is no evidence that
tendencies towards developing bladder cancer are inherited.[40]
-- Clinical Presentation --
Approximately 85% of bladder cancers are diagnosed because they cause
microscopic or grossly visible hematuria.[41] Fewer than 5% of cases present
with constitutional symptoms of metastatic disease, and microscopic or gross
hematuria is also present in the majority of these cases.[42] Very few bladder
cancers are detected because of incidental discovery during cystoscopy for
other diseases; most commonly this occurs during the evaluation of suspected
benign or malignant prostatic diseases.[43,44] Part of the hematuria
evaluation, cystoscopy, indicates that the disease is present; it is then
histologically confirmed by transurethral biopsy or resection (TURBT).
-- Histopathology --
More than 90% of bladder cancers diagnosed in the United States are pure
transitional cell carcinomas (TCCs) or TCCs mixed with other histologies,
primarily squamous cell carcinoma, adenocarcinoma, or both. An additional 3%
to 4% are pure squamous cell carcinomas, which are approximately twice as
likely to occur in women as men. Squamous cell carcinomas also represent a
greater proportion of bladder cancers occurring in individuals who have
Schistosoma hematobium infections of the bladder or who have histories of
long-term indwelling urinary catheters, bladder stones, or recurrent bladder
infections.[23,45,46]
Both the grade and stage at diagnosis of TCC have extremely important
prognostic and therapeutic implications. Nontransitional cell histologies,
however, all behave very aggressively and, in general, are less responsive to
treatments other than extirpative surgery.[47] In general, the prognoses of
patients and the choice of treatments depend on the aggressiveness and grade of
the tumor.
Grade and Stage of Newly Diagnosed Bladder Cancer in an Unscreened Population
Although the critical nature of the histologic grade and stage of index lesions
for individual prognosis and management decisions has been well recognized for
many years, only 1 contemporary study has attempted to evaluate grade and stage
in newly diagnosed bladder tumors in a population-based setting.[48] In this
study, 89% of all newly diagnosed bladder cancers in men aged 50 years and
older reported to the state of Wisconsin tumor registry in calendar year 1988
had blocks and slides reviewed by a single pathologist who did not know the
original diagnoses. Fifty-seven percent of specimens were grade I or II, stage
Ta or T1 TCCs; 19% were grade III, stage Ta or T1 (or TIS) TCCs; and 24% were
muscularis propria invading or deeper (Stage T2+), almost all of which were
grade III lesions or of nontransitional cell histologies. Because of
Wisconsin's small population of black males aged 50 years and older (fewer than
3% of all bladder cancers occurred in nonwhites),[49] differences in grade and
stage at presentation between blacks and whites could not be determined.
Similarly, this study did not look at females or at males younger than 50
years. No other population-based studies have been published that include
central pathology review of grade and stage of bladder tumors at presentation,
with subdivisions of superficial and muscle-invasive lesions. Because of
variability in histological interpretations of bladder cancers recorded by
tumor registries,[47,50] the presenting grade and stage of this malignancy in
Wisconsin is known only for males aged 50 years and older.
References:
1. American Cancer Society: Cancer Facts and Figures-2002. Atlanta, Ga:
American Cancer Society, 2002.
2. Fleshner NE, Herr HW, Stewart AK, et al.: The National Cancer Data Base
report on bladder carcinoma. Cancer 78(7): 1505-1512, 1996.
3. Kiemeney LA, Coebergh JW, Koper NP, et al.: Bladder cancer incidence and
survival in the south-eastern part of The Netherlands, 1975-1989.
European Journal of Cancer 30A(8): 1134-1137, 1994.
4. Mansson A, Anderson H, Colleen S: Time lag to diagnosis of bladder
cancer--influence of psychosocial parameters and level of health-care
provision. Scandinavian Journal of Urology and Nephrology 27(3):
363-369, 1993.
5. Mayer WJ, McWhorter WP: Black/white differences in non-treatment of
bladder cancer patients and implications for survival. American Journal
of Public Health 79(6): 772-775, 1989.
6. National Cancer Institute: 1987 Annual Cancer Statistics Review.
Including Cancer Trends: 1950-1985. Bethesda, Md: NIH Publication No.
88-2789, 1988.
7. Morrison AS: Advances in the etiology of urothelial cancer. Urologic
Clinics of North America 11(4): 557-566, 1984.
8. Burch JD, Rohan TE, Howe GR, et al.: Risk of bladder cancer by source and
type of tobacco exposure: a case-control study. International Journal
of Cancer 44(4): 622-628, 1989.
9. Clavel J, Cordier S, Boccon-Gibod L, et al.: Tobacco and bladder cancer
in males: increased risk for inhalers and smokers of black tobacco.
International Journal of Cancer 44(4): 605-610, 1989.
10. Hoffmann D, Masuda Y, Wynder EL: Alpha-naphthylamine and
beta-naphthylamine in cigarette smoke. Nature 221: 254-256, 1969.
11. Risch A, Wallace DM, Bathers S, et al: Slow N-acetylation genotype is a
susceptibility factor in occupational and smoking related bladder
cancer. Human Molecular Genetics 4(2): 231-236, 1995.
12. Horn EP, Tucker MA, Lambert G, et al.: A study of gender-based cytochrome
P4501A2 variability: a possible mechanism for the male excess of bladder
cancer. Cancer Epidemiology, Biomarkers and Prevention 4(5): 529-533,
1995.
13. Bell DA, Taylor JA, Paulson DF, et al.: Genetic risk and carcinogen
exposure: a common inherited defect of the carcinogen-metabolism gene
glutathione S-transferase M1 (GSTM1) that increases susceptibility to
bladder cancer. Journal of the National Cancer Institute 85(14):
1159-1164, 1993.
14. Lower GM, Nilsson T, Nelson CE, et al.: N-acetyltransferase phenotype and
risk in urinary bladder cancer: approaches in molecular epidemiology.
Preliminary results in Sweden and Denmark. Environmental Health
Perspectives 29: 71-79, 1979.
15. Cartwright RA, Glashan RW, Rogers HJ, et al.: Role of N-acetyltransferase
phenotypes in bladder carcinogenesis: a pharmacogenetic epidemiological
approach to bladder cancer. Lancet 2(8303): 842-846, 1982.
16. Hanke J, Krajewska B: Acetylation phenotypes and bladder cancer. Journal
of Occupational Medicine 32(9): 917-918, 1990.
17. Morrison AS, Cole P: Epidemiology of bladder cancer. Urologic Clinics of
North America 3(1): 13-29, 1976.
18. Steineck G, Plato N, Norell SE, et al.: Urothelial cancer and some
industry-related chemicals: an evaluation of the epidemiologic
literature. American Journal of Industrial Medicine 17(3): 371-391,
1990.
19. King WD, Marrett LD: Case-control study of bladder cancer and
chlorination by-products in treated water (Ontario, Canada). Cancer
Causes and Control 7(6): 596-604, 1996.
20. Stadler WM: Molecular events in the initiation and progression of bladder
cancer (review). International Journal of Oncology 3: 549-557, 1993.
21. Sturgeon SR, Hartge P, Silverman DT, et al.: Associations between bladder
cancer risk factors and tumor stage and grade at diagnosis.
Epidemiology 5(2): 218-225, 1994.
22. Lucas SB: Squamous cell carcinoma of the bladder and schistosomiasis.
East African Medical Journal 59(5): 345-351, 1982.
23. O'Keane JC: Carcinoma of the urinary bladder after treatment with
cyclophosphamide. New England Journal of Medicine 319(13): 871, 1988.
24. Tuttle TM, Williams GM, Marshall FF: Evidence for
cyclophosphamide-induced transitional cell carcinoma in a renal
transplant patient. Journal of Urology 140(5): 1009-1011, 1988.
25. Durkee C, Benson R Jr: Bladder cancer following administration of
cyclophosphamide. Urology 16(2): 145-148, 1980.
26. Cohen SM, Garland EM, St. John M, et al.: Acrolein initiates rat urinary
bladder carcinogenesis. Cancer Research 52(13): 3577-3581, 1992.
27. Habs MR, Schmahl D: Prevention of urinary bladder tumors in
cyclophosphamide-treated rats by additional medication with the
uroprotectors sodium 2-mercaptoethane sulfonate (mesna) and disodium
2,2'-dithio-bis-ethane sulfonate (dimesna). Cancer 51(4): 606-609,
1983.
28. Duncan RE, Bennett DW, Evans AT, et al.: Radiation-induced bladder
tumors. Journal of Urology 118(1 pt 1): 43-45, 1977.
29. Sella A, Dexeus FH, Chong C, et al.: Radiation therapy-associated
invasive bladder tumors. Urology 33(3): 185-188, 1989.
30. Quilty PM, Kerr GR: Bladder cancer following low or high dose pelvic
irradiation. Clinical Radiology 38(6): 583-585, 1987.
31. Buzzeo BD, Heisey DM, Messing EM: Bladder cancer in renal transplant
recipients. Urology 50(4): 525-528, 1997.
32. Steffens J, Nagel R: Tumours of the renal pelvis and ureter.
Observations in 170 patients. British Journal of Urology 61(4):
277-283, 1988.
33. Piper JM, Tonascia J, Matanoski GM: Heavy phenacetin use and bladder
cancer in women aged 20 to 49 years. New England Journal of Medicine
313(5): 292-295, 1985.
34. Derby LE, Jick H: Acetaminophen and renal and bladder cancer.
Epidemiology 7(4): 358-362, 1996.
35. Cole P, Hoover R, Friedell GH: Occupation and cancer of the lower urinary
tract. Cancer 29(5): 1250-1260, 1972.
36. Fraumeni JF Jr, Thomas LB: Malignant bladder tumors in a man and his
three sons. JAMA: Journal of the American Medical Association 201(7):
97-99, 1967.
37. Aherne G: Retinoblastoma associated with other primary malignant tumours.
Transactions of the Ophthalmological Societies of the United Kingdom
94(4): 938-944, 1974.
38. McCullough DL, Lamma DL, McLaughlin AP III, et al.: Familial transitional
cell carcinoma of the bladder. Journal of Urology 113(5): 629-635,
1975.
39. Lynch HT, Ens JA, Lynch JF: The Lynch syndrome II and urological
malignancies. Journal of Urology 143(1): 24-28, 1990.
40. Kiemeney LA, Moret NC, Witjes JF, et al.: Familial aggregation of
transitional cell carcinoma of the urinary tract. Proceedings of the
American Urological Association 155(suppl): A-1520, 691a, 1996.
41. Varkarakis MJ, Gaeta J, Moore RH, et al.: Superficial bladder tumor.
Aspects of clinical progression. Urology 4(4): 414-420, 1974.
42. Messing EM, Vaillancourt A: Hematuria screening for bladder cancer.
Journal of Occupational Medicine 32(9): 838-845, 1990.
43. Kim ED, Ignatoff JM: Unsuspected bladder carcinoma in patients undergoing
radical prostatectomy. Journal of Urology 152(2 pt 1): 397-400, 1994.
44. Wasson JH, Reda DJ, et al, for the Veterans Affairs Cooperative Study
Group on Transurethral Resection of the Prostate: A comparison of
transurethral surgery with watchful waiting for moderate symptoms of
benign prostatic hyperplasia. New England Journal of Medicine 332(2):
75-79, 1995.
45. Kantor AF, Hartge P, Hoover RN, et al.: Urinary tract infection and risk
of bladder cancer. American Journal of Epidemiology 119(4): 510-515,
1984.
46. Locke JR, Hill DE, Walzer Y: Incidence of squamous cell carcinoma in
patients with long-term catheter drainage. Journal of Urology 133(6):
1034-1035, 1985.
47. Messing EM, Catalona W: Urothelial tumors of the urinary tract. In:
Walsh PC, Retik AB, Vaughan ED, et al., eds.: Campbell's Urology. 7th
ed., Philadelphia: W.B. Saunders, 1998, pp 2327-2410.
48. Messing EM, Young TB, Hunt VB, et al.: Comparison of bladder cancer
outcome in men undergoing hematuria home screening versus those with
standard clinical presentations. Urology 45(3): 387-397, 1995.
49. Briggs NC, Young TB, Gilchrist KW, et al.: Age as a predictor of an
aggressive clinical course for superficial bladder cancer in men.
Cancer 69(6): 1445-1451, 1992.
50. Lynch CF, Platz CE, Jones MP, et al.: Cancer registry problems in
classifying invasive bladder cancer. Journal of the National Cancer
Institute 83(6): 429-433, 1991.
** EVIDENCE OF BENEFIT **
Almost all bladder malignancies originate on the uroepithelial surface. The
majority of patients who die from bladder cancer do so from metastatic disease;
treatment for metastatic bladder cancer is rarely, if ever, curative.[1] The
overwhelming majority of patients with metastases have concomitant or prior
muscularis propria (stage T2+) invading lesions.[2] Approximately 90% of
patients with muscularis propria invading bladder cancer present with this
diagnosis, however,[3,4] and do not come from the much larger pool of patients
with recurring superficial transitional cell carcinomas (TCCs). The goal of
screening is the early detection of bladder cancer that is destined to become
muscle invading. Although one study reports that approximately 30% of patients
with superficial TCC followed for 20 years will eventually die from this
disease,[5] these data remain unconfirmed, are at odds with other reports,[6]
and may reflect outmoded patterns of diagnosis, classification, and management.
Because bladder cancer is almost never incidentally found at autopsy, the
preclinical duration in which it has not yet caused symptoms, but in which it
can be detected by cystoscopy, is probably brief. This rapid growth rate is
supported by clinical experience [7] and implies that screening would have to
be performed at frequent intervals.
-- Screening Methods --
Cystoscopy and cytology
The use of cystoscopies and bladder wash/urinary cytologic examinations has
proven quite successful in the surveillance and management of patients with
previously treated bladder cancers.[8] These means are not practical, however,
because of expense, morbidity, and reluctance in individuals without a history
of bladder cancer.
One-time hematuria testing
Two groups have reported on the use of testing a single urine specimen for
blood to detect urologic malignancies, serious urinary tract diseases, and
bladder cancers. Both studies were performed retrospectively to ascertain
information from patients who were seen at a large multispecialty clinic [9] or
who subscribed to a large health maintenance organization (HMO) and were tested
in a "multi-phasic screening."[10] Because of the retrospective nature of each
study, neither was designed to specifically look for bladder cancer detection
or to focus on the population at highest risk (men aged 50 years and older).
Both studies concluded that single hematuria testing was not effective in
diagnosing bladder cancer. A longer follow-up of the HMO study indicated that
individuals with microhematuria were at a higher risk for subsequent
development of muscle-invading bladder cancer, with a latency of 3.5 to 14.5
years.[11] There is insufficient evidence to indicate that single hematuria
testing is effective in screening for bladder cancer, and there is no evidence
that single hematuria testing results in reduced mortality from the disease.
Repetitive hematuria testing
Two studies using Ames Hemastix, a chemical reagent strip for hemoglobin that
correlates with microscopic urinalysis in detecting hematuria,[12] were
conducted in geographically defined (Madison, Wisconsin and Leeds, England)
populations of middle-aged and elderly men using repetitive home reagent strip
testing. In each program, subjects were solicited from patient care
registries. Men with histories of previous urologic malignancies or known
causes of hematuria or who were noncompliant were eliminated. In the 4 studies
performed (1 pilot study and 1 larger study at each site), 45% to 55% of
solicited individuals took part. In these studies, 1.2% to 1.3% of all
participants were found to have bladder cancer (all TCC). Only 1 of the 21
patients in the first study [7,12,13] and none of the 26 detected in the second
study had stage T2 or greater malignancy. As a limitation of repetitive
hematuria screening in a general population of men aged 50 years and older,
more than 90% of individuals with positive tests upon initial work-up were
found not to have bladder cancer.[12] In the Wisconsin hematuria screening
studies, all subjects who were hematuria positive with negative work-ups or who
were found to have no serious disease were followed up at least for 24 months,
with no findings of developing bladder cancer. Similarly, at least 18 months
after their last testing, no screening participant (with or without hematuria)
had died of bladder cancer. It is possible that longer follow-up is necessary
to prove that these participants did not have bladder cancer;[11] such studies
are not, however, available. The relatively low positive predictive value of
repetitive hematuria testing (7.6% for bladder cancer and 11.6% for all
malignancies)[12-14] raises questions about the practicality of this mode of
screening.
The accuracy of voided urine cytology in detecting bladder cancer has been
evaluated primarily in patients with histories of bladder cancer who are
undergoing cystoscopic surveillance, or as a routine test performed in all
patients attending a large urology office in a multispecialty clinic. In the
studies of patients with histories of bladder cancer, voided urinary cytology
was effective in diagnosing 20% to 40% of grade I TCCs, 20% to 50% of grade II
malignancies, and 60% to 80% of grade III/TIS cancers.[15,16] Although such
studies were not performed in subjects without either hematuria or histories of
recurrent bladder tumors, a major concern for screening purposes is the lack of
sensitivity for well-differentiated and moderately differentiated TCCs and the
large proportion of specimens in which an insufficient number of cells were
present for any cytologic diagnosis to be offered. Although false positives
were exceedingly rare, the lack of sensitivity even in this highly suspect
population make voided urine cytology an inappropriate test for screening the
general population. No studies have looked at outcome of cytologic screening
on disease-related mortality in a nonindustrially exposed population. Outcomes
of patients screened at the urology clinic are also not available.[15]
The outcomes of men diagnosed with bladder cancer through a hematuria screening
program were compared with a statewide population-based sample from the
Wisconsin tumor registry.[13] Histologic sections were blindly reviewed,
finding a similar stage distribution but a significantly increased fraction of
patients with grade III (high-grade) disease. At 24 months, 16% of tumor
registry patients had died from bladder cancer (including 35% of those with
grade III lesions); however, at 3 to 8 years of follow-up, no screened patient
had died of bladder cancer. Whether these differences resulted from a
lead-time effect, other biases, or a screening effect cannot be determined.
A variety of urinary antigens, growth factors and/or their receptors, or DNA
analyzed by flow cytometry or image analysis, by in situ hybridization, or by
molecular techniques, have been proposed as ways to diagnose bladder
cancer.[17-30] None of these methods, however, have been sufficiently tested
in a screening setting of the general population (without a history of bladder
cancer) to assess their operational performance and utility in reducing bladder
cancer mortality.
Lewis X immunocytology,[17] microsatellite repeat analysis,[27] and ImmunoCyt
have not been tested in a population of individuals without bladder cancer
histories or a population with findings suggestive of bladder cancer; their
performance in a screening setting is unknown.
-- Special Populations --
In populations at particularly high risk for developing bladder cancer (other
than those with histories of bladder cancer), few screening studies that have
assessed bladder cancer mortality have been published.[31-34] A study of
annual cytology in aluminum workers exposed to coal tar pitch in Quebec showed
a nearly 40% reduction in bladder cancer mortality 6 years after diagnosis,
compared to a historical control group of workers from the same plants who were
not screened;[35] the difference, however, was not statistically significant.
Awareness of adverse outcome in the unscreened predecessors may have influenced
participation in the program and workers' awareness of symptoms, the
willingness of workers and physicians to initiate diagnostic investigations
based on signs and symptoms, and the compliance of workers with medical
recommendations for evaluation and treatment. The brief duration of follow-up
in the screened group may have artifactually improved the outcome.
No randomized controlled bladder cancer screening trials have been conducted in
environmentally or industrially exposed cohorts. Completed studies have
usually not had comparable control groups, have not been of sufficient sample
size to show an effect on outcome, and have been of insufficient length to show
a mortality benefit (or lack thereof) for the modality(ies) being
assessed.[32,33]
References:
1. Saxman SB, Propert KJ, Einhorn LH, et al.: Long-term follow-up of a phase
III intergroup study of cisplatin alone or in combination with
methotrexate, vinblastine, and doxorubicin in patients with metastatic
urothelial carcinoma: a cooperative group study. Journal of Clinical
Oncology 15(7): 2564-2569, 1997.
2. Jewett HJ, Strong GH: Infiltrating carcinoma of the bladder: relation of
depth of penetration of the bladder wall to incidence of local extension
and metastases. Journal of Urology 55: 366-372, 1946.
3. Kaye KW, Lange PH: Mode of presentation of invasive bladder cancer:
reassessment of the problem. Journal of Urology 128(1): 31-33, 1982.
4. Hopkins SC, Ford KS, Soloway MS: Invasive bladder cancer: support for
screening. Journal of Urology 130(1): 61-64, 1983.
5. Holmang S, Hedelin H, Anderstrom C, et al.: The relationship among
multiple recurrences, progression and prognosis of patients with stages
Ta and T1 transitional cell cancer of the bladder followed for at least
20 years. Journal of Urology 153(6): 1823-1827, 1995.
6. Prout GR Jr, Barton BA, et al, for the National Bladder Cancer Group:
Treated history of noninvasive grade 1 transitional cell carcinoma.
Journal of Urology 148(5): 1413-1419, 1992.
7. Messing EM, Young TB, Hunt VB, et al.: Hematuria home screening: repeat
testing results. Journal of Urology 154(1): 57-61, 1995.
8. Whelan P, Britton JP, Dowell AC: Three-year follow-up of bladder tumours
found on screening. British Journal of Urology 72(6): 893-896, 1993.
9. Mohr DN, Offord KP, Owen RA, et al.: Asymptomatic microhematuria and
urologic disease. A population-based study. JAMA: Journal of the
American Medical Association 256(2): 224-229, 1986.
10. Hiatt RA, Ordonez JD: Dipstick urinalysis screening, asymptomatic
microhematuria, and subsequent urological cancers in a population-based
sample. Cancer Epidemiology, Biomarkers and Prevention 3(5): 439-443,
1994.
11. Friedman GD, Carroll PR, Cattolica EV, et al.: Can hematuria be a
predictor as well as a symptom or sign of bladder cancer? Cancer
Epidemiology, Biomarkers and Prevention 5(12): 993-996, 1996.
12. Messing EM, Young TB, Hunt VB, et al.: The significance of asymptomatic
microhematuria in men 50 or more years old: findings of a home screening
study using urinary dipsticks. Journal of Urology 137(5): 919-922,
1987.
13. Messing EM, Young TB, Hunt VB, et al.: Comparison of bladder cancer
outcome in men undergoing hematuria home screening versus those with
standard clinical presentations. Urology 45(3): 387-397, 1995.
14. Kiemeney LA, Coebergh JW, Koper NP, et al.: Bladder cancer incidence and
survival in the south-eastern part of The Netherlands, 1975-1989.
European Journal of Cancer 30A(8): 1134-1137, 1994.
15. Rife CC, Farrow GM, Utz DC: Urine cytology of transitional cell
neoplasms. Urologic Clinics of North America 6(3): 599-612, 1979.
16. Murphy WM, Rivera-Ramirez I, Medina CA, et al.: The bladder tumor antigen
(BTA) test compared to voided urine cytology in the detection of bladder
neoplasms. Journal of Urology 158(6): 2102-2106, 1997.
17. Golijanin D, Sherman Y, Shapiro A, et al.: Detection of bladder tumors by
immunostaining of the Lewis X antigen in cells from voided urine.
Urology 46(2): 173-177, 1995.
18. Grossman HB, Washington RW Jr, Carey TE, et al.: Alterations in antigen
expression in superficial bladder cancer. Journal of Cellular
Biochemistry. Supplement 16I: 63-68, 1992.
19. Fradet Y, Tardif M, et al, and the Laval University Urology Group:
Clinical cancer progression in urinary bladder tumors evaluated by
multiparameter flow cytometry with monoclonal antibodies. Cancer
Research 50(2): 432-437, 1990.
20. Huland E, Huland H, Meier T, et al.: Comparison of 15 monoclonal
antibodies against tumor-associated antigens of transitional cell
carcinoma of the human bladder. Journal of Urology 146(6): 1631-1636,
1991.
21. D'Hallewin MA, Baert L: Initial evaluation of the bladder tumor antigen
test in superficial bladder cancer. Journal of Urology 155(2): 475-476,
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Date Last Modified: 05/2002
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