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Abramson Cancer Center 
NCI CANCERLIT® Search: Diagnosis-Histopathology-Pathogenesis of Bladder Cancer - August 2002
National Cancer Institute®
Ultima Vez Modificado: 1 de agosto del 2002
- Establishment of a mini-gene expression database for bladder tumor.
- Novel chromosome findings in bladder cancer cell lines detected with multiplex fluorescence in situ hybridization.
- Cytologic evaluation of urine is important in evaluation of chronic prostatitis.
- Prostate cancer involving the bladder neck: recurrence-free survival and implications for AJCC staging modification. American Joint Committee on
- Comparison of WHO/ISUP and WHO classification of noninvasive papillary urothelial neoplasms for risk of progression.
- p14ARF promoter hypermethylation in plasma DNA as an indicator of disease recurrence in bladder cancer patients.
- Genome-wide study of gene copy numbers, transcripts, and protein levels in pairs of non-invasive and invasive human transitional cell
- The association of death-associated protein kinase hypermethylation with early recurrence in superficial bladder cancers.
- Prognostic value of matrix metalloproteinase-2 and tissue inhibitor of metalloproteinase-2 in bladder carcinoma.
- Comparative evaluation of the nuclear matrix protein, fibronectin, urinary bladder cancer antigen and voided urine cytology in the
- Clinical use of urinary markers for the detection and prognosis of bladder carcinoma: a comparison of immunocytology with monoclonal
- Interleukin-6 production by human bladder tumor cell lines is up-regulated by bacillus Calmette-Guerin through nuclear factor-kappaB
- [Fluorescent cystoscopy in diagnosing and treating superficial cancer of the urinary bladder]
- Molecular aspects of bladder cancer III. Prognostic markers of bladder cancer.
- Qualitative and quantitative detection of urinary human complement factor H-related protein (BTA stat and BTA TRAK) and fragments of
- Current concepts of tumor markers in bladder cancer.
- Delay and survival in bladder cancer.
- [Endoscopic diagnosis and treatment of superficial bladder tumors]
- [Assessment of loco-regional extension of superficial bladder tumors]
- [Bladder diverticulum and superficial bladder tumors]
- [Pathologic anatomy of superficial tumors of the bladder]
- [Quality criteria in urinary cytology for tumor diagnosis]
- [Etiologies of superficial bladder tumors]
- [Descriptive epidemiology of superficial bladder tumors]
- [Natural history of superficial bladder tumors]
- [Diagnosis of superficial bladder tumors]
- A prospective study on active and environmental tobacco smoking and bladder cancer risk (The Netherlands).
- Alcohol drinking and bladder cancer.
Table of Contents
1
UI - 12099200
AU - Li C; Chen CC; Yang TH; Tzai TS; Huang CH; Liou JT; Su IJ; Tzeng CC;
TI -
Chiu AW; Shieh B
Establishment of a mini-gene expression database for bladder tumor.
SO - J Formos Med Assoc 2002 Feb;101(2):104-9
AD - Institute of Molecular Medicine, National Cheng Kung University Medical
College, Tainan.
BACKGROUND AND PURPOSE: Transitional cell carcinoma has been diagnosed
mostly in urinary bladder in southern Taiwan and has an exceptionally
high mortality rate. To identify the genes associated with bladder
cancer, we investigated differential gene expression. Six bladder tumor
cDNA libraries were constructed and their sequences were compared and
analyzed. METHODS: mRNA from bladder tumor cell lines or tissue samples
were used to construct two regular cDNA libraries and four subtractive
cDNA libraries after subtractive hybridization with cDNA derived from
normal bladder epithelial cells. Subsequently, more than 100 cDNA
inserts from each library were randomly isolated and sequenced, followed
by sequence comparisons with nucleotide and protein sequence databases.
RESULTS: After searching the Basic Local Alignment Search Tool (Blast)
databases, the cDNA nucleotide sequences were grouped into novel, known,
and common gene categories. Since tumor nucleotide sequences are
informative and valuable for research, they were organized as a
mini-gene expression database (http://bladder.nhri.org.tw/).
Interestingly, in one subtractive cDNA library, the ATPase 6 gene was
found to be highly expressed in normal bladder epithelial cells and
elevated levels of ATPase 6 mRNA were later confirmed by reverse
transcription-polymerase chain reaction. However, the role of ATPase 6
in bladder tumorigenesis remains to be investigated. CONCLUSIONS: The
establishment of this database is an important step to enable systematic
screening for bladder tumor-associated genes and may also be useful in
developing diagnostic and/or therapeutic applications.
2
UI - 12127398
AU - Strefford JC; Lillington DM; Steggall M; Lane TM; Nouri AM; Young BD;
TI -
Oliver RT
Novel chromosome findings in bladder cancer cell lines detected with
multiplex fluorescence in situ hybridization.
SO - Cancer Genet Cytogenet 2002 Jun;135(2):139-46
AD - Imperial Cancer Research Fund (ICRF) Medical Oncology Unit, Queen Mary
and Westfield College, Charterhouse Square, Smithfield, London, UK.
j.strefford@icrf.icnet.uk
Bladder cancer is a common neoplasm worldwide, consisting mainly of
transitional cell carcinomas, while squamous, adenocarcinoma, and
sarcomatoid bladder cancers account for the remaining cases. In the
present study, multiplex fluorescence in situ hybridization (M-FISH) has
been used to characterize chromosome rearrangements in eight
transitional and one squamous cell carcinoma cell line, RT112, of
UMUC-3, 5637, CAT(wil), FGEN, EJ28, J82, 253J, and SCaBER. Alterations
of chromosome 9 are the most frequent cytogenetic and molecular findings
in transitional cell carcinomas of all grades and stages, while changes
of chromosomes 3, 4, 8, 9, 11, 14, and 17 are also frequently observed.
In the present study, alterations previously described, including
del(8)(p10), del(9)(p10), del(17)(p10), and overrepresentation of
chromosome 20, as well as several novel findings, were observed. These
novel findings were a del(15)(q15) and isochromosome 14q, both occurring
in three of nine cell lines examined. These abnormalities may reflect
changes in bladder tumor biology. M-FISH represents an effective
preliminary screening tool for the characterization of complex tumor
karyotypes.
3
UI - 12137814
AU - Nickel JC; Ardern D; Downey J
TI -
Cytologic evaluation of urine is important in evaluation of chronic
prostatitis.
SO - Urology 2002 Aug;60(2):225-7
AD - Department of Urology, Queen's University, Kingston General Hospital,
Kingston, Ontario, Canada.
OBJECTIVES: Cytologic examination of the urine has not been a
recommended part of the diagnostic workup for patients presenting with
chronic prostatitis. We identified 3 patients referred to our tertiary
Prostatitis Research Clinic who had carcinoma in situ of the bladder
discovered after evaluation of urine cytology. METHODS: One hundred
fifty consecutive patients referred to the Queen's University
Prostatitis Clinic during 2000 and 2001 underwent extensive evaluation,
including collection of urine specimen for cytologic examination if they
also had symptoms compatible with interstitial cystitis (urinary
frequency, urgency, and suprapubic pain). RESULTS: Three patients, who
were referred to our tertiary prostatitis clinic after being evaluated
and treated by other urologists for an average of 3.5 years for chronic
prostatitis, were eventually diagnosed with carcinoma in situ of the
bladder. The patients were older than the average patient referred to
our specialized clinic (average age 61 years compared with 42 years for
the average patient). All 3 patients complained of pain (suprapubic
and/or perineal) and irritative voiding symptoms, and 2 had dysuria.
Only 1 of these patients had microscopic hematuria. CONCLUSIONS: We
recommend that urine cytology become a diagnostic test for men
presenting with prostatitis-like symptoms, particularly if the symptom
complex includes irritative voiding symptoms, dysuria, and
suprapubic/bladder pain.
4
UI - 12137826
AU - Dash A; Sanda MG; Yu M; Taylor JM; Fecko A; Rubin MA
TI -
Prostate cancer involving the bladder neck: recurrence-free survival and
implications for AJCC staging modification. American Joint Committee on
Cancer.
SO - Urology 2002 Aug;60(2):276-80
AD - Department of Urology, University of Michigan School of Medicine, Ann
Arbor, Michigan 48109, USA.
OBJECTIVES: In the American Joint Committee on Cancer (AJCC) TNM staging
system, prostate cancer involving the bladder neck after radical
prostatectomy is considered pT4 disease, suggesting a high risk of
recurrence. The recurrence risk with pathologic invasion of the bladder
neck, however, has not been definitively compared with that associated
with extra-organ disease. We therefore compared the recurrence risk in
cases with bladder neck involvement with that of cases with
extraprostatic extension and/or seminal vesicle invasion. METHODS: The
study cohort was composed of 1123 men with clinically localized prostate
cancer treated with prostatectomy as monotherapy. The preoperative
prostate-specific antigen (PSA) level, bladder neck involvement, margin
positivity, Gleason score, and other pathologic categories were assessed
as covariates contributing to the PSA-recurrence risk in univariate and
multivariable models. RESULTS: Bladder neck involvement was found in 60
(5%) of 1123 cases. In univariate analysis, the bladder neck was the
site-specific margin with the greatest PSA-recurrence risk of focal
involvement (relative risk 1.52, 95% confidence interval [CI] 1.15 to
2.00, P = 0.0030). The PSA-recurrence relative risk with extraprostatic
extension was 3.05 (95% CI 2.13 to 4.38, P <0.0001) and with seminal
vesicle invasion was 8.59 (95% CI 5.76 to 12.82, P <0.0001). In the
multivariable model, the PSA-recurrence risk with bladder neck
involvement (relative risk 1.19, 95% CI 0.72 to 1.96, P = 0.5) was not a
significant independent prognostic factor. Extraprostatic extension
(relative risk 2.25, 95% CI 1.54 to 3.27, P <0.0001) and seminal vesicle
invasion (relative risk 4.12, 95% CI 2.57 to 6.62, P <0.0001) were
significant independent predictors of PSA recurrence. CONCLUSIONS: Any
staging system should be evidence based. The current AJCC system for
staging bladder neck involvement, however, is contrary to the available
evidence. Reclassification of bladder neck involvement as part of the
pT3 category should be considered.
5
UI - 12137833
AU - Samaratunga H; Makarov DV; Epstein JI
TI -
Comparison of WHO/ISUP and WHO classification of noninvasive papillary
urothelial neoplasms for risk of progression.
SO - Urology 2002 Aug;60(2):315-9
AD - Department of Pathology, Royal Brisbane Hospital, Brisbane, Australia.
OBJECTIVES: To investigate the relation of the World Health
Organization/International Society of Urological Pathology (WHO/ISUP)
system for bladder neoplasia to prognosis. METHODS: A total of 134
patients with pTa bladder tumors were identified. We excluded cases with
prior or concurrent carcinoma in situ or invasion (pT1 or pT2).
Progression was defined as a tumor recurrence with either lamina propria
(pT1) or muscularis propria (pT2) invasion or carcinoma in situ. Age at
diagnosis, sex, tumor size, multifocality, and grade (WHO, WHO/ISUP)
were entered into a Cox multivariate analysis to predict progression.
RESULTS: The distribution of WHO papilloma, WHO G1, WHO G2, and WHO G3
was 5.2%, 31.3%, 59%, and 4.5%, respectively. The distribution of
WHO/ISUP papilloma, tumors of low malignant potential, low-grade
carcinomas, and high-grade carcinomas was 2.2%, 21.6%, 13%, and 21.6%,
respectively. The mean and median follow-up was 56.2 and 50 months,
respectively. The 90-month actuarial risk of progression for WHO
papilloma, G1, G2, and G3 was 0%, 11%, 24%, and 60%, respectively. The
corresponding progression rate for WHO/ISUP papilloma, tumors of low
malignant potential, low-grade carcinoma, and high-grade carcinoma was
0%, 8%, 13%, and 51%, respectively. In separate analyses, WHO grade (P =
0.003) and tumor size (P = 0.03), as well as WHO/ISUP (P = 0.002) and
tumor size (P = 0.04), independently predicted progression. CONCLUSIONS:
WHO G3 has a more rapid progression rate and a slightly worse long-term
progression rate compared with WHO/ISUP high-grade carcinoma. However,
although only 4.5% of tumors were WHO G3, we were able to classify 21.6%
as WHO/ISUP high-grade carcinoma with a poor prognosis. Use of the
WHO/ISUP system allows urologists to more closely follow a larger group
of patients at high risk of progression.
6
UI - 11948103
AU - Dominguez G; Carballido J; Silva J; Silva JM; Garcia JM; Menendez J;
TI -
Provencio M; Espana P; Bonilla F
p14ARF promoter hypermethylation in plasma DNA as an indicator of
disease recurrence in bladder cancer patients.
SO - Clin Cancer Res 2002 Apr;8(4):980-5
AD - Department of Medical Oncology, Clinica Puerta de Hierro, E-28035
Madrid, Spain.
PURPOSE: Several genes are reported to be implicated in bladder
carcinogenesis, including p53, p16INK4a, pRb, erbB-2, Cyclin D1, H-ras,
EGFR, and c-myc. Gene alterations in plasma DNA identical to those
observed within the tumor have been detected in various types of
neoplasia. EXPERIMENTAL DESIGN: We analyzed loss of heterozygosity in
six microsatellite markers (D17S695, D17S654, D13S310, TH2, D9S747, and
D9S161), p53 and K-ras mutations, and the promoter status of p14ARF and
p16INK4a in the mononuclear normal blood cells, tumor, and plasma DNA of
27 bladder cancer patients. We also studied the distribution of several
clinicopathological parameters in these patients in regard to molecular
alterations. RESULTS: Seventeen (63%) cases displayed the same
alteration in plasma and tumor DNA (some patients showed more than one
alteration simultaneously). Plasma p14ARF promoter hypermethylation was
associated with the presence of multicentric foci (P = 0.03), larger
tumors (P = 0.01), and relapse of the disease (P = 0.03). Plasma loss of
heterozygosity was also linked to disease recurrence (P = 0.02).
CONCLUSIONS: The results indicate that p14ARF aberrant promoter
methylation could be involved in bladder carcinogenesis and that plasma
DNA is a potential prognostic marker in urinary bladder cancer.
7
UI - 12096139
AU - Orntoft TF; Thykjaer T; Waldman FM; Wolf H; Celis JE
TI -
Genome-wide study of gene copy numbers, transcripts, and protein levels
in pairs of non-invasive and invasive human transitional cell
carcinomas.
SO - Mol Cell Proteomics 2002 Jan;1(1):37-45
AD - Department of Clinical Biochemistry, Molecular Diagnostic Laboratory,
Aarhus University Hospital, Skejby, DK-8200 Aarhus N, Denmark.
orntoft@kba.sks.au.dk
Gain and loss of chromosomal material is characteristic of bladder
cancer, as well as malignant transformation in general. The consequences
of these changes at both the transcription and translation levels is at
present unknown partly because of technical limitations. Here we have
attempted to address this question in pairs of non-invasive and invasive
human bladder tumors using a combination of technology that included
comparative genomic hybridization, high density oligonucleotide
array-based monitoring of transcript levels (5600 genes), and high
resolution two-dimensional gel electrophoresis. The results showed that
there is a gene dosage effect that in some cases superimposes on other
regulatory mechanisms. This effect depended (p < 0.015) on the magnitude
of the comparative genomic hybridization change. In general (18 of 23
cases), chromosomal areas with more than 2-fold gain of DNA showed a
corresponding increase in mRNA transcripts. Areas with loss of DNA, on
the other hand, showed either reduced or unaltered transcript levels.
Because most proteins resolved by two-dimensional gels are unknown it
was only possible to compare mRNA and protein alterations in relatively
few cases of well focused abundant proteins. With few exceptions we
found a good correlation (p < 0.005) between transcript alterations and
protein levels. The implications, as well as limitations, of the
approach are discussed.
8
UI - 12124340
AU - Tada Y; Wada M; Taguchi K; Mochida Y; Kinugawa N; Tsuneyoshi M; Naito S;
TI -
Kuwano M
The association of death-associated protein kinase hypermethylation with
early recurrence in superficial bladder cancers.
SO - Cancer Res 2002 Jul 15;62(14):4048-53
AD - Department of Medical Biochemistry, Graduate School of Medical Sciences,
Kyushu University, Fukuoka 812-8582, Japan.
Mechanisms for bladder carcinogenesis and the development of
recurrentbladder cancer remain unclear. Aberrant methylation of the 5'
CpG island is thought to play an important role in the inactivation of
the tumor suppressor genes in cancer. To study whether specific or bulk
hypermethylation predicts intrabladder recurrence, we determined the
frequency of aberrant promoter hypermethylation of seven genes, hMLH1,
O(6)-methylguanine-DNA-methyltransferase (MGMT), p16, Von Hippel-Lindau
(VHL), death-associated protein kinase (DAP-kinase), glutathione
S-transferase P1 (GST-P1) and E-cadherin in 55 superficial bladder
cancers and 5 normal urothelial epithelia by methylation-specific PCR
(MSP). These patients of superficial bladder cancer had been followed
prospectively by cystoscopy. Simultaneous hypermethylation of three
genes or more among the seven genes was observed in 2 (7%) of 30
patients in the nonrecurrence group and 7 (28%) of 25 patients in the
recurrence group. There was a significant concordance between the number
of methylated genes and the development of recurrence (P = 0.012). In
particular, the recurrence rate for 24 months was 88% for
hypermethylation of DAP-kinase and 28% for nonmethylation of DAP-kinase.
Hypermethylation of DAP-kinase is, therefore, a strong indicator of the
superficial bladder cancer associated with a high recurrence rate (P <
0.001; hazards ratio, 7.01). Our results suggest that hypermethylation
of DAP-kinase might be a useful prognostic marker for disease recurrence
in superficial bladder cancers.
9
UI - 12133547
AU - Xu K; Hou S; Du Z
TI -
Prognostic value of matrix metalloproteinase-2 and tissue inhibitor of
metalloproteinase-2 in bladder carcinoma.
SO - Chin Med J (Engl) 2002 May;115(5):743-5
AD - Department of Urology, People's Hospital of Peking University, Beijing
100044, China. xuka@hkusua.hku.hk
OBJECTIVES: To detect the level of matrix metalloproteinase-2 (MMP-2)
mRNA and the tissue inhibitor of metalloproteinase-2 (TIMP-2) mRNA in
bladder transitional cell carcinoma (BTCC), and to estimate the
prognosis for bladder tumor based on the quality and quantity of MMP-2
and TIMP-2 mRNA. METHODS: Thirty-five samples of human BTCC and 15
normal fresh bladder tissues were studied by RT-PCR analysis followed by
computer-assisted image analysis. RESULTS: The level of the MMP-2 mRNA
in BTCC was significantly increased compared with that in normal bladder
epithelium. The positive rates of MMP-2 and TIMP-2 mRNA were 71.4% and
65.7% in BTCC, and 66.7% and 60.0% in the normal bladder wall. The
expression intensity of the MMP-2 mRNA by image analysis tended to
increase with tumor grading and staging, which showed statistical
significance. Similarly, the MMP-2 to TIMP-2 ratio also showed
statistically significant difference between normal bladder tissue and
bladder carcinoma (P < 0.01). CONCLUSIONS: A high level of the MMP-2
mRNA exists in BTCC, which may function to damage collagen IV inside the
basement membrane and the extracellular basement of the bladder. The
level of the MMP-2 mRNA is proportional to BTCC grading and staging,
which may have prognostic value. The MMP-2 to TIMP-2 ratio may play a
more significant role in the determination of the aggressiveness and
prognosis of bladder tumor.
10
UI - 12131289
AU - Eissa S; Swellam M; Sadek M; Mourad MS; Ahmady OE; Khalifa A
TI -
Comparative evaluation of the nuclear matrix protein, fibronectin,
urinary bladder cancer antigen and voided urine cytology in the
detection of bladder tumors.
SO - J Urol 2002 Aug;168(2):465-9
AD - Oncology Diagnostic Unit, Biochemistry Department, Faculty of Medicine,
Ain Shams University, Cairo, Eygpt.
PURPOSE: We evaluate the diagnostic efficacy of nuclear matrix
protein-22 (NMP22, Matritech, Newton, Massachusetts), fibronectin and
urinary bladder cancer antigen (UBC, IDL Biotech, Borlange, Sweden)
compared with voided urine cytology in the detection of bladder cancer.
MATERIALS AND METHODS: A total of 168 patients provided a single voided
urine sample for NMP22, fibronectin an ideal monoclonal for urinary
bladder cancer and cytology before cystoscopy. Cystoscopy was done for
all patients as the reference standard for identification of bladder
cancer. Biopsy of any suspicious lesion was performed for
histopathological examination. Of the 168 cases 100 were histologically
diagnosed as bladder cancer, whereas the remaining 68 had benign
urological disorders. A group of 47 healthy volunteers were also
enrolled in this study. Voided urine was evaluated by NMP22, fibronectin
and UBC, and their values were expressed relative to mg. creatinine.
RESULTS: The optimal threshold values for NMP22, fibronectin and UBC
were calculated by receiver operator characteristics curves as 27 units
per mg. creatinine, 198 mg./mg. creatinine and 13 ng./mg. creatinine,
respectively. The levels and positive rates of the 3 parameters were
significantly higher in the malignant group compared to either the
benign group or normal controls. Of the entire group NMP22, fibronectin
and UBC were positive in 93.2%, 91% and 68.2%, respectively in bladder
cancer cases with positive cytology. Moreover, these positive rates were
significantly higher in bilharzial bladder cancer cases (58.8%, 67.5%,
58.8%, respectively) compared to nonbilharzial cases (35.6%, 36.3%,
31.1%). Overall sensitivity and specificity were 85% and 91.3% for
NMP22, 83% and 82.6% for fibronectin, 67% and 80.8% for UBC and 44% and
100% for voided urine cytology. Combined sensitivity of voided urine
cytology with the 3 biomarkers together was higher than either combined
sensitivity of voided urine cytology with 1 of the biomarkers or than
that of the biomarker alone. CONCLUSIONS: Our data indicate that NMP22
and fibronectin had superior sensitivities compared to UBC and voided
urine cytology, while NMP22 and voided urine cytology had the highest
specificities. The combined use of markers increased the sensitivity of
cytology from 44% to 95.3%. The higher sensitivities of markers in
bilharzial than nonbilharzial bladder cancer highlight their clinical
use in screening patients with urinary bilharziasis.
11
UI - 12131290
AU - Friedrich MG; Hellstern A; Hautmann SH; Graefen M; Conrad S; Huland E;
TI -
Huland H
Clinical use of urinary markers for the detection and prognosis of
bladder carcinoma: a comparison of immunocytology with monoclonal
antibodies against Lewis X and 486p3/12 with the BTA STAT and NMP22
tests.
SO - J Urol 2002 Aug;168(2):470-4
AD - Department of Urology, University Hospital, University of Hamburg,
Hamburg, Germany.
PURPOSE: The noninvasive detection of urothelial carcinoma remains
challenging. We prospectively evaluated urine markers for bladder
carcinoma. We compared the NMP22 (Matritech, Cambridge, Massachusetts)
and BTA Stat (Bard Diagnostics, Redmond, Washington) tests with
immunocytology using mAbs 486p3/12 and BG7 against Lewis X antigen.
MATERIALS AND METHODS: The NMP22 and BTA Stat tests were performed in
urine samples and immunocytology with mAbs 486p3/12 and BG7 staining
were performed in bladder washing specimens in 146 samples of 115
patients undergoing transurethral resection for suspected bladder
carcinoma (70) or 45 undergoing followup cystoscopy for a history of
bladder carcinoma (76). Bladder carcinoma was detected in 54 patients,
including stages pTa in 25, pT1 in 20, pT2 in 8 and carcinoma in situ in
1, while 61 had no evidence of bladder carcinoma. The cutoff was 10
units per ml. for the NMP22, 30% positive cells for 486p3/12 and 5%
positive cells for the Lewis X tests. RESULTS: BTA Stat was positive in
65 samples (44.5%) and NMP22 was positive in 69 (47.3%). Immunocytology
with mAbs 486p3/12 and BG7 against Lewis X was positive in 52 (35.6%)
and 109 (74.7%) samples, respectively. Sensitivity was 70.3% for BTA
Stat, 68.5% for NMP22, 68.5% for 486p3/12 and 94.4% for Lewis X.
Specificity was 70.6% for BTA Stat, 65.2% for NMP22, 83.6% for 486p3/12
and 36.9% for Lewis X. Area under the receiver operating characteristics
curve was 0.6804 for NMP22, 0.7226 for Lewis X and 0.8002 for 486p3/12.
False-positive results on BTA Stat in 2 of 22 patients (9%), on NMP22 in
2 of 25 (8%), on 486p3/12 in 3 of 11 (27%) and on Lewis X in 4 of 43
(9.3%) were associated with tumor recurrence. Furthermore, negative
results on BTA Stat in 2 of 39 patients (2%), on NMP22 in 2 of 36
(0.5%), on Lewis X in 0 of 18 (0%) and on 486p3/12 in 1 of 50 (2%) was
associated with tumor recurrence during followup. CONCLUSIONS:
Immunocytology with mAbs against Lewis X showed higher sensitivity than
all commercially available tests evaluated. Because of its high
sensitivity and high negative predictive value, it may be useful for
screening in a high risk population. Patients with a false-positive
486p3/12 test results are at increased risk for tumor recurrence
compared with those with negative results.
12
UI - 12131369
AU - Chen FH; Crist SA; Zhang GJ; Iwamoto Y; See WA
TI -
Interleukin-6 production by human bladder tumor cell lines is
up-regulated by bacillus Calmette-Guerin through nuclear factor-kappaB
and Ap-1 via an immediate early pathway.
SO - J Urol 2002 Aug;168(2):786-97
AD - Division of Urology and Human and Molecular Genetics Center, Medical
College of Wisconsin, Milwaukee, Wisconsin, USA.
PURPOSE: The expression of interleukin-6 (IL-6) by normal and malignant
urothelium in response to bacillus Calmette-Guerin (BCG) may have direct
and indirect effects on the antitumor activity of BCG. We evaluated the
molecular signaling pathway through which BCG induces IL-6 expression in
human transitional cell carcinoma lines. MATERIALS AND METHODS: We
evaluated IL-6 messenger RNA and protein expression by human
transitional carcinoma cell lines in response to BCG. Pharmacological
inhibition of protein synthesis was used to determine if BCG mediated
IL-6 induction occurred via an immediate-early or delayed pathway. We
used 5' deletion analysis and site directed mutagenesis to identify BCG
responsive regions in the human IL-6 promoter. Electrophoretic mobility
shift assays were done to assess nuclear translocation of the putative
signaling proteins AP-1 and nuclear factor-kappaB (NF-kappaB) in
response to BCG. RESULTS: BCG increased IL-6 messenger RNA and protein
in a time and dose dependent manner. IL-6 induction by BCG occurred via
an immediate-early response. Promoter analysis identified 2 areas in the
-1,200 to 14, 5' region of the IL-6 gene, which when deleted were
associated with significant losses of absolute or BCG responsive
activity. Site specific mutation of putative AP-1 or NF-kappaB elements
associated with each region demonstrated that these elements were
necessary but not sufficient for BCG induced IL-6 transcription. Gel
mobility shift assays showed that AP-1 and NF-kappaB were induced in
response to BCG exposure. CONCLUSIONS: Our results show that BCG induced
IL-6 expression by human transitional cell neoplasms occurs as an
immediate-early gene pathway that requires NF-kappaB and AP-1.
13
UI - 11877968
AU - Gorelov SI
TI -
[Fluorescent cystoscopy in diagnosing and treating superficial cancer of
the urinary bladder]
SO - Urologiia 2002 Jan-Feb;(1):25-8
14
UI - 11999461
AU - Kausch I; Bohle A
TI -
Molecular aspects of bladder cancer III. Prognostic markers of bladder
cancer.
SO - Eur Urol 2002 Jan;41(1):15-29
AD - Department of Urology, Research Center Borstel, Medical University of
Lubeck, Germany.
The current pathological and clinical parameters provide important
prognostic information, yet still have limited ability to predict the
true malignant potential of most bladder tumors. In the last years,
investigation of the basic mechanisms involved in carcinogenesis and
tumor progression by molecular biology has provided a host of markers
which are of potential diagnostic or prognostic value for bladder
carcinoma. These markers may serve as tools for early and accurate
prediction of tumor recurrence, progression and development of
metastases and for prediction of response to therapy. The precise
prediction of tumor biological behavior would facilitate treatment
selection for patients who may benefit from radical surgical treatment
or adjuvant therapy. We provide a current, comprehensive review of the
literature on bladder tumor markers with a special emphasis on their
prognostic potential. The literature suggests that currently no single
marker is able to accurately predict the clinical course of bladder
tumors and thus would serve as a reliable prognosticator. A combination
of prognostic markers could predict which superficial tumors need an
aggressive form of therapy and which invasive tumors require adjuvant
therapy. Altogether, the most promising markers are, at this point,
Ki-67 and p53 expression as well as matrixmetalloproteinase complex and
angiogenesis.
15
UI - 11999463
AU - Babjuk M; Kostirova M; Mudra K; Pecher S; Smolova H; Pecen L; Ibrahim Z;
TI -
Dvoracek J; Jarolim L; Novak J; Zima T
Qualitative and quantitative detection of urinary human complement
factor H-related protein (BTA stat and BTA TRAK) and fragments of
cytokeratins 8, 18 (UBC rapid and UBC IRMA) as markers for transitional
cell carcinoma of the bladder.
SO - Eur Urol 2002 Jan;41(1):34-9
AD - Department of Urology, General Teaching Hospital, 1st Medical Faculty,
Charles University, Postgraduate Institute, Prague, Czech Republic.
marko.babjuk@lf1.cuni.cz
OBJECTIVE: To evaluate the role of BTA stat, BTA TRAK, UBC Rapid, UBC
IRMA and voided urinary cytology in the detection of bladder
transitional cell carcinoma (TCC). METHODS: The study included 78
patients with TCC of the bladder (group A), 62 patients with a history
of bladder TCC without tumor recurrence at the time of examination (B,
control group), 20 patients with other malignancy of the urinary tract
(C), 38 patients with non-malignant urinary tract diseases (D), 10
patients with urinary tract infection (E) and 10 healthy volunteers (F).
Except in group F, voided urine was collected before cystoscopy or
cystectomy. RESULTS: The specificity and sensitivity in bladder cancer
detection were 87.1 and 74.4%, respectively with BTA stat, 79.3 and
48.7%, respectively with UBC Rapid, 100 and 33.3%, respectively with
cytology, 72.6 and 75.6%, respectively with BTA TRAK, 64.5 and 70.5%,
respectively with UBC IRMA. CONCLUSIONS: The BTA stat and BTATRAK tests
are superior to UBC Rapid, UBC IRMA and urinary cytology in detection of
bladder TCC. In daily practice however cytology remains the best adjunct
to cystoscopy because of its high sensitivity in Tis and 100%
specificity. Cystoscopy cannot be replaced by any of evaluated methods.
16
UI - 12109349
AU - Droller MJ
TI -
Current concepts of tumor markers in bladder cancer.
SO - Urol Clin North Am 2002 Feb;29(1):229-34
AD - Department of Urology, Mount Sinai Medical Center, 1 Gustave L Levy
Place, New York, NY 10029, USA.
The critical issue in characterizing the usefulness of tumor markers in
screening or monitoring for urothelial cancer and in determining
prognosis revolves around the question, "What do we need to know?"
During surveillance of patients with low-risk disease, highly sensitive
markers may detect disease persistence or early recurrence (on the basis
of field-effect changes or tumor cell implantation); however, they may
not indicate the possibility of progression. If cystoscopy is negative
in these instances, is it appropriate to treat? Does earlier treatment
actually prevent recurrence or progression? Some investigators have
suggested a positive answer to the former question, although lead-time
bias may a role. The issue in the latter question may be moot because
low-risk disease is by definition unlikely to progress. A corresponding
question is whether one should treat the patient if the marker has a low
specificity. In such instances, a marker with low specificity may incur
more frequent instrumentation and a panoply of additional costs. A
marker may have some value in providing earlier diagnosis in low-risk
disease if treatments are available to prevent clinical expression and
recurrence. A tumor marker would have additional value if it could
detect biologic change from low-risk to high-risk disease and permit a
corresponding change in treatment. Moreover, if a marker could provide
earlier diagnosis in high-risk disease, it might permit identification
of those patients likely to progress at earlier and curable stages of
disease. To be successful, such markers must have high sensitivity and
specificity in diagnosis. It has been suggested that "a simple
noninvasive highly sensitive and specific method for detecting bladder
cancer would decrease the morbidity associated with current surveillance
methods, improve quality of life for patients, and reduce costs by
substituting a less expensive test for the more expensive endoscopic
procedures" (Dr. M. Soloway, personal communication 2000). In
considering this statement, it is tempting to question some of its
implications. The term "simple" suggests that point-of-care tests may be
the easiest, but tests that are available may be inconsistent and not
sufficiently sensitive or specific. The need for a "highly sensitive and
specific" test is of critical importance for applicability in the
individual, even when such tests are based on the results in large
populations. When considering the "morbidity of current methods," it is
tempting to question whether cystoscopy is that morbid a procedure.
Given the information it provides, it seems improbable that it can be
readily replaced. Currently, no markers provide information over and
above that provided by cystoscopy and histology- or cytology-based
understanding of the biology of the disease especially in considering
distinctions between low-risk and high-risk disease. The ability to
"improve quality of life" will depend on the use of the predictive value
made on the basis of a test's sensitivity and specificity. A
false-positive test may lead to anxiety and extensive unnecessary
evaluation, whereas a false-negative test may lead to missed diagnosis,
delayed treatment, and the possibility of disease progression until
accurate diagnosis is obtained. In each case, quality of life is
compromised. "Substituting a less expensive test" depends on the
benefits of that substitution and the practicality of omitting or
delaying standard assessment. Costs depend on the frequency of testing,
those incurred by false-positive tests, and those incurred by
false-negative tests. Several caveats emerge when taking into account
these various considerations. In screening for low-risk disease, the
urgency of diagnosis may be less important. High sensitivity is of less
importance because the risk of a missed diagnosis has less ominous
repercussions. Nevertheless, high specificity is important to avoid
unnecessary frequent instrumentations. In considering surveillance for
low-risk disease, cytology may be more useful in indicating a change
from negative (persistent or recurrent low-risk disease) to positive
(high-risk disease) with the consequent need for more aggressive
treatment approach. No urinary "screening" markers reliably provide this
information. In considering surveillance for high-risk disease,
sensitive markers would detect persistence or early recurrence. If such
markers are negative, intervals between repeated cystoscopies may be
prolonged; however, a high specificity is needed to ensure the validity
of a truly negative interpretation. Otherwise, diagnosis may be missed
and the risk from progression and the development of incurability
increased. Markers for urothelial cancer must be expressed exclusively
as a consequence of the presence of cancer cells. The test must be
sensitive in detecting disease and must be validated in nonselected
populations. It must be sensitive in excluding nondisease, and noncancer
conditions must have little influence on its accuracy. There must be
little or no interassay or intra-assay variability. Interpretation of an
assay for a tumor marker should be all or none, or based on a threshold
level. The assays must have sufficient sensitivity and specificity in
populations and in the individual to have practical clinical
applicability.
17
UI - 12010230
AU - Wallace DM; Bryan RT; Dunn JA; Begum G; Bathers S; West Midlands
TI -
Urological Research Group
Delay and survival in bladder cancer.
SO - BJU Int 2002 Jun;89(9):868-78
AD - Department of Urology, The Queen Elizabeth Hospital, Birmingham, UK.
dmwallace@aol.com
OBJECTIVE: To assess in detail and evaluate the effect on survival of
delays in the diagnosis and treatment of cancer (which might lead to a
worse prognosis), dividing the delay from onset of symptoms to first
treatment into several components, comprising patient delay, general
practitioner (GP) delay, and two or more periods of hospital delay.
PATIENTS AND METHODS: Data were prospectively collected on 1537 new
delay times on survival was explored. RESULTS: The median delay from
onset of symptoms to GP referral was 14 days (Delay 1), from GP referral
to first hospital attendance was 28 days (Delay 2), and from first
hospital attendance to first transurethral resection of bladder tumour
was 20 days (Delay 3). The median hospital delay (Delay 2 + 3) was 68
days and the median total delay (Delay 1 + 2 + 3) was 110 days. Patients
with a shorter Delay 1 had a lower tumour stage and a 5% better 5-year
survival. Patients with a shorter hospital delay had worse survival;
total delay had no effect on survival. CONCLUSIONS: There was
significantly better survival for patients referred to hospital within
14 days of the onset of symptoms. The relationship between delay and
survival in bladder cancer is complex. Hospital delays may be influenced
more by comorbidity than by the characteristics of the tumour. However,
the adverse effects of delay seem to be most pronounced for patients
with pT1 tumours.
18
UI - 11769072
AU - Gattegno B; Chopin D
TI -
[Endoscopic diagnosis and treatment of superficial bladder tumors]
SO - Prog Urol 2001 Nov;11(5):1023-30
19
UI - 11769073
AU - Gattegno B; Chopin D
TI -
[Assessment of loco-regional extension of superficial bladder tumors]
SO - Prog Urol 2001 Nov;11(5):1033-44
20
UI - 11769078
AU - Gattegno B; Chopin D
TI -
[Bladder diverticulum and superficial bladder tumors]
SO - Prog Urol 2001 Nov;11(5):1145-8
21
UI - 11769082
AU - Billerey C; Sibony M; Gattegno B; Chopin D
TI -
[Pathologic anatomy of superficial tumors of the bladder]
SO - Prog Urol 2001 Nov;11(5):805-63
22
UI - 11769083
AU - Fontaniere B; Ranchere-Vince D; Landry JL; Colombel M; Chopin D;
TI -
Gattegno B
[Quality criteria in urinary cytology for tumor diagnosis]
SO - Prog Urol 2001 Nov;11(5):867-75
23
UI - 11769085
AU - Chopin D; Vordos D; Gattegno B
TI -
[Etiologies of superficial bladder tumors]
SO - Prog Urol 2001 Nov;11(5):927-52
24
UI - 11769086
AU - Chopin D; Gattegno B
TI -
[Descriptive epidemiology of superficial bladder tumors]
SO - Prog Urol 2001 Nov;11(5):955-60
25
UI - 11769087
AU - Gattegno B; Chopin D
TI -
[Natural history of superficial bladder tumors]
SO - Prog Urol 2001 Nov;11(5):963-90
26
UI - 11769088
AU - Gattegno B; Chopin D
TI -
[Diagnosis of superficial bladder tumors]
SO - Prog Urol 2001 Nov;11(5):993-1019
27
UI - 11899922
AU - Zeegers MP; Goldbohm RA; van den Brandt PA
TI -
A prospective study on active and environmental tobacco smoking and
bladder cancer risk (The Netherlands).
SO - Cancer Causes Control 2002 Feb;13(1):83-90
AD - Department of Epidemiology, Maastricht, The Netherlands.
mpa.zeegers@epid.unimass.nl
OBJECTIVE: In a prospective cohort study among 120,852 adult subjects
the authors investigated the associations between cigarette, cigar,
pipe, environmental tobacco smoking (ETS), and bladder cancer. METHODS:
In 1986 all subjects completed a questionnaire on cancer risk factors.
Follow-up for incident bladder cancer was established by linkage to
cancer registries until 1992. The case-cohort analysis was based on 619
cases and 3346 subcohort members. RESULTS: Compared with lifelong
non-smokers the age- and sex-adjusted incidence rate ratios (RR) for ex-
and current cigarette smokers were 2.1 (95% CI 1.5-3.0) and 3.3 (95% CI
2.4-4.6), respectively. The RR for smoking duration was 1.03 (95% CI:
1.02-1.04) per 1-year increment. The RR per 10 cigarettes/day was 1.3
(95% CI 1.2-1.4). Tar and nicotine exposure increased bladder cancer
risk only weakly. It appeared that associations of cigarette smoking
characteristics with bladder cancer risk were largely attributable to
cigarette smoking duration only. Smoking cessation, age at first
exposure, filter-tip usage, cigar and pipe smoking, and ETS were no
longer associated with bladder cancer risk after adjustment for
frequency and duration of smoking. CONCLUSIONS: The authors conclude
that current cigarette smokers have a three-fold higher bladder cancer
risk than non-smokers. Ex-smokers experience a two-fold increased risk.
About half of male bladder cancer and one-fifth of female bladder cancer
was attributable to cigarette smoking. Other smoking types (cigar, pipe,
or ETS) were not associated with increased risks.
28
UI - 12160910
AU - Pelucchi C; Negri E; Franceschi S; Talamini R; La Vecchia C
TI -
Alcohol drinking and bladder cancer.
SO - J Clin Epidemiol 2002 Jul;55(7):637-41
AD - Istituto di Ricerche Farmacologiche Mario Negri. 20157 Milan, Italy.
pelucchi@marionegri.it
The relation between alcoholic beverage consumption and bladder cancer
risk was investigated using data from a case-control study conducted
between 1985 and 1992 in two areas of northern Italy. Cases were 727
patients with incident, histologically confirmed bladder cancer, and
controls 1,067 patients admitted to the same network of hospitals for
acute, non-neoplastic, nonurologic, or genital tract diseases. Compared
to nondrinkers, the odds ratio (OR) was 0.79 (95% confidence interval,
CI, 0.58-1.08) for drinkers, and 0.84 (95%CI, 0.58-1.22) for > or =6
drinks/day. The OR was 0.86 (95%CI, 0.60-1.23) for > or =5 wine
drinks/day, 0.69 for beer, and 0.85 for spirits. No trend was observed
with duration (OR =1.00 for > or =40 years). ORs were consistent across
various strata of covariates including age, sex, and smoking habits. Our
study, based on a population with high alcohol (mainly wine) intake,
found no association between bladder cancer risk and alcohol intake,
even at high levels of consumption.
The above citations and abstracts reflect those newly added to CANCERLIT for the month and topic listed in the title. The citations have been retrieved from CANCERLIT using a predefined search strategy of indexed subject terms. Although the search strategy has been refined as best as possible, citations may appear that are not directly related to the topic, and occasionally relevant references may be omitted.
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