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Abramson Cancer CenterNCI CANCERLIT® Search: Diagnosis-Histopathology-Pathogenesis of Bladder Cancer - February 2002
National Cancer Institute®
Last Modified: February 1, 2002
Table of Contents
1
UI - 11778548
AU - Sun H; Fan J; Tang X
TI -
[Effect of IGF1 receptor gene antisense oligodeoxynucleotide on T24
urinary bladder cancer cells]
SO - Zhonghua Zhong Liu Za Zhi 2000 Jul;22(4):276-8
AD - Department of Urology, Shanghai First People's Hospital, Shanghai
200080, China.
OBJECTIVE: To evaluate the effects of autocrine blockage on T24 urinary
bladder cancer cells. METHODS: Semiquantitative RT-PCR, MTT
determination, 3H thymidine incorporation, flow cytometry and electron
microscopy were used to study the effects of antisense
oligodexynucleotide (ODN) targeted against insulin-like growth factor 1
receptor (IGF1R) gene on IGF1R gene expression, drug sensitivity,
proliferation and apoptosis of T24 cells. RESULTS: After being treated
with antisense ODN specific for IGF1R gene for 48 hours, the intrinsic
IGF1R mRNA expression of T24 cells reduced approximately by 72.9%, which
caused decrease in survival and increased sensitivity to
mitomycin-induced apoptosis(P < 0.05). CONCLUSION: To block the
autocrine loop with IGF1R antisense oligonucleotide may serve as a
potential therapeutic approach to bladder cancer.
2
UI - 11788727
AU - Collis SJ; Sangar VK; Tighe A; Roberts SA; Clarke NW; Hendry JH;
TI -
Margison GP
Development of a novel rapid assay to assess the fidelity of DNA
double-strand-break repair in human tumour cells.
SO - Nucleic Acids Res 2002 Jan 15;30(2):E1
AD - CRC Experimental Radiation Oncology Group, Paterson Institute for Cancer
Research, Christie Hospital NHS Trust, Wilmslow Road, Manchester M20
4BX, UK.
Cellular survival following ionising radiation-mediated damage is
primarily a function of the ability to successfully detect and repair
DNA double-strand breaks (DSBs). Previous studies have demonstrated that
radiosensitivity, determined as a reduction in colony forming ability in
vitro, may be related to the incorrect repair (misrepair) of DSBs. The
novel rapid dual fluorescence (RDF) assay is a plasmid-based reporter
system that rapidly assesses the correct rejoining of a
restriction-enzyme produced DSBs within transfected cells. We have
utilised this novel assay to determine the fidelity of DSB repair in the
prostate tumour cell line LNCaP, the bladder tumour cell line MGH-U1 and
a radiosensitive subclone S40b. The two bladder cell lines have been
shown in previous studies to differ in their ability to correctly repair
plasmids containing a single DSB. Using the RDF assay we found that a
substantial portion of LNCaP cells [80.4 +/- 5.3(standard error)%]
failed to reconstitute reporter gene expression; however, there was
little difference in this measure of DSB repair fidelity between the two
bladder cell lines (48.3 +/- 3.5% for MGH-U1; 39.9 +/- 8.2% for S40b).
The RDF assay has potential to be developed to study the relationship
between DSB repair fidelity and radiosensitivity as well as the
mechanisms associated with this type of repair defect.
3
UI - 11815965
AU - Cheng L; Gu J; Ulbright TM; MacLennan GT; Sweeney CJ; Zhang S; Sanchez
TI -
K; Koch MO; Eble JN
Precise microdissection of human bladder carcinomas reveals divergent
tumor subclones in the same tumor.
SO - Cancer 2002 Jan 1;94(1):104-10
AD - Department of Pathology, Indiana University School of Medicine,
Indianapolis, IN 46202, USA. lcheng@iupiu.edu
BACKGROUND: Human bladder carcinoma is thought to arise from a field
change that affects the entire urothelium. Whether independently
transformed urothelial cell populations exist in the same patient is
uncertain. METHODS: We studied the clonality of urinary bladder
carcinoma in 18 female patients who underwent cystectomy for urothelial
carcinoma. None had multiple tumors. Tumor samples were obtained from
different areas of the same tumor. Sixty-seven tumor samples were
analyzed. Tumor genomic DNA was microdissected and extracted from
formalin-fixed, paraffin-embedded slides. The clonality of urothelial
tumors was evaluated on the basis of a polymorphism of the X
chromosome-linked human androgen receptor gene (HUMARA) locus. The
technique is dependent on digestion of DNA with the
methylation-sensitive restriction enzyme HhaI, polymerase chain reaction
(PCR) amplification of HUMARA locus, and detection of methylation of
this locus. With this method, only the methylated HUMARA allele is
selectively amplified by PCR. RESULTS: Eleven of 18 patients were
informative. Nonrandom inactivation of the X chromosome was found in 9
of the 11 informative patients (82%). Seven patients showed different
patterns of nonrandom X chromosome inactivation for tumor samples
obtained from different regions of the same tumor. Two patients showed
the same pattern of nonrandom X chromosome inactivation in all samples.
CONCLUSIONS: Some muscle-invasive urothelial carcinomas may arise from
independently transformed progenitor urothelial cells, supporting the
"field effect" theory for bladder carcinogenesis. Copyright 2002
American Cancer Society.
4
UI - 11775223
AU - Cui X; Guo R; Xu Z; Wang B; Li C
TI -
Relationship between metabolic phenotype of N-acetylation and bladder
cancer.
SO - Chin Med J (Engl) 2000 Apr;113(4):303-5
AD - Department of Analytical Chemistry, College of Public Health, Shangdong
Medical University, Jinan 250012, China.
OBJECTIVE: To study the relationship between metabolic phenotype of
acetylation and bladder cancer. METHODS: Totally 203 healthy volunteers
and 67 patients with bladder cancer were investigated with caffeine as a
metabolic probe. Urine samples were collected in 2-6 hours after a cup
of 140 mg coffee was taken, and the caffeine metabolites,
5-acetylamino-6-formylamino-1-methyluracil (AFMU) and 1-methylxanthine
(1X) were analyzed by high performance liquid chromatography (HPLC). The
frequency histogram and probit plot were constructed to select the
critical value which was used to assess slow and fast acetylation status
both in healthy volunteers and patients with bladder cancer. RESULTS:
The peak height ratios of AFMU and 1X (AFMU/1X) were from 0.06 to 6.50
for healthy volunteers and 0.10 to 6.31 for patients with bladder
cancer, both with the critical value of 1.10. Of 203 healthy volunteers
involved in this study, 26.3% were slow acetylacors, as compared to
46.3% with slow acetylacors in patients with bladder cancer. The odds
ratio is 2.376, and the gene frequency for healthy volunteers and
patients with urinary bladder cancer were 0.5218 and 0.6804,
respectively. CONCLUSIONS: N-acetylation status in the Chinese
population is polymorphic and completely concordant with that determined
with other metabolic probes. Slow acetylators are significantly
associated with bladder cancer.
5
UI - 11797447
AU - Radosavljevic V; Jankovic S; Markovic-Denic Lj
TI -
[Risk factors for urinary bladder cancer]
SO - Srp Arh Celok Lek 2001 Jul-Aug;129(7-8):180-2
AD - Institute of Epidemiology, University School of Medicine, Belgrade.
A matched case control study was conducted in order to assess possible
relationships between some habits and risk of bladder cancer. The study
included 130 newly diagnosed bladder cancer patients and the same number
of controls matched with respect to sex, age (+/- 2 years) and type of
residence (rural-urban). According to multivariate logistic regression
analysis, risk factors of bladder cancer were smoking habits (OR =
3.15), consumption of animal fats (RR = 2.10) and pickled food (RR =
21.28). Higher level of educational (RR = 0.51), frequent urination (RR
= 0.21), consumption of greens (RR = 0.10), cherry (RR = 0.03) and
tangerines (RR = 0.02) had a protective effect.
6
UI - 11807796
AU - Sgambato A; Migaldi M; Faraglia B; De Aloysio G; Ferrari P; Ardito R; De
TI -
Gaetani C; Capelli G; Cittadini A; Trentini GP
Cyclin D1 expression in papillary superficial bladder cancer: its
association with other cell cycle-associated proteins, cell
proliferation and clinical outcome.
SO - Int J Cancer 2002 Feb 10;97(5):671-8
AD - Centro di Ricerche Oncologiche "Giovanni XXIII," Istituto di Patologia
Generale, Catholic University, Rome, Italy. asgambato@rm.unicatt.it
Cyclin D1 contributes to regulate G1 progression by forming a complex
with different cyclin-dependent kinases. It has oncogenic properties and
is frequently overexpressed in several human tumor types. In our study,
expression of cyclin D1 and Ki67, a proliferation marker, was evaluated
by immunohistochemistry in human papillary superficial (pTa-pT1) bladder
cancers and was correlated with p27(Kip1), p21(Waf1) and c-erbB-2
expression, with p53 gene status and protein expression, ploidy and
cancer progression. Cyclin D1 expression was neither associated with
tumor stage nor with tumor grade but high cyclin D1 expression (> or
=25% positive nuclei) was significantly associated with p53 gene
mutation (p = 0.012), low p21(Waf1) (p = 0.015) and high p27(Kip1) (p =
0.016) protein expression. Ki67 expression was not associated with tumor
stage but a high proliferation index (> or =10% positive nuclei) was
significantly associated with high tumor grade (p = 0.001) and with DNA
aneuploidy (p = 0.005). There was no significant difference in
proliferative activity between high and low cyclin D1 expressor tumors.
Patients whose tumors showed high expression of cyclin D1 displayed a
significantly longer disease-free survival (p < 0.001 by log-rank test).
Increased Ki67 expression was significantly associated with shorter
disease-free survival (p = 0.003). Both cyclin D1 (p = 0.027; RR =
1.898) and Ki67 (p = 0.047; RR = 1.932) protein expressions were
independent predictors of reduced disease-free survival on a
multivariate analysis that also included p27(Kip1) expression and tumor
stage. The simultaneous presence of low cyclin D1, low p27(Kip1) and
high Ki67 expression defined a "high-risk" group of patients who
displayed a significantly increased risk of recurrence (p < 0.0001).
These results suggest that evaluation of cell cycle-associated markers
can help to identify high-risk patients and may affect the management of
patients with papillary superficial bladder cancer. Copyright 2001
Wiley-Liss, Inc.
7
UI - 11464113
AU - Asci R; Yildiz L; Sarikaya S; Buyukalpelli R; Yilmaz AF; Kandemir B
TI -
p53 and bcl-2 overexpression as associated risk factors in patients 40
years old or less with transitional cell carcinoma of the bladder.
SO - Urol Int 2001;67(1):34-40
AD - Department of Urology, School of Medicine, Ondokuz Mayis University,
Samsun, Turkey. rasci@superonline.com
OBJECTIVES: Transitional cell carcinoma (TCC) of the bladder in younger
patients has historically a favourable prognosis. bcl-2 and p53 genes
are implicated in cell cycle regulation with roles on programmed cell
death. Presence of nuclear accumulation of p53 and cytoplasmic
accumulation of bcl-2 were proposed to confer a growth advantage to
tumour cells. In this study, we investigated the roles of p53 and bcl-2
as prognostic factors in TCC of bladder in patients younger than 40
years. Patients and METHODS: From 1986 to 1998, 25 patients younger than
40 years were treated for TCC of bladder in our hospital. Of the tumour
specimens, 24 were adequate for evaluating p53 and bcl-2 oncoproteins
(group I). As a control (group II), we randomly selected 30 patients
older than 50 years treated for bladder cancer in this period. Two
oncoproteins were detected by immunohistochemical analysis in paired
tumour tissue specimens in both groups. Retrospectively obtained
clinical follow-up data were available, with a mean follow-up of 44 and
25.5 months in groups I and II, respectively. Relations between tumour
recurrences and progression with positivity of bcl-2 and p53 were
investigated. RESULTS: Expression of bcl-2 was observed in 13 (54.1%)
and 11 (36.7%) and nuclear p53 accumulation in 9 (37.5%) and 17 (56.7%)
of groups I and II, respectively. In the presence of p53 expression,
tumours showed significantly more progression in group I (55 vs. 6.7%)
and group II (41.1 vs. 0%). Recurrence rates were not significantly
different in tumours with and without nuclear p53 overexpression in both
groups. Also, recurrence and progression rates were not significantly
different in tumours with and without cytoplasmic bcl-2 overexpression
in both groups. Grade (G) and stage appeared as important prognostic
factors in both groups since 60% of GIII tumours showed progression in
group I, but none of GI and GII tumours. Similarly, 75% of T3 tumours
progressed, while these rates were 25 and 25% for T1-T2 tumours in group
I. In group II, 31.2, 25 and 0% of GIII, GII and GI tumours progressed,
while 50, 41.6 and 0% of T3, T2 and T1 tumours progressed, respectively.
CONCLUSIONS: Nuclear p53 expression in TCC appears to be associated with
a poorer prognosis in both younger and older patients. Although
cytoplasmic bcl-2 overexpression is found in the majority of tumours in
the younger group, it is not associated with tumour progression and
recurrence. Copyright 2001 S. Karger AG, Basel
8
UI - 11743649
AU - Dahse R; Utting M; Werner W; Schimmel B; Claussen U; Junker K
TI -
TP53 alterations as a potential diagnostic marker in superficial bladder
carcinoma and in patients serum, plasma and urine samples.
SO - Int J Oncol 2002 Jan;20(1):107-15
AD - Klinikum der FSU Jena, Institut fur Humangenetik, D-07740 Jena, Germany.
rdah@mti-n.uni-jena.de
Molecular markers are needed for better distinguishing of non-invasive
papillary (pTa) and minimally invasive (pT1) bladder carcinomas and for
identifying individual tumors with a high risk of recurrence or disease
progression. First aim of our study was to evaluate TP53 microsatellite
and mutation analysis as an effective concept for the characterization
of superficial bladder tumors with different biological aggressiveness.
Mutation screening in the TP53 hot spot region was performed in 55
microdissected superficial bladder tumor samples by direct genomic
sequencing. PCR based LOH analysis was done with two markers at 17p13.
Second, there is considerable interest in the development of
non-invasive techniques that would detect recurrent bladder neoplasia.
In order to evaluate TP53 alterations as a potential marker for a
non-invasive diagnosis of recurrences or residuals and to determine
whether tumor-specific DNA exhibiting LOH or sequences harbouring a
mutation, can be detected in body fluids, mutation screening was
performed in urine, plasma and serum of patients with a mutated primary
tumor. LOH analysis with two markers at 17p was done in the
corresponding urine and blood samples of 31 primary tumors. As seen from
our results, TP53 inactivation by mutation seems to characterize higher
malignant superficial bladder tumors which tend to recur and in which
the probability is higher that the rezidives progress to muscle invasive
growth pattern. Only in 2/8 cases, the TP53 mutation from the primary
tumor could be re-detected in patients urine and blood. 17p
microsatellite changes with at least one marker were found in 30/31 body
fluids of the tumor patients (97%). Correlating the 17p status found in
body fluids to the status of the primary tumor, the concordance is only
about 52%. We conclude that TP53 genotyping as a non-invasive diagnostic
tool in outpatient samples is of limited value for clinical practice.
9
UI - 11720438
AU - Le Frere-Belda MA; Cappellen D; Daher A; Gil-Diez-de-Medina S; Besse F;
TI -
Abbou CC; Thiery JP; Zafrani ES; Chopin DK; Radvanyi F
p15(INK4b) in bladder carcinomas: decreased expression in superficial
tumours.
SO - Br J Cancer 2001 Nov 16;85(10):1515-21
AD - Service d'Anatomie et de Cytologie Pathologiques, Centre Hospitalier
Universitaire Henri Mondor, 94010 Creteil Cedex, France.
The p15 gene which encodes a cyclin-dependent kinase inhibitor, is
located in the 9p21 chromosomal region that is frequently deleted in
human bladder transitional cell carcinomas (TCCs). The aim of the
present paper is to study the potential involvement of the p15 gene in
the evolution of TCCs. p15 mRNA expression was investigated by
semi-quantitative RT-PCR in a series of 75 TCCs, 13 bladder cell lines
and 6 normal bladder urothelia by semi-quantitative RT-PCR. p15 was
expressed in the normal urothelium but p15 mRNA levels were
significantly decreased in 66% of the superficial (Ta-T1) TCCs (P =
0.0015). In contrast, in muscle-invasive (T2-T4) TCCs, p15 expression
differed widely between samples. p16 mRNA levels were also studied and
there was no correlation between p15 and p16 mRNA levels, thus
indicating that the two genes were regulated independently. Lower p15
expression in superficial tumours did not reflect a switch from
quiescence to proliferative activity as normal proliferative urothelial
controls did not present decreased p15 mRNA levels relative to quiescent
normal urothelia. We further investigated the mechanisms underlying p15
down regulation. Homozygous deletions of the p15 gene, also involving
the contiguous p16 gene, were observed in 42% of the TCCs with decreased
p15 expression. No hypermethylation at multiple methylation-sensitive
restriction sites in the 5;-CpG island of p15 was encountered in the
remaining tumours. Our data suggest that decreased expression of p15 may
be an important step in early neoplastic transformation of the
urothelium and that a mechanism other than homozygous deletions or
hypermethylation, may be involved in p15 down regulation.
10
UI - 11690548
AU - Irie A; Uchida T; Ishida H; Matsumoto K; Iwamura M; Baba S
TI -
p53 Mutation in bladder cancer patients in Japan and inhibition of
growth by in vitro adenovirus-mediated wild-type p53 transduction in
bladder cancer cells.
SO - Mol Urol 2001 Summer;5(2):53-8
AD - Department of Urology, Kitasato University School of Medicine,
Sagamihara, Kanagawa, Japan. akira_irie@pop07.odn.ne.jp
BACKGROUND: Altered expression of p53 has been described in nearly half
of bladder cancers, and p53 mutations are presumed to play a role in the
multistep progression of these tumors. MATERIALS AND METHODS: The
incidence of mutation in the p53 gene and its correlation with
histopathologic findings and patient survival were evaluated in 105
Japanese patients with bladder cancer. Laboratory experiments were also
performed to confirm the infectivity and efficacy in tumor growth
inhibition of an adenovirus expressing wild-type p53 in EJ bladder
cancer cells. RESULTS: Mutations of p53 were observed in 38 bladder
cancer specimens (36%), with a significantly higher incidence of
mutation being seen in tumors of higher stage and grade. The overall
survival was worse in patients with the p53 mutation. In laboratory
experiments, adenoviral vectors infected bladder cancer cells in a dose-
and cell density-dependent manner. The adenovirus-mediated transduction
of wild-type p53 resulted in dose-dependent growth inhibition of bladder
cancer cells in vitro. No significant cytotoxicity was observed after
infection by a control adenovirus. CONCLUSION: Transduction of wild-type
p53 might be a potential therapeutic option for bladder cancer.
11
UI - 11705862
AU - Durkan GC; Nutt JE; Rajjayabun PH; Neal DE; Lunec J; Mellon JK
TI -
Prognostic significance of matrix metalloproteinase-1 and tissue
inhibitor of metalloproteinase-1 in voided urine samples from patients
with transitional cell carcinoma of the bladder.
SO - Clin Cancer Res 2001 Nov;7(11):3450-6
AD - Department of Surgery, Cancer Research Unit, The Medical School,
University of Newcastle upon Tyne, Newcastle upon Tyne NE2 4HH, United
Kingdom.
PURPOSE: To study the role of urinary matrix metalloproteinase-1 (MMP-1)
and tissue inhibitor of metalloproteinase-1 (TIMP-1) in bladder cancer
and their relationship to tumor progression. EXPERIMENTAL DESIGN: MMP-1
and TIMP-1 were measured by ELISA in urine samples from 131 patients
with bladder tumors (7 cis, 74 Ta, 29 T1, and 21 T2-T4; 46 G(1), 41
G(2), and 37 G(3)), 5 patients with prostate cancer, 33 patients with
benign lower urinary tract disorders, and 36 healthy volunteers.
Complete clinical data were available for 100 patients with bladder
cancer with a median follow-up time of 24 months (range: 4-39 months).
RESULTS: MMP-1 was detected in urine samples from 21 of 131 (16%)
patients with bladder cancer but was undetectable in samples from all
other groups (P < 0.0001). Urinary MMP-1 was detected in a higher
percentage of patients with T2-T4 tumors and G(3) tumors than patients
with cis/Ta/T1 or G(1)-G(2) tumors (P = 0.04 and P = 0.0074,
respectively). Patients with detectable concentrations of urinary MMP-1
had higher rates of disease progression (P = 0.04) and death from
bladder cancer (P = 0.02) than patients with undetectable urinary MMP-1.
All patient groups had higher urinary TIMP-1 concentrations than healthy
volunteers (P = 0.02). Patients with muscle-invasive tumors had higher
concentrations of urinary TIMP-1 than patients with cis/Ta/T1 tumors (P
= 0.037), but there was no association between TIMP-1 and tumor grade.
Urinary TIMP-1 levels strongly correlated with tumor size (P = 0.0002).
Progression-free survival rates were lower for patients with urinary
TIMP-1 concentrations above the median (1.8 ng/ml, P = 0.04), but
urinary TIMP-1 levels were not related to disease-specific survival.
Patients with T2-T4 tumors and G(3) tumors had significantly lower
urinary MMP-1:TIMP-1 ratios than patients with Ta/T1 bladder tumors (P =
0.039) or G(1)-G(2) tumors (P = 0.0415). CONCLUSIONS: Where urinary
MMP-1 is detectable, the patient is more likely to have a bladder tumor
of advanced stage or grade and may be at increased risk of disease
progression and death of bladder cancer. The relationship between
urinary TIMP-1, muscle-invasion, and disease progression in bladder
cancer is at variance with its role as an inhibitor of MMPs and warrants
additional evaluation.
12
UI - 11758874
AU - Williams SG; Buscarini M; Stein JP
TI -
Molecular markers for diagnosis, staging, and prognosis of bladder
cancer.
SO - Oncology (Huntingt) 2001 Nov;15(11):1461-70, 1473-4, 1476; discussion
1476-84
AD - Department of Urology, USC/Norris Comprehensive Cancer Center,
University of Southern California, Los Angeles 90089-9178, USA.
Conventional histopathologic evaluation of bladder cancer, encompassing
tumor grade and stage, is inadequate to accurately predict the behavior
of most bladder tumors. Intense research efforts are under way to
identify and characterize various bladder cancers and their true
biological potential more effectively. The need to predict which
superficial tumors will recur or progress--and which invasive tumors
will metastasize--has led to the identification of a variety of
potential prognostic markers for patients with bladder cancer. The
molecular changes that occur in transitional cell carcinoma of the
bladder are numerous and can be categorized into (1) chromosomal
alterations, leading to carcinogenesis; (2) loss of cell-cycle
regulation, accounting for cellular proliferation; and (3) growth
control events such as angiogenesis, resulting in metastasis. It is
becoming apparent that the accumulation of genetic and molecular changes
ultimately determines a tumor's phenotype and subsequent clinical
behavior. The potential clinical application of new diagnostic
techniques (ie, loss-of-heterozygosity analysis to identify tumor
suppressor genes) and older, well-established, techniques (ie,
immunohistochemistry) combined with improvements in the use of automated
and standardized systems are areas of active investigation.
13
UI - 11747331
AU - Kimura F; Florl AR; Seifert HH; Louhelainen J; Maas S; Knowles MA;
TI -
Schulz WA
Destabilization of chromosome 9 in transitional cell carcinoma of the
urinary bladder.
SO - Br J Cancer 2001 Dec 14;85(12):1887-93
AD - Urologische Klinik, Heinrich-Heine Universitat, Moorenstrasse 5, D-40225
Dusseldorf, Germany.
The most frequent genetic alteration in transitional cell carcinoma of
the urinary bladder (TCC) is loss of chromosome 9 which targets CDKN2A
on 9p. The targets on 9q are not confirmed. Here, 81 advanced TCC
specimens were investigated for loss of heterozygosity (LOH) and
homozygous deletions (HD) on chromosome 9q using multiplex analysis of
microsatellite markers. 41/81 tumours (51%) showed LOH on 9q, with LOH
at all markers in 33 cases. Eight partial losses involved three regions
in 9q12, 9q22.3, and 9q33- 9q34. No mutations were identified in the
candidate tumour suppressor gene DBCCR1 in three tumours showing
restricted LOH at 9q32-33. 22% of the specimens had HD at CDKN2A, but no
HD was found on 9q. Two tumours had lost 9p only and five 9q only. 9q
LOH was not related to tumour grade or stage and present or absent with
equal frequency in recurrent TCC. LOH on 9q correlated with the extent
of genome-wide hypomethylation (P < 0.0001) which extended into
satellite sequences located in 9q12 juxtacentromeric heterochromatin.
While the high frequency of chromosome 9q loss in TCC may reflect
destabilization of the chromosome related to hypomethylation of
repetitive DNA, the data are compatible with the existence of tumour
suppressor genes on this chromosome arm.
14
UI - 11747332
AU - Edwards J; Duncan P; Going JJ; Grigor KM; Watters AD; Bartlett JM
TI -
Loss of heterozygosity on chromosomes 11 and 17 are markers of
recurrence in TCC of the bladder.
SO - Br J Cancer 2001 Dec 14;85(12):1894-9
AD - University Department of Surgery, Glasgow Royal Infirmary, Glasgow, G31
2ER, UK.
Approximately 2/3 of patients diagnosed with superficial transitional
cell carcinoma of the urinary bladder (TCC) will recur within 2 years.
Loss of chromosome 9 and loss of heterozygosity (LOH) at 9q34 in index
TCCs identify a subset of patients at high risk of recurrence. This
study explores genetic alterations on chromosomes 4, 8, 11 and 17 as
predictors of recurrence. A total of 109 carcinomas were investigated at
26 loci. DNA was extracted from microdissected archival normal/tumour
tissue and was analysed for loss of heterozygosity (LOH). Fluorescent
PCR was performed and genotyping carried out on a Perkin Elmer ABI377
sequencer. LOH of D11S490 or D17S928 was significantly more frequent in
index carcinomas of patients who experienced recurrence compared to
those with no recurrence (P = 0.004 and 0.019 respectively). These
results suggest that loss of these regions is associated with recurrence
of TCC. Further investigation is required to identify genes in these
regions, which might be responsible for driving recurrence in TCC of the
urinary bladder.
15
UI - 11834388
AU - Pytel A; Schmeller N
TI -
New aspect of photodynamic diagnosis of bladder tumors: fluorescence
cytology.
SO - Urology 2002 Feb;59(2):216-9
AD - Department of Urology and Andrology, St. Johanns-Spital
Landeskrankenhaus, Salzburg, Austria.
OBJECTIVES: To establish a new diagnostic method for the detection and
follow-up of bladder cancer that combines the principles of photodynamic
diagnosis and urinary cytology. METHODS: We investigated 46 patients
scheduled for transurethral resection of a bladder tumor immediately
before the resection was carried out. After intravesical instillation of
either 5-aminolevulinic acid (ALA) or hypericin, urinary cytology
specimens were obtained. Induced fluorescence of urothelial cells was
detected by fluorescence microscopy. The results were compared with the
conventional cytologic and histologic findings. RESULTS: In the 46
patients, 42 cases of urothelial carcinoma and 4 cases of nonspecific
inflammation were diagnosed. Of the 42 patients with cancer, 19 had
Stage Ta, 9 had T1, 3 had carcinoma in situ, and 11 had invasive bladder
cancer. The grading was G1 in 17 patients, G2 in 6 patients, and G3 in
19 patients. In 38 cases we instilled ALA and in 8 hypericin. All 4
patients diagnosed with nonspecific inflammation had received ALA. We
detected ALA-induced fluorescence in 34 of 38 cases. One of the four
histologically negative cases had a false-positive finding and 1 case of
urothelial carcinoma did not show fluorescence. After instillation of
hypericin we could detect induced fluorescence in all cases.
CONCLUSIONS: Our first results suggest that fluorescence cytology is
more sensitive than other noninvasive tests. After additional
investigation, it may become a valuable diagnostic method and may reduce
the number of cystoscopies in the follow-up of bladder tumors.
16
UI - 11834390
AU - Skemp NM; Fernandes ET
TI -
Routine bladder biopsy after bacille Calmette-Guerin treatment: is it
necessary?
SO - Urology 2002 Feb;59(2):224-6
AD - Department of Urology, Veterans Affairs Medical Center, Minneapolis,
Minnesota 55417, USA.
OBJECTIVES: To evaluate the need for routine biopsy at first follow-up
after intravesical bacille Calmette-Guerin (BCG) therapy for superficial
transitional cell cancer of the bladder (TCCB). We examined the
potential role of voided urine cytology and cystoscopy as screening
tools to determine which patients should undergo biopsy. METHODS: The
records of 71 patients with TCCB who received a total of 95 courses of
BCG were reviewed. The pathology findings before BCG and the
cystoscopic, voided cytologic, and biopsy results after BCG were
recorded. RESULTS: In 54 cases, the cystoscopic and/or cytologic
findings were abnormal. In 19 (35%) of these 54 cases, TCCB was found on
biopsy after BCG. In 41 cases, both cystoscopy and cytology were normal.
In 1 of these 41 cases, a small superficial low-grade TCCB was found on
biopsy. An abnormality on voided cytology or cystoscopy was more likely
to occur after treatment for carcinoma in situ. CONCLUSIONS: Patients
with papillary TCCB who have negative cystoscopic and negative urine
cytologic results can safely be spared routine transurethral bladder
biopsy with its associated cost and morbidity. However, patients with
carcinoma in situ are very likely to have persistent abnormal cytologic
or abnormal cystoscopic findings warranting investigation with biopsy
and may benefit from routine scheduled biopsy.
17
UI - 11834392
AU - Yang MH; Yen CC; Chen PM; Wang WS; Chang YH; Huang WJ; Fan FS; Chiou TJ;
TI -
Liu JH; Chen KK
Prognostic-factors-based risk-stratification model for invasive
urothelial carcinoma of the urinary bladder in Taiwan.
SO - Urology 2002 Feb;59(2):232-8; discussion 238-9
AD - Division of Medical Oncology, Department of Medicine, Taipei Veterans
General Hospital, People's Republic of China, Taipei, Taiwan.
Objectives. To develop a prognostic-factors-based predictive model for
invasive urothelial carcinoma of the urinary bladder derived from
statistical comparison of clinical characteristics.Methods. The medical
records for patients with invasive urinary bladder urothelial carcinoma
were reviewed. Clinical data for age, sex, serum lactate dehydrogenase,
creatinine, albumin, alkaline phosphatase, alanine aminotransferase,
total bilirubin and hemoglobin levels, white blood cell and platelet
counts, positive urine cytology, Eastern Cooperative Oncology Group
performance status score, tumor size, histologic grading, T stage,
presence of lymph node metastases, squamous differentiation,
hydronephrosis, prostatic involvement, Charlson comorbidity index,
surgical procedures, and adjuvant chemotherapy status were recorded.
Univariate and multivariate analyses were performed to test independent
factors for prediction of survival and disease recurrence.Results. After
univariate and multivariate analyses, six independent prognostic factors
were found: T stage, grading, prostatic involvement, Eastern Cooperative
Oncology Group performance status score, and pretreatment serum
creatinine and albumin levels. A scoring system was developed on the
basis the relative risk associated with the proposed prognostic factors
and patients were stratified into three groups according to their
scores, with statistically significant prognostic differences revealed
for each of the between-group comparisons. Independent factors affecting
recurrence-free survival and best predicted disease recurrence were
pretreatment serum creatinine, T stage, and surgical
procedure.Conclusions. This prognostic-factors-based risk-stratification
model for invasive urothelial carcinoma of the urinary bladder may help
clinicians predict outcome and select the most appropriate therapeutic
modalities. The incidence of recurrent disease is significantly higher
for patients with poor renal function before treatment or advanced T
stage and those undergoing transurethral tumor resection instead of
radical cystectomy.
18
UI - 11834395
AU - Pannek J
TI -
Transitional cell carcinoma in patients with spinal cord injury: a high
risk malignancy?
SO - Urology 2002 Feb;59(2):240-4
AD - Department of Urology, Ruhr-Universitat Bochum, Herne, Germany.
OBJECTIVES: To study bladder cancer incidence in patients with spinal
cord injury (SCI) in Germany, Switzerland, and Austria. SCI is
associated with neurogenic bladder dysfunction. These patients are at an
increased risk of developing bladder malignancies. METHODS: A
questionnaire was mailed to all SCI centers in these countries. The
number of patients with SCI treated between 1995 and 1999, and the data
of all patients with SCI with bladder cancer were recorded. RESULTS: The
charts of 43,561 patients were reviewed. Of these, 48 patients (0.11%)
developed bladder cancer. The data of 8 female and 29 male patients were
fully available. The mean age was 53.3 years. Bladder management was
reflex voiding in 18 patients, intermittent catheterization in 12
patients, and an indwelling catheter in 7 patients. Twelve patients were
smokers. The mean time between SCI and the first bladder cancer
diagnosis was 22.6 years. Thirty-two percent had superficial cancers, 8%
had carcinoma in situ, and 60% presented with muscle-infiltrating
tumors; 81% had urothelial cancer and 19% squamous cell cancer. Thirteen
patients rarely had urinary tract infections (UTIs), 9 had more than 10
UTIs annually, and 15 had chronic UTIs. CONCLUSIONS: The bladder cancer
incidence in patients with SCI and in the general population is
comparable. More than 60% of the patients with SCI, however, initially
presented with muscle-infiltrating bladder cancer. Indwelling catheters
and chronic UTIs were common in patients with bladder cancer.
Immunologic pathologic mechanisms and a prolonged exposure to
carcinogens may be involved in bladder cancer carcinogenesis in patients
with SCI.
19
UI - 11783019
AU - Fan Z; Zhang J; Bai J
TI -
[Deletion mapping of chromosome 18q and Smad proteins expression
analysis in urinary bladder carcinomas]
SO - Zhonghua Zhong Liu Za Zhi 2001 Mar;23(2):135-7
AD - Cancer Institute(Hospital), Chinese Academy of Medical Sciences & Peking
Union Medical College, Beijing 100021, China.
OBJECTIVE: To investigate the role of loss of heterozygosity (LOH) on
chromosome 18q in the carcinogenesis and progression of urinary bladder
cancer and to provide clues for early detection and positional cloning
of related genes. METHODS: Deletion mapping was performed on 18q using
12 microsatellite markers. Immunohistochemistry staining was used to
evaluate the expression level of two tumor suppressor candidates Smad 2
and Smad 4 in this region. RESULTS: LOH in at least one of the 12
microsatellites on 18q was detected in 84.2% (32/38) of patients with
bladder cancer. The minimal deletion region included tumor suppressor
candidate Smad 4. Immunohistochemical study revealed that 21.1% (8/38)
of the cases had up-regulated Smad 2 protein and 34.2% (13/38) of the
cases had down-regulated Smad 2 protein. Smad4 protein expression was
down-regulated in 68.4% (26/38) of the cases but up-regulated Smad 4
expression was seen in only one case. CONCLUSIONS: LOH on 18q was
closely linked with bladder cancer. The irregular expression of tumor
suppressor candidates Smad 2 and Smad 4 may play important role in the
initiation and progression of bladder neoplasms.
20
UI - 11801307
AU - Aly MS; Khaled HM
TI -
Chromosomal aberrations in early-stage bilharzial bladder cancer.
SO - Cancer Genet Cytogenet 2002 Jan 1;132(1):41-5
AD - Faculty of Science, Cairo University (Beni-Suef Branch), Cairo, Egypt.
Bilharzial bladder cancer is one of the most common types of malignancy
in both men and women in several developing countries including Egypt.
It has several unique clinical, epidemiological, and histological
characteristics, suggesting that it is an entity distinct from bladder
cancer seen in Western countries. Genetic alterations in
bilharzial-related bladder cancer have been studied infrequently,
especially in the advanced stages of disease, that is, T3 and T4
classifications. The objective of this study was to extend establishing
the baseline cytogenetic profile of this type of malignancy to early T1
and T2 classifications. For this purpose, fluorescence in situ
hybridization was applied to interphase nuclei of frozen-stored samples
with biotinylated repetitive DNA probes specific for all chromosomes to
detect numerical chromosome changes in 35 patients presenting with
relatively early-stage pT1 and pT2 disease. Eleven cases had squamous
cell carcinoma (SCC) and 24 had transitional cell carcinoma. Six of 24
transitional cell carcinomas had diploid chromosome counts with all the
probes. Numerical chromosome aberrations were detected in 18 cases
(75%). In 12 cases, a loss of chromosome 9 was observed. In three cases,
an additional loss of chromosome 17 was detected. One case demonstrated
a loss of chromosome 10, whereas another two cases showed a gain of
chromosome 7, next to a loss of chromosome 9. Loss of chromosome Y was
observed in nine of the 27 male cases studied (33.3%), in which only one
case showed an abnormality whereas four cases were detected next to loss
of chromosome 9, and one case showed gain of chromosome 7. Five cases
showed loss of chromosome 19 whereas gain of chromosome 4 was detected
in two cases. Two of 11 samples of SCC had normal diploid chromosome
counts with all the probes used. In four of 11 cases (36.4%)
underrepresentation of chromosome 9, compared with the other
chromosomes, was detected. An additional loss of chromosome 17 and gain
of chromosome 7, next to loss of chromosome 9, was detected in three
cases. One case showed loss of chromosome 17 as the only numerical
aberration. Loss of the Y chromosome was detected in three cases of
which one case had gain of chromosome 7 and one case had loss of
chromosome 19. No correlation was found between any of the
clinicopathologic parameters examined in this study and the presence or
absence of any numerical chromosomal aberrations except for the
significant association between schistosomal history and loss of Y
chromosome (P=0.007).
21
UI - 11803266
AU - Torabi-Pour N; Nouri AM; Saffie R; Oliver RT
TI -
Comparative study between direct mild acid extraction and immunobead
purification technique for isolation of HLA class I-associated peptides.
SO - Urol Int 2002;68(1):38-43
AD - Uro/Oncology Research Unit, Department of Medical Oncology, St.
Bartholomew's and the Royal London School of Medicine, London, UK.
n.torabi-pour@mds.qmw.ac.uk
Identification of tumour-specific peptide(s) hidden within the groove of
human leucocyte antigens is a crucial prerequisite for peptide vaccine
therapy. Conventionally, the peptide(s) are isolated by mild acid
extraction (MA) technique followed by sequential ultra-filtrations. Here
we describe a new approach for peptide isolation using the immunobead
purification (IB-P) technique in conjunction with reverse-phase
high-performance liquid chromatography. The obtained data were validated
by SDS-PAGE followed by the silver staining technique. The results can
be summarised as follows: (1) Comparison of class I-associated peptides
isolated from a bladder cell line before and after the correction of
class I antigens by gene transfection followed by IB-P technique showed
the presence of peptides only from the class I-corrected cells. The data
were confirmed using the silver staining technique as a way of detecting
individual peptide bands. (2) Whilst peptides could be isolated by both
techniques, the MA method led to the isolation of peptides from both
class I-negative and class I-positive Fen cell lysates. (3) The IB-P
approach could be used for isolation of class I-associated peptides from
a normal kidney tissue. The data showed the high efficiency of the IB-P
approach for isolation of class I-associated peptides. Unlike the MA
technique, where the presence of non- class I-associated peptides was a
problem, the IB-P approach isolated only peptides associated with the
class I antigens. In addition, the data showed the feasibility of
extracting peptides from tissue fragments by the IB-P method. The
approach presented here may assist the future development of peptide
vaccine therapy in urological cancers. Copyright 2002 S. Karger AG,
Basel
22
UI - 11801625
AU - Pelucchi C; Tavani A; Negri E; Franceschi S; La Vecchia C
TI -
Tobacco smoking and bladder cancer in coffee non-drinkers.
SO - J Epidemiol Community Health 2002 Jan;56(1):78-9
23
UI - 11825522
AU - Zhang J; Zheng S; Di X
TI -
[A further study on potential of microsatellite analysis of urine in
diagnosis of bladder cancer]
SO - Zhonghua Yi Xue Za Zhi 2001 Oct 25;81(20):1224-6
AD - Cancer Institute (Hospital), CAMS & PUMC, Beijing 100021, China.
OBJECTIVES: To investigate the application value of microsatellite
analysis of voided urine in diagnosis of bladder cancer and compare the
advantages and disadvantages of this method and urine cytology. METHODS:
Thirteen microsatellite markers, including the nine markers used in the
authors' previous study and another four new markers, were tested on
urine DNA from 143 individuals with or without bladder lesions in a
blinded fashion. Urine cytology was applied at the same time. RESULTS:
The urine DNA from 89% (97/109) of the patients with bladder cancer, 86%
(6/7) of the patients with inverted papilloma of the bladder, 3 out of 7
patients with cystitis and one patient with hematuria of unknown cause
showed alterations, at least, in one of the 13 microsatellite markers,
while the 19 individuals without bladder lesion had no change at any of
these loci. Nucleic atypia or suspicious cancer cells were detected by
routine cytology in the urine of the 3 patients with cystitis and one
patient with hematuria of unknown cause who showed alterations of
microsatellite in their urine sediments. Among the 81 cases of bladder
cancer whose urine was examined by both microsatellite analysis and
routine cytology, 73 cases (90%), of various stage or grade, were
identified by microsatellite analysis, while only 41 cases (51%), mainly
at advanced stage, were detected by cytology. Cancer cells were detected
in the urine sediments of 4 of the 12 cases that were not identified by
microsatellite analysis. CONCLUSION: Microsatellite analysis of urine is
useful for detection of bladder cancer. Microsatellite analysis and
urine cytology could be complementary to each other.
24
UI - 11812940
AU - Oliva E; Amin MB; Jimenez R; Young RH
TI -
Clear cell carcinoma of the urinary bladder: a report and comparison of
four tumors of mullerian origin and nine of probable urothelial origin
with discussion of histogenesis and diagnostic problems.
SO - Am J Surg Pathol 2002 Feb;26(2):190-7
AD - James Homer Wright Pathology Laboratories of the Massachusetts General
Hospital, Harvard Medical School, Fruit Street, Boston, MA 02114, USA.
eoliva@partners.org
Carcinomas of the bladder that resemble clear cell carcinoma of
mullerian type are rare. Whether such neoplasms 1) arise from mullerian
elements in the bladder and are histogenetically identical to the female
genital tract cancer, 2) are a peculiar variant of vesical
adenocarcinoma of nonmullerian derivation, or 3) represent a peculiar
morphologic expression of transitional cell (urothelial) carcinoma with
gland differentiation is often uncertain. We reviewed the clinical,
conventional pathologic, and immunohistochemical features of 13
neoplasms with exclusive, or predominant, morphologic features of clear
cell carcinoma. The 11 female and two male patients were 22-83 (mean 57)
years of age. The clinical and gross features had no unique aspects. On
microscopic examination the most common pattern, present in all cases,
was tubulocystic, with a papillary pattern, present in six tumors and a
predominant solid growth in one. Cells with abundant clear cytoplasm
were conspicuous in nine tumors and hobnail cells were seen in eight.
Four tumors showed focally recognizable patterns of transitional cell
(urothelial) carcinoma in the available material. In five other tumors
pseudostratified epithelium reminiscent of transitional epithelium was
present focally. Endometriosis was present in two cases. In two other
cases benign cysts focally lined by ciliated epithelium and surrounded
by elastosis were interpreted as most likely mullerian.
Immunohistochemistry was performed in 10 cases. All tumors stained for
CA 125 (usually strong, ranging from focal to diffuse) and nine tumors
stained for CK7 (usually strong and diffuse). CK20 was focally and
weakly positive in four tumors and extensively positive in another. The
same immunohistochemical panel was performed on 10 typical transitional
cell carcinomas, 4 transitional cell carcinomas with gland
differentiation, not otherwise specified, and 5 pure adenocarcinomas of
the bladder (one of urachal origin). Minimal CA 125 positivity was seen
in two transitional cell carcinomas. CA 125 staining was seen in the
areas of gland differentiation in three of four transitional cell
carcinomas and three of five pure adenocarcinomas but was focal in most
cases. All transitional cell carcinomas and transitional cell carcinomas
with gland differentiation showed extensive CK7 positivity. In contrast,
only one of four positive pure adenocarcinomas showed >5% CK7-positive
cells. Although all groups showed CK20 positivity, the percentage of
CK20 positive cells was higher in pure adenocarcinomas. Prostate
specific antigen was negative in all tumors. The cytokeratin
immunoprofile of clear cell carcinomas of the bladder is closer to
transitional cell carcinomas and transitional cell carcinomas with gland
differentiation than pure adenocarcinomas arguing against an unusual
form of adenocarcinoma. Our finding of CA 125 expression in bladder
tumors of apparent urothelial origin contrasts with some studies that
have regarded CA 125 expression as evidence for a mullerian origin. The
frequency of gland differentiation in transitional cell carcinomas and
the rarity of vesical endometriosis could be taken to suggest that these
tumors are mostly of urothelial derivation, but the strong female
preponderance in our series argues for a mullerian origin in at least
some cases, and this is almost certain in the four cases with benign
mullerian components. In the absence of endometriosis or conventional
foci of transitional cell carcinoma, it may be impossible to determine
whether a tumor with the morphology of clear cell carcinoma is of
mullerian or transitional (urothelial) cell lineage, and at this time
immunochemistry does not solve this problem.
25
UI - 11812952
AU - McMahon RF; Hunt CR
TI -
In situ adenocarcinoma of the bladder: the role of the urachus.
SO - Am J Surg Pathol 2002 Feb;26(2):271-2
26
UI - 11832713
AU - Neves M; Ciofu C; Larousserie F; Fleury J; Sibony M; Flahault A;
TI -
Soubrier F; Gattegno B
Prospective evaluation of genetic abnormalities and telomerase
expression in exfoliated urinary cells for bladder cancer detection.
SO - J Urol 2002 Mar;167(3):1276-81
AD - Laboratoire d'Histologie, Biologie Tumorale et Genetique Moleculaire,
Service d'Urologie, Hopital TENON, Paris, France.
PURPOSE: To evaluate alternative procedures to cytoscopic examination we
prospectively compared noninvasive procedures for detecting bladder
cancer namely cytology, loss of heterozygosity (LOH), microsatellite
instability and human telomerase catalytic subunit reverse transcriptase
(hTERT) messenger (m) RNA detection. MATERIALS AND METHODS: Specificity
and cutoff values were established in the blood and urine sediment of 50
controls. Sensitivity was analyzed in the urine and tissue samples of 50
patients with bladde
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