PMID- 11830537
OWN - NLM
STAT- MEDLINE
DCOM- 20020305
LR  - 20151119
IS  - 0008-5472 (Print)
IS  - 0008-5472 (Linking)
VI  - 62
IP  - 3
DP  - 2002 Feb 1
TI  - Occurrence of chromosome 9 and p53 alterations in multifocal dysplasia and 
      carcinoma in situ of human urinary bladder.
PG  - 809-18
AB  - To define the genetic changes of flat urothelial lesions, carcinoma in situ (CIS) 
      and moderate dysplasias (DII) were investigated for alterations in the two 
      chromosomal regions most frequently involved in bladder cancer. Overall, 33 CIS 
      and 16 DII from 21 patients were used to microdissect urothelium. Dual color 
      fluorescence in situ hybridization (FISH) using gene locus probes of 9q22 (FACC), 
      9p21 (CDK), 17p13 (p53), and related centromeric probes was applied on interphase 
      nuclei. In parallel, preamplified DNA of these samples was used for loss of 
      heterozygosity (LOH) analyses with eight microsatellite markers on chromosomes 
      9p, 9q and 17p, and for sequencing of exons 5-9 of p53. Data indicated nearly 
      identical deletion frequencies for chromosomes 9 and 17 for CIS (chromosome 9, 
      86%; p53, 84%). DII showed a lower deletion rate in comparison with CIS 
      (chromosome 9, 75%; p53, 53%). A very high correlation between the results of 
      FISH and LOH analyses was found. p53 mutations were detected in 12 of 15 patients 
      (CIS, 72%; DII, 67%). In three of 16 patients with multifocal tumors, oligoclonal 
      lesions were identified by LOH analyses, a finding further supported by 
      sequencing of p53, by which two different p53 deletions were detected in two 
      cases. In conclusion, data from microdissected flat urothelial lesions indicate 
      that chromosome 9 deletions cannot be regarded as indicators of papillary growth, 
      because they are found frequently in both types of flat lesions of the 
      urothelium: those associated with papillary tumors and those that are not. The 
      similar distribution and lower amount of genetic changes in DII render DII a 
      possible precursor lesion of CIS.
FAU - Hartmann, Arndt
AU  - Hartmann A
AD  - Institute of Pathology, University of Regensburg, Franz Josef Strauss Allee 11, 
      D-93042 Regensburg, Germany.
FAU - Schlake, Gudrun
AU  - Schlake G
FAU - Zaak, Dirk
AU  - Zaak D
FAU - Hungerhuber, Edwin
AU  - Hungerhuber E
FAU - Hofstetter, Alfons
AU  - Hofstetter A
FAU - Hofstaedter, Ferdinand
AU  - Hofstaedter F
FAU - Knuechel, Ruth
AU  - Knuechel R
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Cancer Res
JT  - Cancer research
JID - 2984705R
RN  - 0 (Photosensitizing Agents)
RN  - 88755TAZ87 (Aminolevulinic Acid)
SB  - IM
MH  - Aged
MH  - Aged, 80 and over
MH  - Aminolevulinic Acid
MH  - Carcinoma in Situ/*genetics
MH  - *Chromosome Aberrations
MH  - Chromosomes, Human, Pair 17/genetics
MH  - *Chromosomes, Human, Pair 9
MH  - Exons
MH  - Female
MH  - Gene Deletion
MH  - Genes, p53/*genetics
MH  - Humans
MH  - In Situ Hybridization, Fluorescence
MH  - Loss of Heterozygosity
MH  - Male
MH  - Middle Aged
MH  - Photosensitizing Agents
MH  - Precancerous Conditions/*genetics
MH  - Urinary Bladder/pathology
MH  - Urinary Bladder Neoplasms/*genetics
EDAT- 2002/02/07 10:00
MHDA- 2002/03/07 10:01
CRDT- 2002/02/07 10:00
PHST- 2002/02/07 10:00 [pubmed]
PHST- 2002/03/07 10:01 [medline]
PHST- 2002/02/07 10:00 [entrez]
PST - ppublish
SO  - Cancer Res. 2002 Feb 1;62(3):809-18.