PMID- 12647351
OWN - NLM
STAT- MEDLINE
DCOM- 20030417
LR  - 20130520
IS  - 0070-4113 (Print)
IS  - 0070-4113 (Linking)
VI  - 86
DP  - 2002
TI  - [Molecular genetics of urinary bladder cancer progression].
PG  - 49-56
AB  - Extensive cytogenetic and molecular analyses have recently helped to gain a much 
      better understanding of the biology of urinary bladder cancer. Early studies had 
      suggested two different pathways of bladder cancer development, one characterized 
      by chromosome 9 losses and the other by p53 mutations. Subsequent studies have 
      greatly expanded these data. Overall, there is compelling evidence for two 
      entirely different bladder tumor entities. One entity consists of genetically 
      unstable tumors that have many cytogenetic alterations, including p53 alterations 
      in about 50% of the cases. Other cytogenetic alterations that can be found 
      frequently in these tumors are deletions of 8p, 9p, 11p, 11q, and Y as well as 
      gains of 1q, 8q, 17q, and 20q. More than 20 chromosomal regions can undergo high 
      level DNA amplification including 17q21 (HER-2/neu). Phenotypically, these tumors 
      are characterized by a high degree of cytological atypia. Their growth pattern 
      can be non-invasive flat (carcinoma in situ), non-invasive papillary (pTaG3) or 
      invasive (papillary or solid). The other, "benign" bladder cancer entity is 
      composed of tumors with a low level of genetic instability, a low number of 
      cytogenetic alterations, and absence of p53 mutations. Morphologically, these 
      tumors are papillary non-invasive neoplasms with a low degree of cytological 
      atypia. Progression to invasively growing carcinoma is extremely rare. 
      CONCLUSION: Molecular studies have revealed profound genetic differences between 
      invasive and non-invasive bladder cancers. This argues against the previously 
      used combination of pTa and pT1 tumor stages as "superficial bladder cancer". The 
      high frequency of genetic alterations in invasive carcinomas enables a markedly 
      improved detection of bladder cancer cells in voided urine using fluorescence in 
      situ hybridization (FISH) assays.
FAU - Sauter, G
AU  - Sauter G
AD  - Institut fur Pathologie, Universitat Basel, Schoenbeinstrasse 40, CH-4031 Basel, 
      Schweiz.
FAU - Simon, R
AU  - Simon R
FAU - Bubendorf, L
AU  - Bubendorf L
FAU - Mihatsch, M
AU  - Mihatsch M
LA  - ger
PT  - English Abstract
PT  - Journal Article
PT  - Review
TT  - Molekulare Genetik der Progression des Urothelkarzinoms.
PL  - Germany
TA  - Verh Dtsch Ges Pathol
JT  - Verhandlungen der Deutschen Gesellschaft fur Pathologie
JID - 7503704
SB  - IM
MH  - *Chromosome Aberrations
MH  - Chromosome Mapping
MH  - Disease Progression
MH  - Humans
MH  - Molecular Biology/methods
MH  - Urinary Bladder Neoplasms/*genetics/*pathology
RF  - 32
EDAT- 2003/03/22 04:00
MHDA- 2003/04/18 05:00
CRDT- 2003/03/22 04:00
PHST- 2003/03/22 04:00 [pubmed]
PHST- 2003/04/18 05:00 [medline]
PHST- 2003/03/22 04:00 [entrez]
PST - ppublish
SO  - Verh Dtsch Ges Pathol. 2002;86:49-56.