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Bladder cancer, a two phased disease?

Höglund, Mattias LU (2007) In Seminars in Cancer Biology 17(3). p.225-232
Abstract
The processes of intraepithelial migration, intraluminal seeding, and field cancerization as models for initiation, spread, and recurrences of urothelial cell carcinoma (UCC) are reviewed in light of recent molecular investigations. The accumulated molecular data on synchronous and metachronous tumors indicate that the majority of recurrent and multiple tumors are monoclonal. Molecular data has also shown the presence of chromosomal and genetic changes in precursor lesions as well as in normal urothelial cells. Genetic-histological mapping of cystectomized bladders has shown that overt tumors occur as local events in areas of genetically altered urothelium. A model is put forward in which the tumor process is initiated by genetically... (More)
The processes of intraepithelial migration, intraluminal seeding, and field cancerization as models for initiation, spread, and recurrences of urothelial cell carcinoma (UCC) are reviewed in light of recent molecular investigations. The accumulated molecular data on synchronous and metachronous tumors indicate that the majority of recurrent and multiple tumors are monoclonal. Molecular data has also shown the presence of chromosomal and genetic changes in precursor lesions as well as in normal urothelial cells. Genetic-histological mapping of cystectomized bladders has shown that overt tumors occur as local events in areas of genetically altered urothelium. A model is put forward in which the tumor process is initiated by genetically altered but histologically normal cells that produce fields of altered cells by intraepithelial displacement. By the accumulation of further genetic changes the fields of altered urothelium reaches a state of criticality, which locally may produce frank tumors. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Seminars in Cancer Biology
volume
17
issue
3
pages
225 - 232
publisher
Academic Press
external identifiers
  • wos:000246860300006
  • scopus:33947163303
ISSN
1096-3650
DOI
10.1016/j.semcancer.2006.02.002
language
English
LU publication?
yes
id
19de8650-bea8-4efd-af8e-c6ca654de326 (old id 156123)
alternative location
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=16574430&dopt=Abstract
date added to LUP
2007-07-07 07:49:39
date last changed
2017-10-01 04:35:38
@article{19de8650-bea8-4efd-af8e-c6ca654de326,
  abstract     = {The processes of intraepithelial migration, intraluminal seeding, and field cancerization as models for initiation, spread, and recurrences of urothelial cell carcinoma (UCC) are reviewed in light of recent molecular investigations. The accumulated molecular data on synchronous and metachronous tumors indicate that the majority of recurrent and multiple tumors are monoclonal. Molecular data has also shown the presence of chromosomal and genetic changes in precursor lesions as well as in normal urothelial cells. Genetic-histological mapping of cystectomized bladders has shown that overt tumors occur as local events in areas of genetically altered urothelium. A model is put forward in which the tumor process is initiated by genetically altered but histologically normal cells that produce fields of altered cells by intraepithelial displacement. By the accumulation of further genetic changes the fields of altered urothelium reaches a state of criticality, which locally may produce frank tumors.},
  author       = {Höglund, Mattias},
  issn         = {1096-3650},
  language     = {eng},
  number       = {3},
  pages        = {225--232},
  publisher    = {Academic Press},
  series       = {Seminars in Cancer Biology},
  title        = {Bladder cancer, a two phased disease?},
  url          = {http://dx.doi.org/10.1016/j.semcancer.2006.02.002},
  volume       = {17},
  year         = {2007},
}