Bladder cancer, a two phased disease?
(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)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/156123
- author
- Höglund, Mattias LU
- organization
- publishing date
- 2007
- 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
- 2016-04-01 15:34:20
- date last changed
- 2022-01-28 06:00:02
@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 = {{https://lup.lub.lu.se/search/files/4423179/625434.pdf}},
doi = {{10.1016/j.semcancer.2006.02.002}},
volume = {{17}},
year = {{2007}},
}