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An Orthotopic Bladder Cancer Model for Gene Delivery Studies
Published on: December 1, 2013
Can bladder adenocarcinomas be distinguished from schistosomiasis-associated bladder cancers by using array
Hanna Vauhkonen1, Tom Böhling, Saad Eissa
1Department of Pathology, Haartman Institute and HUSLAB, POB 21 (Haartmaninkatu 3), University of Helsinki and Helsinki University Central Hospital, Helsinki, FI-00014, Finland. hanna.vauhkonen@helsinki.fi
Cancer Genetics and Cytogenetics
|September 15, 2007
Summary
Schistosomiasis-associated bladder cancers, particularly adenocarcinomas, exhibit distinct DNA copy number alterations. These genetic changes in bladder cancer may differ based on histology and schistosome infection, revealing unique carcinogenic pathways.
Area of Science:
- Oncology
- Genetics
- Tropical Medicine
Background:
- Bladder cancer is a significant health concern, especially in tropical regions where schistosomiasis is endemic.
- Schistosomiasis-associated (SA) bladder cancers often differ histologically from non-SA cancers, suggesting varied mechanisms of development.
- Adenocarcinomas represent a subset of SA bladder cancers, necessitating detailed genetic investigation.
Purpose of the Study:
- To investigate DNA copy number changes in schistosomiasis-associated bladder adenocarcinomas.
- To compare genetic profiles of SA bladder adenocarcinomas with other bladder cancer subtypes.
Main Methods:
- Oligonucleotide-based comparative genomic hybridization (CGH) array analysis was performed on 10 tumor samples.
- DNA copy number alterations (gains, losses, amplifications) were identified and quantified.
- Genetic profiles were compared with previously reported data for transitional cell carcinoma (TCC) and squamous cell carcinoma (SCC) in the context of schistosomiasis.
Main Results:
- An average of 10 DNA copy number alterations were observed per tumor sample, with frequencies ranging from 2 to 17.
- Frequent gains were identified at chromosomal regions 20q (70%) and 8q (60%).
- Frequent losses were observed at 5q (40%) and 8p (40%). Six regions of amplification were detected in three samples.
- Comparison revealed shared genetic features with SA TCC and SCC, alongside histology-specific alterations, such as gains at 20q for adenocarcinomas.
Conclusions:
- Schistosomiasis-associated bladder adenocarcinomas display characteristic patterns of DNA copy number changes.
- While sharing some genetic similarities with other SA bladder cancers, adenocarcinomas possess unique genetic aberrations.
- These findings contribute to understanding the distinct carcinogenetic pathways in different subtypes of bladder cancer associated with schistosomiasis.
