Frequent amplification of 8q24, 11q, 17q, and 20q-specific genes in pancreatic cancer
(2002) In Genes, Chromosomes and Cancer 35(4). p.353-358- Abstract
- Genetic changes involved in the development and progression of pancreatic cancer are still partly unknown, despite the progress in recent years. In this study, comparative genomic hybridization analysis in 31 pancreatic cancer cell lines showed that chromosome arms 8q, 11q, 17q, and 20q are frequently gained in this tumor type. Copy number analysis of selected genes from these chromosome arms by fluorescence in situ hybridization showed amplification of the MYC oncogene in 54% of the cell lines, whereas CCNDI was amplified in 28%. In the 17q arm, the ERB82 oncogene was amplified in 20% of the cell lines, TBX2 in 50%, and BIRC5 in 58%, indicating increased involvement toward the q telonnere of chromosome 17. In the 20q arm, the... (More)
- Genetic changes involved in the development and progression of pancreatic cancer are still partly unknown, despite the progress in recent years. In this study, comparative genomic hybridization analysis in 31 pancreatic cancer cell lines showed that chromosome arms 8q, 11q, 17q, and 20q are frequently gained in this tumor type. Copy number analysis of selected genes from these chromosome arms by fluorescence in situ hybridization showed amplification of the MYC oncogene in 54% of the cell lines, whereas CCNDI was amplified in 28%. In the 17q arm, the ERB82 oncogene was amplified in 20% of the cell lines, TBX2 in 50%, and BIRC5 in 58%, indicating increased involvement toward the q telonnere of chromosome 17. In the 20q arm, the amplification frequencies varied from 32% to 83%, with the CTSZ gene at 20q 13 being most frequently affected. These results illustrate that amplification of genes from the 8q, 11q, 17q, and 20q chromosome arms is common in pancreatic cancer. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/324509
- author
- Mahlamaki, EH ; Barlund, M ; Tanner, M ; Gorunova, Ludmila LU ; Höglund, Mattias LU ; Karhu, R and Kallioniemi, A
- organization
- publishing date
- 2002
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Genes, Chromosomes and Cancer
- volume
- 35
- issue
- 4
- pages
- 353 - 358
- publisher
- John Wiley & Sons Inc.
- external identifiers
-
- wos:000178878900007
- pmid:12378529
- scopus:0036883715
- ISSN
- 1045-2257
- DOI
- 10.1002/gcc.10122
- language
- English
- LU publication?
- yes
- id
- 2e4b9dcf-561d-4726-8d7d-706c89f3ec32 (old id 324509)
- date added to LUP
- 2016-04-01 12:17:29
- date last changed
- 2022-01-27 01:34:06
@article{2e4b9dcf-561d-4726-8d7d-706c89f3ec32, abstract = {{Genetic changes involved in the development and progression of pancreatic cancer are still partly unknown, despite the progress in recent years. In this study, comparative genomic hybridization analysis in 31 pancreatic cancer cell lines showed that chromosome arms 8q, 11q, 17q, and 20q are frequently gained in this tumor type. Copy number analysis of selected genes from these chromosome arms by fluorescence in situ hybridization showed amplification of the MYC oncogene in 54% of the cell lines, whereas CCNDI was amplified in 28%. In the 17q arm, the ERB82 oncogene was amplified in 20% of the cell lines, TBX2 in 50%, and BIRC5 in 58%, indicating increased involvement toward the q telonnere of chromosome 17. In the 20q arm, the amplification frequencies varied from 32% to 83%, with the CTSZ gene at 20q 13 being most frequently affected. These results illustrate that amplification of genes from the 8q, 11q, 17q, and 20q chromosome arms is common in pancreatic cancer.}}, author = {{Mahlamaki, EH and Barlund, M and Tanner, M and Gorunova, Ludmila and Höglund, Mattias and Karhu, R and Kallioniemi, A}}, issn = {{1045-2257}}, language = {{eng}}, number = {{4}}, pages = {{353--358}}, publisher = {{John Wiley & Sons Inc.}}, series = {{Genes, Chromosomes and Cancer}}, title = {{Frequent amplification of 8q24, 11q, 17q, and 20q-specific genes in pancreatic cancer}}, url = {{http://dx.doi.org/10.1002/gcc.10122}}, doi = {{10.1002/gcc.10122}}, volume = {{35}}, year = {{2002}}, }