High-resolution genomic and expression profiling reveals 105 putative amplification target genes in pancreatic cancer

Eija Mahlamäki, Päivikki Kauraniemi, Outi Monni, Maija Wolf, Sampsa Hautaniemi, Anne Kallioniemi (Corresponding Author)

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Abstract

Comparative genomic hybridization (CGH) studies have provided a wealth of information on common copy number aberrations in pancreatic cancer, but the genes affected by these aberrations are largely unknown. To identify putative amplification target genes in pancreatic cancer, we performed a parallel copy number and expression survey in 13 pancreatic cancer cell lines using a 12,232-clone cDNA microarray, providing an average resolution of 300 kb throughout the human genome. CGH on cDNA microarray allowed highly accurate mapping of copy number increases and resulted in identification of 24 independent amplicons, ranging in size from 130 kb to 11 Mb. Statistical evaluation of gene copy number and expression data across all 13 cell lines revealed a set of 105 genes whose elevated expression levels were directly attributable to increased copy number. These included genes previously reported to be amplified in cancer as well as several novel targets for copy number alterations, such as p21-activated kinase 4 (PAK4), which was previously shown to be involved in cell migration, cell adhesion, and anchorage-independent growth. In conclusion, our results implicate a set of 105 genes that is likely to be actively involved in the development and progression of pancreatic cancer.
Original languageEnglish
Pages (from-to)432 - 439
Number of pages8
JournalNeoplasia
Volume6
Issue number5
DOIs
Publication statusPublished - 2004
MoE publication typeA1 Journal article-refereed

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Gene Amplification
Pancreatic Neoplasms
Comparative Genomic Hybridization
Oligonucleotide Array Sequence Analysis
p21-Activated Kinases
Genes
Cell Line
Gene Dosage
Neoplasm Genes
Human Genome
Cell Adhesion
Cell Movement
Clone Cells
Growth
Neoplasms

Cite this

Mahlamäki, E., Kauraniemi, P., Monni, O., Wolf, M., Hautaniemi, S., & Kallioniemi, A. (2004). High-resolution genomic and expression profiling reveals 105 putative amplification target genes in pancreatic cancer. Neoplasia, 6(5), 432 - 439. https://doi.org/10.1593/neo.04130
Mahlamäki, Eija ; Kauraniemi, Päivikki ; Monni, Outi ; Wolf, Maija ; Hautaniemi, Sampsa ; Kallioniemi, Anne. / High-resolution genomic and expression profiling reveals 105 putative amplification target genes in pancreatic cancer. In: Neoplasia. 2004 ; Vol. 6, No. 5. pp. 432 - 439.
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Mahlamäki, E, Kauraniemi, P, Monni, O, Wolf, M, Hautaniemi, S & Kallioniemi, A 2004, 'High-resolution genomic and expression profiling reveals 105 putative amplification target genes in pancreatic cancer', Neoplasia, vol. 6, no. 5, pp. 432 - 439. https://doi.org/10.1593/neo.04130

High-resolution genomic and expression profiling reveals 105 putative amplification target genes in pancreatic cancer. / Mahlamäki, Eija; Kauraniemi, Päivikki; Monni, Outi; Wolf, Maija; Hautaniemi, Sampsa; Kallioniemi, Anne (Corresponding Author).

In: Neoplasia, Vol. 6, No. 5, 2004, p. 432 - 439.

Research output: Contribution to journalArticleScientificpeer-review

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AB - Comparative genomic hybridization (CGH) studies have provided a wealth of information on common copy number aberrations in pancreatic cancer, but the genes affected by these aberrations are largely unknown. To identify putative amplification target genes in pancreatic cancer, we performed a parallel copy number and expression survey in 13 pancreatic cancer cell lines using a 12,232-clone cDNA microarray, providing an average resolution of 300 kb throughout the human genome. CGH on cDNA microarray allowed highly accurate mapping of copy number increases and resulted in identification of 24 independent amplicons, ranging in size from 130 kb to 11 Mb. Statistical evaluation of gene copy number and expression data across all 13 cell lines revealed a set of 105 genes whose elevated expression levels were directly attributable to increased copy number. These included genes previously reported to be amplified in cancer as well as several novel targets for copy number alterations, such as p21-activated kinase 4 (PAK4), which was previously shown to be involved in cell migration, cell adhesion, and anchorage-independent growth. In conclusion, our results implicate a set of 105 genes that is likely to be actively involved in the development and progression of pancreatic cancer.

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