Abstract
| Original language | English |
|---|---|
| Pages (from-to) | 432-439 |
| Journal | Neoplasia |
| Volume | 6 |
| Issue number | 5 |
| DOIs | |
| Publication status | Published - 2004 |
| MoE publication type | A1 Journal article-refereed |
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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 journal › Article › Scientific › peer-review
TY - JOUR
T1 - High-resolution genomic and expression profiling reveals 105 putative amplification target genes in pancreatic cancer
AU - Mahlamäki, Eija
AU - Kauraniemi, Päivikki
AU - Monni, Outi
AU - Wolf, Maija
AU - Hautaniemi, Sampsa
AU - Kallioniemi, Anne
PY - 2004
Y1 - 2004
N2 - 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.
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.
U2 - 10.1593/neo.04130
DO - 10.1593/neo.04130
M3 - Article
VL - 6
SP - 432
EP - 439
JO - Neoplasia
JF - Neoplasia
SN - 1522-8002
IS - 5
ER -