Cited by 159Pancreatic and Hepatic Oncology ResearchCancer Genomics and DiagnosticsGenomic variations and chromosomal abnormalities

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Genome-wide DNA copy number analysis in pancreatic cancer using high-density single nucleotide polymorphism arrays

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Harada, T, Chelala, C, Bhakta, V, Chaplin, T, Caulee, K, Baril, P, Young, B D, Lemoine, N R·2008·Oncogene

DOI 10.1038/sj.onc.1210832PMC PMC2492386

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Abstract

To identify genomic abnormalities characteristic of pancreatic ductal adenocarcinoma (PDAC) in vivo, a panel of 27 microdissected PDAC specimens were analysed using high-density microarrays representing approximately 116 000 single nucleotide polymorphism (SNP) loci. We detected frequent gains of 1q, 2, 3, 5, 7p, 8q, 11, 14q and 17q (> or =78% of cases), and losses of 1p, 3p, 6, 9p, 13q, 14q, 17p and 18q (> or =44%). Although the results were comparable with those from array CGH, regions of those genetic changes were defined more accurately by SNP arrays. Integrating the Ensembl public data, we have generated 'gene' copy number indices that facilitate the search for novel candidates involved in pancreatic carcinogenesis. Copy numbers in a subset of the genes were validated using quantitative real-time PCR. The SKAP2/SCAP2 gene (7p15.2), which belongs to the src family kinases, was most frequently (63%) amplified in our sample set and its recurrent overexpression (67%) was confirmed by reverse transcription-PCR. Furthermore, fluorescence in situ hybridization and in situ RNA hybridization analyses for this gene have demonstrated a significant correlation between DNA copy number and mRNA expression level in an independent sample set (P<0.001). These findings indicate that the dysregulation of SKAP2/SCAP2, which is mostly caused by its increased gene copy number, is likely to be associated with the development of PDAC.

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Self-citation
Loss of 18q22.3 Involving the Carboxypeptidase of Glutamate-like Gene Is Associated with Poor Prognosis in Resected Pancreatic Cancer
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Sorber, R. A., Teper, Y., Abisoye-Ogunniyan, A., Waterfall, J. J., Davis, S. R., Killian, J. K., Pineda, M. A., Ray, S., McCord, M., Pflicke, H., et al. (2016) · PLoS ONE · doi:10.1371/journal.pone.0149833 · Cited by 26
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“observed frequent gains of chromosome 3 by high-density single nucleotide polymorphism array (78 % of cases), associated with losses in the specific region of chromosome 3p21 [26], this might reflect a propensity for 3p21.”
BackgroundResult
Resequencing Analysis of the Human Tyrosine Kinase Gene Family in Pancreatic Cancer
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Self-citation
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Background
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“In the context of PDAC, chromosome1qamplificationshavebeenpreviouslydescribedthroughSNPar-rays and microarray-based comparative genomic hybridization, as well as most recently in the metastatic setting, but their relevance in noninvasive precursors is relatively unknown (39–41).”
BackgroundResultInfluential
Genomic Instability of Circulating Tumor DNA as a Prognostic Marker for Pancreatic Cancer Survival: A Prospective Cohort Study
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Background

Authors: Harada, T., Chelala, C., Bhakta, V, Chaplin, T., Caulee, K., Baril, P., Young, B. D., & Lemoine, N. R.
Affiliations: University of London (GB)
Corresponding author: Lemoine, N R
ORCID: Harada, T
Chelala, C
Baril, P
Young, B D
Lemoine, N R
Venue: Oncogene
Publisher: Springer Science and Business Media LLC
Published: 2007-10-22
Volume: 27
Issue: 13
Pages: 1951-1960
ISSN: 0950-9232 (ISSN-L)
1476-5594
DOI: 10.1038/sj.onc.1210832
PMC: PMC2492386
OpenAlex: W1997162169
Cited by: 159
References: 34
Citations by year: 2026: 3 · 2025: 3 · 2024: 5 · 2023: 9 · 2022: 9 · 2021: 9 · 2020: 5 · 2019: 5 · 2018: 7 · 2017: 4 · 2016: 10 · 2015: 7 · 2014: 8 · 2013: 8 · 2012: 10
FWCI: 6.56
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.springer.com/tdm (tdm)
www.springer.com/tdm (vor)
Locations: Oncogene (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
HAL (submittedVersion)
Funders: Cancer Research UK (A6438, A6789, A6253)
Topics: Health Sciences › Medicine › Oncology › Pancreatic and Hepatic Oncology Research
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genomic variations and chromosomal abnormalities
Keywords: pancreatic ductal adenocarcinoma, DNA copy number alterations, single nucleotide polymorphism array, gene amplification, gene expression, pancreatic carcinogenesis, chromosomal gains and losses
MeSH terms: Adenocarcinoma, Adult, Aged, Chromosome Aberrations, Chromosomes, Human, DNA, Neoplasm, Female, Humans, Male, Middle Aged, Nucleic Acid Hybridization, Pancreatic Neoplasms, RNA, Neoplasm, In Situ Hybridization, Fluorescence, Gene Dosage, Loss of Heterozygosity, Reverse Transcriptase Polymerase Chain Reaction, Oligonucleotide Array Sequence Analysis, Polymorphism, Single Nucleotide, Carcinoma, Pancreatic Ductal, Microdissection, Intracellular Signaling Peptides and Proteins

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Genome-wide DNA copy number analysis in pancreatic cancer using high-density single nucleotide polymorphism arrays

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