Genome-wide DNA copy number analysis in pancreatic cancer using high-density single nucleotide polymorphism arrays
Open accessAbstract
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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Previously described hallmark genomic events characteristic of PDAC lesions were observed in pseudo-bulk summary, in some cases only in a subset of genomic subclones for each line.
“In this “pseudo-bulk” summary, previously described hallmark genomic events characteristic of PDAC lesions1–6 were readily observed, albeit in some cases only in a subset of genomic subclones for each line.”
From Occult polyclonality of preclinical pancreatic cancer models drives in vitro evolution (2022) · cites this paper as [3]
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Cites
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BackgroundMethodInfluentialHigh-Resolution Analysis of DNA Copy Number Using Oligonucleotide MicroarraysPreprint
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“…arrays has allowed genome-wide, high-resolution analysis of both DNA copy number (DCN) alterations and loss of heterozygosity (LOH) events in cancer cells (Lindblad-Toh et al., 2000; Bignell et al., 2004; Huang et al., 2004; Janne et al., 2004; Zhao et al., 2004, 2005; Midorikawa et al., 2006).”
BackgroundMolecular karyotyping of human hepatocellular carcinoma using single-nucleotide polymorphism arrays
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“Analysing matched normal DNA in parallel with tumour DNA, SNP arrays can be a powerful tool for the genome-wide detection of LOH/UPD regions because we could completely exclude consanguinity as a cause of homozygosity (Fitzgibbon et al., 2005; Raghavan et al., 2005; Andersen et al., 2007).”
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ResultConsistent chromosome abnormalities in adenocarcinoma of the pancreas
Griffin, C. A., Hruban, R. H., Morsberger, L. A., Ellingham, T. J., Long, P. P., Jaffee, E. M., Houda, K. M., Bohlander, S. K., & Yeo, C. J. (1995) · Cancer Genetics and Cytogenetics · doi:10.1016/0165-4608(96)85235-6 · Cited by 53 · cited 1× · see citing works
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“Chromosome arm 7p has long been suspected to include critical oncogenes in PDAC (Griffin et al., 1995; Harada et al., 2002a; Karhu et al., 2006).”
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“87, respectively, corresponding to ±2 standard deviation (see Harada et al., 2007 for more details).”
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“SCAP2 was originally described as a substrate for the src family kinases able to regulate the phosphorylation of the presynaptic protein a-Synuclein; a process considered to be crucial in the pathogenesis of several neurodegenerative diseases including Parkinson’s disease (Takahashi et al., 2003).”
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“These results are in agreement with previous reports (Schleger et al., 2000; Harada et al., 2002, 2008, 2009; Karhu et al., 2006).”
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“In human cancers, LOH at chromosome 3p is frequently observed (Yamano et al. 2000; Harada et al. 2008; Toma et al. 2008).”
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BackgroundLi, X., Galipeau, P. C., Sanchez, C. A., Blount, P. L., Maley, C. C., Arnaudo, J., Peiffer, D. A., Pokholok, D., Gunderson, K. L., & Reid, B. J. (2008) · Cancer Prevention Research · doi:10.1158/1940-6207.capr-08-0121 · Cited by 75 · see citing works
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“Recently, Peutz-Jeghers syndrome, single nucleotide polymorphisms (SNPs), hereditary pancreatitis, and a 5-10% family history of PC have also been added as PC risk factors [16, 35, 39].”
BackgroundPancreatic cancerDNMT1expression and sensitivity toDNMT1inhibitors
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PI3K keeps the balance between metabolism and cancer
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Transcriptional dissection of pancreatic tumors engrafted in mice
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“Pancreas ductal adenocarcinoma (PDAC) is usually diagnosed in advanced stages after it has metastasized to regional lymph nodes, liver or lung [15] and the median survival after diagnosis is approximately 8 months [16].”
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Genomic Heterogeneity of Pancreatic Ductal Adenocarcinoma and Its Clinical Impact
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The Genomic Landscape of Pancreatic and Periampullary Adenocarcinoma
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Copy Number Variations in Pancreatic Cancer: From Biological Significance to Clinical Utility
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“2) to further confirm their role in the disease [75,76,115–129].”
BackgroundMethodInfluentialDiNAMIC: a method to identify recurrent DNA copy number aberrations in tumors
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NPAS3 Demonstrates Features of a Tumor Suppressive Role in Driving the Progression of Astrocytomas
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Genomic heterogeneity in pancreatic cancer organoids and its stability with culture
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“The copy number of some genes, including the four most common driver mutation genes 27 : KRAS , CDKN2A , TP53 , and SMAD4 , are also frequently altered in PDAC 28 .”
Implementing precision cancer medicine in the genomic era
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Molecular Subtyping of Pancreatic Cancer: Translating Genomics and Transcriptomics into the Clinic
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Occult polyclonality of preclinical pancreatic cancer models drives in vitro evolution
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Molecular changes in pancreatic cancer
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Genome-Wide Mapping Of Copy Number Variations using SNP Arrays
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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.”
BackgroundResultResequencing Analysis of the Human Tyrosine Kinase Gene Family in Pancreatic Cancer
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Genome-wide analyses of cell-free DNA for therapeutic monitoring of patients with pancreatic cancer
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“3B) ( 45 , 46 ).”
The molecular landscape of pancreatic ductal adenocarcinoma
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Molecular Genetics of Pancreatic Neoplasms
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Immunodeficiency in Pancreatic Adenocarcinoma with Diabetes Revealed by Comparative Genomics
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CYLD deficiency promotes pancreatic cancer development by causing mitotic defects
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“Analysis of copy number of DNA in patients with pancreatic ductal adenocarcinoma indicate numerous regions in DNA where losses and gains of copies appears [23, 24].”
BackgroundGenetic Load and Potential Mutational Meltdown in Cancer Cell Populations
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Deletion of 17p in cancers: Guilt by (p53) association
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“…aberration observed in many cancers [1 – 4]. del17p is particularly common in solid cancers such as pancreatic ductal adenocarcinomas and colorectal carcinomas where more than 60% of tumours have been reported to contain malignant cells bearing this copy number alteration (CNA) [1, 5 – 7].”
Pancreatic ductal adenocarcinoma in the era of precision medicine
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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).”
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Genetic Variant Associated With Survival of Patients With Stage II-III Colon Cancer
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Basic Principles and Technologies for Deciphering the Genetic Map of Cancer
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“High-throughput screening analyses have identified a multitude of differences between malignant and benign processes in the pancreas, as well as between different malignant tumor entities, on the genome [16–19], transcriptome [20–33], proteome [34–38], and epigenome [39–42] levels.”
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
- Venue
- Oncogene
- Published
- 2007-10-22
- Volume
- 27
- Issue
- 13
- Pages
- 1951-1960
- ISSN
- 0950-9232 (ISSN-L)
- 1476-5594
- 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
- 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
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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