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Updated: Aug 16, 2026
Array Comparative Genomic Hybridization (Array CGH) for Detection of Genomic Copy Number Variants
Published on: February 21, 2015
Array-based comparative genomic hybridization identifies localized DNA amplifications and homozygous deletions in
Murali D Bashyam1, Ryan Bair, Young H Kim
1Department of Pathology, Stanford University, Stanford, CA, USA.
Abstract:
Pancreatic cancer, the fourth leading cause of cancer death in the United States, is frequently associated with the amplification and deletion of specific oncogenes and tumor-suppressor genes (TSGs), respectively. To identify such novel alterations and to discover the underlying genes, we performed comparative genomic hybridization on a set of 22 human pancreatic cancer cell lines, using cDNA microarrays measuring approximately 26,000 human genes (thereby providing an average mapping resolution of <60 kb). To define the subset of amplified and deleted genes with correspondingly altered expression, we also profiled mRNA levels in parallel using the same cDNA microarray platform. In total, we identified 14 high-level amplifications (38-4934 kb in size) and 15 homozygous deletions (46-725 kb). We discovered novel localized amplicons, suggesting previously unrecognized candidate oncogenes at 6p21, 7q21 (SMURF1, TRRAP), 11q22 (BIRC2, BIRC3), 12p12, 14q24 (TGFB3), 17q12, and 19q13. Likewise, we identified novel polymerase chain reaction-validated homozygous deletions indicating new candidate TSGs at 6q25, 8p23, 8p22 (TUSC3), 9q33 (TNC, TNFSF15), 10q22, 10q24 (CHUK), 11p15 (DKK3), 16q23, 18q23, 21q22 (PRDM15, ANKRD3), and Xp11. Our findings suggest candidate genes and pathways, which may contribute to the development or progression of pancreatic cancer.
Insights
Researchers identified novel gene amplifications and deletions in pancreatic cancer cell lines. These findings highlight potential new oncogenes and tumor suppressor genes (TSGs) crucial for understanding pancreatic cancer development and progression.
Area of Science:
- Genomics
- Cancer Biology
- Molecular Oncology
Background:
- Pancreatic cancer is a leading cause of cancer death in the US.
- Genetic alterations, including oncogene amplification and tumor suppressor gene (TSG) deletion, are common in pancreatic cancer.
- Identifying novel genetic changes is crucial for understanding cancer development.
Purpose of the Study:
- To identify novel genetic alterations in human pancreatic cancer cell lines.
- To discover candidate oncogenes and TSGs involved in pancreatic cancer.
- To correlate genomic changes with gene expression.
Main Methods:
- Comparative genomic hybridization (CGH) using cDNA microarrays on 22 pancreatic cancer cell lines.
- Analysis of approximately 26,000 human genes with <60 kb mapping resolution.
- Parallel mRNA expression profiling using the same microarray platform.
Main Results:
- Identified 14 high-level amplifications (38-4934 kb) and 15 homozygous deletions (46-725 kb).
- Discovered novel amplicons suggesting candidate oncogenes at specific chromosomal locations (e.g., 6p21, 7q21, 11q22).
- Identified novel PCR-validated homozygous deletions indicating candidate TSGs at various loci (e.g., 6q25, 8p22, 9q33).
Conclusions:
- The study identified novel candidate oncogenes and TSGs in pancreatic cancer.
- These genetic alterations and associated pathways may play a role in pancreatic cancer initiation and progression.
- Findings provide a foundation for further research into therapeutic targets for pancreatic cancer.
