ArticleGenome biology2007
Genome position and gene amplification.
Article in Genome biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed.
- Recent advances and application of whole genome amplification in molecular diagnosis and medicine.MedComm · 2022Review
- Article
- Complex chromosomal neighborhood effects determine the adaptive potential of a gene under selection.eLife · 2017Article
- Engineering targeted chromosomal amplifications in human breast epithelial cells.Breast cancer research and treatment · 2015Article
- Genomic organization and evolution of double minutes/homogeneously staining regions with MYC amplification in human cancer.Nucleic acids research · 2014Article
- Regulatory mechanisms that prevent re-initiation of DNA replication can be locally modulated at origins by nearby sequence elements.PLoS genetics · 2014Article
- Cancer quasispecies and stem-like adaptive aneuploidy.F1000Research · 2013Article
- Article
- Amplification of c-MYC and MLL Genes as a Marker of Clonal Cell Progression in Patients with Myeloid Malignancy and Trisomy of Chromosomes 8 or 11.Balkan journal of medical genetics : BJMG · 2011Article
- Gene amplification in human cells knocked down for RAD54.Genome integrity · 2011Article
- Germline variation controls the architecture of somatic alterations in tumors.PLoS genetics · 2010Article
- Gene amplification as double minutes or homogeneously staining regions in solid tumors: origin and structure.Genome research · 2010Article
- The DNA damage-binding protein XPC is a frequent target for inactivation in squamous cell carcinomas.The American journal of pathology · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
backgroundAmplifications, regions of focal high-level copy number change, lead to overexpression of oncogenes or drug resistance genes in tumors. Their presence is often associated with poor prognosis; however, the use of amplification as a mechanism for overexpression of a particular gene in tumors varies. To investigate the influence of genome position on propensity to amplify, we integrated a mutant form of the gene encoding dihydrofolate reductase into different positions in the human genome, challenged cells with methotrexate and then studied the genomic alterations arising in drug resistant cells.
resultsWe observed site-specific differences in methotrexate sensitivity, amplicon organization and amplification frequency. One site was uniquely associated with a significantly enhanced propensity to amplify and recurrent amplicon boundaries, possibly implicating a rare folate-sensitive fragile site in initiating amplification. Hierarchical clustering of gene expression patterns and subsequent gene enrichment analysis revealed two clusters differing significantly in expression of MYC target genes independent of integration site.
conclusionThese studies suggest that genome context together with the particular challenges to genome stability experienced during the progression to cancer contribute to the propensity to amplify a specific oncogene or drug resistance gene, whereas the overall functional response to drug (or other) challenge may be independent of the genomic location of an oncogene.
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