ArticleScientific reports2017
Palindromic amplification of the ERBB2 oncogene in primary HER2-positive breast tumors.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 41 citations in OpenAlex.
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- Short Inverted Repeats as Mutational Hotspots and Putative Drivers of Genome Instability in Osteosarcoma.Genes · 2025Article
- Breakage fusion bridge cycles drive high oncogene number with moderate intratumoural heterogeneity.Nature communications · 2025Article
- RNA polymerase II at histone genes predicts outcome in human cancer.Science (New York, N.Y.) · 2025Article
- RNA Polymerase II hypertranscription at histone genes in cancer FFPE samples.bioRxiv : the preprint server for biology · 2024Article
- Depicting Biomarkers for HER2-Inhibitor Resistance: Implication for Therapy in HER2-Positive Breast Cancer.Cancers · 2024Review
- HER2 copy number determination in breast cancer using the highly sensitive droplet digital PCR method.Virchows Archiv : an international journal of pathology · 2024Article
- Insights into the mechanisms and structure of breakage-fusion-bridge cycles in cervical cancer using long-read sequencing.American journal of human genetics · 2024Article
- Aneuploidy and complex genomic rearrangements in cancer evolution.Nature cancer · 2024Review
- A Practical Approach for Targeting Structural Variants Genome-wide in Plasma Cell-free DNA.Research square · 2024Article
- A unifying model that explains the origins of human inverted copy number variants.PLoS genetics · 2024Review
- Breakage fusion bridge cycles drive high oncogene copy number, but not intratumoral genetic heterogeneity or rapid cancer genome change.bioRxiv : the preprint server for biology · 2023Article
- Genome-Wide Analysis of Palindrome Formation with Next-Generation Sequencing (GAPF-Seq) and a Bioinformatics Pipeline for Assessing De Novo Palindromes in Cancer Genomes.Methods in molecular biology (Clifton, N.J.) · 2023Article
- HER2 Overexpression and Cytogenetical Patterns in Canine Mammary Carcinomas.Veterinary sciences · 2022Article
- Extrachromosomal DNA in Cancer.Annual review of genomics and human genetics · 2022Review
- Multi-omic cross-sectional cohort study of pre-malignant Barrett's esophagus reveals early structural variation and retrotransposon activity.Nature communications · 2022Article
- The Mammalian Ecdysoneless Protein Interacts with RNA Helicase DDX39A To Regulate Nuclear mRNA Export.Molecular and cellular biology · 2021Article
- Alternative DNA StructuresMicrobiology and molecular biology reviews : MMBR · 2021Review
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Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Oncogene amplification confers a growth advantage to tumor cells for clonal expansion. There are several, recurrently amplified oncogenes throughout the human genome. However, it remains unclear whether this recurrent amplification is solely a manifestation of increased fitness resulting from random amplification mechanisms, or if a genomic locus-specific amplification mechanism plays a role. Here we show that the ERBB2 oncogene at 17q12 is susceptible to palindromic gene amplification, a mechanism characterized by the inverted (palindromic) duplication of genomic segments, in HER2-positive breast tumors. We applied two genomic approaches to investigate amplification mechanisms: sequencing of DNA libraries enriched with tumor-derived palindromic DNA (Genome-wide Analysis of Palindrome Formation) and whole genome sequencing (WGS). We observed significant enrichment of palindromic DNA within amplified ERBB2 genomic segments. Palindromic DNA was particularly enriched at amplification peaks and at boundaries between amplified and normal copy-number regions. Thus, palindromic gene amplification shaped the amplified ERBB2 locus. The enrichment of palindromic DNA throughout the amplified segments leads us to propose that the ERBB2 locus is amplified through the mechanism that repeatedly generates palindromic DNA, such as Breakage-Fusion-Bridge cycles. The genomic architecture surrounding ERBB2 in the normal genome, such as segmental duplications, could promote the locus-specific mechanism.
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