ArticleAmerican journal of human genetics2004
The breakpoint region of the most common isochromosome, i(17q), in human neoplasia is characterized by a complex genomic architecture with large, palindromic, low-copy repeats.
Article in American journal of human genetics, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
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Who cites it
63 citing papers in PubMed, 125 citations in OpenAlex.
- Identification of novel NUP98::RARA fusion transcripts in acute promyelocytic leukemia with i(17)(q10) abnormality.American journal of cancer research · 2025Article
- Sex-specific DNA-replication in the early mammalian embryo.Nature communications · 2024Article
- Article
- Breaking the paradigm: early insights from mammalian DNA breakomes.The FEBS journal · 2022Review
- Myelodysplastic/myeloproliferative neoplasms-unclassifiable with isolated isochromosome 17q represents a distinct clinico-biologic subset: a multi-institutional collaborative study from the Bone Marrow Pathology Group.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2022Article
- Whole-chromosome arm acquired uniparental disomy in cancer development is a consequence of isochromosome formation.Neoplasia (New York, N.Y.) · 2022Article
- Clan genomics: From OMIM phenotypic traits to genes and biology.American journal of medical genetics. Part A · 2021Article
- Article
- The fragility of a structurally diverse duplication block triggers recurrent genomic amplification.Nucleic acids research · 2021Article
- A reference catalog of DNA palindromes in the human genome and their variations in 1000 Genomes.Human genome variation · 2020Article
- Cruciform DNA in mouse growing oocytes: Its dynamics and its relationship with DNA transcription.PloS one · 2020Article
- From gene editing to genome engineering: restructuring plant chromosomes via CRISPR/Cas.aBIOTECH · 2020Review
- Chromosomal Density of Cancer Up-Regulated Genes, Aberrant Enhancer Activity and Cancer Fitness Genes Are Associated with Transcriptional Cis-Effects of Broad Copy Number Gains in Colorectal Cancer.International journal of molecular sciences · 2019Article
- 2018 Victor A. McKusick Leadership Award: Molecular Mechanisms for Genomic and Chromosomal Rearrangements.American journal of human genetics · 2019Article
- The dark side of centromeres: types, causes and consequences of structural abnormalities implicating centromeric DNA.Nature communications · 2018Review
- Mutation, methylation, and gene expression profiles in dup(1q)-positive pediatric B-cell precursor acute lymphoblastic leukemia.Leukemia · 2018Article
- Unusual de novo Partial Trisomy 17p12p11.2 due to Unbalanced Insertion into 5p13.1 in a Severely Affected Boy.Journal of pediatric genetics · 2017Article
- Myeloid neoplasms with isolated isochromosome 17q demonstrate a high frequency of mutations in SETBP1, SRSF2, ASXL1 and NRAS.Oncotarget · 2016Article
- Nonrecurrent 17p11.2p12 Rearrangement Events that Result in Two Concomitant Genomic Disorders: The PMP22-RAI1 Contiguous Gene Duplication Syndrome.American journal of human genetics · 2015Article
- Jumping translocations, a novel finding in chronic lymphocytic leukaemia.British journal of haematology · 2015Article
3 more citing papers are in PubMed but not listed here.
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Authors and funding
12 authors at 5 institutions in 3 countries.
Funding
Abstract
Although a great deal of information has accumulated regarding the mechanisms underlying constitutional DNA rearrangements associated with inherited disorders, virtually nothing is known about the molecular processes involved in acquired neoplasia-associated chromosomal rearrangements. Isochromosome 17q, or "i(17q)," is one of the most common structural abnormalities observed in human neoplasms. We previously identified a breakpoint cluster region for i(17q) formation in 17p11.2 and hypothesized that genome architectural features could be responsible for this clustering. To address this hypothesis, we precisely mapped the i(17q) breakpoints in 11 patients with different hematologic malignancies and determined the genomic structure of the involved region. Our results reveal a complex genomic architecture in the i(17q) breakpoint cluster region, characterized by large ( approximately 38-49-kb), palindromic, low-copy repeats, strongly suggesting that somatic rearrangements are not random events but rather reflect susceptibilities due to the genomic structure.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.