ArticleJournal of autism and developmental disorders2008
Sequencing and analyzing the t(1;7) reciprocal translocation breakpoints associated with a case of childhood-onset schizophrenia/autistic disorder.
Article in Journal of autism and developmental disorders, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 1 synthesis or guideline pooled it, 8 citations in OpenAlex.
- Childhood-Onset Schizophrenia: A Systematic Overview of Its Genetic Heterogeneity From Classical Studies to the Genomic Era.Frontiers in genetics · 2019Pooled it
- Cellular reprogramming: a novel tool for investigating autism spectrum disorders.Trends in molecular medicine · 2012Review
- Sex chromosome anomalies in childhood onset schizophrenia: an update.Molecular psychiatry · 2008Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
We characterized a t(1;7)(p22;q21) reciprocal translocation in a patient with childhood-onset schizophrenia (COS) and autism using genome mapping and sequencing methods. Based on genomic maps of human chromosome 7 and fluorescence in situ hybridization (FISH) studies, we delimited the region of 7q21 harboring the translocation breakpoint to a approximately 16-kb interval. A cosmid containing the translocation-associated 1:7 junction on der(1) was isolated and sequenced, revealing the positions on chromosomes 1 and 7, respectively, where the translocation occurred. PCR-based studies enabled the isolation and sequencing of the reciprocal 7:1 junction on der(7). No currently recognized gene on either chromosome appears to be disrupted by the translocation. We further found no evidence for copy-number differences in the genomic regions flanking the translocation junctions in the patient. Our efforts provide sequence-based information about a schizophrenia/autism-associated translocation, and may facilitate future studies investigating the genetic bases of these disorders.
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