Refined physical mapping of chromosome 16-specific low-abundance repetitive DNA sequences (original) (raw)
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1993
This article was originally published in
Cytogenetics and Cell Genetics
Research Articles| May 14 2008
aDepartment of Human Genetics, University of Pittsburgh, Pittsburgh, PA (USA);
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bDepartment of Cytogenetics and Molecular Genetics, Adelaide Children’s Hospital, North Adelaide, South Australia (Australia); and
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cCenter for Human Genome Studies and Life Sciences Division, Los Alamos National Laboratory, Los Alamos, NM (USA)
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bDepartment of Cytogenetics and Molecular Genetics, Adelaide Children’s Hospital, North Adelaide, South Australia (Australia); and
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Cytogenetics and Cell Genetics (1993) 63 (2): 97–101.
Abstract
Repetitive DNA sequences have been implicated in the origin of several disease phenotypes, including fragile X syndrome, myotonic dystrophy, and spinal bulbar atrophy. In addition, complex family of chromosome 16-specific low-abundance repetitive (CH16LAR) DNA sequences have been mapped by fluorescence in situ hybridization to regions of chromosome a 16 that undergo breakage/rearrangement in acute nonlymphocytic leukemia (ANLL) cells. It has been hypothesized that these repetitive sequences are causally related to the chromosome rearrangements found in ANLL. Here, we further refine the mapping of CHI 6LAR sequences with respect to the ANLL inversion breakpoints, using a panel of somatic cell hybrids containing 51 different chromosome 16 breakpoints. These studies indicate that CH16LAR sequences at 16p13 are in close proximity to the ANLL short-arm breakpoint region. However, the region containing the highest density of CH16LAR sequences on the long arm appears to be distal to the region where the ANLL long-arm breakpoint has been mapped. These studies further show that CHI 6LAR sequences map in close proximity to FRA16D and FRA16A.
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© 1993 S. Karger AG, Basel
1993
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