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The Molecular Basis of Fragile Site FRA16B and its Role in inv(16)(p13q22) in Acute Myeloid Leukemia

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abstract
Fragile sites are regions of the human genome especially susceptible to DNA breakage and have been suggested to play a role in cancer development. Several studies have determined that fragile site locations correspond to DNA breakpoints in a number of chromosomal rearrangements observed in tumor cells, but there has been no comprehensive examination of the location of fragile sites relative to breakpoints in all known cancer-specific abnormalities, or direct evidence of a role for fragile sites in tumorigenesis. Furthermore, the mechanism of fragile site breakage remains unclear, making it difficult to identify potential risk factors or determine the involvement of fragile site breakage in chromosomal rearrangements. With an increasing number of fragile sites being mapped and cancer cases on the rise, it is becoming even more important to identify a role for these highly breakable regions in cancer development and the molecular basis of their breakage. The purpose of the studies in this work was to investigate the involvement of fragile sites in the formation of cancer-specific chromosomal rearrangements and the underlying mechanism of fragile site breakage.
subject
acute myeloid leukemia
DNA secondary structure
FRA16B
fragile site
inv(16)(p13q22)
contributor
Weckerle, Allison Burrow (author)
Wang, Yuh-Hwa (committee chair)
Ornelles, David (committee member)
Perrino, Fred W (committee member)
Koty, Patrick P (committee member)
Wilkinson, John C (committee member)
date
2011-07-14T20:35:50Z (accessioned)
2012-01-14T09:30:13Z (available)
2011 (issued)
degree
Biochemistry and Molecular Biology (discipline)
embargo
2012-01-14 (terms)
identifier
http://hdl.handle.net/10339/33465 (uri)
language
en (iso)
publisher
Wake Forest University
title
The Molecular Basis of Fragile Site FRA16B and its Role in inv(16)(p13q22) in Acute Myeloid Leukemia
type
Dissertation

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