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Wake Forest University

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

Abstract

dc:description.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.

Degree

thesis:*
Grantor dc:publisher
Wake Forest University
Year dc:date.issued
2011

Author and committee

dc:creator, dc:contributor.*
Author dc:creator
  • Weckerle, Allison Burrow

Subjects

dc:subject × 1

Rights

Language dc:language.iso
en

Identifiers

dc:identifier.*
Handle dc:identifier.uri
http://hdl.handle.net/10339/33465
OAI identifier oai:identifier
oai:wakespace.lib.wfu.edu:10339/33465

Chain of custody

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Wake Forest University
Base URL
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Last updated
2026-07-27
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citation

Weckerle, Allison Burrow. The Molecular Basis of Fragile Site FRA16B and its Role in inv(16)(p13q22) in Acute Myeloid Leukemia. Wake Forest University, 2011. http://hdl.handle.net/10339/33465