Genetic rearrangements beget genomic instability
Author:
Affiliation:
1. KING'S COLLEGE LONDON
Publisher
American Society of Hematology
Subject
Cell Biology,Hematology,Immunology,Biochemistry
Link
http://ashpublications.org/blood/article-pdf/104/12/3424/1703588/zh802304003417i.pdf
Reference5 articles.
1. Lengauer C, Kinzler KW, Vogelstein B. Genetic instability in colorectal cancers. Nature. 1997;386: 623-627.
2. Mills KD, Ferguson DO, Alt FW. The role of DNA breaks in genomic instability and tumorigenesis. Immunol Rev. 2003;194: 77-95.
3. Brady N, Gaymes TJ, Cheung M, Mufti GJ, Rassool FV. Increased error-prone NHEJ activity in myeloid leukemias is associated with DNA damage at sites that recruit key nonhomologous end-joining proteins. Cancer Res. 2003;63: 1798-1805.
4. Rassool FV. DNA double strand breaks (DSB) and nonhomologous end joining (NHEJ) pathways in human leukemia. Cancer Lett. 2003;193: 1-9.
5. Loeb L. Cancer cells exhibit a mutator phenotype. Adv Cancer Res. 1998;72: 25-55.
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1. Genomic instability in myeloid malignancies: Increased reactive oxygen species (ROS), DNA double strand breaks (DSBs) and error-prone repair;Cancer Letters;2008-10
2. Up-regulation of WRN and DNA ligase IIIα in chronic myeloid leukemia: consequences for the repair of DNA double-strand breaks;Blood;2008-08-15
3. Reactive Oxygen Species, DNA Damage, and Error-Prone Repair: A Model for Genomic Instability with Progression in Myeloid Leukemia?;Cancer Research;2007-09-15
4. Targeting Signal Transduction Pathways in Hematopoietic Disorders;Molecular Basis of Hematopoiesis
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