Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2006-1-10
pubmed:abstractText
Recurrent reciprocal translocations are present in many hematologic and mesenchymal malignancies. Because significant sequence homology is absent from translocation breakpoint junctions, non-homologous end-joining (NHEJ) pathways of DNA repair are presumed to catalyze their formation. We developed translocation reporters for use in mammalian cells from which NHEJ events can be selected after precise chromosomal breakage. Translocations were efficiently recovered with these reporters using mouse cells, and their breakpoint junctions recapitulated findings from oncogenic translocations. Small deletions and microhomology were present in most junctions; insertions and more complex events also were observed. Thus, our reporters model features of oncogenic rearrangements in human cancer cells. A homologous sequence at a distance from the break site affected the translocation junction without substantially altering translocation frequency. Interestingly, in a direct comparison, the spectrum of translocation breakpoint junctions differed from junctions derived from repair at a single chromosomal break, providing mechanistic insight into translocation formation.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/16195334-10467413, http://linkedlifedata.com/resource/pubmed/commentcorrection/16195334-10864328, http://linkedlifedata.com/resource/pubmed/commentcorrection/16195334-11074004, http://linkedlifedata.com/resource/pubmed/commentcorrection/16195334-11607811, http://linkedlifedata.com/resource/pubmed/commentcorrection/16195334-11751629, http://linkedlifedata.com/resource/pubmed/commentcorrection/16195334-11870614, http://linkedlifedata.com/resource/pubmed/commentcorrection/16195334-11902580, http://linkedlifedata.com/resource/pubmed/commentcorrection/16195334-11915950, http://linkedlifedata.com/resource/pubmed/commentcorrection/16195334-11983152, http://linkedlifedata.com/resource/pubmed/commentcorrection/16195334-12508246, http://linkedlifedata.com/resource/pubmed/commentcorrection/16195334-12760073, http://linkedlifedata.com/resource/pubmed/commentcorrection/16195334-12951583, http://linkedlifedata.com/resource/pubmed/commentcorrection/16195334-14506474, http://linkedlifedata.com/resource/pubmed/commentcorrection/16195334-15485900, http://linkedlifedata.com/resource/pubmed/commentcorrection/16195334-15780943, http://linkedlifedata.com/resource/pubmed/commentcorrection/16195334-15829534, http://linkedlifedata.com/resource/pubmed/commentcorrection/16195334-9071577, http://linkedlifedata.com/resource/pubmed/commentcorrection/16195334-9536079, http://linkedlifedata.com/resource/pubmed/commentcorrection/16195334-9560248, http://linkedlifedata.com/resource/pubmed/commentcorrection/16195334-9826756, http://linkedlifedata.com/resource/pubmed/commentcorrection/16195334-9869637, http://linkedlifedata.com/resource/pubmed/commentcorrection/16195334-9881706
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0006-4971
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
107
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
777-80
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
A model of oncogenic rearrangements: differences between chromosomal translocation mechanisms and simple double-strand break repair.
pubmed:affiliation
Department of Medicine and Molecular Biology Program, Memorial Sloan-Kettering Cancer Center, New York, NY, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural