Amplifying mechanisms of lymphomagenesis.
Mice doubly deficient for either XRCC4 or DNA ligase IV and p53 invariably develop lymphomas bearing characteristic chromosome translocations with gene amplification. A recent study highlights the importance of nonclassical end joining mechanisms in the formation of these oncogenic DNA rearrangements.
Roth
David B
DB
Howard Hughes Medical Institute and Department of Immunology, Baylor College of Medicine, 1 Baylor Plaza, Houston, TX 77030, USA.
D000818:Animals; D000072481:DNA Ligase ATP; D011088:DNA Ligases / Q000172:deficiency / Q000235:genetics / Q000378:metabolism*; D004260:DNA Repair; D004268:DNA-Binding Proteins / Q000172:deficiency / Q000235:genetics / Q000378:metabolism*; D005784:Gene Amplification / Q000235:genetics*; D006801:Humans; D008223:Lymphoma / Q000201:enzymology / Q000235:genetics* / Q000473:pathology*; D051379:Mice; D016159:Tumor Suppressor Protein p53 / Q000172:deficiency / Q000235:genetics / Q000378:metabolism*
D004268:DNA-Binding Proteins; C000607893:LIG4 protein, human; D016159:Tumor Suppressor Protein p53; C101467:XRCC4 protein, human; D011088:DNA Ligases; D000072481:DNA Ligase ATP