The MYC family of cellular oncogenes includes c-Myc, N-myc, and L-myc, which 
encode transcriptional regulators involved in the control of cell proliferation 
and death. Accordingly, these genes become aberrantly activated and expressed in 
specific types of cancers. For example, c-Myc translocations occur frequently in 
human B lymphoid tumors, while N-myc gene amplification is frequent in human 
neuroblastomas. The observed association between aberrations in particular MYC 
family genes and specific subsets of malignancies might reflect, at least in 
part, tissue-specific differences in expression or function of a given MYC gene. 
Since c-Myc and N-myc share substantial functional redundancy, another factor 
that could influence tumor-specific gene activation would be mechanisms that 
target aberrations (e.g., translocations) in a given MYC gene in a particular 
tumor progenitor cell type. We have previously shown that mice deficient for the 
DNA Ligase4 (Lig4) nonhomologous DNA end-joining factor and the p53 tumor 
suppressor routinely develop progenitor (pro)-B cell lymphomas that harbor 
translocations leading to c-Myc amplification. Here, we report that a modified 
allele in which the c-Myc coding sequence is replaced by N-myc coding sequence 
(NCR allele) competes well with the wild-type c-Myc allele as a target for 
oncogenic translocations and amplifications in the Lig4/p53-deficient pro-B cell 
lymphoma model. Tumor onset, type, and cytological aberrations are similar in 
tumors harboring either the wild-type c-Myc gene or the NCR allele. Our results 
support the notion that particular features of the c-Myc locus select it as a 
preferential translocation/amplification target, compared to the endogenous 
N-myc locus, in Lig4/p53-deficient pro-B cell lymphomas.