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Table 2 Tumor susceptibility in mice defective in 53BP1 and related DNA damage response genes.

From: Tying the loose ends together in DNA double strand break repair with 53BP1

Defective Gene(s) B cell lymphoma T cell lymphoma References
53BP1 None Low-mild [29, 69]
p53 None All aneuploid with no clonal breaks [109–111]
53BP1/p53 t(12;15) translocations that amplify c-myc Aneuploidy and clonal translocations that include TCRα locus [14, 85]
H2AX None Low-mild [73, 74]
H2AX/p53 t(12;15) translocations that amplify c-myc 75% of animals clonal translocations; H2AX+/- p53-/- animals are aneuploid or possess clonal translocations [71, 72]
NHEJ None None [77]
NHEJ/p53 Pro-B cell lymphoma None [77, 89–92]
Mdc1 None Low [39]
ATM None 100% of animals with clonal translocations at TCR locus of chromosome 14 [75]
  1. Phenotypes of 53BP1 -deficient murine animals relative to those of its related DSB repair factors with particular emphasis on tumor susceptibility. Murine animals defective in 53BP1 function share overlapping features to H2AX, Mdc1 and ATM -deficient animals in that they are growth retarded, sensitive to IR and immune deficient as they are impaired in isotype switching. Like H2AX and any of several components of the NHEJ apparatus, 53BP1-/- animals are relatively non-tumor prone unless combined with p53 deficiency. See text for details.