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

Cell Division

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

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]

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.

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