Figure 4.
Figure 4. Tet2-deficient abnormal B cells share features with human B-cell tumors. (A) Coding sequence somatic mutations. Frequencies of the type of mutations observed in the exome analysis of abnormal B-cell populations obtained from 6 independent tumors. The type of point mutations is indicated as well as insertions and deletions (indels). Transversion mutations (green) and transitions (red) are indicated. Note the statistically significant high frequency of C > T and G > A mutations. (B) Survival curves of Aid+/+Tet2+/+ (control [CTR]), Aicda-deficient mice: Aid−/− Tet2+/+ (Aid−/−); Tet2-deficient mice: Aid+/+Tet2−/− (Tet2−/−); and double-deficient mice: Aid−/−Tet2−/− strains. Only mice sacrificed because of B-cell tumors are scored. (C) Venn diagram of exome mutations from the literature of human CLL27,31,34-36 and DLBCL32,37-39 in comparison with exome mutations from the Tet2-deficient sorted abnormal B cells. The name of the mutated genes in the overlaying zones is indicated. *P < .05.

Tet2-deficient abnormal B cells share features with human B-cell tumors. (A) Coding sequence somatic mutations. Frequencies of the type of mutations observed in the exome analysis of abnormal B-cell populations obtained from 6 independent tumors. The type of point mutations is indicated as well as insertions and deletions (indels). Transversion mutations (green) and transitions (red) are indicated. Note the statistically significant high frequency of C > T and G > A mutations. (B) Survival curves of Aid+/+Tet2+/+ (control [CTR]), Aicda-deficient mice: Aid−/− Tet2+/+ (Aid−/−); Tet2-deficient mice: Aid+/+Tet2−/− (Tet2−/−); and double-deficient mice: Aid−/−Tet2−/− strains. Only mice sacrificed because of B-cell tumors are scored. (C) Venn diagram of exome mutations from the literature of human CLL27,31,34-36  and DLBCL32,37-39  in comparison with exome mutations from the Tet2-deficient sorted abnormal B cells. The name of the mutated genes in the overlaying zones is indicated. *P < .05.

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