a frank leukemia, we concluded that miR-29 transgenics developed a disease similar to indolent CLL [55]. Moreover, miR-29 mice showed significant increases in % of leukemic cells with age. In mice younger than 15 months, CD5+ leukemic cells were only ~20% of total B-cells; on the other hand, at the age of 20–26 months, >65% of all B-cells were CD5+. These results showed a gradual progression of indolent CLL in miR-29 transgenics [55]. To determine whether leukemic cells from miR-29 mice divide, we did measure the proliferative capacity of CD5+ leukemic B-cells compared to WT CD19+ spleen lymphocytes. BrdU incorporation experiments showed significant proliferation in miR-29 transgenic B-cells, while no proliferation was found in CD19+ WT lymphocytes [55]. These results suggest that miR-29 over-expression plays an important role in promoting B-cell proliferation. Because progressive hypogammaglobulinemia and immune incompetence are important features of human CLL [6], we analyzed serum levels of immunoglobulins and the immune response to SRBC antigen in the serum of miR-29 mice and wild type littermates. We showed that in miR-29 transgenics immune response to SRBC antigen and serum levels of immunoglobulins were significantly decreased [55]. Thus, these findings confirmed our initial observations that miR-29 transgenics develop a
