PI3Kδ^−/− mice in additional hematologic and nonhematologic tumor models. (A) PI3Kδ protein expression in murine leukemic cell lines. Naive murine PI3Kδ^+/− and PI3Kδ^−/− bone marrow preparations served as controls. Kaplan-Meier plot after injection of EL4 cells intravenously into PI3Kδ^+/−RAG2^+/− and PI3Kδ^−/−RAG2^+/− recipients (log-rank test; P = .045). (B) PI3Kδ protein is expressed in Eμ-myc–derived leukemic cells. Upon injection of Eμ-myc–derived cells, PI3Kδ^−/−RAG2^+/− recipients succumbed to disease significantly faster than PI3Kδ^+/−RAG2^+/− littermate controls (log-rank test; P = .039). (C) B16 melanoma cells were injected intravenously and numbers of metastatic infiltrates per lung were counted under the binocular microscope. RAG2^+/−PI3Kδ^−/− recipient mice showed a significantly higher number of metastatic infiltrates than RAG2^+/−PI3Kδ^+/− (P = .005), and this was also true on the RAG2^−/− background (P = .015). Horizontal lines indicate data mean. Thus, increased tumor formation in PI3Kδ^−/− mice is not restricted to lymphoid malignancies. Formation of lung metastasis in littermate controls (top panels: photographs, digital camera, Canon EOS 300D; bottom panels: H&E-stained histologic sections of lungs; magnification, ×20 Zeiss AxioImager 71; see Figure 2B).