The IL-12Rβ2 gene functions as a tumor suppressor in human B cell malignancies
J. Clin. Invest. Irma Airoldi, et al. 113:1651 doi:10.1172/JCI20303 [Go to this article.]

Figure 7
Tumorigenicity of IL-12Rβ2_transfected Raji cells in SCID-NOD mice. (A) The mean size ± SD of tumors formed by IL-12Rβ2_transfected Raji cells in SCID-NOD mice treated with hrIL-12 (black bar) or PBS (gray bar) is shown. The difference between mean size of tumors from hrIL-12 treated and PBS treated mice was statistically significant (P < 0.0001). (B) Two representative tumors grown in hrIL-12_treated and PBS-treated mice are shown. (C) Histological and immunohistochemical features of tumors from PBS treated (C, G, E, and I) and hrIL-12 treated (D, F, H, and J) SCID/NOD mice. IL-12Rβ2 gene_transfected Raji tumors from PBS-treated mice are formed by medium- to large-sized neoplastic cells with round to oval nuclei showing two or more nucleoli. The “starry sky” pattern determined by macrophages that have ingested apoptotic tumor cells is also present (arrows) (C). The tumor is well vascularized (E) and does not express detectable level of Mig/CXCL9 (G). An extremely high proliferation rate is evidenced by Ki-67 immunostaining (I). In tumors from hrIL-12 treated mice the above described architectural features are altered by frequent and extensive areas of ischemic-hemorrhagic necrosis (N) (D), which are associated with defective intratumoral microvessel network (F), and expression of Mig/CXCL9 in the cytoplasm and in the proximity of intact tumor cells (H). In addition, the number of proliferating cells in the viable neoplastic tissue surrounding necrotic areas, as assessed by Ki-67 staining, is strongly reduced (J). Magnification, ∞400, for all pictures shown.