The antitumor effects of IFN-α are abrogated in a STAT1-deficient mouse
J. Clin. Invest. Gregory B. Lesinski, et al. 112:170
doi:10.1172/JCI16603 [Go to this article.]

Figure 6
Absence of STAT1 in the host results in decreased signaling in response to IFN-α and decreased survival after tumor challenge. (a) A DNA probe specific for activated murine STAT1 reacted with whole-cell lysates from IFN-α–treated splenocytes of C57BL/6 but not STAT1-deficient mice. Similar results were obtained in other tissues, including liver and kidney (data not shown). STAT1–/– and C57BL/6 mice (n = 10 mice per group) were injected intraperitoneally with 106 B16F1 melanoma cells. As compared with PBS-treated controls (filled circles), IFN-α treatment (2 × 104 U per day) (open triangles) prolonged the survival of C57BL/6 mice but not STAT1–/– mice challenged with B16F1 melanoma cells (b and c) or JB/MS melanoma cells (n = 6 mice per group) (d and e).