AuthOr’s VIew AuthOr’s VIew

Signal transducer and activator of tran-scription 1 (STAT1) has been classically defined as an oncosuppressive transcription factor. Early studies showed that STAT1 activates anti-proliferative and pro-apop-totic genes in tumor cells. Moreover, a large body of evidence demonstrated that the interferon γ (IFNγ)-mediated activa-tion of STAT1 is associated with antiviral and antitumor immunity.1 In line with this notion, Stat1−/ − mice are more prone to mammary tumorigenesis than their wild-type counterparts.2,3 Nonetheless, evidence is mounting against the univo-cal role of STAT1 as a tumor suppressor. For example, STAT1 expression is upreg-ulated in several late-stage human can-cers, including metastatic lesions,4,5 and high STAT1 levels have been suggested to constitute a predictive marker for poor survival, as well as for chemo/radiother-apy resistance among breast carcinoma patients.6 Still, many of these studies only provided a correlative association between STAT1 and disease progression. We have recently provided direct, causal evidence suggesting that STAT1 exerts tumorigenic effects in a syngeneic mouse model of breast cancer.7 In this model, TM40D-MB cells implanted into the mammary fat pads of BALB/c mice generated mammary tumors that were more aggressive and exhibited an increased Novel function of STAT1 in breast cance