Mig, the Monokine Induced By Interferon-γ, Promotes Tumor Necrosis In Vivo
Cecilia Sgadaria b c d, Joshua Marion Farbera b c d, Anne L. Angiolilloa b c d, Fang Liaoa b c d, Julie Teruya‐Feldsteina b c d, Parris R. Burda b c d, Lei Yaoa b c d, Ghanshyam Guptaa b c d, Chiharu Kaneganea b c d, Giovanna Tosatoa b c d
- aFrom the Center for Biologics Evaluation and Research, Bethesda, MD; the Laboratory of Clinical Investigation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD; the Department of Hematology/Oncology, Children's National Medical Center, Washington, DC; and the Laboratory of Pathology, Hematopathology Section, National Cancer Institutes, Bethesda, MD
- bFrom the Center for Biologics Evaluation and Research, Bethesda, MD
- cthe Department of Hematology/Oncology, Children's National Medical Center, Washington, DC
- dthe Laboratory of Pathology, Hematopathology Section, National Cancer Institutes, Bethesda, MD
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Abstract
Mig, the monokine induced by interferon-gamma, is a CXC chemokine active as a chemoattractant for activated T cells. Mig is related functionally to interferon-inducible protein 10 (IP-10), with which it shares a receptor, CXCR3. Previously, IP-10 was found to have antitumor activity in vivo. In the present study, murine Mig RNA was found to be expressed at higher levels in regressing Burkitt's lymphoma tumors established in nude mice compared with progressively growing tumors. Daily inoculations of purified recombinant human Mig into Burkitt's tumors growing subcutaneously in nude mice consistently caused tumor necrosis associated with extensive vascular damage. These effects were indistinguishable from those produced by intratumor inoculations of Burkitt's tumors with IP-10. These results support the notion that Mig, like IP-10, has antitumor activity in vivo.