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Laboratorio di Ricerca Oncologica, Istituti Ortopedici Rizzoli, 40136 Bologna [K. S., S. B., M. S., M. C. M., P. P., N. B.]; Istituto di Cancerologia, Università di Bologna, 40126 Bologna [P. N., P-L. L.]; and Unità Satellite di Biotecnologie, Istituto Nazionale per la Ricerca sul Cancro-Genova, 40126 Bologna [G. N., L. L.], Italy
Innovative, more effective treatment modalities are needed for Ewing's sarcoma (ES), a neoplasm with a disappointingly low survival rate despite the use of aggressive multimodal therapeutic approaches. We have previously shown (K. Scotlandi et al., Cancer Res., 56: 45704574, 1996) the existence and the pathogenetic relevance of an autocrine loop that is mediated by the insulin-like growth factor-I receptor (IGF-IR) and is crucial for the survival and proliferation of ES cells in vitro. In this study, we report that the IGF-IR-blocking monoclonal antibody
IR3 may also significantly inhibit ES cell growth in vivo. In particular, in almost one-half of the animals tested, after s.c. inoculation with TC-71 ES cells, the blockage of IGF-IR by
IR3 induced a complete regression of tumors that developed, which suggests that IGF-IR is valuable as a specific target for novel therapeutic strategies. In addition, suramin, a drug that can interfere with growth factor binding with their receptors, inhibited the tumorigenic and the metastatic ability of TC-71 cells and, therefore, is a promising agent to be combined with conventional cytotoxic drugs for the design of more effective therapeutic regimens.
1 This work was supported by the Istituti Ortopedici Rizzoli, Ricerca Corrente; by the Ministero della Sanità, Ricerca Finalizzata; and by Consiglio Nazionale delle Ricerche/Progetto Finalizzato. Applicazioni Cliniche della Ricerca Oncologica.
2 To whom requests for reprints should be addressed, at the Laboratorio di Ricerca Oncologica, Istituti Ortopedici Rizzoli, Via di Barbiano 1/10, 40136 Bologna, Italy. E-mail: gis2278@iperbole.bologna.it.
Received 4/22/98. Accepted 7/17/98.
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