Affiliations: [a] Aging Research Center, University G. d'Annunzio Foundation, Chieti, Italy | [b] Department of Clinical and Biological Sciences, University of Torino, Italy | [x] Karmanos Cancer Institute, Wayne State University, Detroit, MI 48201, USA | [y] Department of Microbiology and Immunology, University of Miami School of Medicine, Miami, FL 33136, USA
Correspondence:
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Corresponding author: Dr. Piero Musiani, Aging Research Center (Ce.S.I.), University G. d'Annunzio Foundation, Via Colle dell'Ara, 66013 Chieti, Italy. Tel.: +39 0871 541 276; Fax: +39 0871 541 545; E-mail: musiani@unich.it
Abstract: Development of the mammary gland is controlled by hormones and many other growth factors. Hyperplasia and neoplasia are thus a likely consequence of alterations in their number and type, or the number and function of their receptors. p185neu, a member of the epidermal growth factor family, is coded by the ErbB-2 oncogene. It is expressed in the normal human breast, but overexpressed and associated with a poor prognosis in 15–30% of breast tumours. Employment of ErbB-2 sequences as vaccinal antigens to induce an immune rejection of such tumours is being investigated in several transgenic animal models. One of the most aggressive models of mammary p185neu-dependent carcinogenesis is that of BALB-neuT mice, which are transgenic for the rat transforming Her-2/neu oncogene (a homologue of the human ErbB-2 oncogene). The progression of their early neoplastic lesions can be prevented with both cellular and DNA vaccines coadjuvated by antiangiogenic and immunostimulatory molecules. This suggests that induction of a specific immune reaction against a tumor target antigen may provide a way of preventing the onset of tumours in subjects with a high genetic risk of developing cancer.
DOI: 10.3233/BD-2004-20105
Journal: Breast Disease, vol. 20, no. 1, pp. 33-42, 2004
