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• W2740691100 abstract "TO THE EDITOR The remarkable clinical benefit of donor-lymphocyte infusions, as well as the finding that human T cells can destroy chemotherapy-resistant cell lines from chronic myeloid leukemia and multiple myeloma, has encouraged the development of immunotherapeutic strategies against hematological cancers. Vaccination with leukemia-associated antigen peptides might constitute one way to induce clinical responses in patients (Van et al., 2010). The survivin protein is expressed in high levels in most hematopoietic malignancies and solid cancers (Adida et al., 2000), but is absent in normal, differentiated tissues. Survivin is a survival protein that has been implicated in protection from apoptosis and regulation of mitosis. Thus, the attractiveness of using survivin as a target for clinical intervention is based on the fact that tumor escape by downregulation or loss of expression of this protein would impair sustained tumor growth. Consequently, several clinical trials targeting survivin with a collection of different approaches from small-molecule antagonists to immunotherapy are currently under way. With regard to the latter, spontaneous anti-survivin T-cell reactivity was first described in cancer patients suffering from a wide range of cancers of different origin, including chronic lymphocytic leukemia and acute myeloid leukemia, about 10 years ago (Andersen et al., 2007). When used in an oral DNA vaccine, the survivin-directed immune response affected both tumor cells and tumor-associated angiogenesis, eradicating pulmonary metastases without toxicity, including wound healing or fertility in preclinical studies (Xiang et al., 2005). Furthermore, although activated B and T cells express survivin, it has been described that survivin-specific cytotoxic T lymphocytes (CTLs) did not recognize and kill such cells ex vivo (Schmidt et al., 2003). These and several other preclinical studies justified clinical testing to evaluate the efficacy and safety of survivin-based vaccinations. Consequently, survivin-directed immunotherapy was quickly moved to the clinic, and several survivin-based vaccination trials are currently ongoing at different institutes (Andersen et al., 2007). T-cell responses toward survivin have almost only been studied in the context of HLA-A2. Only very few studies have examined additional HLA-restricted survivin immunity (Reker et al., 2004a, b). The set of HLA molecules expressed in a particular person is highly individual and allows each person to present a specific pattern of foreign peptides to the immune system. Nevertheless, specific HLA class I alleles have a high degree of sequence homology and share similar peptide-binding motifs, resulting in the presentation of identical epitopes, owing to which they are referred to as HLA superfamilies (Sette and Sidney, 1998). To date, nine major HLA class I superfamilies have been classified according to similar peptidebinding motifs. A highly interesting non-HLA-A2– restricted survivin-derived epitope is the HLA-A11–restricted epitope Sur53-62 (DLAQCFFCFK) (Reker et al., 2004b). On monitoring T-cell reactivity against survivin in a melanoma patient in complete regression following IL-2–based immunotherapy, we found persistence of HLA-A11–restricted Sur53-62–specific T cells for more than 7 years (Hadrup et al., 2006). This could suggest that T-cell responses against Abbreviations: CTL, cytotoxic T lymphocyte; MM, malignant melanoma; TILs, tumor-infiltrating lymphocytes" @default.
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• W2740691100 date "2012-01-01" @default.
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• W2740691100 title "A Promiscuous Survivin-Derived T-Cell Epitope Restricted to the HLA-A3 Super-Type Alleles" @default.
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