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Peptide-Based Active Immunotherapy in Cancer 123 PROSPECTS The growing number of TAA identified in many tumor types becomes a solid basis for peptide vaccine development. However, the antigenic profile of human tumors is very complex and consists of many peptides originating from various classes of protein. This fact should be considered carefully in designing anticancer vaccines. An important question is which tumor antigens are the most important in tumor regression in vivo. In any case, the ideal peptide vaccine most likely will consist of a cocktail of tumor antigenic peptides. However, the number of epitopes in the vaccine cocktail should be evaluated carefully since CTL responses in AIDS patients directed to fewer epitopes are associated with better clinical outcome (89). In this case it appears that the stimulation of multiple simultaneous CTL responses is clinically inefficient. The dose of antigen and the speed of antigen release in the vaccine formulations are also very important. High doses of antigen released faster may induce T-cell tolerance (90). Immune tolerance may be due to fast expansion and subsequent elimination of specific T-cell clones, or to apoptosis induced by repeated stimulation of already stimulated T-cells in cell cycle (91,92). Therefore, it is essential to select as immunogens those epitopes against which tolerance has not been induced (93,94). Currently, clinical responses to peptide vaccines, as determined by the criteria set for chemotherapy and radiation, have been difficult to assess. However, the lack of toxicity of peptide vaccines in patients with many different tumor types, and the clearly observed efficacy in some studies, support the use of peptide vaccination. Future peptide vaccine strategies will most likely focus on more potent and combined approaches for immunization. Applied in conjunction with surgery, radiotherapy, and/or chemotherapy, peptide vaccines can be effective in eliminating micro-metastases, in decreasing the immunosuppressive effects of the chemotherapy or radiotherapy, and in increasing the resistance to viral or bacterial infections frequently occurring in cancer patients. Recent advances in the design of polyvalent vaccines targeting several antigens are also very promising. In addition, the possibility to treat patients with peptide vaccines earlier in the course of the disease and to combine vaccines with other treatment modalities may also improve the vaccine efficacy. As a result, immunotherapy with peptide vaccines may become a major treatment modality of cancer in the near future. REFERENCES 1. Rammensee HG, Friede T, Stevanoviic S. MHC ligands and peptide motifs: first listing. Immunogenetics 1995; 41:178–228. 2. Rammensee HG. Antigen presentation—recent developments. Int Arch Allergy Immunol 1996; 110:299–307. 3. Yewdell JW, Norbury CC, Bennink JR. Mechanisms of exogenous antigen presentation by MHC class I molecules in vitro and in vivo: implications for generating CD8þ T cell responses to infectious agents, tumors, transplants, and vaccines. Adv Immunol 1999; 73:1–77.
124 Schroter and Minev 4. Heemels MT, Ploegh H. Generation, translocation, and presentation of MHC class I-restricted peptides. Annu Rev Biochem 1995; 64:463–491. 5. Spies T, Cerundolo V, Colonna M, et al. Presentation of viral antigen by MHC class I molecules is dependent on a putative peptide transporter heterodimer. Nature 1992; 355:644–646. 6. Lehner PJ, Cresswell P. Processing and delivery of peptides presented by MHC class I molecules. Curr Opin Immunol 1996; 8:59–67. 7. Liu CC, Young LH, Young JD. Lymphocyte-mediated cytolysis and disease. N Engl J Med 1996; 335:1651–1659. 8. Van Pel A, van der Bruggen P, Coulie PG, et al. Genes coding for tumor antigens recognized by cytolytic T lymphocytes. Immunol Rev 1995; 145:229–250. 9. De Plaen E, Lurquin C, Lethe B, et al. Identification of genes coding for tumor antigens recognized by cytolytic T lymphocytes. Methods 1997; 12:125–142. 10. Rosenberg SA. Cancer vaccines based on the identification of genes encoding cancer regression antigens. Immunol Today 1997; 18:175–182. 11. Wang RF. Human tumor antigens: implications for cancer vaccine development. J Mol Med 1999; 77(9):640–655. 12. Nestle FO, Alijagic S, Gilliet M, et al. Vaccination of melanoma patients with peptide- or tumor lysate-pulsed dendritic cells. Nat Med 1998; 4(3):328–332. 13. Rosenberg SA, Yang JC, Schwartzentruber DJ, et al. Immunologic and therapeutic evaluation of a synthetic peptide vaccine for the treatment of patients with metastatic melanoma. Nat Med 1998; 4(3):321–327. 14. Thurner B, Haendle I, Reoder C, et al. Vaccination with mage-3A1 peptide-pulsed mature, monocyte-derived dendritic cells expands specific cytotoxic T cells and induces regression of some metastases in advanced stage IV melanoma. J Exp Med 1999; 190(11):1669–1678. 15. Kawakami Y, Nishimura MI, Restifo NP, et al. T-cell recognition of human melanoma antigens. J Immunother 1993; 14:88–93. 16. Storkus WJ, Zeh HJD, Maeurer MJ, et al. Identification of human melanoma peptides recognized by class I restricted tumor infiltrating T lymphocytes. J Immunol 1993; 151:3719–3727. 17. Cox AL, Skipper J, Chen Y, et al. Identification of a peptide recognized by five melanoma-specific human cytotoxic T cell lines. Science 1994; 264:716–719. 18. Sahin U, Teureci O, Pfreundschuh M. Serological identification of human tumor antigens. Curr Opin Immunol 1997; 9(5):709–716. 19. Minev B, Hipp J, Firat H, et al. Cytotoxic T cell immunity against telomerase reverse transcriptase in humans. Proc Natl Acad Sci U S A 2000; 97(9):4796–4801. 20. Mitchell MS, Kan-Mitchell J, Minev BR, et al. A novel melanoma gene (MG50) encoding the interleukin 1 receptor antagonist and six epitopes recognized by human cytolytic T lymphocytes. Cancer Res 2000; 60(22):6448–6456. 21. Romero P, Cerottini JC, Speiser DE. The human T cell response to melanoma antigens. Adv Immunol 2006; 92:187–224. 22. Takahashi T, Makiguchi Y, Hinoda Y, et al. Expression of MUC1 on myeloma cells and induction of HLA-unrestricted CTL against MUC1 from a multiple myeloma patient. J Immunol 1994; 153:2102–2109. 23. Coussens L, Yang-Feng TL, Liao YC, et al. Tyrosine kinase receptor with extensive homology to EGF receptor shares chromosomal location with neu oncogene. Science 1985; 230:1132–1139.
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Translational Medicine Series 6 Can
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TRANSLATIONAL MEDICINE SERIES 1. Pr
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Informa Healthcare USA, Inc. 52 Van
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Preface Throughout the last 20 year
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Preface vii Table 1 A Diverse Techn
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Preface . . . . v Contributors . .
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Contributors Pedro Alves Ludwig Ins
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1 Factoring in Antigen Processing i
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Factoring in Antigen Processing in
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2 Outlining the Gap Between Preclin
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Preclinical Models and Clinical Sit
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Table 1 Examples of Preclinical Act
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56 Srinivasan disease agents. Garda
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58 Srinivasan expressing various kn
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60 Srinivasan The above-mentioned a
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62 Srinivasan (69). In another stud
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64 Srinivasan patients with prostat
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70 Teofilovici and Wentworth In 190
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206 Index Antigenic peptides degrad
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208 Index Chromogens, enzymatic act
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210 Index Freund’s adjuvants. See
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212 Index Langerhans cells, 133, 13
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214 Index [Peptide vaccines] invest
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216 Index TCRL. See TCR-like immuno
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Oncology and Immunology about the b
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