Immunotherapy
Tumor vaccines have a long history, but the search for effective methods to induce active immunity against tumors has been difficult. Repeated attempts have been made to inhibit the outgrowth of tumors and influence the natural history of melanoma by immunization against tumor cells or extracts of tumor cells. More recently, purified antigens recognized by the host antibody response, as well as the epitopes defined by T-cell responses, have been identified and prepared for use as vaccines. In addition, genetically modified melanoma cells, recombinant vaccines, and antiidiotype antibodies that represent the antibody-recognized antigens of melanoma have entered into clinical trials. Evidence is mounting that vaccination can induce immune responses to melanoma. Efforts to vaccinate patients against the antigens of melanoma can be classified categorically into trials of allogeneic tumor cell immunization, autologous tumor cell immunization, and immunization against synthetic chemically defined antigens.
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The last category can be subclassified into approaches directed at the induction of antibody responses, such as the gangliosides noted below, and approaches directed at the induction of a T-cell response to antigens that may include either proteins or peptides. Formal phase III trials have been initiated to evaluate the potential efficacy of relatively few tumor vaccines as adjuvant therapy in high-risk patients.
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At this point, it remains unclear which approaches will be most effective. The multitude of different ongoing trials listed indicate that there is no consensus on vaccine strategies. Early clinical trials of each of the categories of vaccines have been conducted in patients with metastatic disease, for reasons of safety evaluation. Despite early concerns, no reports of tumor enhancement have been documented with the whole-cell vaccination trials conducted to date. Antitumor responses have been recorded in a small fraction of subjects with metastatic disease, receiving varied programs of tumor cell immunization against allogeneic tumor cells incorporating two of three cell lines of hapten-coupled autologous [autochthonous] tumor cells. Most subsequent clinical studies have been performed in patients after resection of regional lymph node metastases or high-risk primary lesions. A more interesting observation is that patients who develop evidence of immune responses have improved disease-free survival or overall survival. This intriguing correlation does not directly imply that vaccines improve the clinical course (for instance, patients who a priori have a better prognosis may be more likely to develop an immune response to vaccination), but is consistent with the hypothesis that an immune response induced by vaccination may have antitumor benefit. A number of problems exist in the construction of tumor vaccines, including the weak immunogenicity of tumor antigens, heterogeneity of tumor-restricted antigen expression in tumors, and the ability of tumors to escape any immune responses that may be induced naturally, or therapeutically. Most melanoma antigens on tumor cells are not tumor-restricted or specific (i.e., present only on cancer cells) but are shared with certain normal cells.
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Active specific vaccination trials in melanoma (as opposed to nonspecific vaccination with BCG) have progressed from the use of unmodified, irradiated allogeneic or autologous melanoma cells for immunization, either alone or in combination with BCG and other nonspecific immunomodulators. It has been difficult to demonstrate any benefit or specific immune responses in the course of these trials. One exception has been immune responses to gangliosides, the major acidic glycolipid of melanoma cells, in some patients immunized with selected allogeneic melanoma cells.
Melanoma information
Efforts have been made to improve immunogenicity of allogeneic tumor cells by treating with the enzyme neuraminidase to remove sialic acid residues from the cell surface. Strategies have been developed to augment the immune response to tumor antigens by infecting tumor cells with nonpathogenic viruses. Viral proteins presented on the cell membrane of tumors have been shown to augment the immunogenicity of tumor antigens.