title: Site specific therapy: an integrative approach to treating melanoma.
abstract: There have been many proposed theories for effectively treating melanoma, especially through the regulation of histamine. Histamine has been proven to be a major regulator of the immune system's T-helper cell subset balance and major shifts in this balance towards TH2 cytokines have contributed to diseases such as asthma, lupus and cancer. Histamine also causes suppression of interferon-induced proteins needed for anti-tumor response and activates T-suppressor cell function in cancers such as squamous cell carcinoma and melanoma. Scientific evidence has suggested the possibility of an anthistamine approach as treatment to these diseases and for melanoma, there has been great promise. This is due to the fact that melanotic cells have been elucidated to express histamine receptors and as a result, regulation of histamine could occur specifically at the site of these epidermal growths. Another factor to consider is how effective an inflammatory response can be when combined with regulation of histamine. Inflammation is a very powerful tool against pathogenic environments by causing cytokine recruitment and migration of dendritic cells to infected sites. Adequate stimulation of an inflammatory response at the specific site of any cancerous region would greatly weaken its evasive mechanisms. However, there are no reports showing high efficacy utilizing the benefits of regulating inflammation and histamine that could cause TH1 subset levels to predominate, down-regulate T-suppressor cells, up-regulate interferon-induced proteins and properly sustain migration of dendritic cells concurrently. These benefits have been proven in separate instances for a range of diseases but have not been assessed as a combined modality for melanoma therapy. Therefore successful melanoma treatment should integrate these principles involving: the use of H2 antagonists for preventing the negative effects of histamine, monoclonal antibodies to ensure an effective dendritic cell response, and routine pro-inflammatory induction at the specific site of the melanotic tissue to ensure recognition of the cancer that has evaded immunity.
authors.affiliation: Department of Immunology, Center for Molecular Cell Biology, Florida Atlantic University, 777 Glades Road, P.O. Box 3091 Boca Raton, FL 33431-0991, USA. mannykav@netzero.com
authors.forename: Manuel
authors.initials: M
authors.lastname: Kavekos
mesh_terms: D000970:Antineoplastic Agents / Q000494:pharmacology / Q000627:therapeutic use*; D017679:Cryotherapy; D006632:Histamine / Q000378:metabolism*; D006634:Histamine H1 Antagonists / Q000494:pharmacology / Q000627:therapeutic use*; D006635:Histamine H2 Antagonists / Q000494:pharmacology / Q000627:therapeutic use; D006801:Humans; D008545:Melanoma / Q000188:drug therapy* / Q000276:immunology / Q000378:metabolism / Q000532:radiotherapy / Q000628:therapy; D018448:Models, Immunological; D009363:Neoplasm Proteins / Q000096:biosynthesis / Q000187:drug effects* / Q000235:genetics; D011968:Receptors, Histamine / Q000187:drug effects*; D011970:Receptors, Histamine H2 / Q000096:biosynthesis / Q000187:drug effects / Q000235:genetics
chemical_list: D000970:Antineoplastic Agents; D006634:Histamine H1 Antagonists; D006635:Histamine H2 Antagonists; D009363:Neoplasm Proteins; D011968:Receptors, Histamine; D011970:Receptors, Histamine H2; D006632:Histamine