title: Spontaneous regression of neoplasms: new possibilities for immunotherapy.
abstract: In mammalian cells, neoplastic transformation is directly associated with the expression of oncogenes, loss or simple inactivation of the function of tumour suppressor genes and the production of certain growth factors. Genes for suppression of the development of the neoplastic cellular immunophenotype, as well as inhibitory growth factors, have regulatory functions within the normal processes of cell division and differentiation. Telomerase (a ribonucleoprotein polymerase) activation is frequently detected in various neoplasms. Telomerase activation is regarded as essential for cell immortalisation and its inhibition may result in spontaneous regression of neoplasms. This phenomenon of neoplasms occurs when the malignant tissue mass partially or completely disappears without any treatment or as a result of a therapy considered inadequate to influence systemic neoplastic growth. This definition makes it clear that the term 'spontaneous regression' applies to neoplasms in which the overall malignant disease is not necessarily cured and to cases where the regression may not be complete or permanent. A number of possible mechanisms of spontaneous regression are reviewed, with the understanding that no single mechanism can completely account for this phenomenon. The application of the newest immunological, molecular biological and genetic insights for more individualised and adequate antineoplastic immunotherapy (alternative biotherapy) is also discussed.
authors.affiliation: Department of Pathology, Keck School of Medicine, University of Southern California, Los Angeles, USA. Bodey18@aol.com
authors.forename: Bela
authors.initials: B
authors.lastname: Bodey
mesh_terms: D000818:Animals; D002454:Cell Differentiation; D002471:Cell Transformation, Neoplastic / Q000187:drug effects; D006728:Hormones / Q000502:physiology; D006801:Humans; D007167:Immunotherapy; D016219:Immunotherapy, Adoptive; D009365:Neoplasm Regression, Spontaneous / Q000235:genetics / Q000276:immunology*; D009369:Neoplasms / Q000473:pathology; D009857:Oncogenes / Q000502:physiology; D013602:T-Lymphocytes, Cytotoxic / Q000276:immunology
chemical_list: D006728:Hormones