title: The spontaneous regression of neoplasms in mammals: possible mechanisms and their application in immunotherapy.
abstract: In mammalian cells, neoplastic transformation is directly associated with the expression of oncogenes, with the mutation, loss or simple inactivation of the function of tumor suppressor genes, and the production of certain growth factors. Genes for suppression of the development of the malignant 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 observed in various cancers. Telomerase activation is regarded as essential for cell immortalization and its inhibition may result in the spontaneous regression (SR) of neoplasms. SR of neoplasms occurs when the malignant tumor mass partially or completely disappears without any treatment or as a result of a therapy considered inadequate to influence systemic neoplastic disease. This definition makes it clear that the term SR applies to neoplasms in which the malignant disease is not necessarily cured, and to cases where the regression may be neither complete nor permanent. A number of possible mechanisms of SR 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 individualized anticancer immunotherapy (biotherapy) is also discussed.
authors.affiliation: Department of Pathology, School of Medicine, University of Southern California, Los Angeles, USA.
authors.forename: B
authors.initials: B
authors.lastname: Bodey
authors.forename: B
authors.initials: B
authors.lastname: Bodey
authors.forename: S E
authors.initials: SE
authors.lastname: Siegel
authors.forename: H E
authors.initials: HE
authors.lastname: Kaiser
mesh_terms: D000818:Animals; D006801:Humans; D007167:Immunotherapy; D008322:Mammals; D009365:Neoplasm Regression, Spontaneous; D009369:Neoplasms / Q000276:immunology* / Q000628:therapy*