title: Spontaneous neoplastic regression: the significance of apoptosis.
abstract: In mammalian cells, neoplastic transformation has a direct relationship with the expression of oncogenes, the production of certain growth factors and with the mutation, loss or simple inactivation of the function of tumor suppressor genes. 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 types of neoplastic cell transformation. Telomerase activation is regarded as essential for cell immortalization and its inhibition may result in 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 not be complete or 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. In conclusion, of all the possible mechanisms of SR of neoplasms, programmed cell death (PCD) or apoptosis is involved in each. The immunological mechanism is probably the main effector mechanism of SR in human neoplasms with its trigger being apoptosis. The treatments of the tumor, such as with various anti-neoplastic drugs or radiation or immunotherapy, all include the basic mechanism of programmed cell death or apoptosis. Without apoptosis, there is practically no tumor regression, none of any kind.
authors.affiliation: Department of Pathology, School of Medicine, University of Maryland, Baltimore, MD, USA.
authors.forename: H E
authors.initials: HE
authors.lastname: Kaiser
authors.forename: B
authors.initials: B
authors.lastname: Bodey
authors.forename: S E
authors.initials: SE
authors.lastname: Siegel
authors.forename: A M
authors.initials: AM
authors.lastname: Gröger
authors.forename: B
authors.initials: B
authors.lastname: Bodey
mesh_terms: D000328:Adult; D017209:Apoptosis / Q000276:immunology*; D001254:Astrocytoma / Q000276:immunology / Q000473:pathology; D001932:Brain Neoplasms / Q000276:immunology / Q000473:pathology*; D002528:Cerebellar Neoplasms / Q000276:immunology / Q000473:pathology*; D002648:Child; D006098:Granulocytes / Q000473:pathology; D006801:Humans; D007150:Immunohistochemistry; D007694:Killer Cells, Natural / Q000473:pathology; D008527:Medulloblastoma / Q000276:immunology / Q000473:pathology*; D008545:Melanoma / Q000473:pathology; D009000:Monocytes / Q000473:pathology; D009365:Neoplasm Regression, Spontaneous / Q000276:immunology / Q000473:pathology*; D018242:Neuroectodermal Tumors, Primitive / Q000276:immunology / Q000473:pathology*; D013601:T-Lymphocytes / Q000473:pathology