Document 0206
 DOCN  M9580206
 TI    [Apoptosis or programmed cell death: regulatory and pathophysiological
       mechanisms (editorial)]
 DT    9506
 AU    Silvestris F; Ribatti D; Nico B; Silvestris N; Romito A; Dammacco F
 SO    Ann Ital Med Int. 1995 Jan-Mar;10(1):7-13. Unique Identifier : AIDSLINE
       MED/95244238
 AB    Apoptosis is an active death process genetically encoded to eliminate
       abnormal or unwanted cells. The phenomenon is induced by a cascade of
       molecular events leading to nucleolysis by endonucleases and involves a
       number of membrane receptors and cytoplasmic proteins. These structures
       (including Fas, mullerian inhibiting substance, p53 and the c-myc
       oncogene) contribute, by interactive regulatory mechanisms, to the
       promotion or inhibition of apoptosis, on the basis of both external
       stimulus and cell activation state. Since apoptosis is a selective
       process to suppress defective cells, deregulation of genes encoding for
       such apoptosis-related proteins could be relevant in the growth of
       several tumors. Remarkably, overexpression of the bcl-2 gene in a few
       experimental lymphomas has been associated with neoplastic proliferation
       because of its inhibitory effect on apoptosis. Conversely, early
       activation of Fas, an apoptosis-inducing gene on HIV-infected CD4+
       lymphocytes, is thought to aggravate T cell lymphopenia in HIV infection
       by increasing the level of normal apoptosis. Genetic deregulation of
       apoptosis has also been postulated in the pathogenesis of several
       diseases. Indeed, while preliminary studies suggest that apoptosis plays
       a role in autoimmune disorders including systemic lupus erythematosus,
       the pathogenesis of a few degenerative neuropathies, such as Alzheimer's
       disease, could depend on a similar altered mechanism in apoptosis of
       neuronal cells. However, no studies are presently available to suggest
       that exploitation of molecular events of apoptosis would imply
       therapeutic progress.
 DE    Acquired Immunodeficiency Syndrome/GENETICS/PATHOLOGY  Alzheimer's
       Disease/GENETICS/PATHOLOGY  Apoptosis/*GENETICS/*PHYSIOLOGY  Autoimmune
       Diseases/GENETICS/PATHOLOGY  Comparative Study
       Dexamethasone/PHARMACOLOGY  Endonucleases/METABOLISM  English Abstract
       Enzyme Activation  Genes, myc  Genes, pX  Human
       Neoplasms/GENETICS/PATHOLOGY  T-Lymphocytes/DRUG EFFECTS/PHYSIOLOGY
       EDITORIAL  REVIEW  REVIEW, TUTORIAL  JOURNAL ARTICLE

       SOURCE: National Library of Medicine.  NOTICE: This material may be
       protected by Copyright Law (Title 17, U.S.Code).