Important note: Information in this article was accurate in 1992. The state of the art may have changed since the publication date.
HTLV-I AS AGENT INDUCING GENETIC CHANGES IN INFECTED HUMAN LYMPHOCYTES (MEETING ABSTRACT)
Fifteenth Symposium of the International Association for Comparative Research on Leukemia and Related Disease. October 6-11, 1991, Padova/Venice, Italy, p. 54, 1991.. Unique Identifier : AIDSLINE ICDB/92682404 Maruyama K; Fukushima T; Mochizuki S; Kawamura K; Miyauchi M; Dept. of Pathology, Chiba Cancer Center Res. Inst., Chiba 280,; Japan
Abstract:
HTLV-I is etiologically associated with adult T-cell leukemia (ATL). However, the relative low incidence of ATL among virus carriers in ATL-endemic areas suggests host and/or environmental cofactors for the development of ATL. In a search for host cofactors, members in 3 generations of a suspected carrier family were studied. By Western blot analysis, sera of a man, his mother, wife, 2 daughters and newborn son were found to carry antibodies to HTLV-I proteins. In Southern blot analysis of DNAs extracted from lymphocytes of each member and amplified by PCR using specific primers, signals for gag and tax, but not pol, sequences of HTLV-I were more clearly detected in adults than in children of the family. In order to examine a possible role of proviral sequences in neoplastic change of the carrier cell following exposure to environmental carcinogens, human T cells that were infected in vitro with HTLV-I and, IL-2-dependent for their continuous growth, were treated with MNNG and maintained in medium containing TPA. Cells achieved independence from IL-2 but became TPA-dependent. Multiple ultraviolet irradiation of TPA-dependent cells resulted in their autonomous growth and allowed the establishment of several transformed cell lines. Abnormalities of chromosome 1 were commonly seen in cells of all cell lines. In addition, abnormalities of chromosome 7, known to carry a number of oncogenes including met, were commonly observed shared or not shared in TPA-dependent and in transformed cells. Rearrangements of certain cellular genes were detected in all cell lines, but none was found to be associated with cellular transformation. These results suggest that retroposon-like sequences homologous to HTLV-I genes might be present in carrier cells more tightly repressed in children than in adults. Continuous transcription of these sequences may produce the genomic instability leading to the increased risk of formation of chromosome abnormalities and further for genetic mutations required for neoplastic change of the carrier cell upon exposure to environmental carcinogens.
Keywords: Cell Transformation, Neoplastic Chromosome Abnormalities Chromosomes, Human, Pair 1 Chromosomes, Human, Pair 7 Female Gene Products, gag/GENETICS Gene Products, pol/GENETICS Gene Products, tax/GENETICS Gene Rearrangement Human HTLV-I Antibodies/ANALYSIS HTLV-I Infections/COMPLICATIONS/*GENETICS Interleukin-2/GENETICS Leukemia, T-Cell/ETIOLOGY/*GENETICS Male Sequence Homology, Nucleic Acid T-Lymphocytes/DRUG EFFECTS/RADIATION EFFECTS Tetradecanoylphorbol Acetate/PHARMACOLOGY Transcription, Genetic ABSTRACT
920830
M9281102
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Important note: Information in this article was accurate in 1992. The state of the art may have changed since the publication date.
