Important note: Information in this article was accurate in 1988. The state of the art may have changed since the publication date.
BURKITT'S LYMPHOMA, A HUMAN CANCER MODEL FOR THE STUDY OF THE MULTISTEP DEVELOPMENT OF CANCER: PROPOSAL FOR A NEW SCENARIO
Adv Viral Oncol; 7:173-206 1987. Unique Identifier : AIDSLINE ICDB/88640299 Lenoir GM; Bornkamm GW; International Agency for Res. on Cancer, 69372 Lyon Cedex 08,; France
Abstract:
Evidence supporting a multistep scenario for the development of Burkitt's lymphoma (BL), focusing on the Epstein-Barr virus (EBV)-associated BL that occurs in areas in Africa, is reviewed. In view of new knowledge gained from molecular studies, from studies of acquired immunodeficiency syndrome (AIDS)/BL cases, and of the BL animal model (murine plasmacytoma), the authors propose that the sequence of events leading to the appearance of a Burkitt's cell be reconsidered. A three-step model for BL development is proposed as an alternative to the one originally proposed by G Klein. The first step is the generation of lymphoid cells at high risk for occurrence of translocations involving the Ig loci, which is achieved by chronic, persistent immunological stimulation of the B-cell subset by holoendemic malaria or AIDS-associated opportunistic infections, superimposed on the extremely high physiological turnover of B cells (about 5 x 10(7)/day in mice). Step two is the acquisition of the translocation involving c-myc and Ig loci in one or a few B cells. This, the first genetic event, is not sufficient to transform cells to a neoplastic state, but the first molecular event has made the lymphoid cells competent and responsive to external growth factors upon which cell proliferation still depends. The third step is the infection by EBV of a B cell carrying the specific translocation; this is the second genetic event. The acquisition of viral functions renders the cell independent of exogenous growth factors and, thus, autonomous for its growth. The third step could be achieved by a second cellular event, such as activation of another oncogene, and this may be the case in most EBV-negative BLs occurring in low-incidence areas. The implications of this new model of BL development in comparison with the previous model are discussed. (160 Refs)
Keywords: Acquired Immunodeficiency Syndrome/GENETICS Animal Burkitt's Lymphoma/*GENETICS Cell Division *Cell Transformation, Neoplastic Chromosome Mapping DNA, Neoplasm/GENETICS Gene Expression Regulation Herpesvirus 4, Human/GENETICS Human HIV/GENETICS *Oncogenes Proto-Oncogene Proteins/GENETICS Translocation (Genetics) JOURNAL ARTICLE
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Important note: Information in this article was accurate in 1988. The state of the art may have changed since the publication date.
