Deregulated c-myc Gene Expression and Persistence of EBV are Not Sufficient to Maintain the Malignant Phenotype in Burkitt’s Lymphoma x B-Lymphoblastoid Hybrid Cells

Abstract

Evidence for loss of specific genetic information as an essential event in the multistep process of malignant transformation has been provided by somatic cell hybrid studies which demonstrated suppression of the malignant phenotype for a wide spectrum of murine and human tumor cells after fusion with nonmalignant fibroblasts or keratinocytes (Sager 1986, Klein 1987). The model of recessive tumorigenesis seems to be confirmed by the detection of specific allele losses in several human tumors of epithelial and mesenchymic origin (Ponder 1988), however, has not mainly been involved in scenarios for the development of hematopoietic malignancies. Especially malignant lymphomas still are considered to be models for the dominant action of oncogenes activated by specific chromosomal translocations. This concept was supported by transfection experiments which demonstrated tumorigenic conversion of Epstein-Barr virus (EBV)-immortalized human B-lymphocytes after introduction of a constitutively expressed c-myc gene (Lombardi et al. 1987). Accordingly, no tumor suppression has been demonstrated yet in lymphoma/lymphocyte hybrid cells (Harris 1988).