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Forward and reverse changes in Ig/myc translocation carrying tumors
1Department of Tumor Biology, Karolinska Institute, Stockholm, Sweden.
Translocation of the c-myc protooncogene to an immunoglobulin locus is a rate-limiting step in the genesis of three B cell derived tumors: Burkitt lymphoma (BL) in humans, mouse plasmacytoma (MPC), and rat immunocytoma (RIC). The translocation appears as a rate-limiting step in the genesis of all three tumors. Its consequences have been best analyzed in BL. They involve a non-immunological and an immunological component. The former acts by preventing the B cell from leaving the cycling compartment and entering the resting stage when programmed to do so. The latter acts by the down-regulation of certain human leucocyte antigen (HLA) class I polymorphic specificities, adhesion molecules and Epstein-Barr virus (EBV) encoded proteins. Together, they contribute to the escape of the BL cell from the host immune response. We have also described a non-clonogenic, non-tumorigenic "revertant", subline among five EBV-convertants of an originally highly tumorigenic, EBV-negative BL line. The other four convertants have remained highly tumorigenic. Suppression of tumorigenicity is associated with a switch to a lymphoblastoid line (LCL)-like phenotype, accompanied by the appearance of several activation markers. It is suggested that the LCL-type immunoblast comes under the influence of host feedback that normally contribute to the constancy of the B cell pool.
Translocation of the c-myc protooncogene to an immunoglobulin locus is a rate-limiting step in the genesis of three B cell derived tumors: Burkitt lymphoma (BL) in humans, mouse plasmacytoma (MPC), and rat immunocytoma (RIC). The translocation appears as a rate-limiting step in the genesis of all three tumors. Its consequences have been best analyzed in BL. They involve a non-immunological and an immunological component. The former acts by preventing the B cell from leaving the cycling compartment and entering the resting stage when programmed to do so. The latter acts by the down-regulation of certain human leucocyte antigen (HLA) class I polymorphic specificities, adhesion molecules and Epstein-Barr virus (EBV) encoded proteins. Together, they contribute to the escape of the BL cell from the host immune response. We have also described a non-clonogenic, non-tumorigenic "revertant", subline among five EBV-convertants of an originally highly tumorigenic, EBV-negative BL line. The other four convertants have remained highly tumorigenic. Suppression of tumorigenicity is associated with a switch to a lymphoblastoid line (LCL)-like phenotype, accompanied by the appearance of several activation markers. It is suggested that the LCL-type immunoblast comes under the influence of host feedback that normally contribute to the constancy of the B cell pool.