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Forward and reverse changes in Ig/myc translocation carrying tumors
1Department of Tumor Biology, Karolinska Institute, Stockholm, Sweden.
Princess Takamatsu Symposia
|January 1, 1989
Summary
The c-myc protooncogene translocation is key in B cell tumors like Burkitt lymphoma (BL). This genetic change prevents B cells from resting and helps tumors evade immune responses.
Area of Science:
- Oncology
- Immunology
- Genetics
Background:
- Translocation of the c-myc protooncogene to an immunoglobulin locus is a critical step in B cell tumor development.
- This process is observed in human Burkitt lymphoma (BL), mouse plasmacytoma (MPC), and rat immunocytoma (RIC).
Purpose of the Study:
- To analyze the consequences of c-myc translocation in B cell tumors, particularly BL.
- To investigate the mechanisms by which these tumors escape host immune surveillance.
Main Methods:
- Analysis of c-myc translocation in BL, MPC, and RIC.
- Examination of EBV-convertants of a BL cell line to study tumorigenicity.
- Phenotypic analysis including activation markers and HLA class I expression.
Main Results:
- C-myc translocation prevents B cells from entering resting phase and contributes to immune escape through down-regulation of HLA class I and adhesion molecules.
- A non-tumorigenic revertant subline with a lymphoblastoid line (LCL)-like phenotype was identified among EBV-convertants.
- Tumorigenicity suppression correlated with an LCL-like phenotype and activation markers.
Conclusions:
- C-myc translocation has both non-immunological and immunological consequences that promote B cell lymphomagenesis.
- The host immune system may exert feedback control on B cell populations, influencing tumor development.
- Reversion to an LCL-like phenotype suggests a potential mechanism for host control over B cell proliferation.