Ben-David Y, Yefenof E, Kotler M
The Lautenberg Center for General and Tumor Immunology, Hebrew University, Hadassah Medical School, Jerusalem, Israel.
Cancer Res. 1987 Dec 15;47(24 Pt 1):6590-4.
Clonality of radiation leukemia virus (RadLV)-induced thymic lymphomas was determined by detection of rearrangements in the genetic locus coding for the beta chain of the T-cell receptor (T beta). Unique T beta rearrangements were detected in four of six lymphomas. Two of the T beta-rearranged thymic lymphomas and two in which such a rearrangement was not detected had a biallelic deletion of C beta 1. With an anti-RadLV monoclonal antibody it was found that 1-2 days after virus inoculation more than one-third of the cells in the thymus were infected by the virus. The frequency of virus-positive cells gradually declined and persisted at 1-2% until the appearance of a clonal lymphoma at which time virtually all the cells in the thymus were virus positive. Transfer of thymocytes from a single, preleukemic mouse 21 days post-virus inoculation into several adoptive recipients resulted in donor-type thymic lymphomas in the majority of the mice. T beta rearrangement analysis revealed that these lymphomas were clonal and derived from different potentially leukemic (preleukemic) cells in the thymus of the donor mouse. Eleven of 15 lymphomas had a biallelic deletion of C beta 1. These results suggest that clonal, RadLV-induced thymomas are selected from an oligoclonal, RadLV-infected preleukemic T-cell population.