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    THE E-MU-MYC TRANSGENIC MOUSE - A MODEL FOR HIGH-INCIDENCE SPONTANEOUS LYMPHOMA AND LEUKEMIA OF EARLY B-CELLS
    HARRIS, AW ; PINKERT, CA ; CRAWFORD, M ; LANGDON, WY ; BRINSTER, RL ; ADAMS, JM (ROCKEFELLER UNIV PRESS, 1988-02-01)
    Mice transgenic for a c-myc gene driven by the IgH enhancer (E mu-myc) were shown to almost invariably develop lymphomas, 90% succumbing in the first 5 mo of life. The tumors typically presented as rapidly progressive lymphadenopathy with thymic involvement and were highly malignant by transplantation assay. Morphologically, they were lymphoblastic lymphomas, usually accompanied by lymphoid leukemia and granulocytosis, and were distinct from the tumors that arose much later in 37% of nontransgenic mice of the same (C57BL/6 x SJL)F2 genetic background. Cell-surface markers on 31 E mu-myc tumors identified 52% as pre-B lymphomas, 29% as mixed pre-B and B lymphomas, and 19% as B lymphomas. The tumors appeared to arise at random from a population of pre-B cells expanded by constitutive expression of the myc transgene. A majority of the animals initiated malignancy at the rate of 17% per week. The rate at which the cycling, benign pre-B cells spontaneously convert to malignancy was estimated to about 10(-10) per cell per generation. A transient leukocytosis identified in young E mu-myc mice was developed into a rapid assay for inheritance of the transgene.
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    A SEARCH FOR MESSENGER-RNA MOLECULES BEARING IMMUNOGLOBULIN VH NUCLEOTIDE-SEQUENCES IN T-CELLS
    KEMP, DJ ; ADAMS, JM ; MOTTRAM, PL ; THOMAS, WR ; WALKER, ID ; MILLER, J (ROCKEFELLER UNIV PRESS, 1982)
    Expression of VH-coded mRNA molecules in T cells, antigen-specific T cell lines, or T cell hybridomas was not detected using four different VH DNA probes under conditions that permitted cross-hybridization between distantly related VH genes. In contrast, VH gene expression was readily detected in two B cell lymphomas and in splenic B cells. Less than one molecule per cell of RNA, exactly complementary to the DNA probes used, would have been detected in these T cell populations. The results thus seriously question the proposition that T cells use the B cell VH repertoire to code for antigen receptors.