Abstract
A cell line (BS) carrying a variant 11;19 translocation was established following exposure to Epstein-Barr virus (EBV) of the blast cells from an infant with null (B precursor) acute lymphoblastic leukaemia (ALL). Morphology, cytochemistry and immunophenotype were identical to those of the original leukaemic blasts and characteristic of an early B cell neoplasm. Both the cell line and the patient's blasts had an identical karyotype, 46.XY, t(11;19) (q23;p13), t(11;19)(q13;q13). Immunoglobulin heavy chains were rearranged without concomitant light chain rearrangement. No rearrangements of the β, γ or δ chain of the T cell receptor, the proto-oncogene c-ets 1 or the insulin receptor gene which maps to 19p13 were detected. Exposure of the BS line to phorbol ester (PMA) induced a myelomonocytic phenotype with coexpression of B and myeloid cell surface antigens and myeloid cytochemistry. No EBV nuclear antigens (EBNA 1,2) were detectable in the cell line using either immunocytochemical or molecular analyses and the mechanism of "immortalization" by EBV remains unknown. With its unique karyotype, BS provides a useful cell line to study the four translocation breakpoints which occur frequently in both acute lymphoblastic and acute myeloid leukaemias.
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