of platelet aggregation . Fibrinogen mediated activation

diagnosed by morphological, cytochemical, immunological, and ultrastructural methods.' Following remission induction with daunorubicin, vincristine, prednisolone, and L-asparaginase she received maintenance treatment with methotrexate, 6 mercaptopurine, cytosine arabinoside, vincristine, and prednisolone for 12 months before this was stopped due to neutropenia. She remained well until August 1985 (28 months after diagnosis) when she relapsed. Full blood count at this time showed haemoglobin 10-4 g/dl, white cell count 67-0 x 109/1 (differential 95% blasts, 4% neutrophils, 1% lymphocytes), and platelet count 55-0 x 109/1. Examination of MayGrunwald-Giemsa stained smears showed two distinct blast cell populations with about 70% having lymphoblastic and 30% myeloblastic features. The Table shows details of the immunological studies at diagnosis and relapse, and, apart from an increased expression of OKTl1 at relapse, they are remarkably similar. She was treated with vincristine, prednisolone, daunorubicin, and L-asparaginase, but her disease was totally refractory and she died 14 days after relapse. Necropsy examination was not performed. Biphenotypic leukaemia may either result from a single mutation in a pluripotential progenitor cell with maintained capacity for bilineage differentiation, or, alternatively, may be two unrelated transformations. The fact that the relapse occurred with similar proportions of T cell and myeloid blasts (as found at diagnosis) strongly suggests that in this case they had arisen from a single malignant progenitor. Recently blasts in a proportion of cases of acute myeloid leukaemia have been shown to express membrane sheep red blood cell (E) receptors, or the OKTI 1 determinant.2 Our case, however seems to differ from these, as the lymphoblasts were positive with more than one T cell antibody (OKT17, 3A1, RFT2) and also because we were able to show mutual exclusion of myeloperoxidase and T cell specific antigens, confirming true biphenotypic leukaemia. AN STARK