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Characterisation of acute leukaemia has greatly progressed due to the discovery of a large number of molecules using monoclonal antibody techniques. In acute lymphoblastic leukaemia, these techniques not only demonstrate the lymphoid origin of the proliferation but also allow to distinguish between T and B lymphoblasts at various stages of differentiation. This information is useful in establishing prognosis and making therapeutic choices. In acute myeloid leukaemia, immunologic phenotyping confirms the French-American-British (FAB) classification, allowing diagnosis of undifferentiated acute myeloid leukaemia (LAM 0) and can itself constitute a prognostic element.

By immunizing mice with bone marrow cells of a patient with acute lymphoblastic leukemia, monoclonal antibodies have been produced against differentiation antigens of hemopoietic cells. These antibodies also recognize cells in different parts of the normal human kidney. Two antibodies, ALB1 et ALB2, which recognize the common acute lymphoblastic leukemia antigen, (CALLA), label the podocytes and the epithelial cells of the proximal tubules of the kidney; ALB6, which recognizes the "p 24" antigen of lymphocytes, labels the distal tubules; ALB9, which recognizes lymphoblasts and granulocytes, labels the thick ascending loop of Henle and the collecting tubules; PM1, which recognizes immature granulocytic cells, labels the thick ascending loop of Henle.

Animal immune RNA used for the induction of the human lymphoblastoid cell line LDV/7, induces the appearance of receptor sites on the surface of these cells and the synthesis of specific immunoglobulins which are liberated into the culture medium. Furthermore, RNA has been extracted from these cells, which possesses the same properties of specific cytotoxicity as the RNA used for induction. It is supposed that the immune RNA derepresses specific genes on the genome of the induced cells.

Between January, 1982 and April, 1983, 92 adult patients with acute leukaemia were investigated in our department. According to classical criteria (cytology and optical cytochemistry), 34 were classified as "non-myeloid". These were further tested with a panel of monoclonal antibodies against cell membrane, including ALB1-2 (anti-CALLA), ALB6 (anti-p24), ALB7-8-9 (BA1), OKT and HLA DR; they were also tested for E rosettes, Slg and terminal transferase (TDT). When all these markers but HLA DR were negative, patients were investigated for ultrastructural peroxidases which were found to be present in 2 cases. Among all non-myeloid leukaemias, 18 (56%) were CALLA-positive and TDT-positive acute lymphoblastic leukaemias (ALL), 2 (6%) were ALL T, 7 (22%) were CALLA-negative and TDT-positive ALL and 5 (16%) were acute leukaemias null for our markers, a phenomenon the significance of which is discussed. Patients with the CALLA-negative TDT-positive phenotype were peculiar with regard to age (mean: 50 years), female predominance, L2 cytological pattern according to the FAB classification, good prognosis (complete remission in 100% of the cases) and median survival (p less than 0,03).

In a retrospective study of 112 adult patients with acute leukaemia (AL), the percentage of undifferentiated leukaemia was reduced to almost 1% by an analysis of routine cytochemical reactions (PAS, peroxidase, esterases and esterase inhibition), B and T lymphocyte markers (IgS, E-rosettes, HuTLA) cAll antigen and ultrastructural detection of peroxidase activity (PO-ME). A simultaneous study of cALL antigen and PO-ME showed reciprocal exclusion of these markers, except in one case of mixed leukaemia. Therapeutically, the value of these tests lies in that patients with typical PAS reaction and cALL antigen consistently respond to vincristine- corticosteroid treatment, whereas patients without cALL and with PO-ME are frequently resistant to that combination of drugs.

A specific determination of fibrin degradation product (FbDP) is essential for the monitoring of thrombolytic therapy. In patients under thrombolytic therapy, even with tpA (tissue type plasminogen activator) fibrinogen is degraded, and fragment D derived from fibrinogen degradation, is evidenced in the plasma of treated patients. In order to determine specifically the FbDP, even in the presence of fragment D, we take into account the fact that FbDP are complexes such as DDE complex. Therefore a new Elisa technique is proposed. FbDP and fragment D are captured from plasma by immobilized anti D neo monoclonal antibody which recognizes an epitope accessible on fragment D but does not react with undegraded fibrinogen. DDE complexes are then detected specifically using a peroxidase-labelled anti E antibody. The advantage of this technique is discussed in this paper.