[Localization of acid phosphatase in the cells of the hemolymphopoietic tissue and inflammatory exudates at pH 5 and 6.3].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to D Catovsky.
Explore the source record for details and available documents.
The expression of two membrane antigens identified by the monoclonal antibodies (McAb) My9 and 3C5 has been investigated in cells from 80 acute leukemias. My9 was positive in the blasts of 33 out of the 38 (87 per cent) cases of acute myeloid leukemia (AML) tested, regardless of FAB subtype, and in 13 of 18 (72 per cent) cases of chronic granulocytic leukemia (CGL) in myeloid blast crisis. The reactivity of 3C5 was confined to myeloblastic (M1) AML, 85 per cent of cases, and to lymphoblastic leukemia (ALL) of B-lineage, 70 per cent of cases, including CGL in lymphoid transformation. My9 was negative in ALL except for an unusual case. The phenotype My9+, 3C5+ was seen exclusively in M1 (69 per cent) and M2 (14 per cent) AML. Ultrastructural analysis with the immunogold method in combination with the myeloperoxidase (MPO) reaction showed that expression of My9 increased in parallel with MPO activity whereas 3C5 was expressed mainly in myeloblasts with little MPO content. We conclude that the use of these two McAb will contribute to the diagnosis and classification of AML and may throw some light to the pathogenesis of biphenotypic acute leukemias, including TdT + AML.
The distribution of T cell subsets and the T colony-forming capacity were assessed in 22 patients with hairy-cell leukemia. An overall increase in the proportion of T gamma cells (31 +/- 15%) and a decrease in Tmu cells (38 +/- 11%) were observed if compared with normal controls (16 +/- 6% for T gamma and 51 +/- 13% for Tmu). In half of the patients, however, these values were normal. T gamma cells were highest in the splenectomized patients and in the 15 non-splenectomized patients T gamma cells were higher in those with active disease. Patients with stable disease or in remission had values close to normal. The T colony-forming capacity of unseparated and enriched T lymphocytes was normal regardless of the T cell subset distribution and clinical stage of the disease. These findings suggest that in HCL, unlike B cell chronic lymphocytic leukemia, the imbalance in Tmu/T gamma ratio does not result in an impairment of the in vitro T colony-forming capacity.
In the past few years important advances have been made in our understanding of the biology and natural history of CLL; also, new strategies and agents offer promise in the treatment of this form of leukemia. Now, patients can be treated on a more rationale basis and with real prospects for a sustained control of their disease, and improved quality of life. Hopefully, progresses in CLL will continue to accumulate in the coming years.
10 neutropenic leukaemic patients had septicaemia caused by viridans streptococci, organisms not commonly recognised as opportunist pathogens. 1 patient died; in the remainder recovery was generally dependent on an adequate circulating granulocyte count (seven patients) rather than specific antimicrobial therapy. Seven of the infections were caused by Streptococcus mitis, and seven of the eight strains tested were resistant to cotrimoxazole, which the patients had received as prophylaxis against infection. It is suggested that oral ulceration caused by cytotoxic chemotherapy provided a portal of entry for cotrimoxazole-resistant viridans streptococci. The increasing incidence of infections with gram-positive organisms as a complication of neutropenia prompts a reconsideration of current empirical antimicrobial therapy.
T-cell prolymphocytic leukaemia (T-PLL) is an aggressive disease often resistant to conventional chemotherapy. Long lasting remissions with the monoclonal antibody CAMPATH-1H (anti-CD52) have been documented. We describe two unusual T-PLL patients treated successfully first with CAMPATH-1H in whom, at the time of relapse, the cells underwent a phenotypic switch with loss of CD52 expression. In one of them, cytogenetic analysis demonstrated the same chromosome abnormalities in the cells at diagnosis and relapse. The reasons for the immunophenotypic changes are unknown but it is likely that loss of CD52 antigen expression contributed to the resistance to CAMPATH-1H in one of the patients when re-treated.
The Fourier transformation is proposed as a technique for the description of cell volume histogram data. In order to test the applicability of this transformation, peripheral blood leucocytes were studied as model populations and the technique assessed by determining the extent to which the Fourier coefficients could be applied as descriptors of various pathologic abnormalities of the differential leucocyte count. Histograms of leucocyte volume distribution were plotted for 87 cases with a variety of abnormalities of the peripheral blood leucocyte population. These histograms were submitted to Fourier analysis and the coefficients thus obtained were used as the basis of a multivariate classification system designed to distinguish certain predefined abnormalities of the differential count. The results obtained suggest that Fourier analysis may prove a valuable technique for the interpretation of cell volume histogram data, and its potential applications are discussed.
Explore the source record for details and available documents.
BACKGROUND AND OBJECTIVE: A minority of acute leukemias have features characteristic of both the myeloid and lymphoid lineages and for this reason are designated mixed-lineage, hybrid or biphenotypic acute leukemias (BAL). There have been difficulties in establishing whether BAL represents a distinct clinico-biological entity due to a lack of objective criteria for distinguishing BAL from acute myeloid leukemias (AML) or acute lymphoblastic leukemias (ALL) with aberrant expression of a marker from another lineage. In this work we analyze diagnostic criteria for BAL. METHODS: We describe the features of 26 patients (19 adults and 7 children) with BAL diagnosed at the Royal Marsden Hospital. BAL was defined according to a scoring system devised by our group and the European Group for the Immunological Classification of Leukemia (EGIL). This system is based on the number and degree of specificity of the markers (lymphoid and myeloid) expressed by the blasts. RESULTS: According to the FAB criteria, BAL may present as "ALL" or as one of the "AML" subtypes, often M1. It is not infrequent to identify two distinct blast populations: one of small size resembling lymphoblasts and the other larger. The most common immunophenotype is coexpression of B-lymphoid and myeloid markers and less frequently, T-lymphoid and myeloid markers. Cases with a B and T lymphoid phenotype or with trilineage differentiation are rare. BAL has a high incidence of clonal chromosomal abnormalities, the most common being the t(9;22) (q34;q11) (Ph chromosome) and structural abnormalities involving 11q23. Data are emerging that BAL has a negative prognosis in both children and adults and this may be related to the underlying chromosome abnormalities. INTERPRETATION AND CONCLUSIONS: In summary, BAL is an uncommon type of leukemia which probably arises from a multipotent progenitor cell and carries a poor prognosis. Although there are no uniform criteria about whether to treat these patients as ALL or AML, it is likely that an intensive approach with high-dose therapy followed by bone marrow transplantation will be required to eradicate the disease permanently.