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Biomedical subjects

E Matutes

Publications and source records attributed to E Matutes.

287 records · Page 16Linked to original sources
PubMed1981

Unusual T-cell phenotype in advanced B-chronic lymphocytic leukaemia.

T-lymphocytes isolated by E-rosetting from 22 patients with B-cell chronic lymphocytic leukaemia (B-CLL) showed membrane phenotype features distinct from those of normal T-lymphocytes. These changes were particularly marked in advanced disease (Rai stages II, III, IV and WBC over 100x10(9)/l). The most significant finding was the demonstration, in 10 cases, of a major population of E-rosette positive cells (40-80%) unreactive with the OKT monoclonal antibodies against mature or immature T-cells; 15-30% of the cells were unreactive in seven other cases. A significant reduction in OKT4 positive (helper) lymphocytes was seen in 18 cases. The proportion of OKT8 positive cells was increased in two and normal or low in the rest. Only four patients with early disease (stages 0 and I) had a normal T-cell phenotype. These findings could explain abnormalities previously described in the T-lymphocytes of B-CLL and provide new insights into the pathogenesis of the disease.

Antibodies, Monoclonal↗
PubMed1981

Megakaryoblastic leukemia presenting as acute myelofibrosis -- a study of four cases with the platelet-peroxidase reaction.

Acute myelofibrosis (AM) or malignant myelosclerosis is a myeloprofilerative syndrome in which bone marrow fibrosis is associated with a proliferation of immature myeloid cells. In four patients with typical AM, investigated by the platelet-peroxidase reaction at ultrastructural level, the blast cells were found to be megakaryoblasts. One patient, treated with the drug combination DAT, achieved a complete remission of 5 mo duration. This study supports the view that megakaryoblastic leukemia is the most frequent underlying cause of AM and proposes that it should be classified as a form of acute myeloid leukemia.

Acute Disease↗
PubMedDate not supplied

Characterization of myeloid leukemias with monoclonal antibodies 3C5 and MY9.

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.

Antibodies, Monoclonal↗
PubMedDate not supplied

T lymphocyte subsets and colony growth in hairy-cell leukemia.

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.

Animals↗
PubMedDate not supplied

Comparative morphology of granulocytes collected by three methods of leukapheresis. A light microscopy and transmission electron microscopy study.

The morphology of granulocytes collected by continuous-flow centrifugation (CFC), discontinuous-flow centrifugation (DFC), and continuous-flow filtration (CFF) was investigated in 18 healthy donors by means of light microscopy and transmission electron microscopy. Light microscopy study of semithin sections of granulocytes collected by CFC and DFC showed minimal morphologic abnormalities, compared to granulocytes procured by CFF. Ultrastructural study of granulocytes procured by CFF showed more conspicuous qualitative and quantitative abnormalities (the most prominent being "microvilli," degranulation, and bazarre chromatin) than in granulocytes obtained by the other two methods. Controls showed that the bulk of CFF-cell abnormalities was due to the "tapping" of the filters. Factors such as the mechanical compression (plasma extractor) used in DFC method, donor pretreatment with anticoagulants and steroids, hydroxyethyl starch, and duration of leukapheresis scarcely influenced granulocyte morphology.

Adult↗
PubMedDate not supplied

Immunophenotype changes and loss of CD52 expression in two patients with relapsed T-cell prolymphocytic leukaemia.

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.

Adult↗
PubMedDate not supplied

Definition of acute biphenotypic leukemia.

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.

Acute Disease↗