Serum selenium levels in untreated children with acute lymphoblastic leukemia. I.

Serum selenium in the control group of 79 children aging 1 to 16 years was measured. A slight increase in serum selenium values with age occurred. The 89 patients of the test group were suffering from malignant proliferative diseases. The largest number of patients was suffering from acute lymphatic leukemia (78 patients), then Hodgkin's and non-Hodgkin's lymphoma (5 patients) and other malignant proliferative diseases (6 patients). Samples were taken before any therapeutic treatment at the time of diagnosis. Patients were of the same ages as the control group. Statistical analysis of the data shows that a significant difference exists in the selenium level of most of the patients as compared with the control group. They have a lower serum selenium. Only patients with Hodgkin's and non-Hodgkin's lymphoma have same selenium content as the control group.

Defect of NK activity in children with untreated acute lymphocytic leukemia (ALL). I. Dependence on the blast count and phenotype, and response to exogenous and endogenous alpha-interferon.

Endogenous NK-activity (eNK) against K-562 cells was determined in peripheral blood of 68 children with acute lymphocytic leukemia (ALL) before treatment. In 53% of them it was depressed, and in 47% it was within the range of control children (27) and adults (104). There was a significant negative correlation between blast contamination of peripheral blood and the level of eNK-activity. In spite of this general trend, 8 patients with high blast count have had normal eNK-activity, and 10 patients with relatively low blast count (below 50%) have had depressed eNK-activity. Examples of T ALL showed significantly lower eNK-activity than CALLA ALL. The ability of exogenous alpha-interferon (IFN) to stimulate eNK-activity was impaired in 18 of 40 examples of ALL and preserved in 22. The IFN-induced NK-response was also negatively correlated to the blast burden, but again with exceptions: Six nonresponders in spite of low blast count, and six responders in spite of high blast count in peripheral blood. IFN-inducer, poly-IC, stimulated eNK-activity only in 6 of 26 ALL samples. Surprisingly, positive correlation was found between poly-IC-induced NK-stimulation and blast count in peripheral blood. Poly-IC induced significant IFN production only in one of six cultures of ALL. Impaired eNK-activity has been attributed, in part, to "dilution" of NK cells by the blasts. Defects in production of IFN, and in response to it, may be additional reasons for depressed NK-activity in about 50% of children with untreated ALL.

Expression of haematopoietic progenitor cell-associated antigen BI-3C5/CD34 in leukemia.

The expression of progenitor cell-associated antigen CD34, defined with monoclonal antibody BI-3C5, was investigated in cells from 109 patients with leukaemia. No reactivity was found in chronic leukaemias, whereas 31% of acute myelogenous leukaemia (AML) and most non-T, non-B acute lymphoblastic leukaemia (ALL) expressed CD34. Examples of BI-3C5+ AML included M1 and M2 FAB types only; all but one were myeloperoxidase positive. In combination with pan-myeloid markers, BI-3C5 is useful for identification of immature myeloid cells.

Premature chromosome condensation in children with acute lymphocytic leukemia (L1) and malignant histiocytosis.

In this study we report the observation of premature chromosome condensation (PCC) in two children with acute lymphocytic leukemia L1 and one child with malignant histiocytosis. Cytogenetic analysis was performed on peripheral blood or bone marrow cells cultivated for 24 hours without mitogen. In all three reported cases the modal karyotype was normal, while 12.9%, 5.5%, and 5% of spreads with PCC was observed, respectively.

Defects of natural killer cell activity in children with untreated acute lymphocytic leukemia.

Natural killer (NK) activity against cells of the K-562 line was significantly depressed in 12 of 18 children (66%) with untreated acute lymphocytic leukemia (ALL). No suppression of allogeneic NK activity was observed with sera of the patients, regardless of the level of NK depression. The ability of peripheral blood lymphocytes (PBLs) to suppress allogeneic NK activity was tested in two ALL patients - one with no detectable NK activity, and one with high NK activity. No NK-suppressive activity was found with PBLs of the areactive patient; PBLs of the reactive patients exhibited some suppressive activity, but only at a particular suppressor-to-effector cell ratio. Leukemic blasts were resistant to killing by autologous NK cells stimulated by IFN, as well as to killing by allogeneic, IFN-stimulated PBLs. Leukemic blasts of an ALL patient inhibited lysis of K-562 cells in an 18-h, but not in a 4-h NK assay. The inhibition could partly be reversed by pretreatment of ALL cells with alpha interferon, suggesting that the blasts might inhibit the lysis of K-562 targets in a competitive manner. Disturbed function and/or regulation of NK cells may influence attempts at NK cell activation by lymphokines.

Subsets of childhood acute lymphoblastic leukaemia in Croatia.

As a contribution to epidemiological studies on distribution of acute lymphoblastic leukaemia (ALL) subsets in different countries, we investigated blast cell immunophenotype in 54 children with ALL from the western part of Yugoslavia. The subtype incidences were: common, 75.9%; null, 7.4%; T, 11.1%; B, 1.9%; and unclassifiable, 3.7%. This resembles the ALL pattern registered in developed countries. Hence, differences in socioeconomic status between our population and developed European countries do not result in an appreciably altered incidence of childhood leukaemia subtypes.

Cytogenetic analysis of a child with malignant histiocytosis.

This report presents the results of cytogenetic analysis of a child with malignant histiocytosis. The analysis was carried out on slides obtained following short-term cultures of peripheral blood cells. The malignant cells had a deletion of the long arm of chromosome #7, 46,XX,del(7)(q22).

Heterochromatic segment length of Y chromosome in 55 boys with malignant diseases.

By investigating heterochromatic segment variability in a group of boys with malignant disease a significantly greater value of the Yc:F index in relation to the control subjects was established.

Marker chromosome 1q+ in acute lymphocytic leukemia.

This paper presents the results of a cytogenetic analysis on a patient with acute lymphocytic leukemia (ALL) type L2 according to the FAB classification. Of the metaphases examined, 69.3% belong to the aberrant clone of pseudodiploid karyotype. Marker chromosome 14q+ has been identified in all the cells of the clone. Duplication was found in 30% of the metaphases, and in 15% triplication of the proximal segment of the long arm of chromosome #1 (q11-q21). In one metaphase the long arm of chromosome #1 is made up of segment q11-q21 four times repeated. Aberrations of chromosome #1 support the idea that heterochromatic region may be related to the higher degree of the cell malignity.

Variability of chromosomes 1, 9, and 16 in children with malignant diseases.

Heterochromatic segments of chromosomes #1, #9, and #16 were analyzed in 38 children with malignant disease and 42 healthy persons. The analysis was carried out on C-banded metaphases obtained by peripheral blood culture. Using a quantitative method of analysis, an association was established between C-segment length of chromosome #9 and malignant disease in children. A disturbed quantitative relation of C-heterochromatin of chromosomes #1, #9, and #16 was also found in the group of children with malignant disease.

[Treatment of bone marrow aplasia in phase I of acute lymphatic leukemia treatment in children]. / Pokusaji suzbijanja i lijecenja aplazije kostane srzi u I fazi lijecenja akutne limfaticne leukemije u djece.

In the first phase of treatment of acute lymphatic leukemia in children (ALL) with aggresive cytostatic protocols, the doctor is, in some patients, forced to modify the antitumor therapy over a certain period of time because of bone marrow depression. The authors attempted to pull patients with ALL through this critical phase of the disease - by administering "profilactically" Lithium Carbonate (Li2CO3) ( in order to stimulate granulopoiesis) or, if anaemia, leukopenia and thrombocytopenia had already occurred, by administering concentrates of erythrocytes, leukocytes and platelets - without discontinuing the administration of cytostatics. The results of these attempts are reported.