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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report on the characterization of four monoclonal antibodies which were prepared against membrane markers of human myeloid lineage. Fusion, isolation of hybridoma cells and their cloning and testing of the monoclonal antibodies by indirect immunofluorescence and FACS 440 analysis were performed by means of standard procedures. The results indicate that the monoclonal antibodies have a specificity against membrane markers of human myeloid lineage (exactly promyelo-granulocytes). These monoclonal antibodies do not react with human T and B lymphocytes, monocytes, erythrocytes and thrombocytes of peripheral blood. In normal bone marrow reactivity to matured myeloid cells was found to occur in promyelocytes and expressed on all granulocytes. These monoclonal antibodies also react with cells of myeloid cell lines and with other precursor cell lines represented by NALM-1, NALM-16, HEL, K-562, REH no reactivity was detected. The produced antibodies react with some leukaemic cells from patients with more mature myeloid cells (AML with promyelocytes, myelocytes and CML) they do not react with pathological cells from patients with CLL, AML (with myeloblasts), ALL, hairy cell leukaemia, erythroleukaemia and several types lymphoma. All antibodies have a IgM class and express granulocytotoxic and granuloagglutination activity. Using flow cytometry comparative analysis with other monoclonal antibodies was performed to detect the membrane structure (X-haptene) included in standard International classification as CD 15 group.
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PMID:Human leukocyte markers defined by monoclonal antibodies. I. Expression of X-hapten structure on cells of myeloid lineage. 246 63

T and NK cell blood subpopulations were determined in 33 patients with B-CLL and in 14 patients with B-MLUS by two-color immunofluorescence. CLL patients had significantly higher total numbers of Leu-7+ and CD8+ cells and lower numbers of CD16+/Leu-7- cells as well as a higher Leu-7/CD16 ratio and a lower CD4/CD8 ratio than MLUS patients and control donors. Moreover, MLUS patients exhibited a significantly lower Leu-7/CD16 ratio as well as a higher frequency of CD16+/Leu-7- cells than healthy donors. These results suggest that B-CLL patients have higher numbers of circulating immature NK cells compared to B-MLUS, while B-MLUS patients have a larger proportion of NK cells with a high lytic capability as compared to both CLL and normal controls. The imbalance between CD4+ and CD8+ cells was prominent in CLL with a low CD4/CD8 ratio, but within the upper normal range in MLUS. Differences in immunoregulatory cell subpopulations between B-CLL and B-MLUS might therefore contribute to the different clinical behavior of these two disorders.
Leukemia 1989 Jul
PMID:Differences in blood T and NK cell populations between chronic lymphocytic leukemia of B cell type (B-CLL) and monoclonal B-lymphocytosis of undetermined significance (B-MLUS). 247 2

In the present study plasma fibronectin levels were determined in patients with hematopoietic malignancy, particularly leukemias, in an effort to clarify their clinical implications. Among leukemia patients, those with AML, ALL, ATL or CLL had various plasma fibronectin levels that were higher in some cases, while lower in others, as compared to normal control values. An elevation of the fibronectin level was noted often in APL, while lower fibronectin values were observed in many instances of CML. In these types of leukemia, acute exacerbation as well as supervention of infection tended to be associated with lower than normal levels of fibronectin. An especially marked depression of fibronectin occurred, when leukemia was complicated by sepsis or DIC, in which a good parallel was noted between the progress of disease and the fibronectin level. In lymphoproliferative diseases, the fibronectin value varied widely, but low fibronectin levels were frequently associated with intercurrent infection or an extreme deterioration of the general physical conditions.
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PMID:Variation of plasma fibronectin levels in leukemia patients. 248 45

The occurrence and frequency of aphidicolin-induced common chromosomal fragile sites were examined in 12 B-cell chronic lymphocytic leukemia (B-CLL) patients (ten males and two females) and three normal individuals. The mononuclear cells separated by Ficoll-Hypaque gradient were cultured in vitro for 96 hours stimulated by pokeweed mitogen (PWM) in combination with T-leukemia cell conditioned medium or 10% B-cell growth factor. For the final 24 hours the cells were treated with aphidicolin (0.07 microgram/ml). Results indicate that there was a significant reduction in the overall mean frequency of common fragile sites in CLL patients with a wide individual variation. Fragile sites were found to be localized either on a single chromatid or both chromatids, but rarely involved homologous chromosomes. No definite relationship between the frequency of fragile sites and the staging of CLL disease was observed. A significant reduction and variability in the frequency of fragile sites suggest the heterogenous nature of B-CLL and probably a different mechanism of induction of fragile sites in CLL cells compared to controls.
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PMID:Reduced expression of aphidicolin-induced common fragile sites in peripheral lymphocyte chromosomes of patients with B-cell chronic lymphocytic leukemia. 249 14

Large granular lymphocytes (LGL) may exert regulatory influences on B cell immunoglobulin synthesis. We, therefore, investigated the influence of LGL from controls and B cell chronic lymphocytic leukemia patients (B-CLL) on control B cell proliferation to costimulation with the F(ab')2 fragment of goat antihuman mu and B cell growth factor (BCGF). Purified LGL (greater than 90% by morphology) from control and B-CLL peripheral blood were added in various concentrations to purified control B cells and incubated with anti-mu and BCGF for 3 days. [3H]-thymidine uptake of B cells was then measured. There was no proliferation of control or CLL LGL alone to the costimulatory signals of the F(ab')2 fragments of goat antihuman mu chain and BCGF. Addition of control LGL to equal numbers of control B cells did not blunt control B cell responsiveness to BCGF (with control LGL 8,649 +/- 298 cpm vs. control B cells alone 8,336 +/- 556 cpm, mean +/- SEM). When control LGL were increased to 10:1 LGL:B cell ratio, the maximal inhibition by control LGL of control B cell proliferative response to BCGF was 23%. In contrast, addition of CLL LGL at a 1:1 LGL:B cell ratio resulted in marked impairment of the control B cell proliferative response to BCGF (with CLL LGL 3,586 +/- 954 cpm vs. control B cells alone 8,649 +/- 298 cpm). Inhibition by CLL LGL occurred in a cell-concentration-dependent manner. No difference in CLL LGL's inhibitory effect on either resting or activated control B cell responsiveness to BCGF was noted. Inhibition of de novo protein synthesis (by cycloheximide inhibition) of CLL LGL did impair CLL LGL's inhibitory capacity for BCGF-induced B cell proliferation. A possible explanation for these findings includes the possibility that a subgroup of LGL with B cell suppressive activity may have expanded as a host response to the B cell leukemia or as part of the disordered cell regulation in B-CLL.
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PMID:Large granular lymphocytes from B-chronic lymphocytic leukemia patients inhibit normal B cell proliferation. 250 Aug 49

A 78-year-old woman, who had axillary lymphadenopathy but no hepatosplenomegaly, was admitted because of lymphocytosis. The leukocyte count was 18.1 x 10(9)/l with 72% abnormal cells. Neither anemia nor thrombocytopenia was present. Many abnormal cells and erythroblasts were seen in the bone marrow. These abnormal cells had irregular nuclei but no granules in the cytoplasm. The surface markers of these cells were positive for E-rosette, CD 2, CD 3, and Leu 7 but negative for CD 4, CD 8, CD 11 (OKM 1), CD 16 (Leu 11), and HLA-DR. The DNA analysis revealed the rearrangement of T-cell receptor beta-chain genes. Direct Coombs test was positive and red-cell life-span (51Cr) was T 1/2 = 19.5 days. The patient was diagnosed as having T-CLL with mild autoimmune hemolysis and was followed without treatment. Seven months later, the leukemia cells of peripheral blood increased to 62.6 X 10(9)/l and the frank autoimmune hemolytic anemia developed. After prednisolone, vincristine and cyclophosphamide were administered, leukemia cells of blood decreased. Anemia with reticulocytopenia, however, persisted and direct Coombs test became negative. In the bone marrow at that time, many neutrophils and megakaryocytes besides leukemia cells were preserved, but erythroblasts were hardly seen, namely a pattern of red cell hypoplasia was observed. The patient deteriorated rapidly and died 26 months after initial recognition of lymphocytosis. When complement was added, the patient's serum obtained during red cell hypoplasia but not during autoimmune hemolysis inhibited BFU-E and CFU-GM in in vitro colony assays. This case indicates that not only B-CLL but also T-CLL is accompanied by immune hematocytopenia.
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PMID:[Red cell hypoplasia following autoimmune hemolytic anemia associated with T-CLL: report of a case and review of the literature]. 250 1

The frequencies of HLA-DP alleles in 50 acute lymphocytic, 43 acute non-lymphocytic, 50 chronic myelogenous and 51 chronic lymphocytic leukaemia patients were compared with 254 controls using primed lymphocyte typing. In CLL and ANLL there were significantly decreased frequencies of DPw1. Decreased DPw1 and DPw3 was observed in ALL, but after correction for the number of comparisons made this was no longer significant. However, in ALL, even after correction, there were significantly increased frequencies of DPw2 and DPw5, whereas in ANLL and CLL the only significant increases were of DP-blank, and in CML there were no positive or negative associations at all. These results suggest an influence of DP alleles in disease susceptibility and resistance in three of the four major types of leukaemia.
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PMID:Frequencies of HLA-DP alleles in the four major types of leukaemia. 251 65

The distribution of a carbohydrate antigen, the sialyl SSEA-1 (sialyl Lex-i), in human lymphoid cells was investigated by flow cytometry with a specific monoclonal antibody, MoAb FH-6. We concluded that the lymphocytes positive for the sialyl SSEA-1 antigen present in normal peripheral blood (PB) are natural killer (NK) cells since the positive cells had an NK activity toward K562 cells, and most of the sialyl SSEA-1+ cells were simultaneously positive for Leu-11 (CD-16) and Leu-19. Essentially, no T and B cells, defined by Leu-4 (CD3) and Leu-16 (CD20), were positive for the sialyl SSEA-1 antigen in PB samples taken from healthy donors and patients with disorders unrelated to lymphoid malignancies. Among the malignant lymphoid cells, many sialylated SSEA-1+ cells were observed in large granular lymphocyte (LGL) leukemia cells and some acute lymphoblastic leukemia (ALL) blasts, but not in CLL cells or malignant lymphoma cells. Sialyl SSEA-1 was also positive in some cultured human lymphoid cell lines. We conclude that expression of the sialyl SSEA-1 antigen is strictly limited to a distinct population of NK cells among the mature lymphocytes in normal PB, but the antigen is present in a wide range of immature lymphoblasts of T- and B-cell lineages as well as the NK-cell lineage. The sialyl SSEA-1 antigen disappears from the surface of immature lymphocytes of T- and B-cell lineages during the course of maturation.
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PMID:Sialyl SSEA-1 antigen as a carbohydrate marker of human natural killer cells and immature lymphoid cells. 256 58

Trisomy 12 is the most common chromosomal aberration in chronic B lymphocytic leukemia (B-CLL). In this study we have investigated trisomy 12 and posed two major questions: (a) What is the origin of the third copy of chromosome 12? and (b) What is the proportion of trisomy 12 cells in malignant clones with this aberration? The origin of an extra copy of chromosome 12 in lymphocytes from patients with B-CLL was studied by the use of probes detecting restriction fragment length polymorphisms on this chromosome. In all six patients that were evaluable, the third copy was derived from a simple duplication of one of the original chromosomes. In none of these patients nor in four patients with two copies of chromosome 12 were losses of the homologue observed. When studying metaphase cells from some CLL patients with trisomy 12, a large proportion of the cells are found to have a normal karyotype. In this study the fraction of normal metaphases was not matched by a similar fraction of cells lacking trisomy 12, as judged by scanning densitometry of hybridization bands. Thus, normal metaphases appear to be derived from a small fraction of easily stimulated probably nonmalignant cells and not from a large second population of malignant cells with a normal karyotype.
Leukemia 1989 Dec
PMID:Molecular analyses of chromosome 12 in chronic lymphocytic leukemia. 258 80

We have previously described a monoclonal antibody (MoAb), H2, which recognized a tumour-unique antigen on a human T-cell chronic lymphatic leukaemia (T-CLL, CD3,4+). However, further characterization of H2 has revealed a reactivity with the majority of T lymphocytes and a minority of B lymphocytes, some malignant T cells and a few cell lines of leukaemia or of hematopoietic tumour origin. The molecular weight of the antigen (80,000) precipitated by the MoAb H2 from the cell lines NALM-6 and Reh corresponded to that previously found. When PBL were stimulated with PHA, IL-2, or Con A a reduced reactivity of H2 could be seen. The MoAb H2 was submitted to the Fourth International Conference on Human Leucocyte Differentiation Antigens, Vienna, 1989. H2 did not cluster in any of the 78 clusters of differentiation (CD 1-78) discussed at the conference, indicating its unique reactivity. This suggests that we have defined a new antigen on lymphocytes with a possible role along the resting-proliferating axis.
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PMID:A monoclonal antibody, H2, defines a new surface antigen expressed on human lymphocytes. 258 34


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