Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A MCA raised against the human acute myelogenous leukaemia cell line KG1 reacted with only KG1 among 26 haematopoietic cell lines covering the major lineages. It reacted with early myeloid (M1/2), 1 of 2 acute myelomonocytic (M4) and most non-B non-T leukaemias, including blast crises of CGL. Among M1-AML cells, both MPO+ and MPO- blasts were BI-3C5+. Blasts in 3 Tdt+ M1-AMLs were simultaneously BI-3C5+. BI-3C5 reacted with 4% cells in normal BM, many of which were histologically recognisable as myeloid precursors. 8-15% of BI-3C5+ cells in BM were simultaneously Tdt+, and all were weakly Ia antigen+. BI-3C5 was unreactive with all peripheral leucocytes, with M3 and M5 AMLs, with lymphoid and myeloid leukaemias of "mature" phenotype (T-ALL, B-ALL, CLL, CGL) and with non-haematopoietic cell lines. BI-3C5 precipitated a 120K moiety from 125I-labelled KG1 membranes. It was not blocked by J5 anti-cALLA. The potential use of BI-3C5 in the classification of acute leukaemias is discussed.
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PMID:A novel monoclonal antibody BI-3C5 recognises myeloblasts and non-B non-T lymphoblasts in acute leukaemias and CGL blast crises, and reacts with immature cells in normal bone marrow. 385 2

A panel of monoclonal antibodies were used to define acute myeloblastic leukaemia (AML) and acute lymphoblastic leukaemia (ALL) with its different subgroups. Thirty-three patients were studied in a period of one year. ALL was diagnosed in 80% of the children and 20% of the adults. AML was present in 22% of the children and 78% of adults. In children, only one of seven was common ALL, three of seven were T-ALL and three of seven were B-ALL. Five of 12 were unclassifiable (U-ALL). In adults the 4 ALL were U-ALL.
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PMID:Cell markers and acute leukaemia subtypes in Chile. 385 23

We have classified 200 cases of lymphoid leukemia and non-Hodgkin lymphoma (LL and L) typed with as many monoclonal antibodies as possible for each case in the WHO Leukemia and Lymphoma categorisation modified according to the today knowledge of normal cell differentiation. We have found that the lymphoid acute leukemias correspond respectively to normal differentiation steps: the [microblastic] to the polyvalent stem cell TdT+, Ia+, B4- or to the lymphoid progenitor TdT+, Ia+, B4-; the [prolymphoblastic T] to the prothymocyte TdT+, OKT11+, OKT10+, 9+, 6-, 4-, 8-; the [prolymphoblastic non T] to the B precursor B4+, B1+, J5+, C mu-, sIg-; the [T-macrolymphoblastic] to the OKT6+ thymocyte; the [B-macrolymphoblastic] to the large pre-B C mu+; the [prolymphocytic T] to the OKT6-, 3+, 4+ and 8+ thymocyte; the [prolymphocytic B] to the small pre-B C mu+; the Burkitt's leukemia to a pre-B cell transformed into a lymphoblastoid cell sIg mu. The B-CLL is constituted of sIg mu+, gamma-, Ia+, B4+, B1+, FC+ virgin lymphocytes and the T-cell either of OKT3+, 4+ or of 8+ peripheral T-lymphocyte, the mantle zone B- lymphoma is constituted of sIg mu+, FC- primary lymphocytes. The B-centro-follicular lymphomas are made of sIg mu+, delta+, gamma+ either small cell cleaved, or large cell. The Burkitt's and non-endemic Burkitt's lymphomas are made of transformed cells into sIg mu+ lymphoblastoid B-cells. We have described a non-blastic, non-Burkitt's, non-follicular, medium cell lymphoma sIg+. The B-immunoblastic lymphoma is sIg mu+, delta-, gamma+, FC+.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lymphoid leukemia and non-Hodgkin's lymphoma type continuum, superimposed to lymphocyte differentiation step continuum. A proposition for a revised W. H. O. lympiioid leukemia-lymphoma categorisation. 386 94

Leukemia cells were mixed with normal human bone marrow cells to simulate bone marrow from leukemia patients; the mixture was then treated with a combination of stabilized derivative of cyclophosphamide [Mafosfamide (ASTA Z 7557)] and pokeweed antiviral protein-containing immunotoxin. The ability of this protocol for selective elimination of B-ALL cells was evaluated by clonogenic assay. The monoclonal antibody (B43) portion of the immunotoxin was directed against human B-cells and was linked to pokeweed antiviral protein by a disulfide bond. The combination of ASTA Z 7557 and immunotoxin was superior to either ASTA Z 7557 or the immunotoxin alone and produced nearly 7 logs of elimination of leukemia cells from the cell mixtures. About 5 logs of contaminating tumor cells were eliminated from a 200-fold excess of normal marrow under conditions where fewer than 50% of pluripotent stem cells were lost. Moreover, this manipulation did not inhibit subsequent production of pluripotent stem cells in long-term bone marrow cultures, indicating that the more primitive progenitors were not harmed.
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PMID:Increased efficiency in selective elimination of leukemia cells by a combination of a stable derivative of cyclophosphamide and a human B-cell-specific immunotoxin containing pokeweed antiviral protein. 387 Nov 74

Adequate tumour material was obtained for phenotypic classification using a standard library of monoclonal antibodies from 81 previously untreated patients with acute lymphoblastic leukaemia (ALL), chronic lymphocytic leukaemia (CLL), or lymphocytic lymphoma (LL). Sixty-one individuals were adults and 20 were children of 14 yr or younger. Fifty-eight of the patients (72%) had acute lymphoblastic leukaemia and the remaining 23 (28%) had chronic lymphocytic leukaemia or lymphocytic lymphoma. Considering only the patients with acute lymphoblastic leukaemia (n = 58) the median age was 19 yr (range 3-69 yr): 9% were black, 43% were coloured, 48% were white, and the distribution between adult (n = 38) and paediatric patients (n = 20) was comparable. Complete remission rate in the adults was 58% and in the paediatric group 85%. For the total group (n = 58) median duration of survival was 59 weeks for common, 39 weeks for null, 63 weeks for T-ALL, and 13 weeks for B-ALL subtypes. In both the common and the null groups overall and disease-free survival was superior in the children. In contrast, no difference was evident in the T-ALL group, which was also notable for its high incidence in young coloured males. The 15 patients with CLL and eight with LL were adults and all the cells were phenotypically of B lineage: in view of the small numbers no comments are possible about ethnic differences. A multi-centre collaborative study is needed to define the epidemiology of haematologic malignancy in South Africa, with emphasis on differences among ethnically distinct subpopulations.
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PMID:Immunophenotypic classification of lymphoblastic leukaemia and lymphocytic lymphoma--an experience in the south-western area of the Cape Province of South Africa. 387 33

A multicentre phenotypic study was carried out in Italy combining conventional immunological techniques with monoclonal antibody (MoAb) analysis in 190 cases of adult and childhood acute lymphoblastic leukaemia (ALL), in an attempt to define better the lineage relationship of the neoplastic cells. Of the 140 children evaluated, 79.3% expressed the common ALL (cALL) antigen (all analyses performed by MoAb), 11.4% were T-ALL and 9.3% were non-T, non-B, non-common ('null') ALL. The proportion of adult cALL cases was slightly lower (64% of the 50 cases studied) than that of childhood ALL, whilst the incidence of T-ALL was significantly higher in adults than in children (26% v. 11.4%, P less than 0.05). Because of the high proportion of cALL cases, the incidence of 'null' ALL in adult patients was similar (10%) to that of children, and lower than previously reported. The recognition of early pre-T-ALL cases (T1+, RFT2+, T10+, T6-, T11-, E-) contributed to the overall low proportion of 'null' ALL; prior to the use of MoAb, such cases would probably have been classified as undifferentiated acute leukaemia or 'null' ALL. The search for B-cell-related markers showed that the incidence of pre-B-ALL cases (cytoplasmic immunoglobulin positive cases) was similar in adults and in children (25.6% and 32%, respectively). Furthermore, the great majority of cases studied expressed the BA-1 antigen (92.8% of adults and 79% of children), whilst the BA-2 antigen was found in 53% of cases (tested only in children), confirming a hierarchy in the expression of B-cell related markers in cALL: BA-1, BA-2, CyIg. Several of the 'null' cases also expressed the BA-1 antigen on a variable proportion of cells, pointing to a possible B-cell origin of the blasts. This multicentre study shows that both in adult and in childhood ALL the combined use of conventional immunological markers and of a panel of MoAb allows identification of the cell lineage of the great majority of cases, thus reducing the number of 'null' ALL. Furthermore, these findings suggest that practically all cases of ALL belong either to the T or to the B cell compartment and that the neoplastic cells appear blocked at different levels along the lymphoid differentiation pathway.
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PMID:Multimarker phenotypic characterization of adult and childhood acute lymphoblastic leukaemia: an Italian multicentre study. 387 7

One of several human leukocyte interferon subtypes A (LeIF-A), obtained in purified form from a gene cloned in Escherichia coli, stimulated human peripheral blood natural killer cell activity, whereas another human leukocyte interferon subtype D (LeIF-D) had no effect with the use of K562 as target cells. With Daudi as target cells, both LeIF-A and LeIF-D stimulated natural killer cell activity. A hybrid human leukocyte interferon, NH2-terminal 61 amino acids and COOH-terminal 104 residues of LeIF-A and LeIF-D, respectively (LeIF-AD) showed greater stimulation than did LeIF-A, but the stimulation did not exceed that of natural buffy coat interferon. A mixture of equal antiviral units of LeIF-A and LeIF-D was no more effective than was LeIF-A alone. The cloned interferon subtypes showed differential effects on the proliferation of three human leukemic cell lines: Daudi (B-cell lymphoblastoid leukemia); BALL 1 (B-cell acute lymphoblastic leukemia); CCRF-HSB-2 (T-cell acute lymphoblastoid leukemia). Growth of Daudi cells was generally most sensitive to all the interferons tested, LeIF-A, -D, -AD, and a buffy coat preparation; no viable cells remained after 120-hr exposure to 1000-unit/ml doses of the interferons. BALL 1 was relatively resistant to the interferon subtypes tested including LeIF-AD, but this cell lines was very sensitive to a preparation of natural buffy coat interferon. CCRF-HSB-2 showed some sensitivity to all the interferons with greatest sensitivity to LeIF-A (10% of the viable cells were detected after 1000 units/ml exposure for 120 hr). In contrast to the leukemic cell lines tested, human amnion cells (WISH) and the human erythroid leukemia, K562, were resistant to the antiproliferative activity of the interferons.
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PMID:Stimulation of natural killer cell activity and inhibition of proliferation of various leukemic cells by purified human leukocyte interferon subtypes. 617 22

Antiserum was produced in white rabbit by intravenously injecting living cells of a B cell acute lymphoblastic leukemia (ALL) line (BALL-1). The reactivity of the antiserum against various lymphoid cell lines was examined by membrane immunofluorescence after appropriate absorption. Serum absorbed with non-T, non-B (NALL-1) and T-ALL (TALL-1) cells recognized B cell antigens distinct from Ia-like antigens on both normal and neoplastic B cells. After further absorption with tonsillar cells or normal B cell line (KO-HL-3), it reacted only with BALL-1 cells and did not react with other leukemia/lymphoma and normal B cell lines. The serum absorbed with tonsillar cells reacted only with BALL-1 and some B cell lines. Thus we were able to obtain antisera with specificity to B cell antigen, B-ALL antigen, and B cell line antigen.
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PMID:Characterization of xenoantiserum produced against B cell acute lymphoblastic leukemia cell line. 618 55

The 3-fucosyl-N-acetyllactosamine structure, a sugar sequence contained in the human milk oligosaccharide lacto-N-fucopentaose III, is recognized by most of the granulocyte-specific monoclonal antibodies (MoAb) reported in the literature, including the six MoAb from our laboratory. Blast cells from patients with acute myeloblastic leukemia (AML) displayed a heterogeneous reaction pattern when they were exposed to MoAb against this moiety, and the proportion of reactive cells in individual cell samples was highly variable. The intensity of the reaction was strongly enhanced by neuraminidase treatment of AML blasts, and reactive structures were exposed on previously negative AML blast cells. Surprisingly, this granulocyte-associated antigen was exposed by desialylation not only on malignant myeloid precursor cells but also on common acute lymphoblastic leukemia cells. No such effect was seen when normal peripheral blood lymphocytes, lymphocytes from patients with chronic lymphatic leukemia, or blast cells from patients with B-cell acute lymphoblastic leukemia, acute erythroid leukemia, and acute megakaryoblastic leukemia were treated with neuraminidase.
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PMID:Exposure by desialylation of myeloid antigens on acute lymphoblastic leukemia cells. 620 96

The clinical application of blast cell immunophenotype testing is important in childhood ALL for the following reasons. (1) Knowledge of the immunologic group is important in predicting prognosis. Prognostic grouping may prove to be accomplished best by using a combination of traditional risk factors and immunologic phenotyping. However, definition of traditional risk factors may vary within the immunologic groups of ALL. (2) In assessing the relative effectiveness of different treatment regimens for children with ALL it is important to make comparisons among patients within the same major immunologic groups of ALL. (3) Identification of specific immunologic groups of patients within ALL may help in designing therapy for each group. The POG has already made preliminary attempts in this direction for T-ALL and B-ALL. However, leukemia species-specific therapy is still only a long-range goal. Laboratory research must endeavor to identify additional biologic characteristics peculiar to each major immunologic group of ALL. These characteristics may dictate therapeutic maneuvers in the future.
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PMID:Pediatric oncology group utilization of immunologic markers in the designation of acute lymphocytic leukemia subgroups: influence on treatment response. 623 34


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