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

The human thymus leukemia-like antigens (CD1a-c) consist of three similar glycoproteins found on subpopulations of normal thymocytes, T cell acute leukemias, and cutaneous dendritic cells. The CD1c antigen recognized by the M241 monoclonal antibody was detected on the circulating mononuclear cells of three children with severe combined immunodeficiency disease (SCID). Two-color immunofluorescence analysis demonstrated that M241 expression (43 to 95%) was limited to cells expressing the B cell-restricted antigens B4 (CD19), B1 (CD20), and surface immunoglobulin. To confirm M241 expression on normal cells of the B lineage rather than aberrant expression limited to SCID B cells, its expression was demonstrated serologically and biochemically on purified B cells from spleen, tonsil, and peripheral blood. Parallel analyses with monoclonal antibodies NA1/34 and 4A76 demonstrated that the CD1a and CD1b molecules were negative on all B cells that were studied. It has been hypothesized that the CD1 molecules represent the human counterpart of the murine thymus leukemia antigens due to their similar size, limited tissue distribution, and association with beta 2-microglobulin. This study suggests that a subset of CD1 antigens detected by M241 (CD1c) may represent a human analog of a murine Qa antigen due to its extended distribution on normal peripheral B cells.
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PMID:M241 (CD1) expression on B lymphocytes. 310 92

A previously established human leukemia cell line, designated THP-6, was further characterized with respect to cell surface antigen expression and immunoglobulin(Ig) and T-cell receptor(TCR) gene status. THP-6 cells were positive for CD7 and CD5 antigens and terminal deoxynucleotidyl transferase, but negative for CD2, CD1, CD4, CD8, CD10, cytoplasmic and surface CD3 and HLA-DR antigens, suggesting a precursor T-cell line. Analysis of Ig and TCR beta chain genes revealed that THP-6 had a rearranged TCR beta chain gene and a germline Ig gene. These results, in agreement with its phenotype, confirmed that THP-6 was of the T-cell lineage.
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PMID:Characterization of a precursor T-cell line (THP-6) with rearranged T-cell receptor beta chain gene. 313 May 28

Rearrangement of germ-line genes coding for T and B cell antigen receptor molecules is an early event in lymphoid development which eventually leads to the generation of clonal diversity in receptor-positive lymphocytes. Three T cell-associated rearranging genes have been described. Two, T alpha and T beta, code for the two polypeptide chains that form the T cell receptor heterodimer. The function of the third gene, the gamma-gene (T gamma), is not known. To learn more about the behavior of T gamma during lymphoid ontogeny, we compared rearrangement of T gamma and T beta genes in leukemic cells arrested at varied stages of lymphoid and myeloid development. We analyzed 38 fresh cell lines and 15 established cell lines from a total of 53 leukemic patients. Cells were immunophenotyped with a panel of monoclonal antibodies recognizing T-, B-, or myeloid-associated surface markers. Sixteen T-lineage cases were studied; 15 displayed both T beta and T gamma rearrangements. The exception (germ-line for T beta and T gamma) was an immature CD2(T11)+, CD3(T3)-, CD7(3A1)+, CD1(T6)+, CD5(T101)+ phenotype. Fourteen non-T non-B leukemias were analyzed; eight were germ-line for both T beta and T gamma, four had rearrangements involving both T beta and T gamma, and two were germ-line for T beta and rearranged to T gamma. Four cases with acute biphenotypic leukemia were studied; two had rearrangements of T beta and T gamma, and two were germ-line for both genes. Cells from nonlymphocytic leukemias were studied in 19 cases. All were found to be germ-line for both T beta and T gamma. Fifty-one of 53 genomic DNA samples were concordant for T gamma and T beta rearrangement. These results indicate that rearrangement of T gamma can occur in leukemic cells of B cell as well as T cell precursor origin, as has been reported previously for T beta.
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PMID:Human T cell gamma-chain gene rearrangements in acute lymphoid and nonlymphoid leukemia: comparison with the T cell receptor beta-chain gene. 348 46

Two new amino acid derivatives with the fluorene substituent, when administered ip to female inbred ICR-CD1 mice inoculated with Friend murine leukemia virus, significantly inhibited virus-induced splenomegaly, reduced viable virus titers in spleen and plasma, and significantly prolonged survival time. These compounds also inhibited multiplication of the strains of the Friend and Moloney murine leukemia viruses in a cell culture system. The action of these compounds on murine leukemia virus was presumely different from that of tilorone.
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PMID:Antiviral effects of amino acid derivatives with the fluorene substituent on murine leukemia viruses. 657 36

Recent studies of the TCR alpha and beta chains expressed by normal human IELs suggest that these intestinal lymphocytes are directed at a limited set of antigens, presumably on intestinal epithelial cells in view of their anatomic location. The direct sequence analysis of these cells has indicated that they are oligoclonal and cannot, therefore, be responding to the complex mixture of antigens which are present in the lumen. The abundant expression of the CD8 accessory molecule by the IELs, in addition, indicates that these putative intestinal epithelial cell antigens are presented by MHC class I or I-like molecules. The expression of CD8 also suggests that these cells function biologically in part as cytolytic T lymphocytes which is consistent with a variety of functional studies. Taken together with their expression of the CD45RO isoform, these phenotypic and functional observations suggest that iIELs are cytolytic, memory cells which are responsive to an extremely limited number of antigens bound to major histocompatibility complex (MHC) class I or class I-like molecules. Several non-polymorphic MHC class I-like molecules such as Qa, the thymus leukemia antigen (TL) and CD1 in the mouse and CD1 in human represent important candidate ligands for these oligoclonal iIELs. TL and CD1 are expressed specifically by murine intestinal epithelial cells. In humans, CD1d is constitutively expressed by intestinal epithelial cells. In addition, we have isolated iIEL T cell clones which specifically recognize members of the CD1 gene family when expressed on a transfected B cell line that lacks HLA-A and B and have shown that the proliferation of peripheral blood T cells to intestinal epithelial cells is CD1d dependent. Thus, the evidence to date strongly implicate the nonpolymorphic, class Ib molecules as novel restriction elements for unique populations of lymphocytes within the intestinal epithelium.
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PMID:Intraepithelial lymphocytes and their recognition of non-classical MHC molecules. 752 51

We report a novel human thymocyte differentiation antigen ICT-1 with a molecular weight of 49 kDa that is noncovalently associated with another 12-kDa protein. The ICT-1 antigen is expressed in 50-70% of total thymocytes, but not in resting or PHA-activated peripheral blood T-cells and bone marrow cells. The thymocytes expressing ICT-1 antigen appear after the 18th week of gestation during fetal development. Since the distribution pattern of the ICT-1 antigen within thymus partly overlaps with that of the CD1 antigens, we investigated whether ICT-1 was one of the CD1 antigen family. However, the failure of anti-ICT-1 antibody to react with mouse L cells transfected with cDNA of CD1a, -b, and -c and the different histologic distribution patterns from that of CD1d strongly suggest that the anti-ICT-1 antibody recognizes an antigen distinct from CD1. Furthermore, ICT-1 is also expressed in human neuroglial cells such as oligodendroglioma, glioblastoma multiforme, Ewing's sarcoma, and cerebellar astrocyte. Hence we believe that the ICT-1 antigen may be a novel thymus-leukemia (TL) antigen or a nonclassical MHC class I antigen.
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PMID:A novel T-cell differentiation antigen expressed in immature human thymocytes and neuroglial cells. 754 48

A long-term T-cell line, termed SP+, was developed from a human T-cell leukemia virus type I (HTLV-I)-infected patient with adult T-cell leukemia that is dependent on exogenous IL-2 for growth. The SP+ expresses a full complimentation of HTLV-I-specific viral proteins, and contains replication competent viral particles. Restriction enzyme digestion followed by Southern blot analysis demonstrated the presence of a single integrated proviral copy and limiting dilution analysis confirmed the clonality of the cell line. Interestingly, phenotypically, the SP+ cell line is CD2+, CD3+ and coexpresses CD4 and CD8, yet lacks TCR alpha beta and TCR tau delta expression. Further ontogenetic characterization of the SP+ cell line demonstrated the lack of thymic T-cell precursor markers, including absence of cell surface expression of CD1, intracellular thymic terminal deoxynucleotidyl transferase (TdT) enzyme, as well as message expression for V(D)J recombinase activating gene-1 (RAG-1). Furthermore, the SP+ cell did express the message for the CD3 delta chain. Taken together, these data suggest that the SP+ cell line resulted from HTLV-I infection of a mature CD4+/CDB+ lymphocyte. This cell line can be potentially useful as a model, both for regulation of cellular functions by HTLV-I and for immunologic functions of mature dual CD4/CD8 positive T-cells.
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PMID:Characterization of a HTLV-I-infected cell line derived from a patient with adult T-cell leukemia with stable co-expression of CD4 and CD8. 756 72

To get more insight into the phenotypic changes of childhood acute lymphoblastic leukemia (ALL) at relapse, a detailed morphological and immunophenotypic study in 40 childhood ALL cases (32 precursor B-ALL and 8 T-ALL) was performed. Expression patterns of non-lineage specific markers (terminal deoxynucleotidyl transferase (TdT), CD34, and HLA-DR), B-lineage markers (CD10, CD19, CD20, and CD22), T-lineage markers (CD1, CD2, CD3, CD4, CD5, CD7, and CD8), and cross-lineage myeloid markers (CD14, CD15, and CD33) were compared at diagnosis and relapse. In case of low blast counts (< or = 70%) at relapse, double labeling for membrane markers and TdT was used in order to define the precise immunophenotype of the TdT+ leukemic cells. An immunological marker-shift was defined as either a conversion from positive to negative and vice versa or a difference in positivity of > or = 50%. Morphological differences between diagnosis and relapse were detected in 34% of precursor B-ALL and 14% of T-ALL. Differences in immunological marker expression were found in 72% of precursor B-ALL and in 75% of T-ALL, and generally concerned minor shifts with loss or acquisition of a few markers. The morphological shifts and immunophenotypic shifts were not correlated. Immunophenotypic shifts were found for all markers tested in precursor B-ALL, except for HLA-DR. Shifts in CD10 expression (16% of cases) were only observed in relapses occurring 30 months or more after diagnosis. In four precursor B-ALL an intra-lineage shift was found at relapse (one common ALL to null ALL and three pre-B-ALL to common ALL or null ALL) and two precursor B-ALL cases were diagnosed as acute non-lymphocytic leukemia at relapse based on morphology and immunophenotype. In T-ALL, neither intra-lineage nor inter-lineage shifts were observed, although shifts were detected in all T cell markers tested, except for the lineage specific CD3 and T cell receptor (TcR) markers. In conclusion, immunophenotypic shifts at relapse frequently occur in precursor B-ALL and T-ALL, in a small percentage leading to an intra-lineage shift (10%) or inter-lineage shift (5%). Therefore immunophenotypic monitoring of minimal residual disease in ALL patients should be based on multiple marker combinations, preferably together with polymerase chain reaction analysis of rearranged immunoglobulin and/or TcR genes or chromosome aberrations.
Leukemia 1995 Sep
PMID:Immunophenotypic changes between diagnosis and relapse in childhood acute lymphoblastic leukemia. 765 22

A portion of patients with acute myeloid leukemia also display surface antigens associated with lymphoid development (Ly+AML). The incidence of Ly+AML varies considerably between independent studies, both overall and with regard to individual antigens. On average, lymphoid-associated antigen expression is relatively low in AML. The reasons for some striking differences between conflicting reports are not clear, but are most probably due to various technical aspects including several arbitrary parameters. The data accumulated from the literature lead to the following conclusions: (i) use of different reagents against the CD surface antigens, different positive/negative cut-off levels, analysis of fresh or frozen cell material and variable sensitivities of the analytical instruments (expression of lymphoid-associated antigens was commonly weaker than myeloid-associated markers) seriously influence the results; (ii) most antigens (CD1, CD2, CD3, CD5, CD8, CD10, CD19, CD20, CD21, CD22) were expressed on less than 10% of AML cases; (iii) the CD4 and CD7 antigens, also found on normal monocytic and immature myeloid progenitor cells, were detected in 24% and 15% of AML cases, and their expression correlated with FAB M4/M5 and M1/M2 morphology, respectively; (iv) differences between pediatric and adult Ly+AML were restricted to CD4 and CD19 expression being detected more often in childhood cases; (v) there is no cytogenetic anomaly specific for Ly+AML; anomalies exclusively associated with lymphoid malignancies were not seen; aberrations involving 11q23, 14q32, and the 9;22 translocation seem to be increased; (vi) in most studies, expression of lymphoid-associated antigens (with the exception of CD7) on AML blasts lacked prognostic significance; CD7+AML appears to be a particular subset of malignant myeloid progenitors. In summary, these findings suggest that in general, Ly+AML may not represent a biologically distinct form of leukemia as these cases have similar clinical features and respond to therapy in a comparable manner.
Leukemia 1993 Apr
PMID:Acute myeloid leukemias expressing lymphoid-associated antigens: diagnostic incidence and prognostic significance. 768 17

We describe here a case of T-cell lymphocytic leukemia (T-CLL) which coexpressed CD4 and CD45RA cell-surface antigens and functioned as suppressor inducer cells. The patient, an 81 year-old man, had massive generalized lymphadenopathy. His hemoglobin was 9.4g/dl, the platelet count 94,000, and the WBC was 895,000/microliters with 98% abnormal lymphoid cells. He had massive hepatosplenomegaly. Serum LDH was elevated to 3,990 u/l. The T-CLL cells coexpressed antigens detected by MAbs CD2, CD3, CD4, CD5, Ti(TcR alpha/beta; WT31) CD45 and CD45RA, but did not express any other antigens including CD1, CD8, CD29, and TCR gamma/delta, Ti gamma A and TQ-1. The cell-surface phenotypes of the cultured cells established by utilizing recombinant interleukin 2 were basically the same as those of the uncultured peripheral blood lymphoid cells. Both the peripheral blood and cultured cells clearly showed gene rearrangement for T cell receptors, TcR beta and TcR gamma. No association with human T-cell leukemia virus-1 (HTLV-1) was found by means of electron microscopic studies or the application of MAbs to p19 and p24 of HTLV-1. No anti-HTLV-1 antibody was detected. By the means of two color fluorescence, it was clearly demonstrated that the leukemic cells possessing CD4 in the peripheral blood and cell cultures coexpressed CD45RA, but did not express either CD29 or TQ-1. In vitro immunoglobulin synthesis by normal T and B cells was remarkably reduced in the presence of CD8+ T and leukemic cells. This suggests suppressor inducer T cell activity for the leukemic cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:CD4+, CD45RA+, CD29- T-cell lymphocytic leukemia functioning as T suppressor inducer for B-cell immunoglobulin synthesis. 769 6


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