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

Presenting features of 120 consecutive children with T-cell acute lymphoblastic leukemia (ALL), representing 15% of all patients diagnosed as having ALL during the study period, were analyzed to determine relationships with treatment outcome. Patients' ages ranged from 1.7 to 18.8 years (median, 10.3 years) and their leukocyte counts from 1.7 to 1,070 x 10(9)/L (median, 100 x 10(9)/L). Central nervous system (CNS) leukemia was present in 12.5% of the cases, a mediastinal mass in 61%, and L2 lymphoblast morphology in 32%. A relatively high proportion of cases, 26%, had normal karyotypes at presentation. Of the cases tested, membrane CD1 expression was found in 38% of cases, CD3 in 33%, CD4 in 50%, CD5 in 94%, CD8 in 55%, and CD10 in 35%. Four presenting features were found to confer an increased risk of treatment failure: age greater than or equal to 15 years, L2 lymphoblast morphology, abnormal karyotype, and membrane CD3 expression. This study illustrates the heterogeneity of presentations of childhood T-cell ALL and suggests that the relative importance of risk factors in ALL differs according to immunophenotype and treatment strategy.
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PMID:Heterogeneity of presenting features and their relation to treatment outcome in 120 children with T-cell acute lymphoblastic leukemia. 213 2

Until recently, T cells were believed not to be involved in chronic myeloid leukemia. We describe an example of CML in T lymphoblastic crisis with massive generalized lymphadenopathy in which the blasts were CD2(+), CD5(+), and CD7(+), variably CD1(+) and CD3(+), and both responded to and could be induced to produce the T cell growth factor, interleukin-2. Additionally, the blasts were shown to contain the CML-related tyrosine kinase P210bcr-abl rather than the smaller kinase associated with Ph1(+) ALL. Finally, the participation of the T lymphoid lineage in the CML clone was proven by the presence of the same BCR rearrangement in blasts as in granulocytes, suggesting the existence of a bone marrow progenitor common to the T cell and myeloid lineages.
Leukemia 1990 Sep
PMID:Chronic myeloid leukemia arising in a progenitor common to T cells and myeloid cells. 216 6

We report here the establishment of a new cell line, Karpas 620 (K620), from the peripheral blood of an elderly woman with an IgG-kappa plasma cell leukaemia (PCL). The line has the same hypotetraploid karyotype as the fresh cells from the patient. The cultured cells have the ultrastructural appearance of plasma cells with abundant rough endoplasmic reticulum (RER) and secrete kappa light chain. They are positive for surface antigens HLA DR, and WR17 (CD 37) and negative for CD1, CD3, CD4 and CD8. Using high resolution (HR) cytogenetic analysis it has been possible to identify all the marker chromosomes including several rearrangements commonly seen in malignancies of B cell lineage. These are a 14q+ marker with a typical 'Burkitt' morphology der(14)(pter----q32.3::8q24.1----qter) but with no reciprocal 8q-, and three translocations involving chromosome 11 at q13 with partners other than chromosome 14, namely 1q32.1, 8q24.22 and 13q14.3. An earlier report of molecular studies on the DNA of K620 has shown a rearrangement near the region on 11q13 designated BCL-1 (Rabbitts et al. 1988). This is the first report of a rearrangement in the region of 11q13 in a cell line originating from a case of plasma cell leukaemia.
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PMID:A new human plasma cell line, Karpas 620, with translocations involving chromosomes 1, 11 and 14. 231 Jun 98

We have examined subfractions of human thymocytes for the expression of novel differentiation antigens. Non-HLA alloantisera procured from multiparous women served as antibody probes. Thymocytes from five individuals were sequentially separated by discontinuous Percoll density gradient centrifugation and a peanut agglutinin (PNA) panning technique. Subfractions were selected and examined for their relative intensity of HLA class I and CD1 antigens as determined by cytofluorometric analysis. Two subfractions were characterized as follows: an immature population (Fr6 PNA-) expressed a high level of CD1 (OKT6 binding) antigen and a low level of class I HLA antigen; and a more mature fraction (Fr3 PNA-) expressed minimal amounts of CD1 antigen and relatively high levels of HLA class I molecules. Fr6 PNA+ and Fr3 PNA- thymocytes were tested for their reactivity with a panel of non-HLA alloantibodies as determined by cytofluorometric analysis. We observed that three alloantibodies demonstrated strong fluorescence staining with Fr6 PNA+ thymocytes only, whereas three other alloantibodies reacted with both the Fr6 PNA+ and the Fr3 PNA- subfractions. All six alloantibodies failed to react with peripheral T cells. However, the six antibodies did react with a panel of cultured T lymphoblastoid leukemic cells and fresh leukemic T cells. Blocking studies demonstrated that these alloantibodies do not bind beta 2-microglobulin-associated determinants. These results suggest that the alloantibodies detect thymocyte differentiation antigens (TDA) that are shared by or are cross-reactive with antigens expressed on certain leukemia T cells. The non-beta 2m-associated TDA antigens are not expressed on normal resting T cells.
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PMID:Serological identification of thymocyte differentiation antigens. 245 87

A case of large granular lymphocyte (LGL) leukemia with ascites and CNS involvement was reported. A 39-year-old Japanese female was admitted to our hospital in March, 1987 because of high fever. Her clinical and hematological features were characterized by generalized lymphadenopathy, marked hepatosplenomegaly, high serum LDH level (3,257 mU/ml), marked leukocytosis (71,000/microliters) with 74% LGLs and bone marrow infiltration with 57% LGLs. Despite of chemotherapy, ascites, retroperitoneal mass and CNS involvement developed and she died of sepsis after three months. LGLs from the patient's blood, marrow and ascites, stained positively for acid phosphatase. These LGLs were E rossete+ and Fc (IgG) receptor+ and were positive for CD2, OKM1, HLA-DR and Leu11, but were negative for CD1, CD3, CD4, CD8 and Leu7 as well as for terminal deoxynucleotidyl transferase activity. The natural killer activity against K562 target cells was high and was significantly augmented after stimulation by recombinant human interleukin 2. These LGLs also demonstrated normal antibody-dependent cytotoxicity activity. Cytogenetic study on bone marrow cells and ascitic cells revealed clonal chromosomal abnormalities. These clinical, hematological, immunological and cytogenetic findings suggest that this patient had a neoplastic proliferation of natural killer cells.
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PMID:[CD3-, OKM1+, Leu7-, Leu11+ large granular lymphocyte leukemia with ascites and CNS involvement]. 247 53

Pretreatment peripheral and/or bone marrow blasts from 14 patients with acute unclassifiable leukemia (AUL) expressing myeloid related cell-surface antigen (CDII) or megakaryocyte-platelet related cell-surface antigen (OKM6), were isolated for further analysis in this study. Among 11 cases of CD11+AUL, despite a lack of myeloperoxidase (MPO) activity, one patient's blasts possessed Auer rod in a basophilic cytoplasm and another one's blasts expressed MPO maintaining the same surface phenotype after 20 months of his clinical course. The blast from 2 cases possessed both myelomonocytic and monocyte-specific antigens on the cell-surface, whereas the remaining nine cases completely lacked monocyte-specific antigen which is detectable by monoclonal antibodies, Mo2, My4 and Leu M3 (CD14). In addition, we revealed the presence of MPO protein in the cytoplasm of 3 cases of AUL patients by cytoplasmic immunofluorescence test utilizing monoclonal antibody (MA1). Following these results, the former was diagnosed as acute myelomonocytic leukemia (AMMoL) and the latter as acute myelogenous leukemia (AML) by immunophenotypic analysis using flow cytometry (FACS IV) and cytoplasmic immunofluorescence test. We have also described three cases of acute megakaryocytic leukemia which were demonstrated by the presence of megakaryocyte-platelet-related cell-surface antigens detected by utilizing flow cytometry and monoclonal antibodies in addition to both the PPO activity which was shown by ultrastructural cytochemistry, and the emergence of differentiation antigens while culturing these leukemic cells. The blast of 1 case possessed both platelet GPIb and GPIIb/IIIa cell-surface antigens detected by 5F1 (CD36), AN51 (CDw42), and J15, P2 and HPL2 (CDw41), respectively, whereas the remaining two cases almont lacked the GPIb cell-surface antigen. Hence, the former was diagnosed as immature (pro) megakaryocytic leukemia and the latter as acute megakaryoblastic leukemia from the viewpoint of immunophenotypic analysis as will be discussed in this article. These leukemic blasts did not express both T-cell lineage antigens which are detectable by monoclonal antibodies, T6 (CD1), T11 (CD2), T3 (CD3), T4 (CD4), T1 (CD5), Tp40, Leu9 (CD7), T8 (CD8), and B-cell lineage antigens which are detectable by monoclonal antibodies, B4 (CD19), B1 (CD20), B2 (CD21) and J5 (CD10).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Flow cytometric analysis of myeloperoxidase negative acute unclassifiable leukemias by monoclonal antibodies. Acute myelogenous and acute megakaryocytic leukemia]. 254 Dec 76

Configuration of the T cell receptor (TCR) beta, gamma, and delta chain genes, as well as immunoglobulin (Ig) heavy and light chain genes, was studied in 29 cases of E rosette-negative (pre-T cell) acute lymphoblastic leukemias that lack early B cell (CD19), myeloid (CD33), as well as most T cell associated membrane antigens such as CD1, C4, and CD8, but express CD7, cytoplasmic CD3 (cCD3), and TdT strongly, as well as CD5 and/or CD2 heterogeneously. Hematopoietic progenitor cell markers, namely HLA-DR, J5 (CD10), and My10 (CD34), further characterized this immature T ALL of putative prothymocytic phenotype. Eleven ALLs showed a germline configuration of TCR as well as Ig genes. In three cases, only TCR delta sequences were rearranged, and four additional cases were characterized by recombination of both, TCR gamma as well as TCR delta sequences. Eleven patients showed concurrent rearrangements of TCR beta, gamma, and delta chain genes. An Ig heavy chain rearrangement was observed in one case. These data support the hypothesis that, analogous to pre-B development, a cascade of TCR rearrangements occurs in pre-T cells. Moreover, findings reported here suggest that CD7, as well as CD2 and CD5, antigens appear on precursor cells prior to entry into the thymus and support a model for the developmental hierarchy of TCR genes during early T cell ontogeny.
Leukemia 1989 Jun
PMID:Rearrangement of T cell receptor beta, gamma, and delta gene loci in human pre-T cell acute lymphoblastic leukemia. 254 99

A 26-year-old male was admitted to our hospital because of fever and leukocytosis. On admission, a white blood cell count was 28,300/microliters with 46.5% blast cells and 16.0% atypical monocytoid cells, a hemoglobin level 13.7 g/dl, and a platelet count 15.0 X 10(4)/microliters. Bone marrow contained 58.8% of peroxidase-negative blast cells. He was diagnosed as acute lymphoblastic leukemia (ALL L2) according to the FAB classification. Chromosome analysis revealed the marrow cells to contain 45, XY, -7, t(9; 22) (q34; q11). On surface marker analysis, the leukemic cells were positive for both lymphoid (CD10) and myeloid markers (CD13). Two color flow-cytometric analysis showed two distinct populations with CD10 and CD1 3, respectively. Rearrangements of both immunoglobulin heavy chain and T cell receptor beta-chain were observed. The "breakpoint cluster region" on chromosome 22 was not rearranged. On the basis of these findings, we thought this case being acute mixed leukemia. He was refractory to AdVP therapy and BHAC-DMP therapy. He is now under treatment with A-Triple-V therapy.
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PMID:[Philadelphia-positive acute mixed leukemia with monosomy 7]. 255 34

The article reports a case of acute T-cell leukemia (T-ALL) with the unusual CD3+, WT31 phenotype. On surface marker analysis, the blast cells were found to be CD7+, CD2-, CD5-, CD1-, CD4-, CD8-, CD3+ and negative for B-lymphoid and myeloid lineage. The cells had both TCR beta and TCR gamma gene rearrangement but had negative results with the monoclonal antibody WT31, which reacts with a framework epitope on the T alpha/beta heterodimer (Ti) of the conventional T-cell receptor (TCR). This suggests an association of the CD3 molecular complex with a different polypeptide (the alternate TCR gamma). In two similar reported cases of T-ALL (WT31-, CD3+, CD4-, CD8-), the CD3 molecular complex was found to be associated with a product of the T gamma gene.
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PMID:A case of CD3+, CD4-, CD8-, WT31- acute T-cell leukemia. 278 96

Thymocyte antigens CD1 [Thy,gp45,12] are thought to be the human counterparts of mouse thymus leukaemia (TL) antigens. Serological and biochemical analyses indicate that at least three subsets exist, the first of which (HTA 1/T6) was initially identified by the monoclonal antibody NA1/34. Like TL, CD1 are expressed on cortical thymocytes as well as on some lymphoid neoplasias, and resemble in structure major histocompatibility complex (MHC) class I antigens. However HTA 1/T6 is loosely associated with beta 2-microglobulin and is also found linked by a disulphide bridge to CD8(T8). A molecular genetic approach is needed to investigate the CD1 system, to clarify its relationship to TL antigens and to understand its regulation. We report the isolation of complementary DNA (cDNA) clones encoding a CD1 antigen. These clones reveal a novel family of genes which are MHC-related but are neither equivalent to mouse TL antigens nor linked to the MHC.
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PMID:A novel family of human major histocompatibility complex-related genes not mapping to chromosome 6. 309 94


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