Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0026764 (multiple myeloma)
 36,148 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The monoclonal antibody WR16 was secreted by a hybridoma produced by fusing splenocytes from a BALB/c mouse immunized with human T-cell chronic lymphocytic leukaemia cells and the murine myeloma cell line NS-O. WR16 reacts specifically with human lymphocytes and binds to 48% of OKT4+ T lymphocytes and the majority of B lymphocytes. Human OKT4+ tonsil lymphocytes were subfractionated into WR16-/OKT4+ and WR16+/OKT4+ subpopulations by the panning technique. The capacity of these cells to help or suppress pokeweed mitogen-induced immunoglobulin (Ig) secretion by autologous B lymphocytes was monitored after 9 days of coculture. Cells of phenotype WR16-/OKT4+ enhanced Ig secretion in excess of that found with non-fractionated OKT4+ lymphocytes, whilst WR16+/OKT4+ lymphocytes suppressed Ig secretion when added to a mixture of B lymphocytes and non-fractionated OKT4+ cells. The WR16-/OKT4+ subpopulation was further fractionated by use of the MoAb Leu 8. Forty-two percent of WR16-/OKT4+ lymphocytes bound Leu 8, and cells of the phenotype WR16-/OKT4+/Leu 8+ were found to induce B-lymphocyte Ig secretion, whilst WR16-/OKT4+/Leu 8- lymphocytes were less active in this system. These data confirm the heterogeneity of the human T helper/inducer subset and indicate the existence of a population of OKT4+ lymphocytes that can suppress Ig secretion in the absence of OKT8+ lymphocytes.
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PMID:Identification and isolation of OKT4+ suppressor cells with the monoclonal antibody WR16. 294 65

We screened serum samples from patients with various hematological disorders and healthy individuals for the presence of adult T-cell leukemia/lymphoma associated antigen (anti-ATLA) antibodies. These antibodies were detected not only in all patients with ATL but frequently in those diagnosed as T-cell malignant lymphoma or T-cell chronic lymphocytic leukemia; the positivity rate of anti-ATLA antibody was lower in B- and null-cell-type lymphoma, B-cell chronic lymphocytic leukemia, and multiple myeloma. Patients with aplastic anemia or acute leukemia who had received frequent and massive blood transfusions also possessed anti-ATLA antibodies. About 5.5% of the healthy individuals over 40 years of age in the endemic area (Kumamoto) were carriers. The rate of positivity gradually increased with age, and was higher in females than in males. In addition, the peripheral blood mono-nuclear cells and/or lymph node cells from patients with various hematological disorders, including ATL, were examined. The presence of human T-cell leukemia/lymphoma virus type I (HTLV-I) proviral DNA was confirmed in all patients with ATL and in some with T-cell-type malignant lymphomas. However, in HTLV-I carriers or other patients with hematological disorders without ATL, proviral DNA was not detected. In endemic areas, detection of proviral DNA is essential for the classification and diagnosis of T-cell malignancies.
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PMID:Clinical aspects of adult T-cell leukemia/lymphoma (ATL). 615 59

Four consistent markers, involving chromosomes 8, 11, 14, 18, 21 and 22, were found in the majority of metaphases obtained after stimulation of peripheral blood and bone marrow from a patient with a T-cell chronic lymphocytic leukemia (CLL) and a concomitant IgA/lambda myeloma with phytohemagglutinin (PHA), lipopolysaccharide of E. coli (LPS) and S. aureus strain Cowan I bacteria (Cowan). A second malignant clone with three additional markers was observed after stimulation with Concanavalin A (Con A). A chromosome 14 aberration, inv(14) (q11-q32), may be of significance in the T-cell malignancy and may suggest a common clonal origin of the two tumors.
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PMID:Chromosomal aberrations in a case of T-cell CLL with concomitant IgA myeloma. 641 31

Acid phosphatase (AcP) in neoplastic cells from various lymphoid leukemias was examined. In the cytochemical studies, tartrate-resistant AcP (T-rAcP) activity was observed in the neoplastic cells from well-differentiated lymphoid leukemias such as adult T-cell leukemia (ATL), B-cell chronic lymphocytic leukemia (B-CLL), T-cell chronic lymphocytic leukemia (T-CLL), and hairy-cell leukemia (HCL). T-rAcP activity was also detected in a small number of leukemic cells obtained from T-cell acute lymphoblastic leukemia (T-ALL), while it was not detected in the neoplastic cells from null-ALL, macroglobulinemia, and multiple myeloma (MM). In the electrophoretical studies, fraction 1 (F-1), F-3, F-3b, and F-4 were completely tartrate-sensitive, while F-2 was partially resistant and F-5 was completely resistant. T-rAcP activity (F-5) was observed in ATL cells, B-CLL cells, and HCL cells, while it was not detected in ALL cells, macroglobulinemia cells, and MM cells. The present study indicates that T-rAcP activity is observed not only in HCL cells but also in the well-differentiated lymphoid cells such as ATL cells, B-CLL and T-CLL cells except the most highly differentiated forms of B-cells of MM and macroglobulinemia.
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PMID:Existence of tartrate-resistant acid phosphatase activity in differentiated lymphoid leukemic cells. 680 73

In order to elucidate the possibility of costimulatory molecules-mediated immuno or immuno-gene therapy for human hematological malignancies, we analyzed 30 hematopoietic cell lines and cells obtained from 48 patients with hematological malignancies for the expression of costimulatory molecules such as CD80 and CD86. The 30 hematopoietic cell lines were composed of 4 cell lines derived from the patients with T-cell acute lymphoblastic leukemia (T-ALL), 3 from Philadelphia chromosome positive ALL (Ph1+ALL), 8 from acute myeloblastic leukemia (AML), 3 from acute promyelocytic leukemia (APL), 8 from chronic myeloid leukemia at blast crisis (CML-BC), 3 from Burkitt's lymphoma and one from follicular cell lymphoma. The expression of CD80 or CD86 was frequent on cell lines derived from the patients with CML-BC or Burkitt's lymphoma, while it was rare on cell lines from T-ALL. Subsequently we analyzed the cells obtained from 48 patients with hematological malignancies, which consisted of 6 samples from patients with ALL, 30 from AML, 2 from CML-BC, 3 from B-cell lymphoma and one from each acute mixed leukemia (AMixL), adult T cell leukemia (ATL), T-cell large granular lymphocytic leukemia (T-LGL leukemia), chronic lymphocytic leukemia (CLL), myelodysplastic syndrome (MDS)-RAEB in T, multiple myeloma (MM) or T-cell lymphoma. Among all the 48 cases, all cases except one case with CLL and two with B cell lymphoma were demonstrated to be negative for CD80 on the neoplastic cells. CD86 and HLA-DR were shown to be expressed in 50% and 88% of total 48 cases respectively. In 30 AML samples, CD86 was positive in 15 cases (50%), which was sharply in contrast with the finding that CD80 was not detected in any AML samples. HLA-DR was expressed in 25 AML samples (83%). We also treated seven human hematopoietic cell lines with IFN-gamma, IL-12 or IL-15 and observed whether these cytokines could induce or enhance the expression of CD40, CD54, CD58 and HLA-DR as well as CD80 and CD86. The present study demonstrated that the expression of CD86 could be upregulated not only by IFN-gamma, but also by IL-12 or IL-15 in some cell lines. These findings suggested the possibility that the absence of CD80 on neoplastic cells may be associated with the lack of efficient anti-tumor immunity in most patients with hematological malignancies and that the immuno or immuno-gene therapy manipulating the expression of costimulatory molecules such as CD80 may be a useful treatment modality for hematological malignancies.
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PMID:Expression patterns of costimulatory molecules on cells derived from human hematological malignancies. 989 58

Fibromodulin is an extracellular matrix protein normally produced by collagen-rich tissues; the fibromodulin gene has been found to be the most overexpressed gene in B-cell chronic lymphocytic leukemia. In this study, fibromodulin was expressed at the gene level (reverse transcription-polymerase chain reaction [RT-PCR]) in all patients with B-CLL (n = 75) and in most (5 of 7) patients with mantle cell lymphoma (MCL). No mutations in the fibromodulin gene were detected. Fibromodulin was also detected at the protein level in the cytoplasm of the B-CLL cells and in the supernatant after in vitro cultivation, but not at the cell surface. Fibromodulin was not found in patients with T-cell chronic lymphocytic leukemia (T-CLL), B-cell prolymphocytic leukemia (B-PLL), T-cell prolymphocytic leukemia (T-PLL), hairy cell leukemia, follicular lymphoma, lymphoplasmacytic lymphoma, multiple myeloma, acute lymphoblastic leukemia (ALL), acute myelogenous leukemia (AML), or chronic myelogenous leukemia (CML) or in 36 hematologic cell lines. Normal blood mononuclear cells (T and B lymphocytes, monocytes), tonsil B cells, and granulocytes did not express fibromodulin. Activation (phorbol 12-myristate 13-acetate [PMA]/ionomycin) of normal T and B lymphocytes induced weak fibromodulin gene expression, but not to the extent seen in freshly isolated B-CLL cells. The reason for the exclusive ectopic expression of fibromodulin in B-CLL and MCL is unknown. However, its unique protein expression makes it likely that fibromodulin is involved in the pathobiology of B-CLL and MCL.
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PMID:Fibromodulin, an extracellular matrix protein: characterization of its unique gene and protein expression in B-cell chronic lymphocytic leukemia and mantle cell lymphoma. 1574 Dec 14

The development and function of hematopoietic cells depends on complex signaling pathways that are mediated by numerous cytokines and their receptors. The Janus kinase-signal transducer and activator of transcription (JAK-STAT) pathway is prominent both in normal hematopoiesis and in hematological malignancies. STATs are phosphorylated on tyrosine residues via JAK kinases and on serine residues by a variety of serine/threonine kinases. STATs then dimerize, translocate to the nucleus and bind DNA, initiating the transcription of target genes. STAT proteins mediate cell growth, differentiation, apoptosis, transformation, and other fundamental cell functions. Recently, mutations in the JAK2 gene driving the proliferation of the neoplastic clone have been identified in myeloproliferative disorders. In addition constitutive activation of the JAK-STAT pathway has been reported in various types of leukemias such as acute myelogenous leukemia, T-LGL leukemia, and multiple myeloma. This review describes the pathophysiological role of this pathway in hematological malignancies and the potential benefits of JAK-STAT inhibition.
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PMID:The JAK-STAT pathway: a therapeutic target in hematological malignancies. 1716 72

We report the first case of T-cell large granular lymphocyte leukemia of donor origin after a second cord blood transplantation for acute myeloid leukemia, and review the literature regarding rare cases of T-cell-origin posttransplantation lymphoproliferative disorders.
Clin Lymphoma Myeloma 2007 Jul
PMID:T-cell large granular lymphocyte leukemia of donor origin after cord blood transplantation. 1787 38

Large granular lymphocyte (LGL) leukemia is a rare disorder of mature cytotoxic T or natural killer cells. Large granular lymphocyte leukemia is characterized by the accumulation of cytotoxic cells in blood and infiltration in the bone marrow, liver, and spleen. Herein, we review clinical features of LGL leukemia. We focus our discussion on known survival signals believed to play a role in the pathogenesis of LGL leukemia and their potential therapeutic implications.
Clin Lymphoma Myeloma 2009
PMID:Never say die: survival signaling in large granular lymphocyte leukemia. 1977 48

We report a CD20dim- positive T-cell large granular lymphocytic (T-LGL) leukemia in a patient with concurrent hairy cell leukemia and plasma cell myeloma. This patient was first diagnosed with T-LGL leukemia with dim CD20 expression, which by itself was a rare entity. He received no treatment for T-LGL leukemia. The patient later developed a hairy cell leukemia, which went into complete clinical remission after one cycle of 2-CdA. Five years later, he was diagnosed with a third malignancy, plasma cell myeloma. Complex cytogenetic aberrancies were present at the time when plasma cell myeloma was diagnosed. This is the first report, to the best of our knowledge, in the English literature with the aforementioned three distinct hematopoietic malignancies in one patient.
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PMID:CD20dim-positive T-cell large granular lymphocytic leukemia in a patient with concurrent hairy cell leukemia and plasma cell myeloma. 2115 94


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