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

Monolayer cultures of ARH-77 cells, a human myeloma cell line propagated in vitro, display a variety of morphologic entities ranging from small lymphocytes to classic plasma cells. The cells show intense pyronin and periodic acid-Schiff affinity but are negative for colloidal iron, sudan black, and naphtol AS-D chloroacetate esterase. The cells exhibit phenotypic markers pertaining to each stage of the B-cell lineage. They fail to display sheep erythrocyte and bovine erythrocyte-IgG antibody complex rosettes, common acute lymphocytic leukemia (ALL) antigens and T-cell antigens, but most cells display surface complement receptors, Ia-like antigens, and surface and intracytoplasmic Ig. Monoclonal antibodies were negative for T-antigens, myelomonocytic cell antigens, leukemia-associated antigens, and BA-1 and OKT-10 antigens. However, 100% of the cells were positive with OKT-9 and B3/25 antibodies that are specific for transferrin receptors. About 50% to 80% of the cells were positive for surface membrane immunoglobulin (kappa IgG) and about 10% to 50% for cytoplasmic immunoglobulin (kappa IgG). Virtually all cells were positive when tested for nuclear Epstein-Barr virus antigens.
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PMID:ARH-77, an established human IgG-producing myeloma cell line. I. Morphology, B-cell phenotypic marker profile, and expression of Epstein-Barr virus. 609 3

Enzyme histochemical and immunohistochemical study was carried out on 16 cases of Hodgkin's disease in order to elucidate the origin of Hodgkin's cell and Reed-Sternberg cell. Both Hodgkin's cell and Reed-Sternberg cell do not have tumor markers such as lysosome enzyme, alpha-fetoprotein, and fibronectin, and these cells do not form either Es or EoxACm rosettes. A great number of cells in most cases contained intracytoplasmic immunoglobulin and showed gamma-glutamyl transpeptidase activity on the cell membrane and in cytoplasm. Since gamma-glutamyl transpeptidase is an enzyme related to the transport of amino acid into cell, it is assumed that there is an intake of amino acid in these cells followed by synthesis of protein. Enzyme histochemically, both Hodgkin's cells and Reed-Sternberg cells resemble multiple myeloma cells rather than B-cells in acute lymphocytic leukemia and chronic lymphocytic leukemia and T-cells or monocytes.
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PMID:Hodgkin's disease--a histochemical study with special emphasis on the character of Hodgkin's cell and Reed-Sternberg cell. 613 29

Hybridomas were produced against the T-cell CLL derived-cell line, SKW3, by the fusion of hyperimmune spleen cells with P3 myeloma cells. One clone, designated DU-SKW3-1, was shown to produce a murine IgG2b antibody reactive with an antigen expressed on normal thymocytes and peripheral blood T cells. This antigen was not detected on human B cells, erythrocytes, monocytes, granulocytes, or platelets. D-SKW3-1 also reacted with T-ALL, T-CLL, and B-CLL cells, but did not react with common ALL or acute myelocytic or monocytic leukemias. Immunoprecipitation of lactoperoxidase-iodinated, detergent-solubilized PBL demonstrated that DU-SKW3-1 reacted with a protein with an apparent mass of 67,000 daltons (p67), which had identical mobility to the antigen precipitated by L17F12, Cocapping experiments suggested that DU-SKW3-1 and L17F12 detected the same molecule: however, DU-SKW3-1 was unable to block the binding of L17F12. In addition, DU-SKW3-1 reacted with the T lymphocytes of both the great apes and old world monkeys, in contrast to L17F12 and two other p67 monoclonals, T101 and 10.2, which reacted only with the cells of the great apes. This data suggests that DU-SKW3-1 may react with a second, less phylogenetically restricted epitope on the p67 T cell-/CLL-associated molecule.
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PMID:A monoclonal antibody reactive with a second epitope of the 67,000-dalton human T cell antigen. 619 Jul 92

This study delineated the distribution of reactivity of malignant human lymphoid cells with monoclonal antibodies Leu 1 and OKT1, and correlated this expression with that of conventional lymphoid cell markers. The presence of Leu 1 on benign lymph nodal T-cells and its absence from benign lymph nodal B-cells was confirmed. Twenty-two T-cell neoplasms, expressing a variety of intrathymic and mature peripheral phenotypes, expressed Leu 1, but this expression was heterogeneous with respect to percent-positive cells and antigenic density, and appeared to correlate with stages of T-cell differentiation. This study demonstrated the expression of Leu 1 by 33 of 36 cases of B-CLL, by 10 of 15 cases of the closely allied small lymphocytic cell lymphoma, and by 9 of 29 follicular center-cell lymphomas. This included B-cell malignancies of each surface immunoglobulin isotype, and some cases associated with a monoclonal protein spike. Leu 1 was not expressed by myeloma plasma cells, and was absent from non-B, non-T acute lymphoblastic leukemia cells in each of 15 cases studied. Finally, Leu 1 and OKT1 were expressed in parallel, with respect to percent-positive cells and staining intensity, on benign and malignant T-cells, and on malignant B-cells, wherever studied. Possible explanations for this shared antigen are the existence of a minor Leu 1+ B-cell subset, a transformation-associated event, or glycosylation.
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PMID:Reactivity of monoclonal antibodies Leu 1 and OKT1 with malignant human lymphoid cells. Correlation with conventional cell markers. 619 56

Hybrids formed between human acute lymphoblastic leukemia (ALL) cells and mouse myeloma have been used to determine the chromosomal location of genes required for the expression of several monoclonal antibody (mAb)-defined cell surface antigens on ALL cells. Cloned hybrids were tested for antibody binding, immunoprecipitation of the relevant protein, chromosome isoenzyme markers and karyotype. Two antigens of those studies could be definitively mapped, OKT10/p45 to chromosome 4 and BA-2/p24 to chromosome 12. mAb BA-2 reacts with the same protein as another mAb designated 609-29 (anti-teratocarcinoma). Reactivity with the latter mAb has been previously shown to segregate with chromosome 12.
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PMID:Chromosome assignment of monoclonal antibody-defined determinants on human leukemic cells. 619 79

Age-adjusted incidence rates for males and females for 36 cancer sites across 29 census sub-divisions of the province of Alberta were correlated with one another. It was hypothesized that cancers which vary together across geographical areas may have common aetiological factors. The correlations were measured by the Pearson product moment coefficient, r, and illustrated by scatter graphs and regression lines. For males moderate correlations were found between prostate and skin cancer and between prostate cancer and non-Hodgkin's lymphoma. Also moderately correlated were male stomach and small intestine cancers and cancers of the bladder and the buccal cavity and pharynx. Specific site correlations for cancers in females were generally higher than for cancers in males. The highest correlations were found between cancer of cervix (invasive) and cancer of trachea, bronchus and lung, between multiple myeloma and cancer of brain and nervous system, between acute lymphatic leukemia and cancer of the bone and connective tissue, and between melanoma and cancer of bone and connective tissue. Although all these correlations are moderate they nevertheless indicate substantial relationships. Possible common aetiologic factors for correlating pairs of cancers are discussed.
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PMID:Correlation of incidence rates for selected cancers in 29 census sub-divisions of Alberta, Canada, 1961-1981. 633 9

Two distinct antigen systems (L26 and L27) specifically expressed in human B lymphocytes were identified using TB2-2B3 (2B3) and T3-5B3 (5B3) monoclonal antibodies, respectively. Whereas L26 antigen defined by 2B3 were rarely expressed on the surface of B cells but abundant in the cytoplasm, 127 antigens detected by 5B3 was clearly expressed on the cell surface. These two antigens appeared to be restricted in their expression to B cells, as they were found in most B cells but not other cell types including thymocytes, T cells, monocytes and granulocytes. Functional studies demonstrated that L27 was more easily lost from B cells after activation with pokeweed mitogen than was L26. Likewise, plasma cell myeloma, as well as normal plasma cells, was devoid of both L26 and L27, whereas immunoblastic sarcoma of B cell type expressed L26 but not L27. These two antigens co-existed in the same B cell lines including Epstein-Barr virus transformed B cell lines, B cell type acute lymphatic leukaemia (B-ALL) cell line, Burkitt's lymphoma cell lines and myeloma cell lines, but pre-B and common ALL cell lines were entirely negative for both L26 and L27. Immunoprecipitation studies showed that L26 consisted of at least two polypeptide chains with molecular weights of 30K and 33K daltons, which were clearly distinct from HLA-DR antigens. The antigen L27 is presently under study.
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PMID:Two distinct antigen systems in human B lymphocytes: identification of cell surface and intracellular antigens using monoclonal antibodies. 633 92

Twenty-three T-cell neoplasms were divided, according to their reactivity with the OKT monoclonal antibodies as follows: Fourteen neoplasms of diverse histopathology expressed the OKT3+ OKT4+ phenotype, commonly associated with the helper T-cell subset; seven histologically similar lymphoblastic neoplasms expressed diverse phenotypes consistent with various stages of intrathymic differentiation and two neoplasms expressed the uncommon OKT3+ OKT10+ phenotype. Thus, T-cell neoplasms are divisible into phenotypes that correspond to normal stages of T-cell differentiation and functionally distinct T-cell subsets. Benign and malignant lymphoid cells were investigated in cell suspension and in cryostat tissue sections for their reactivity with OKB1, OKB2, OKB4, and OKB7, monoclonal antibodies known to detect distinctive B lymphocyte antigens. Fetal liver pre-B cells, cases of pre-B acute lymphoblastic leukemia, and common-type acute lymphoblastic leukemia were OKB2+ but unreactive with the other OKB antibodies. All mature lymphoid tissue B cells and 47/47 surface immunoglobulin (SIg)-positive B-cell neoplasms were OKB2+. Interfollicular, follicular center, and many, but not all, mantle zone B cells were OKB1+ OKB7+. Follicular center B cells were OKB4+ but mantle zone and interfollicular B cells were OKB4-. 45/47 SIg+ B-cell neoplasms were OKB1+ OKB4+. 45/46 SIg+ B-cell neoplasms were OKB7+. Benign and myeloma plasma cells were OKB-. T-cell neoplasms were OKB2- OKB4- but were occassionally OKB1+ and OKB7+. The OKB antibodies appear to detect distinctive antigens that may be expressed at different stages of B-cell differentiation.
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PMID:The application of monoclonal antibodies to the characterization and diagnosis of lymphoid neoplasms: a review of recent studies. 633 55

A clinical study on human lymphoblastoid interferon (HLBI) in various advanced malignant diseases was performed. HLBI was administered to a total of 25 patients with various advanced malignant diseases in order ot investigate antitumor effect and toxicity. The diseases evaluated were as follows: 8 multiple myeloma (MM), 2 chronic lymphocytic leukemia (CLL), 2 adult T cell leukemia (ATL), 1 acute lymphocytic leukemia (ALL), 8 breast cancer, 3 gastric cancer and 1 ovarian cancer. Twenty-three patients received either 3 million or 6 million units of HLBI by daily intramuscular injection or every other day. One patient with ATL received 18 million units of HLBI by i. v. daily and 1 patient with ALL received 30.32 million units of HLBI i. v. daily. Tumor regression (PR) was observed in 2 patients with MM, each one patient with ATL and ALL, respectively. Major toxicities were pyrexia, myelosuppression, general malaise and G.I. toxicity. Several patients showed abnormality of hepatic or renal function. Two patients who received HLBI for more than a year developed cardiac toxicity.
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PMID:[Clinical trial of human lymphoblastoid interferon on advanced malignancy]. 635 2

The present AML protocol which only applies one anthracycline associated with arabinosyl-cytosine gives a first remission plateau of 65% and a 75% survival plateau at five years. Contrary to other teams, we do not apply the allogenic bone marrow graft at the first remission but at the second one. The new protocol comprises application of two anthracyclines, adriamycin and aclacinomycin, a possible autologous bone marrow graft at first remission upon reinforcement, a combination of methotrexate and thioguanine as maintenance chemotherapy and immunotherapy with bestatine. The two protocols respectively applied to the ALL good prognosis and reserved prognosis, give 85% global survival. The autologous bone marrow graft is added at first remission to B or T forms or voluminous CALLA + types. The advantage of CNS radiotherapy is compared with its disadvantages. Bestatine is employed in immunotherapy. The immunoprevention protocol applied to CML blastic crisis (vaccination with a pool of CB blasts) from the second year has prolonged survival of patients suffering from this affection and also treated by splenectomy and hydroxyurea. Allogeneic or autologous bone marrow graft is added to the protocol. The same protocol is applied to not very aggressive LLC and LNH (lymphocytic and centrofollicular with small cleaved nucleus cells) and includes maximum remission induced by chemotherapy followed by immunotherapy (by thymuline and then, if immunity disorders are not corrected, by zinc, then bestatine and finally tuftsin). A similar sequence was applied to the myeloma, comprising MLP-PDN-CPM chemotherapy to induce remission, combination of MLP-PDN and CPM and, if there is resistance, CLB, 6-TG, PDN and TNP. Interferon is appropriate with certain cytopenic forms. A protocol comprising VCR, ADM, PDN, CPM and TNP is applied to centrofollicular NHL with small non cleaved nucleus cells or large cells. As Hoerni and Jones have obtained significant benefits with BCG, its terminal application is compared with that of bestatine. Finally a less mutagenic protocol than MOPP and/or ABVD is proposed for Hodgkin's disease. In this protocol, two cycles alternate, and they combine: a) firstly VCR, PDN, THP-ADM and VPS, and b) secondly VLB, DXM, ACM and TNP with alternatively BLM and PPM between the cycles. This chemotherapy is followed by the same immunorestoration protocol as that applied to LLC and myeloma.
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PMID:[Protocols for the treatment of leukemia and lymphoma: toward escalation or toward reduction of degree?]. 638 Jun 5


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