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)

One hundred one patients were treated for Ph' positive chronic granulocytic leukemia (CGL) in the blastic phase. In seven of these (6.9 per cent), meningeal leukemia developed. Of the 99 patients who died of their disease, a complete remission was achieved in 12 with a median survival of 12 months (three to 28 months). Incomplete responders had a median survival of only 2.5 months (one to 14 months). In five of the 12 complete responders (42 per cent), but in only two of the incomplete responders (2.3 per cent), meningeal leukemia developed. The principal neurologic signs were cranial nerve palsies and papilledema. All patients had pleocytosis with myeloblasts in the cerebrospinal fluid. As in patients with acute leukemia and diffuse histiocytic lymphoma, increased survival of patients in whom hematologic remission from the blastic phase of CGL is achieved may allow sufficient time for the development of meningeal leukemia. Intrathecal methotrexate is extremely successful in treating this complication. Cerebrospinal fluid pleocytosis was eradicated in all seven of our patients, and neurologic symptoms and signs were completely eliminated in five patients. No evidence of meningeal leukemia was found in three of the five patients in whom an autopsy was performed.
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PMID:Meningeal leukemia in the blastic phase of chronic granulocytic leukemia. 105 28

A human cell line established in culture from a histiocytic lymphoma patient synthesizes and secretes the monocyte-granulocyte specific enzyme lysozyme. 18 other human cell lines with characteristics of T-lymphocyte, B-lymphocyte, Burkitt's lymphoma, non-Burkitt's lymphoma, myeloma, and bone marrow epithelial cells were not associated with lysozyme. Among murine cell lines, lysozyme was produced by (a) three histiocytic lymphoma or macrophage lines, which mediate antibody-dependent phagocytosis and cytolysis; (b) myelomonocytic leukemia line which also secretes myeloid colony-stimulating factor; and (c) a spontaneous lymphoma and an Abelson leukemia virus-induced lymphoma. Lysozyme-negative lines include another Abelson lymphoma, myelomas, T lymphomas, and mastocytoma.
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PMID:Lysozyme synthesis by established human and murine histiocytic lymphoma cell lines. 108 90

Studies were made on the effects of 665 sera, from normal donors or patients with various diseases, on B-lymphocyte colony formation in agar by mouse spleen cells. Undiluted serum from most normal donors inhibited colony formation, but 43-53% of sera from patients with histiocytic lymphoma, lymphocytic lymphoma or Hodgkin's disease stimulated colony formation, serum activity correlating with the stage of the disease. Moderate colony-stimulating activity was observed with serum taken from patients with acute lymphoid or myeloid leukaemia following, but not prior to, chemotherapy. Colony stimulating activity was not correlated with the blood group of serum donors and could not be ascribed to the presence of endotoxin, red cells or mouse red cell haemagglutinins in the active sera. Elevated colony stimulating activity was not observed in sera from patients with non-neoplastic disorders ot haemopoiesis or with diseases of other organ systems.
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PMID:Stimulation of B-lymphocyte colony formation in vitro by sera from patients with leukaemia or lymphoma. 108 58

The clinical and pathological features of 64 children with non-Hodgkin's malignant lymphoma seen between April 1962 and June 1973 are described. Forty-one children had diffuse, undifferentiated, non-Burkitt lymphoma (lymphoblastic lymphoma). They tended to be boys under 10 years of age and their median survival was 1 year. Almost one-third are surviving for 1-11 years, most in initial complete remission. Nineteen children had diffuse, poorly differentiated, histiocytic lymphoma. They tended to be boys more than 10 years of age, their median survival was only 6 months, and only the 3 patients with Stage I peripheral node tumour survived. Two children had nodular, lymphocytic, poorly differentiated lymphoma and 2 had lymphoma resembling the Burkitt type. From our clinical and pathological observations, we conclude that non-Hodgkin's malignant lymphomata in children cannot be separated from the acute lymphocytic, histiocytic and unclassified leukaemias by cytological or histological methods. What is called diffuse, undifferentiated, non-Burkitt type, or lymphoblastic lymphoma is actually acute lymphocytic leukaemia without apparent invasion of marrow and peripheral blood by neoplastic lymphocytes at time of diagnosis. What is termed diffuse, histiocytic lymphoma is acute histiocytic leukaemia without apparent infiltration of marrow and peripheral blood at initial presentation. One could say just as well that acute lymphocytic leukaemia is Stage IV lymphoblastic lymphoma and that acute histiocytic leukaemia is Stage IV histiocytic lymphoma. Further classification of lymphocytic and histiocytic cancers by newer functional, chemical and morphological methods should include both what is called lymphocytic or histiocytic leukaemia and what is called non-Hodgkin's lymphoma as one group of diseases, susceptible to subclassification by the new methods. We recommend that Stage I lymphocytic and histiocytic cancers be treated with local irradiation. Patients with Stages II-IV tumours should receive anti-leukaemic forms of therapy including prolonged multiple agent chemotherapy and preventive central nervous system irradiation. Staging laparotomy should be considered in patients with Stage I tumour in low cervical, axillary and inguinal nodes.
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PMID:Non-Hodgkin's lymphoma in children. 110 24

A rare case of spinal epidural granulocytic sarcoma (GS) preceding acute myelogenous leukemia is described. A 10-year-old boy presented with lower leg weakness. The initial diagnosis was a histiocytic lymphoma, and he was treated accordingly. No evidence of bone marrow involvement was found at that time. The correct diagnosis of epidural GS was made possible in retrospect by using immunoperoxidase staining for lysozyme fourteen months later when the patient showed the full-blown features of leukemia. This rare tumor should be considered in the differential diagnosis of an epidural mass with cord compression in patients with or even without acute leukemia, because early diagnosis followed by appropriate combined chemotherapy and radiation may obviate surgical intervention and eventually prevent leukemic transformation.
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PMID:Spinal epidural granulocytic sarcoma preceding acute myelogenous leukemia. 128 31

Adult T cell leukemia-derived factor (ADF) is a human homologue of thioredoxin with many biologic functions including IL-2R induction, growth promotion, thiol-dependent reducing activity, and radical scavenging activity. The regulatory effect of ADF on the cytotoxic activity of TNF was examined by using a human histiocytic lymphoma cell line, U937. When U937 cells were preincubated with recombinant ADF (rADF) (0.1-100 micrograms/ml) at 37 degrees C for 30 min, TNF-dependent cytotoxicity on U937 cells was markedly inhibited. This inhibitory effect was as high as 95% in the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide assay (rADF 100 micrograms/ml) and 85% in the 51Cr-releasing assay (rADF 10 micrograms/ml). After pretreatment of U937 cells with IFN-gamma to augment the sensitivity to TNF, an inhibitory effect of rADF was also found. When U937 cells were washed after preincubation with rADF, resistance to TNF-dependent cytotoxicity was still observed, indicating that rADF inhibited the sensitivity of U937 to TNF-dependent cytotoxicity rather than modifying TNF molecules. Scatchard analysis of TNF receptors on U937 cells using 125I-TNF showed that rADF modulated neither the density nor the affinity of the cell membrane significantly. rADF also reduced the cytotoxicity induced by anti-Fas IgM mAb which shows cytotoxicity quite similar to TNF. rADF (10 micrograms/ml) reduced 90% of the cytotoxicity by anti-Fas IgM mAb, without a detectable change either in Fas Ag expression (MFI 58.1 vs 53.3) or in the degradation of anti-Fas IgM mAb as determined by flow cytometric analysis. These findings indicated that the rADF-induced resistance to the cytotoxic effect of TNF and anti-Fas mAb was not related to the modulation of the TNF receptor or Fas Ag.
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PMID:Protective activity of adult T cell leukemia-derived factor (ADF) against tumor necrosis factor-dependent cytotoxicity on U937 cells. 171 91

The expression of neutral glycosphingolipids (GSL) in 37 B-cell neoplasms [7 acute lymphocytic leukemia (ALL), 5 Burkitt's lymphoma (BL), 7 chronic lymphocytic leukemia (CLL), 5 diffuse, poorly differentiated lymphoma (DPDL), 6 diffuse histiocytic lymphoma (DHL), 3 hairy-cell leukemia (HCL), and 4 multiple myeloma (MM)] was examined. Patterns of expression of simple (GlcCer, LacCer) and globo-series GSL (Gb3, Gb4) were found for each tumor type. In addition, pre-B ALL expressed the neo-lacto series GSL, paragloboside, which was not significantly seen at later stages of maturation. As a group, leukemias expressed about 10 times higher ratios of simple GSL to Globo-series GSL as compared to lymphomas, regardless of stage of differentiation. Significant amounts of GSL of other series were not found except in one CLL which contained asialo-GM2. GSL phenotype in these cells was not grossly affected by cell genotype since pre-B ALL containing Philadelphia chromosome t(9q;22q) translocations were similar to other ALL; and DHL with t(8q;14q) translocations had GSL patterns similar to other DHL samples and dissimilar to GSL patterns found in Burkitt's lymphomas with t(8q;14q). Differences in GSL expression among the different types of B-cell neoplasm suggested that GSL patterns form a phenotypic map that may complement the traditional glycoprotein immunophenotypic map and contribute to our understanding of the biology of these diseases and B-cell differentiation.
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PMID:Neutral glycosphingolipid expression in B-cell neoplasms. 195 88

Human and mouse bone marrow cells were cultured for 1 h in the presence of either the antileukaemia drug amsacrine or its 4-methyl,5-[N-methyl]carboxamide disubstituted analogue CI-921, before being plated in methylcellulose medium to determine the survival of granulocyte-macrophage colony forming units (CFU-GM). The drug concentration required for 50% reduction in survival was approx. 0.4 microM for both drugs and was similar for both human and mouse cells. A comparison of the two drugs was then made, at an added drug concentration of 0.5 microM, using cultured mouse L1210 and P388 leukaemia, Lewis lung carcinoma cell lines LLAK and LLTC, human Jurkat leukaemia, human histiocytic lymphoma U937 and human colon carcinoma SW620. The sensitivity of the mouse lines for amsacrine was in the order L1210 greater than P388 greater than LLAK greater than LLTC, similar to the in vivo sensitivity. The selectivity of CI-921 for L1210 versus bone marrow, and for LLAK versus L1210 or P388, was greater than that of amsacrine, again in keeping with its in vivo properties. The sensitivity of the human Jurkat and U937 lines for amsacrine was intermediate between that of L1210 and P388, while SW620 was resistant. The selectivity of CI-921 for Jurkat and U937 versus bone marrow was greater than that of amsacrine, suggesting that CI-921 could have additional advantages over amsacrine in the treatment of some tumours.
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PMID:Comparison of the cytotoxicity of amsacrine and its analogue CI-921 against cultured human and mouse bone marrow tumour cells. 213 78

We have studied the expression of vimentin in the human histiocytic lymphoma cell line U937, induced to differentiate along the monocyte/macrophage pathway. Normal monocytes possess a network of vimentin intermediate filaments (IFs) at all stages of maturation. The undifferentiated U937 leukemia cells contain very low amounts of vimentin, but express a conspicuous IF network when exposed to phorbol myristate acetate. In parallel, they acquire functional properties typical of cells of the monocyte lineage. These concomitant variations suggest that vimentin IFs could play a role in the process of differentiation. However, we observed that all-trans-retinoic acid and 1,25-dihydroxyvitamin D3 confer monocyte-like properties upon U937 cells without inducing vimentin expression. We obtained increased phenotypic changes, yet in the absence of a vimentin network, by combining the effects of both inducers. These results show that vimentin expression is not crucial for the acquisition of some of the functions characteristic of the monocyte/macrophage lineage.
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PMID:Induction of differentiation of the human histiocytic lymphoma cell line U937 in the absence of vimentin expression. 229 64

The possible presence of tumor cells in remission bone marrow (BM) is one of the major problems for the success of autologous BM transplantation (ABMT), because the reinfusion of viable malignant cells may result in relapse. In this study we attempted the purging of the malignant cells by the use of VP-16-213 (VP-16) and nitrogen mustard (NM) either alone or in combination. Four cell lines from various hematological malignancies were utilized: SK-DHL-2 was established from a B-cell diffuse histiocytic lymphoma; RAJI was from an Epstein-Barr virus (EBV)-infected B-cell lymphoma cell line; K-562 were from a chronic myelogenous leukemia (CML) blastic crisis; and HL-60, derived from a human promyelocytic leukemia, were used in exponential growth phase. Four logs of tumor cell-elimination were observed after 1-h incubation of RAJI cells with 25 micrograms/ml of VP-16. K-562 and SK-DHL-2 cells showed a greater than 4 logs reduction after 1-h exposure to 75 micrograms/ml of VP-16, and HL-60 cell line growth was inhibited by 3.2 logs. Under the same conditions (i.e., the treatment with 75 micrograms/ml), we observed a mean recovery of 2.7% of BM granulocyte-macrophage colonies (granulocyte-macrophage colony-forming units, CFU-GM), 3.2% of erythroid (erythroid burst-forming units, BFU-E), and 2.5% of pluripotent (granulocyte erythrocyte macrophage megakaryocyte colony-forming units, CFU-GEMM) progenitors, respectively. More than 3 logs reduction of leukemia and lymphoma cell lines were reached following 1-h treatment with 1 micrograms/ml of NM. After exposure to the same concentration of the drug we obtained 2.5% CFU-GM, 1.2% BFU-E, and 2% CFU-GEMM recovery. A drug mixture containing constant doses of VP-16 (10 and 20 micrograms/ml) and NM (1 micrograms/ml) reduced HL-60 and SK-DHL-2 cell growth to undetectable levels (i.e., 4 and 5 logs elimination) in the presence of an excess of irradiated BM cells, whereas it did not further affect the recovery of the BM precursors as compared to the single drugs used alone. These results suggest that the combination of these two drugs at the selected dose level could provide a better therapeutic index (i.e., higher tumor cell killing coupled with no additional cytotoxic effect on normal BM cells) than the same chemotherapeutic agent used alone and that this mixture may be useful for the "ex vivo" treatment of BM grafts.
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PMID:In vitro cytotoxicity of VP-16-213 and nitrogen mustard: agonistic on tumor cells but not on normal human bone marrow progenitors. 239 48


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