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)

Three murine monoclonal antibodies, named 2H9, 1E9 and 1A2, were produced after immunization of BALB/c mice with cells of the SU-DHL-1 cell line from a true histiocytic lymphoma. In frozen sections from various lymphomas, 2H9 and 1A2 selectively stained the cell membranes of neoplastic cells in true histiocytic lymphoma and Hodgkin's disease. Antibody 1E9 stained the nuclear membranes of the tumor cells in true histiocytic lymphoma and malignant histiocytosis. No staining was seen in 56 cases of B and T cell lymphoma. Several tissue culture cell lines, including T cell acute lymphoblastic leukemia and pre-B cell lines, were not stained. With 2H9, however, a positive reaction was noted for two Epstein-Barr virus (EBV)-positive African Burkitt's lymphoma cell lines (Daudi and P3HRI), one human T cell lymphoma/leukemia-virus-positive cell line (HUT 102), and one EBV-transformed normal B lymphoblastoid cell line (RPMI 8057). In normal lymphoid tissues, 2H9 and 1E9 reacted with the nuclear membranes of histiocytes and interdigitating reticulum cells, whereas 1A2 stained only rare cells of an unknown type. All three antibodies failed to react with B or T cells in frozen tissue sections of normal lymphoid tissues. The use of these three antibodies should facilitate the diagnosis of histiocyte and interdigitating reticulum (IR) cell-related neoplasms, namely, true histiocytic lymphoma, malignant histiocytosis, and Hodgkin's disease. True histiocytic lymphoma and Hodgkin's disease exhibit similar reactivities with these three and with two other monoclonal antibodies (HeFi-1 and Tac), suggesting that these two types of lymphoma are related. In contrast, malignant histiocytosis was negative for 2H9, 1A2, Tac, and HeFi-1. The difference in the phenotypic expression of true histiocytic lymphoma and malignant histiocytosis indicates that they are two different disease entities.
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PMID:Monoclonal antibodies against SU-DHL-1 cells stain the neoplastic cells in true histiocytic lymphoma, malignant histiocytosis, and Hodgkin's disease. 242 24

A patient is described who, after completing treatment for diffuse histiocytic lymphoma, remained disease-free for 7 years (presumably cured), then developed acute nonlymphocytic leukemia (ANLL) after a brief preleukemic phase. Marrow cytogenetic analysis at the onset of frank leukemia revealed loss of chromosomes 5 and 7, which is consistent with secondary leukemia. She received only chemotherapy for her lymphoma, including high doses of an alkylating agent and a nitrosourea, which may have contributed to the development of the leukemia. This case report suggests that secondary ANLL may complicate the course of some long-term disease-free survivors of diffuse histiocytic lymphoma.
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PMID:Acute leukemia in a patient cured of diffuse histiocytic lymphoma. 242 76

A human histiocytic lymphoma cell line, U937, is highly sensitive to L-asparaginase with an ID50 of about 0.0001 U/ml after 72 hr of culture. When U937 cells were made resistant to either L-asparaginase (1 U/ml) or asparagine deprivation, the activity of asparagine synthetase increased to 80- or 7-fold of the wild type, respectively. The phenotype of the resistance to L-asparaginase turned out to be stable under nonselective conditions for over several months. The hybrids between L-asparaginase sensitive (Molt4) and resistant (HL-60) cell lines revealed the latter phenotype in terms of L-asparaginase sensitivity and the activity of asparagine synthetase. Furthermore, U937 cells resistant to L-asparaginase could survive in glutamine-free media with 1.5-fold elevation of glutamine synthetase activity. These results altogether clarify the role of asparagine synthetase in L-asparaginase toxicity and have a good implication for the clinical use of L-asparaginase.
Leukemia 1989 Apr
PMID:Biochemical characterization of U937 cells resistant to L-asparaginase: the role of asparagine synthetase. 256 53

Adenosine deaminase (ADA) deficiency is associated with a fatal severe combined immunodeficiency. Because most patients do not have a suitable marrow donor, the introduction of a normal ADA gene into the patient's marrow cells is a potentially useful alternative therapy. To identify vectors that provide optimal gene expression in human hematopoietic cells, we investigated retroviral vectors containing the ADA gene under the transcriptional control of the promoter/enhancers of Moloney murine leukemia virus, the simian virus 40 early region, the cytomegalovirus immediate-early gene, the lymphotropic papovavirus, and the human beta-globin gene. ADA expression from these vectors was monitored in the ADA- human histiocytic lymphoma cell line DHL-9, and in the multipotential chronic myeloid leukemia cell line K562. ADA expression in infected K562 cells was also measured after induction of megakaryoblastic differentiation by phorbol ester, and after induction of erythroid differentiation by sodium n-butyrate or hemin. In these hematopoietic cell lines, the vectors that contained ADA controlled by either the Moloney murine leukemia virus promoter (LASN) or the cytomegalovirus promoter (LNCA) expressed ADA at much higher levels than the other vectors tested. Furthermore, in K562 cells infected with LASN and LNCA vectors, induction of terminal differentiation resulted in the same or higher level expression of ADA. These cell lines have permitted the evaluation of transduced gene expression in proliferating and differentiating hematopoietic cells that provide a model for bone marrow-targeted gene therapy.
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PMID:Expression of human adenosine deaminase from various strong promoters after gene transfer into human hematopoietic cell lines. 275 48

The specificity of the expression of dipeptidylaminopeptidase-IV (DAP-IV) was examined in cells from leukemia patients and in 33 normal and leukemic human cell lines widely used in various studies. There was no correlation between DAP-IV activity and OKT4 positivity or maturation stage in T cells. In addition, DAP-IV was unexpectedly expressed by 4 B cell lines and 1 histiocytic lymphoma cell line, indicating either lack of specificity of DAP-IV or infidelity of gene expression under unnatural culture environment.
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PMID:Expression of dipeptidylaminopeptidase-IV in some human T and B cell lines. 287 56

The classification of non-Hodgkin's lymphomas (NHLs) is an important factor in treatment. Most clinical protocols divide these tumors into two broad categories--indolent, or low-grade, and aggressive, or high-grade. Patients with low-grade NHLs usually have a relatively long survival, with or without the use of aggressive therapy. Although the tumors can be controlled with conventional chemotherapeutic approaches, they are rarely cured. Patients with high-grade tumors usually die within 1 to 2 years without therapy. However, with aggressive treatment, many patients can be cured if complete remissions can be sustained for at least 2 years. Several types of NHLs represent distinct clinicopathologic entities--lymphoblastic lymphoma, adult T cell leukemia/lymphoma, true histiocytic lymphoma, Burkitt's lymphoma, and hairy cell leukemia. Immunologic concepts are now used to classify NHLs. Identifying the cell of origin of a malignant lymphoma has important therapeutic implications, since malignant cells retain phenotypic and functional properties of their precursors. It is possible, therefore, to predict both the sites of involvement and the patterns of dissemination. Clinical applications are beginning to be developed. These include the use of monoclonal antibodies, monoclonal antibodies coupled to a toxin, alpha interferon, and monoclonal anti-idiotype antibodies. Human leukocyte interferon has been used experimentally to induce spontaneous regressions. Excellent results have been achieved so far only for patients with low-grade lymphomas.
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PMID:Relationship of classification to biologic behavior of non-Hodgkin's lymphomas. 287 56

Laser photoradiation therapy was tested in an in vitro model for its efficacy in the elimination of non-Hodgkin's lymphoma cells. Results show that at 31.2 J/cm2 of laser light in the presence of 20 micrograms/mL of merocyanine 540 (MC540) there was greater than 5 log reduction in Burkitt's lymphoma (Daudi) cells. Similar tumor cell kill was obtained for leukemia (HL-60) cells at a laser light dose of 93.6 J/cm2. However, to obtain the same efficiency of killing for histiocytic lymphoma (U-937) cells, a higher dose of MC540 (25 micrograms/mL) was required. Clonogenic tumor stem cell colony formation was reduced by greater than 5 logs after laser photoradiation therapy. Under identical conditions for each cell line the percent survival for granulocyte-macrophage colony-forming units (CFU-GM, 45.9%, 40%, 17.5%), granulocyte/erythroid/macrophage/megakaryocyte (GEMM, 40.1%, 20.1%, 11.5%), colony-forming units (CFU-C, 16.2%, 9.1%, 1.8%), and erythroid burst-forming units (BFU-E, 33.4%, 17.8%, 3.9%) was significantly higher than the tumor cells. Mixing of gamma ray-irradiated normal marrow cells with tumor cells (1:1 and 10:1 ratio) did not interfere with the elimination of tumor cells. The effect of highly purified recombinant interferon alpha (rIFN) on laser photoradiation therapy of tumor cells was also investigated. In the presence of rIFN (30 to 3,000 U/mL), the viability of leukemic cells was observed to increase from 0% to 1.5% with a concurrent decrease in membrane polarization, suggesting an increase in fluidity of cell membrane in response to rIFN. However, at higher doses of rIFN (6,000 to 12,000 U/mL) this phenomenon was not observed. The viability of lymphoma cells remained unaffected at all doses of rIFN tested. These results may have therapeutic relevance in patients undergoing interferon treatment who require bone marrow transplantation, as the complete elimination of tumor cells by marrow-purging procedures may be hampered by this increased survival in the presence of interferon.
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PMID:Elimination of clonogenic tumor cells from HL-60, Daudi, and U-937 cell lines by laser photoradiation therapy: implications for autologous bone marrow purging. 292 Feb 7

One hundred four cases of malignant lymphomas, including 90 cases of non-Hodgkin's lymphoma, 5 cases of histiocytic malignancy, and 9 cases of Hodgkin's disease were analyzed pathologically and immunologically using a panel of monoclonal and conventional antibodies for T-, B-, histiocyte, and Hodgkin's neoplastic cells. Our results revealed a high frequency of T-cell lymphoma (42.3%), a low percentage of follicular lymphoma (10.5%), and Hodgkin's disease (8.7%) in Taiwan. More than half of the malignant lymphomas belonged to the high-risk unfavorable group. Peripheral T-cell lymphomas (33 cases) showed characteristic clinical and histologic features, which can sometimes be confused with Hodgkin's disease. Monoclonal antibodies Leu-M1 and 2H9 were an important aid for their differential diagnosis. Five of the 33 peripheral T-cell lymphomas were positive for antibody to adult T-cell lymphoma/leukemia (ATL) virus associated antigen (ATLA). Four patients were from the northeast coast of Taiwan, I-Lan county. Five (4.8%) were diagnosed as true histiocytic malignancies, including two true histiocytic lymphoma and three malignant histiocytosis. Two cases each of large cell lymphoma and immunoblastic lymphoma showed no identifiable marker expression. The distribution of lymphoproliferative disorders in Taiwan is similar to that in Japan but much different from western countries.
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PMID:Pathologic and immunologic characterization of malignant lymphoma in Taiwan. With special reference to retrovirus-associated adult T-cell lymphoma/leukemia. 300 Jan 62

Antibodies reactive against human T-cell leukemia virus I (HTLV-I) were detected by indirect immunofluorescence assay using MT-2 as target cells, enzyme linked immunosorbent assay screen and competition assay, and Western blot analysis in three sera (one collected in 1979) from a captive gorilla which developed diffuse histiocytic lymphoma in 1983. The sera from four other healthy gorillas housed separately were HTLV-I antibody negative. All sera were negative for HTLV-III antibodies by enzyme linked immunosorbent assay. Southern blot analysis of DNA from lymphoma tissue after digestion with BamHI and using complete HTLV-I genome probe gave one 10-kilobase fragment and a characteristic 1.05-kilobase internal fragment detected in all known HTLV-I isolates. These results indicate that the gorilla was infected with HTLV-I or a closely related simian virus several years before the development of lymphoma.
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PMID:Human T-cell leukemia virus I provirus and antibodies in a captive gorilla with non-Hodgkin's lymphoma. 301 96

A B-cell lymphoma was induced in athymic NIH Swiss nu/nu mice by challenging the animals with NIH3T3 cells, previously transfected with a recombinant DNA carrying a human oncogene hhcM, ligated to an SV40 promoter with a neomycin-resistance marker. The gross pathology of the tumor-bearing animal revealed generalized lymphadenopathy and the histopathology indicated widespread infiltration of lymphocytes into organs, such as brain, liver, kidney and lung, in addition to the lymphoid tissues and spleen; the appearance was consistent with diffuse histiocytic lymphoma. Direct immunofluorescence assays with specific typing anti-sera on live cells prepared from spleen and various lymph nodes in short-term culture, suggested the cells were B-cells. This B-cell lymphoma provides an experimental model, not only for studying possible oncogene activation but also for studying the various interactions involved in signal transduction essential for the activation of B-cell proliferation and differentiation.
Leukemia 1988 Dec
PMID:Induction of B-cell lymphomas in athymic NIH Swiss nu/nu mice. 326 64


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