Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0023473 (chronic myeloid leukemia)
 18,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Q fever is caused by Coxiella burnetii, a strictly intracellular bacterium that lives within the phagolysosome of infected cells. We report here five cases of Q fever in patients with cancer. Three of them had a solid tumor, one had a B cell lymphoma, and one had chronic myeloid leukemia. One patient had acute Q fever, and the four others had chronic Q fever endocarditis. Two patients with endocarditis had no previous history of valvulopathy. C. burnetii was isolated from the valves of two patients. One of the patients with endocarditis died. Patients with cancer who have unexplained fever and live in areas in which C. burnetii is endemic should undergo serological testing for infection with this microorganism.
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PMID:Acute and chronic Q fever in patients with cancer. 157 16

A new non-T cell, non-B cell lymphoma cell line, designated IN-1, was established from the ascitic fluid of a patient with non-Hodgkin lymphoma. The IN -1 cells did not show any T cell and B cell immunophenotypes. There were rearrangements of T cell receptor beta- and gamma-chain gene, but no rearrangement of T cell receptor delta-chain gene and immunoglobulin JH gene. Electron microscopically, the cell had numerous pseudopods, mitochondria, vesicles, a conspicuous nucleolus, and scattered heterochromatin at the periphery of the nucleus. They reacted with only OKT9 monoclonal antibody. Molecular analysis revealed that cellular DNA from the IN-1 cells did not hybridize with Bam HI W fragment of EB virus DNA. Cytogenetic analysis showed that the chromosome number of the IN-1 was in the range of 61 -63 whose karyotype analysis demonstrated multiple numerical and structural chromosome changes. The IN-1 cells were resistant to etoposide in comparison with an IC50 of K562 (human chronic myelogenous leukemia). Interestingly, this IN-1 cell possessed 85 KD protein, but not P-glycoprotein, both of which are considered to be multidrug resistance-related proteins.
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PMID:Establishment and characterization of a non-T, non-B cell lymphoma cell line with T cell receptor beta- and gamma-chain gene rearrangement and possessing MRK 20 monoclonal antibody-defined 85KD protein. 196 85

The v-abl gene in Abelson virus induces pre-B-cell lymphoma in mice while the BCR/ABL oncogene is associated with chronic myelogenous leukemia and some cases of acute lymphocytic leukemia in humans. Understanding the mechanisms by which these oncogenes affect various cell types has been hampered by a paucity of experimental systems that reproduce the range of biological effects associated with them. We have developed an experimental system in which murine hematopoietic stem cell populations are infected with either v-abl or BCR/ABL retroviruses and are used to reconstitute lethally irradiated mice. Irrespective of the form of activated abl, greater than 90% of the animals reconstituted with such cells develop tumors. About 50% of them develop a myeloproliferative syndrome that shares several features with the chronic phase of chronic myelogenous leukemia; the remaining animals succumb to pre-B-cell lymphomas. The myeloproliferative syndrome is characterized by large numbers of clonally derived, infected myeloid cells. This model will allow study of the mechanism by which activated abl genes affect hematopoietic precursors in chronic myelogenous leukemia. Furthermore, our results demonstrate that introduction of an activated abl gene into the appropriate target cell, not the structure of the gene, is the major determinant in myeloid cell specificity.
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PMID:Induction of a chronic myelogenous leukemia-like syndrome in mice with v-abl and BCR/ABL. 220 61

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

Mouse monoclonal antibodies were produced against MT-2 cell line derived from adult T-cell leukemia or human T-cell leukemia virus-rich fraction therefrom. Two IgG1 antibodies, Ta60a and Ta60b, were found to be reactive not only with cell lines derived from adult T-cell leukemia or cutaneous T-cell lymphomas, but also with activated peripheral blood lymphocytes, suggesting the similarity of Ta60 antigen group to Tac antigen which is present on interleukin 2 receptor. Thus, the relationship among these antigens was studied. Two Ta60 antibodies and Tac antibody immunoprecipitated the molecule with almost identical electrophoretic mobility, approximately a Mr 60,000 antigen from [3H]glucosamine-labeled activated peripheral blood lymphocytes or MT-2, MT-1, or ATN-1 cells from adult T-cell leukemia and a Mr 53,000 antigen from HUT-102 cells derived from cutaneous T-cell lymphomas. Further, Tac antibody was found to immunoprecipitate Ta60b molecule on 125I-labeled MT-2 cells by sequential immunoprecipitation, indicating that these two epitopes are on the same molecule. Antibody binding inhibition assays with either 3H-labeled Ta60a or Ta60b antibody demonstrated that Ta60a and Tac are the same epitope, but different from Ta60b. Thus, at least two epitopes were demonstrated to be present on interleukin 2 receptor molecule. However, Ta60b antibody showed almost no blocking effects on proliferation of an interleukin-2-dependent cell line, whereas Ta60a antibody did. Various hematopoietic tumor cells were typed with these two antibodies, but the results with Ta60b antibody were described, because they showed a similar specificity. Ta60b antibody reacted with all adult T-cell leukemia cases, but did not react with T-cell acute lymphoblastic leukemia, lymphoblastic lymphoma, or mature T-cell lymphoma. Interestingly, 3 of 12 acute myeloblastic leukemia and 2 of 5 chronic myelocytic leukemia in blastic crisis showed positive reactions. One-third of B-cell chronic lymphocytic leukemia and B-cell lymphoma as well as a few B-cell lines were also weakly reactive with this antibody. A part of the results with direct tests was confirmed by the absorption tests. The results obtained demonstrated the presence of Ta60b on a certain fraction of malignant hematopoietic cells of other than T-cell origin.
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PMID:Two mouse monoclonal antibodies detecting two different epitopes of an activated lymphocyte antigen on adult T-cell leukemia cells. 257 77

The expression of the enzyme marker terminal deoxynucleotidyl transferase (TdT) was examined by immunofluorescence assay in the cells from 333 cases with various types and subtypes of leukemia or lymphoma. More than 90% of cALL and T-ALL, 70% of Null-ALL and 80% of pre-B-ALL were TdT-positive. One case in the commonly TdT-negative group of B-ALL showed TdT-positive cells. All cases of mature B-cell malignancies (B-CLL, hairy cell leukemia, B-cell lymphoma) have been TdT-negative. In the group of mature T-cell malignancies, T-CLL and mycosis fungoides were negative and 2 out of 6 mature T-cell lymphomas were TdT-positive. 13% of acute myeloid leukemias and 36% of CML in blast crisis expressed TdT. Therefore, these TdT-positive cases of CML in blast crisis also carrying the common ALL-antigen belong to the lymphoid subtype. CML and erythroleukemia were invariably TdT-negative. TdT has become an indispensable indicator of immature lymphoid leukemia cells and is particularly valuable as part of the panel of markers used in leukemia phenotyping.
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PMID:Incidence of TdT positivity in cases of leukemia and lymphoma. 308 80

Non-Hodgkin's lymphoma is the commonest secondary cancer following bone marrow transplantation (BMT). We report the case of a 42-year-old man who developed a laryngeal high-grade B-cell lymphoma 5 years following a matched T depleted BMT for CML. Polymerase chain reaction (PCR) analysis using the microsatellite marker Cyp 19 demonstrated the donor origin of involved tissue. Epstein-Barr virus (EBV) genomic sequences were identified by PCR. Although EBV related B-cell lymphoproliferative disorders (BLPD) post BMT are difficult to treat, there was a complete remission in this patient following three courses of chemotherapy (CHOP) administered with G-CSF. This case of late-onset BLPD appears clinically distinct from the well-defined, aggressive, early post-transplant BLPD.
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PMID:Localized, late-onset, high-grade lymphoma following bone marrow transplantation: response to combination chemotherapy. 751 97

The distribution of S-100 protein in normal tissue has been studied extensively. However, little is known about its expression in pathologic states. The aim of the present study was to investigate the expression of S-100 protein in diseased human liver, especially in Kupffer cells. One hundred cases of autopsy livers originating from patients with various diseases were examined. Increased S-100-immunoreactivity of Kupffer cells was observed in six cases. Of the six cases, four were derived from a lymphohematologic malignancy, such as B cell lymphoma, B cell lymphoblastic leukemia, multiple myeloma and chronic myelogenous leukemia with lymphoblastic crisis. Lymphohematologic malignancy accounted for 16 out of the 100 cases examined. Thus, increased S-100-positive Kupffer cells was significantly associated with lymphohematologic malignancy (P < 0.01); 25% (4/16) in cases with lymphohematologic malignancy versus 2.4% (2/84) in the remaining cases. Moreover, some of these S-100-positive Kupffer cells were positive for S-100 beta-subunit, which is not normally expressed by Kupffer cells. Although the reason for this increased S-100-immunoreactivity is speculative, the authors' hypothesis is that tumor cells may produce some factor(s) that induce the expression of S-100 protein in Kupffer cells.
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PMID:Increased S-100 protein-immunoreactivity of Kupffer cells is associated with lymphohematological malignancy. 856 35

p21 is induced by and mediates the effects of p53 in response to DNA damage arresting the cell in G1 or G2, by inhibiting multiple cyclin-cyclin-dependent kinases (CDK) or binding to proliferating-cell nuclear antigen (PCNA), respectively. To determine whether p21 mutants occur in tumors we examined DNA from 188 primary non-Hodgkin's B-cell lymphoma (NHL) tumors and 84 chronic myelogenous leukemia samples for mutational changes in the coding region of p21 by single-strand conformation polymorphism (SSCP) analysis and direct sequencing of polymerase chain reaction (PCR)-amplified DNA. We did not find mutations in the coding region in these two tumor types. We identified a polymorphic nucleotide change in codon 31 in which a transversion from C to A substituted amino acid arginine for serine. Three of 188 NHL tumors were homozygous for this change, but they were not identified in 84 CMLs or in 97 normal controls. On the other hand, in one CML case a transition from G to A in codon 64 substituted amino acid threonine for alanine. These data do not indicate that derangements in the coding region of p21 contribute to the initiation and/or progression of these tumors.
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PMID:Absence of somatic changes in p21 gene in non-Hodgkin's lymphoma and chronic myelogenous leukemia. 865 61

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


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