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

Optimized biochemical assays and cytoimmunofluorescence tests were used to detect terminal deoxynucleotidyl transferase, TdT, in malignant cells of 36 leukemias and 75 lymphomas from patients not receiving chemotherapy. TdT was virtually absent from normal lymph nodes and from leukocytes of chronic lymphocytic leukemia, CLL, taken as controls. Its quantitative distribution in the neoplasms matched the current knowledge. Appreciable amounts of TdT were found in all the 10 lymphomas of lymphoblastic type, LL, and in the white blood cells of: 16 out of 19 acute lymphoblastic leukemia, AAL, perhaps with modulation in the various phenotypes; 2 out of 3 acute undifferentiated leukemias, AUL; and 3 out of 7 blastic crises in chronic myelogenous leukemia, b.c. CML. Biochemical and cytoimmunological analyses yielded concordant responses and even roughly comparable estimates in the same patients. TdT immunofluorescence was clearly nuclear in most cells and was cytoplasmic occasionally. Definite correlations between concentrations of enzymatic activity and percentage of immunofluorescent cells could not e established. Further detailed work will be required to identify putative subgroups in TdT-positive blast populations.
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PMID:Studies of terminal deoxynucleotidyl transferase in normal and neoplastic human cells. 681 Jun 61

Rabbit antisera have been produced to an acute myelomonocytic leukaemia (AMML)-derived cell line (RC2a) and a histiocytic lymphoma derived cell line (U937) having macrophage characteristics. The antisera were screened by complement-mediated cytotoxicity and immunofluorescence (cytofluorograph analysis) against separated leukaemic (122 patients plus 13 cell lines) and normal haematologic cell populations (60 preparations from 20 donors plus 10 B-lymphoblastoid cell lines). The sera were absorbed with pooled B-lymphoblastoid cell lines including the autologous B-lymphoblastoid cell line to RC2a (CESS-B) or alternatively with B-CLL and T-CLL cells. All leukaemic cell populations were confirmed using the markers SIg, E-rosette receptor, cALL antigen, alpha-naphthyl butyrate esterase and myeloperoxidase. Rabbit anti-RC2a (Adherent cells) (RARC2a(Ad) ) and rabbit anti-U937 (RAU937) recognised antigens common to immature myeloid monocyte and T-lymphocyte lineage but did not react by cytotoxicity, absorption or cytofluorographic analysis with cells of B-lymphocyte lineage (B-lymphoblastoid or B-CLL) and reacted only occasionally with cALL patients' cells (includes pre B phenotype). These sera reacted with peripheral blood monocytes but not with other mature blood leucocytes. RAU937 reacted with a major mononuclear population from normal marrow and with more differentiated myeloid leukaemia cells. RARC2a(Ad) and RAU937 detected overlapping subgroups of myeloid leukaemia (AMoL, AMML, AML and CML) patients and Null-ALL and T-ALL patients. These subgroups are now being examined for prognostic significance.
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PMID:Rabbit antisera to cell lines RC2a and U937: antigens expressed on human leukaemic cells of myeloid, monocyte and T-lymphocyte lineage. 681 43

m-AMSA is a synthetic aminoacridine DNA intercalator found to have experimental murine antitumor activity. A phase I investigation was undertaken in 71 patients with solid tumors and acute leukemia. Using an intermittent every 3-week schedule in solid tumors, toxicity encountered was primarily hematologic, predominantly leukopenia with relative platelet sparing. The recommended dose for phase II evaluation in patients with solid tumors is 90 mg/m2 every 3 weeks; patients with minimal prior therapy could be treated at 120 mg/m2 and patients with hepatic dysfunction or marginal bone marrow reserve should have an initial dose reduction to 70 mg/m2. Therapeutic activity was seen in Hodgkin's disease, hepatoma, and epidermoid carcinoma of the esophagus. Various dose schedules were studied in leukemia. The recommended dose for phase II evaluation is 120 mg/m2 daily for 5 days as a daily 30-minute infusion. At this dose, nausea, vomiting, mucositis, alopecia, and hepatic toxicity were noted. Therapeutic activity was seen in AML, blastic CML, and CLL. Further clinical trials with this agent are warranted.
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PMID:Phase I study of m-AMSA in patients with solid tumors and leukemias. 689 83

In an attempt to investigate the utility of glucocorticoid receptor determination to predict clinical responsiveness in human leukemias we have studied glucocorticoid receptors in the leukemic cells from 46 patients and in the lymphocytes from 18 normal donors. In the normal lymphocytes there were 3,875 (Median) specific binding sites per cell. The blasts from 17 patients with ANLL had on average higher levels of binding sites per cell (Median = 7,250, range: 0 to 15,295) than the other leukemias. Of the 15 patients with CLL, six had received glucocorticoid treatment for 3 to 5 years. Their lymphocytes had lower number of receptors (Median = 2,000) than the other cases which were newly diagnosed (Median = 4,500). Four patients had ALL/AUL, three patients had blast crisis as terminal phase of CML, and seven had leukemic Non-Hodgkin lymphomas (Median = 3,500 sites/cell). In 24 patients we have also studied the in vitro sensitivity of the leukemic cells to dexamethasone. There was no marked correlation between glucocorticoid receptor levels and in vitro sensitivity. An attempt to correlate receptor levels with clinical responsiveness demonstrated that glucocorticoid receptor determination might be of value in patients with lymphoid malignancies but probably not in patients with other leukemias.
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PMID:Glucocorticoid receptors and sensitivity in leukemias. 693 62

The biochemical activities of 8 lysosomal acid hydrolases in leukemic cells from 48 patients were examined. Characteristic alterations were found in alpha-mannosidase, beta-galactosidase and N-acetyl-beta-glucosaminidase activities of leukemic cells. The level of alpha-mannosidase activity was much higher in myelo(mono)genous leukemias (AML, AMoL, AMMoL, CML and CMMoL) than in lymphogenous ones (ALL, T-cell leukemia, hairy cell leukemia and CLL) without exception. The beta-galactosidase activity also differed as a result of alpha-mannosidase, except in T-cell leukemia. In T-cell leukemia it was within the range of normal lymphocytes, but in the other lymphogenous leukemias it was significantly below normal. N-acetyl-beta-glucosaminidase activity in myelo(mono)genous leukemic cells was above the range of normal granulocytes. The changes in these enzyme levels were consistent. The lymphocytic or myelocytic nature of three cases of acute undifferentiated leukemia could be determined by enzyme studies. In two cases it was lymphocytic and in one it was myelocytic. The enzymatic abnormalities were also found in morphologically mature neutrophils from patients but not only chronic types (CML, CMMoL) but also acute types (AMoL, AMMoL) of leukemias, and were similar to those of their respective leukemic cells. Analysis of lysosomal enzymes (at least three of those mentioned above), can elucidate one of the biochemical properties of leukemic cells and may be valuable in the differentiation of leukemias.
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PMID:Biochemical activities of lysosomal acid hydrolases in leukemic cells. 694 81

The behaviour of phagocytosis and that of PGE1 and PGE2 in the circulating granulocytes of normal and leukaemic subjects was investigated by the comparison of latex particles and the PAP (peroxidase-antiperoxidase) immuno-enzymatic method respectively. Generally speaking, it was found that chronic myeloid leukaemia and acute myeloblastic leukaemia were accompanied by a marked reduction in phagocyting capacity, whereas this is apparently normal in CLL and ALL. PCE values, on the other hand, were well down in lymphatic leukaemia, AML and AMML, but not in CML, where high PGE (especially PGE2) was noted both basally and after phagocytosis. That the PGE take part in phagocytosis is shown by their redistribution in phagocyting cells, with elective accumulation in the membrane and around the engulfed material.
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PMID:[Behavior of PGE1 and PGE2 in the granulocytes of normal and leukemic subjects during phagocytosis in vitro]. 695 84

Monocyte chemotaxis was studied in 35 patients with ALL, six with CLL, six with AML, and 10 with CML before beginning chemotherapy. Function was contrasted to age-matched control groups. Significant inhibition of chemotaxis was seen in patients with ALL (p less than 0.001) and CLL (p less than 0.01), whereas function in CML and AML patients was not significantly depressed. The deficient monocyte chemotaxis was not due merely to decreased percentages of peripheral blood monocytes. Thus, in addition to numerical deficiencies in monocyte numbers, qualitative deficiencies in monocyte function exist in patients with ALL and CLL.
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PMID:Monocyte chemotaxis in leukemia patients. 696 98

Two of our preparations of rabbit immune sera against Non-T, Non-B ALL cells were characterized. After a previously described absorption schedule used at present with some modifications, the sera were tested by indirect immunofluorescence and by a complement-dependent microcytotoxicity technique on a panel of cells: various types of ALL, lymphoblastoid cell lines of T, B and Non-T, Non-B surface characteristics, other leukemias (AML, CLL, Ph1 positive CML-BC), nonleukemic tissue of normal bone marrow, lymph-nodes and tonsils and also PBL. About 70% of Non-T, Non-B ALL, the Non-T, Non-B ALL line "REH" and CML cells in Ph1 positive "lymphoid" blast crisis were reactive in both test systems. Non-regenerating normal bone marrow, peripheral blood lymphocytes, and lymph node cells were non-reactive. CLL cells and tonsil cels, however, showed a positive fluorescence, yet gave a negative reaction in the complement-dependent microcytotoxicity test. This phenomenon might be explained by unspecific binding to Fc receptors. The antisera thus appear to detect a common Non-T, Non-B ALL antigen.
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PMID:Expression of a non-T, non-B ALL associated antigen on leukemic cells, lymphoblastoid cell lines and normal blood cells. 696 42

A marked sensitivity of CLL lymphocytes to hydrocortisone in vitro was demonstrated in each of the 25 patients tested. The sensitivity was manifested by the eventual lysis of the affected cells. Malignant lymphocytes from 8 out of 14 ALL patients were found also to be in vitro sensitive, whereas CML cells, AML cells, normal BM cells, thymocytes, peripheral blood lymphocytes, and polymorphonuclear cells were resistant. Within a tested CLL lymphoid suspension it is proven that the hydrocortisone causes the specific lysis of the malignant cells leaving the normal lymphocytes undamaged. The cytolysis is not an immediate action, but is expressed within 7-8 hr of incubation. However, 30 min incubation with the hormone is sufficient for the cytolytic effect to occur 20 hr later. The possible mechanisms involved in the specific glucocorticoid induced cytolysis are discussed.
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PMID:The in vitro sensitivity of leukemic and normal leukocytes to hydrocortisone induced cytolysis. 696 96

By means of the multiple marker analysis, a total of 55 human leukemia-lymphoma cell lines which included 15 T-cell, 30 B-cell, four myelomonocytic-cell, and six non-T, non-B cell lines was characterized for their marker profiles. The multiple markers used included a number of cell surface markers as detected by either rosette or immunofluorescence tests, enzyme assays, cytogenetic analysis, and certain functional assay. Based on the criteria previously defined it was found that all the cell lines were proved to represent original leukemia-lymphoma of ALL, AML, CLL, CML in blastic phase or variety of lymphomas. The monoclonality, a "frozen" state at a specific state of differentiation-maturation, and cytogenetic marker in each leukemia-lymphoma cell line were remarkable common properties and were stable for years of cultivation. Similar, if not identical, general characteristics were observed in the study on 344 cases of uncultured fresh leukemia-lymphomas by the multiple marker analysis. While no single marker specific to any type of tumor was found, the study offers not only a basis for better understanding of the biology of leukemia-lymphoma but also an insight into normal hematopoietic cell differentiation in man.
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PMID:Marker profiles of human leukemia and lymphoma cell lines. 697 76


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