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)

Blast cells were obtained from 17 patients with acute undifferentiated leukemia and 13 patients with chronic myelogenous leukemia in blast crisis. The blasts were tested with anti-i serum in cytotoxicity tests and with antisera to myeloblastic leukemia-associated antigens in immunofluorescence tests. The terminal deoxynucleotidyl transferase (TDT) content of the blasts was also measured. Lymphoblasts react strongly with anti-i, do not react with anti-myeloblast serum, and have high levels of TDT; myeloblasts react weakly with anti-i, do not react with anti-myeloblast serum, and have very low levels of TDT. Of the 17 patients with acute undifferentiated leukemia, there were six with blasts which reacted like lymphoblasts, six with blasts which reacted like myeloblasts, and five with blasts bearing different combinations of these lymphoblastic and myeloblastic markers. Eight of the 11 patients with lymphoblastic or mixed lymphoblastic-myeloblastic markers, but only one of the six with myeloblastic markers, achieved complete or partial remission in response to therapy. Thus, in acute undifferentiated leukemia, classification of blasts with these markers may be of prognostic value. Of the 13 patients with chronic myelogenous leukemia in blast crises, the markers were concordant (for myeloblasts) in only two cases. Three of the 13 patients had TDT-positive blasts, but the reactions of these cells with anti-i and with anti-myeloblast serum differed from those seen with lymphoblasts from patients with acute lymphoblastic leukemia. Although the cell involved in "lymphoid" blast crisis of chronic myelogenous leukemia is similar in many respects to that involved in acute lymphoblastic leukemia, these cells are not identical.
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PMID:Myeloblastic and lymphoblastic markers in acute undifferentiated leukemia and chronic myelogenous leukemia in blast crisis. 693 37

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

Terminal deoxynucleotidyl transferase (TdT) is a unique DNA polymerase which is only found in immature cells of lymphoid lineage (pre-T/pre-B). Because of this restricted distribution of TdT, biochemical and immunofluorescence techniques have been employed to determine the distribution of TdT phenotypes in human leukemias and lymphomas, showing high levels of TdT in approximately 95% of acute lymphoblastic leukemia (ALL) and lymphoblastic lymphoma (LBL), approximately 50% of patients with acute undifferentiated leukemia (AUL), approximately 10 of patients with acute nonlymphoblastic leukemia (ANLL), and approximately 30% of patients with chronic myeloid leukemia (CML) and other myeloproliferative (MPS) or myelodysplastic (MDS) syndromes in blast crisis. High levels of TdT activity are associated with a clinical response to remission inducing therapy with vincristine and prednisone in a high proportion of patients (50%-90%), irrespective of clinical and morphologic diagnosis. Preliminary studies furthermore suggest that TdT might serve as a sensitive indicator of subclinical disease in ALL in complete remission.
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PMID:Methods and clinical relevance of terminal deoxynucleotidyl transferase determination in leukemic cells. 694 40

A monoclonal antibody designated PI153/3, which reacts with neuroblastoma and fetal brain, is shown to identify also a cell surface determinant shared by pre-B and mature B cells and their corresponding leukemias including chronic lymphocytic leukemia, non-Hodgkin's lymphoma, B acute lymphoblastic leukemia, and hairy cell leukemia, but not plasmacytoma. Almost all non-T, non-B acute "lymphoid" leukemias bind PI153/3. The latter includes 71 of 74 common ALL tested, most but not all "unclassified" or "null" ALL and cases of both acute undifferentiated leukemia and Ph1 positive chronic myeloid leukemia in blast crisis with common ALL phenotypes. The antigen is absent or present at very low density on normal and leukemic T lymphocyte, myeloid and erythroid cells. The determinant appears to co-redistribute with cell surface immunoglobulin in B lymphocytes and segregates independently of other cell surface antigens associated with B cells and/or cALL including HLA-DR (Ia-like antigens) and the cALL (gp 100) antigen.
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PMID:A monoclonal antibody identifying a cell surface antigen shared by common acute lymphoblastic leukemias and B lineage cells. 696 98

Forty-five patients with various forms of acute leukemia refractory to usual methods of treatment were treated with AMSA at doses of 100-200 mg/m2 iv daily for 5-7 days, for total doses of 500-1000 mg/m2/course. Among 41 evaluable patients, six (15%) achieved complete remissions, including two of 19 patients with typical acute nonlymphocytic leukemia, none of four with atypical acute nonlymphocytic leukemia, two of nine with chronic granulocytic leukemia in blast crisis, two of eight with acute lymphoblastic leukemia, and none of one with acute undifferentiated leukemia. Durations of complete remissions were 6, 7, 8, 12, 13, and 14 weeks. Four of the patients who died with infection during marrow hypoplasia 2-5 weeks after receiving AMSA had no evidence of leukemia on premortem bone marrow aspirates or postmortem examination. The primary toxic effects of AMSA were severe myelosuppression, stomatitis, and alopecia. One incident of life-threatening liver failure occurred. AMSA appears to be a promising agent for use in heavily pretreated patients with acute leukemia and chronic granulocytic leukemia in blast crisis.
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PMID:AMSA--a promising new agent in refractory acute leukemia. 704 28

Terminal Transferase (TdT), Adenosine Deaminase (ADA), immunological membrane markers, cytochemical reactivity and cytogenetics were analyzed in 226 patients with ALL, AUL and AML, in 70 patients with CML and in 3 cases of Ph' positive acute leukemia presenting as ALL. TdT was tested in peripheral blood and bone marrow with both the biochemical and immunofluorescence (IF) methods, and ADA was determined biochemically only in peripheral blood cells. By using conventional cytochemistry, cell surface markers determinations, TdT and ADA analysis, three distinct groups are recognized in ALL at presentation: T-ALL with TdT+ and very high ADA values; non-T, non-B ALL with TdT+ and intermediate levels of ADA; B-ALL with TdT absence and low levels of ADA. Clinical presentation and responses to therapy in adult and children ALL were correlated to TdT determinations. The median survivals in adults, calculated for TdT+ and TdT- groups, were 14.2 and 5.6 months, respectively. TdT and ADA were determined in ALL during remission. The wide fluctuation observed for TdT IF and ADA values prevented a reliable monitoring of remissions. At relapse, TdT and ADA values were similar to those found for ALL at presentation; TdT IF determinations were diagnostic in cases showing CNS involvement as the only localization. Forty per cent of AUL and 11% of AML cases were positive for TdT; the medians of ADA values of the TdT+ cases in both AML and AUL were several times higher than those obtained in the TdT- group. While TdT positivity and high ADA had a favorable prognostic value in AUL, similar conclusions can not be drawn at the moment for AML. In chronic phase of CML, TdT was strictly negative and ADA values were increased over the control line only in cases showing initial signs of transformation. In acute phase, the cases positive for TdT (32%) presented a significantly higher ADA activity than the TdT negative ones. The actuarial survival curves for the TdT+ and TdT- groups differ significantly, presenting median survivals from onset of phase of 11 and 4.8 months respectively. The three cases of Ph' positive ALL were all TdT+, presented high ADA values and entered chronic phase of CML after therapy.
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PMID:Clinical relevance of terminal transferase and adenosine deaminase in leukemia. 705 80

We evaluated the in vitro proliferative response to exogenous IL-1 beta in terms of tritiated thymidine (3H-TdR) incorporation in leukemic cells obtained from 119 patients with various types of acute leukemia. The content of IL-1 beta in leukemic cells was measured by enzyme-amplified sensitivity immunoassay. We observed a significant proliferative response to exogenous IL-1 beta in leukemic cells from 27/66 patients with de novo AML, 1/29 patients with ALL, 2/3 patients with AUL, 8/12 patients with AML arising from MDS, 4/7 patients with myeloid crisis of CML, and 0/4 patients with lymphoid crisis of CML. Proliferation was marked in myeloid leukemic cells of a more premature stem cell origin. There were no significant differences in proliferative responses among the different FAB classes of de novo AML. The IL-1 beta content of leukemic cells was low in patients with lymphoid leukemia, but there was no significant difference among the various types of myeloid leukemia. There was no correlation between the proliferative response to exogenous IL-1 beta and the IL-1 beta content of leukemic cells. When we correlated the proliferative response to exogenous IL-1 beta with treatment outcome in patients with de novo AML, we found the rate of complete remission (CR) to be lower in those with a high proliferative response. We noted a longer duration of CR (p = 0.07) and of survival (p < 0.05) in patients with a low proliferative response. Thus, a high proliferative response to IL-1 beta in the cells of AML patients may indicate a poor prognosis.
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PMID:Interleukin-1 beta (IL-1 beta) and acute leukemia: in vitro proliferative response to IL-1 beta, IL-1 beta content of leukemic cells and treatment outcome. 783 16

In 67 cases of newly diagnosed blood malignancies, NonT-ALL, T-ALL, AMLL, AML, CML, CLL, HCL, PLL, MDS, B splenic lymphoma, AUL, as well as in 9 cell lines (U937, HEL, Jurkat, HL60, UHKT2, KG1, Raji, K562, REH), we have analysed the expression and distribution of 2 relatively incompletely studied antigenic markers from the CD nomenclature: CDw12 and CD17, individually and in combination with well characterized ones. We present our data for the usefulness of these molecules in immunodiagnosis of leukemias and lymphomas.
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PMID:Expression of CDw12 and CD17 cell surface antigens on leukemic cells from patients with blood malignancies. 815 32

To help elucidate the mechanism responsible for graft failure (GF) following a T-cell depleted bone marrow transplant (BMT) from an unrelated donor, five patients (2 chronic myelogenous leukemia, 1 acute undifferentiated leukemia, 2 myelodysplastic syndrome) who experienced this complication were studied. All patients were HLA class I identical with their donors as determined by serology and one-dimensional isoelectric focusing (IEF); two were serologically matched with their donors for HLA class II antigens, whereas three donor-recipient pairs were serologically mismatched for one HLA-DR antigen. All patients received total body irradiation (fractionated, 1,500 rads), VP-16 (750 mg/m2), and cyclophosphamide (120 mg/kg) pre-BMT and antithymocyte globulin (15 mg/kg every other day) and methylprednisolone (2 mg/kg) post-BMT. Three patients experienced primary nonengraftment and two experienced secondary GF. Peripheral blood mononuclear cells obtained from the patients at the time of GF were studied to examine their functional and phenotypic characteristics. Emerging cells were of host origin and were found to be specifically cytotoxic to donor target cells and suppressive to the in vitro growth of donor BM, especially in the cases of primary nonengraftment. Peripheral blood mononuclear cells from these patients were expanded to form T-cell lines (TcLs). The cytotoxic activities of TcLs were tested in the presence of blocking MoAbs directed against various HLA determinants in an attempt to determine if HLA antigens expressed on donor cells were the target for cytotoxicity. The observed cytotoxic activity was blocked by antibodies to HLA-B, -C (1 patient), HLA-DR (1 patient), and HLA-DQ (1 patient). In two cases, antidonor cytotoxicity could not be blocked by MoAb directed against HLA-A, -B, -C, or -DR. Phenotypic characterization of four successfully maintained TcLs showed 100% CD3+ cells with 100% CD4+ (3 patients) or 50% CD4+/50% CD8+ (1 patient). In two of the three patients with 100% CD4+ cells, antidonor cytotoxicity was blocked by an anti-HLA class II MoAb. In contrast to our previous findings in cases of GF following T-cell-depleted HLA nonidentical family member BMT in which host T cells were CD8+ and cytotoxicity was directed against HLA class I antigens, our present study indicates host T cells emerging at the time of GF following BMT from an HLA class I IEF-identical unrelated donor can be of the CD4+ subset and seem to be capable of recognizing antigenic disparities in the HLA class II region.
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PMID:Characterization of cells emerging at the time of graft failure after bone marrow transplantation from an unrelated marrow donor. 833 33


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