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)

These experiments have investigated cellular mechanisms involved in the generation of cellular immune responses to human acute leukemic blasts. Because normal human lymphocytes are not able to recognize immunologically, in vitro, lymphocytes from MHC identical siblings, the present studies have examined the in vitro proliferative and cytotoxic responses of normal lymphocytes to MHC identical AML and ALL blasts. In those cases where acute leukemic cells were unable to induce a proliferative response by MHC identical lymphocytes, the generation of effective anti-leukemic cytotoxicity required the addition of unrelated stimulating cells to the sensitization culture. In contrast, leukemic blasts that induced a proliferative response by MHC identical lymphocytes were also able to stimulate anti-leukemic cytotoxicity. This could be augmented by the addition of unrelated stimulating cells to the sensitization culture. The specificity of anti-leukemic cell cytotoxicity was demonstrated in all instances by simultaneous testing of putative killer cells on 51Cr leukemic blasts as well as 51Cr-labeled MHC identical phytohemagglutinin blasts or normal lymphocytes. Simultaneous sensitization to MHC identical leukemic blasts and unrelated stimulating lymphocytes did not invariably generate anti-leukemic cytotoxicity even when allogeneic cytotoxicity was observed; the absence of demonstrable suppressor activity in these nonreactive combinations suggested that some individuals may be specifically immunoincompetent, and thereby unable to generate effective anti-leukemic CML.
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PMID:Cell-mediated destruction of human leukemic cells by MHC identical lymphocytes: requirement for a proliferative trigger in vitro. 106 27

Rabbit antisera to myelogenous leukemia (ML) cells were raised; ML cells from line K-562 that has the Philadelphia (Ph) chromosome were used as antigen. Antibodydependent, complement-mediated cytotoxicity was demonstrated by the trypan blue test and Cr release assay for cultured ML cells, whereas no cytotoxicity was demonstrated for cells from B (SB) and T (MOLT 4) lymphoblastoid cell lines. The antisera showed no cross-reactivity for normal human peripheral leukocytes or purified granulocytes. A low level (less than 8%) of cytotoxicity was directed against cell membrane associated fetal bovine serum proteins. Absorption of the immune serum with normal human bone marrow cells of first trimester human whole embryo cells reduced the cytotoxic titer to a similar extent; this suggested the possibility of crossreactivity between ML cells and fetal antigen(s). However, the ML antigen(s) was unrelated to carcinoembryonic antigen (CEA), since absorption with CEA had no effect on the serum cytotoxic titer. The anti-ML sera were cytotoxic for cells taken from 10 patients with chronic myelogenous leukemia and from 3 with acute myelogenous leukemia. In contrast, the leukocytes of 1 of 4 patients with acute lymphocytic leukemia, and 3 of 7 with chronic lymphocytic leukemia shared similar antigenic determinants as demonstrated by cytotoxicity tests. The significance of the cross-reactivity of some lymphatic and ML cells may be the result of the use of rabbit sera that did not distinguish antigens common to both granulocytic and lymphocytic cells, or it may reflect an "immature" or "blastic" antigen present on many leukemia cells.
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PMID:Cytotoxicity of antisera to a myelogenous leukemia cell line with the Philadelphia chromosome. 106 37

The antiserum was obtained from horses immunized with cells from patients with blastic crisis of CML and completely absorbed with normal white blood cells (WBC). The absorbed antiserum remained cytotoxic to blast cells from nearly half of the patients in blastic crisis and did not react with WBC from patients with Acute Myeloid Leukemia (AML), Acute Lymphoid Leukemia (ALL), Chronic Lymphoid Leukemia (CLL) and Chronic Myeloid Leukemia (CML) in its chronic phase as well as with cells of human normal bone marrow or fetal liver.
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PMID:Specific xenogenous antiserum to cells of chronic myeloid leukemia (CML) in blastic crisis. 106 94

Occurrence of immune complexes in leukemia has been investigated by the 125I-Clq-binding test. A highly significant serum Clq-binding activity (Clq-BA) was demonstrated in 37% of patients with acute myelocytic leukemia, in 23% of patients with acute lymphocyte leukemia,and in 32% of those in blastic crisis of chronic myelocytic leukemia. Such a high Clq-BA is found only in 13% of cases with chronic leukemia. Incidence of increased serum Clq-BA is significantly higher during the blastic stage of leukemia than in complete remission. There is no correlation between the elevated Clq-BA and infections complicating acute leukemia, or with the chemotherapy given to the patients. The Clq-binding material exhibits properties similar to those of immune complexes.
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PMID:[Circulating immune complexes in human leukemias]. 107 Jan 56

The relationship between changes in the bone marrow labeling index and the patient's subsequent response to cycle-specific agents was studied by the South-eastern Cancer Study Group in adults with acute leukemia. Ninety-eight patients were randomized to one of two treatment regimens. Schedule 1 consisted of a single intravenous (i.v.) push of cytosine arabinoside followed in 48 hours by a large dose of oral methotrexate distributed over 24 hours and i.v. vincristine. Leucovorin rescue was employed to control the toxic effects of the high dose methotrexate and the cycle was repeated every 7 days. Schedule 2 differed only in that there were three daily injections of cytosine arabinoside preceding vincristine and methotrexate injections and each cycle was given every 10 days. Cell kinetic studies were performed in 30 patients and revealed that the majority of patients who had a response to therapy had some increase in the marrow labeling index 48 hours after cytosine arabinoside injection. In general, those patients who had no response to therapy had little change. There was no significant difference between schedules in the ability to induce an increase in labeling index 48 hours after cytosine arabinoside or in the increment achieved by the responders. However, there was a significant difference in the response rate seen with these schedules. Schedule 1 achieved only a 24% remission rate in acute nonlymphocytic leukemia (ANLL) while schedule 2 was associated with a 52% remission rate. In acute lymphoblastic leukemia (ALL) both schedules induced a 60% remission rate while none of the four patients with blast crisis of chronic granulocytic leukemia (CGL) responded. Analysis of the characteristics associated with remission revealed that more females achieved a remission than males and that the presence of pretreatment infection was the greatest contributing cause of early death and thus severely limited the ability to achieve a remission. As opposed to the current regimens used in ANLL, schedule 2 did not require significant bone marrow hypoplasia (as judged by the degree of hematological toxicity) to achieve a remission and there was no decrease in response seen with increasing age. The data suggest that increased efficiency of cycle-specific, antitumor agents may occur by increasing the proportion of human leukemic cells in DNA synthesis.
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PMID:An attempt at synchronization of marrow cells in acute leukemia: relationship to therapeutic response. 108 65

217 sera from 33 patients with acute myeloid leukemia (AML), 42 with chronic myeloid leukemia (CML), 12 with acute lymphatic leukemia (ALL), 22 with lymphoma, and 20 with other malignant diseases were examined by a radioimmunological technique for the presence of antibodies against DNA. The levels of single-stranded DNA binding activity was significantly higher in all 3 types of leukemia and lymphoma compared to those of healthy controls. In contrast, none of these sera exhibited a positive reaction with double-stranded DNA. In some cases of leukemia, the level of serum anti-DNA antibodies increased after the decrease of the leukocytes count.
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PMID:Anti--DNA antibodies in patients with leukemia and lymphoma. 108 60

Patients with myeloproliferative disorders were prospectively studied by in vitro agar-gel marrow culture technics to evaluate factors involved in the evolution of abnormal granulopoiesis. Marrow granulocytic colony-forming capacity was determined in 78 patients with chronic myeloid leukemia, subacute myeloid leukemia, preleukemia, Di Guglielmo's syndrome, polycythemia vera or essential thrombocythemia. A wide range of marrow colony-forming capacity values was noted early in disease courses; however, in 26 of 33 patients decreased colony-forming capacity was associated with disease transformation into acute myeloid leukemia or other clinically aggressive stages. An increased proportion of abnormally light buoyant density (less than 1.062 g/cm3) colony-forming cells was present in the marrow and peripheral blood of 15 of 16 patients with chronic myeloid leukemia, subacute myeloid leukemia, preleukemia or essential thrombocythemia; in seven of eight patients with greater than 35 per cent abnormally light colony-forming cells their disease subsequently underwent transformation. Elevated levels of urinary colony-stimulating factor output were noted in 17 of 31 patients, and in 10 of 12 patients whose disease subsequently underwent acute transformation within 10 months of study. In six of seven patients who simultaneously had an increased urinary output of colony-stimulating factor and low colony-forming capacity in marrow, transformation occurred within 10 months. These findings indicate that progressive abnormalities of both marrow clonal growth patterns and levels of possible humoral regulatory substances develop during evolution of these diseases. In contrast, patients with idiopathic sideroblastic ineffective erythropoiesis had normal values for marrow colony-forming capacity, proportion of light density colony-forming cells and urinary colony-stimulating factor output, and in none has their disease transformed into acute myeloid leukemia. These in vitro studies appear useful for clinical staging, evaluating prognosis and categorizing patients with myeloproliferative disorders.
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PMID:The myeloproliferative disorders. Correlation between clinical evolution and alterations of granulopoiesis. 108 34

Eight cases of Hodgkin's disease and acute leukemia are reported. An additional 74 cases of acute myelocytic leukemia or one of its variants, 11 cases of acute lymphocytic leukemia, 12 cases of chronic myelocytic leukemia and 37 cases of chronic lymphocytic leukemia associated with Hodgkin's disease are reviewed from the literature. In 3 of the 82 patients with acute myelocytic leukemia and Hodgkin's disease, the two diseases occurred simultaneously. Of the remaining 79 patients, 76 had received radiation therapy for their Hodgkin's disease and acute myelocytic leukemia had developed 1.2 to 19 years later (mean 6.5 years). Thirty-four of these patients also received antineoplastic chemotherapy. Only three patients with Hodgkin's disease were treated with multiple chemotherapy alone; in these, Hodgkin's disease developed 1.2, 1.5 and 3.2 years later. In 4 of 11 patients with acute lymphocytic leukemia and Hodgkin's disease, the two disorders occurred simultaneously. The other seven patients were all treated with radiation for their Hodgkin's disease, and acute lymphocytic leukemia developed 2 to 8 years later (mean 4.5 years). Three of the 7 patients also received alkylating agents. It is concluded that the development of acute leukemia, mostly acute myelocytic leukemia but also acute lymphocytic leukemia, during the course of Hodgkin's disease, is most likely related to radiation therapy. There is as yet insufficient evidence to implicate intensive chemotherapy in the causation of acute leukemia since in only three patients with Hodgkin's disease treated with chemotherapy alone has the development of acute leukemia been reported. It is possible, however, that chemotherapy potentiates the effect of radiotherapy. 2t is also possible that acute leukemia is part of the natural history of Hodgkin's disease and is occurring with greater frequency because of improved survival in Hodgkin's disease since the introduction of better radiotherapeutic and chemotherapeutic treatment regimens.
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PMID:Hodgkin's disease and acute leukemia. Report of eight cases and review of the literature. 109 Jan 58

Remission induction therapy with 6MP and adriamycin in combination was administered to 19 adult leukemic patients refractory to previous therapy. Eight patients also received vincristine and prednisone. Thirteen patients had acute myelogenous leukemia, 3 undifferentiated leukemia, and 3 blastic transformation of chronic myelogenous leukemia. Four patients achieved remission but in only 2 were the remissions complete. Eleven patients failed to respond. Ten of the 19 patients developed unexpected severe liver toxicity manifested by a clinical picture of cholestasis (in the majority) or ascending cholangitis (in 2 patients). In the postmortem examination of 8 patients there was cholestasis and mild to severe hepatocellular damage in all.
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PMID:Combination 6-mercaptopurine-adriamycin in refractory adult acute leukemia. 110 Mar 9

Bone marrow chromosomes obtained from 50 of 55 consecutive adult patients with acute nonlymphocytic leukemia were analyzed with quinacrine fluorescence. Twenty-five patients showed a normal karyotype and 25 an abnormal karyotype on the initial samples available for analysis. Among the 25 patients with abnormalities, the marrow cells contained 48 chromosomes in one case, 47 in two, 46 in ten, 45 in nine, 43 in two, and 42 chromosomes in one case. Seven of the ten patients with 46 chromosomes had abnormalities, primarily balanced translocations, that were not detected with the standard Giemsa stains. The analysis of all of the data available revealed the presence of nonrandom chromosome changes such as the addition of No. 8, the loss of No. 7, and a gain or loss of one No. 21. the most frequent structural rearrangement was the translocation between the long arm of No. 8 and No. 21, which may also be associated with the loss of a sex chromosome. Chromosomal abnormalities decreased or disappeared during remission; the same abnormality recurred in relapse. Chemotherapy did not appear to produce a stable clone of aberrant cells. Evolution of the karyotype occurred in eight patients, in five of whom an additional No. 8 was observed. This pattern of chromosomal evolution in patients with acute leukemia was very similar to that observed in patients with chronic myelogenous leukemia in the blast phase.
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PMID:Chromosomal banding patterns in acute nonlymphocytic leukemia. 126 Jan 31


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