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Query: UMLS:C0023473 (chronic myeloid leukemia)
18,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two unique cell lines, NALM-1 and BALM-2 derived from lymphoblast-like cells of chronic myelogenous leukemia and rare B cell acute lymphoblastic leukemia patients, respectively, were compared with fresh parent cells from the patients and with a Philadelphia chromosome positive K-562 cell line previously established from a chronic myelogenous leukemia patient in blastic phase. NALM-1 resembled the parent cells in the presence of Philadelphia chromosome, non-T/non-B acute lymphoblastic leukemia specific antigens and lack of T or B cell markers, whereas BALB-2, like the parent cells, had two chromosome markers and bore kappa, delta and mu immunoglobulins. NALM-1 lacked Epstein-Barr virus genome, whereas BALM-2 showed the presence of Epstein-Barr virus genome. K-562 cells lacked all the antigen markers examined. All cells had high DNA polymerase alpha activity and low DNA polymerase gamma activity. NALM-1, like the parent cells and unlike K-562 cells, had high terminal deoxynucleotidyl transferase activity of about 200 mu/mg DNA, whereas BALM-2, like its parent cells, had terminal deoxynucleotidyl transferase activity of 1-2 mu/mg DNA (1 u = 1 nmole Mn++-dGTP/h on dA12-18 initiator). Terminal deoxynucleotidyl transferase was characterized by its chromatographic and sedimentation behavior, thermal sensitivity and specific inhibition by streptolydigin and terminal deoxynucleotidyl transferase antisera. These results indicate that NALM-1 and K-562 may represent different phenotypes of cells in CML blastic crisis. Moreover, NALM-1 and BALM-2 seem to have retained the characteristics of original leukemic cells from which they may have been derived.
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PMID:Terminal deoxynucleotidyl transferase activity and cell surface antigens of two unique cell lines (NALM-1 and BALM-2) of human leukemic origin. 7 Apr 13

Four patients who demonstrated unusually prolonged survival with Philadelphia chromosome positive Ph' (+) chronic myeloid leukemia (CML) were analyzed for factors associated with survival. Survival duration from initial diagnosis ranged from 120 to 222 months, with a mean of 170 months. At diagnosis, age, symptoms, liver or spleen size, hematocrit, white blood cell count, absolute peripheral myeloblast plus promyelocyte count, and uric acid did not have unique prognostic significance. At diagnosis all four patients had normal or low-normal platelet counts, (range: 170,000 to 248,000/mm3). Thrombocytopenia occurred during treatment in three patients. None of the four patients, however, developed severe marrow hypoplasia or leukopenia during treatment for the chronic phase. Cytogenic studies performed from 103 to 156 months after diagnosis did not reveal a large subpopulation of marrow cells with a normal karyotype or cells with the XO genotype in the male patients. These observations suggest that prolonged survival in CML 1) is not contingent upon intensive treatment resulting in marrow hypoplasia, and 2) does not require the persistence of a clone of karyotypically-normal bone marrow cells or a clone of marrow cells in males which has lost the Y chromosome. A normal or low-normal platelet count at diagnosis may be a favorable prognostic indicator.
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PMID:Factors associated with prolonged survival in chronic myeloid leukemia. 28 Apr 16

A child with chronic myelocytic leukemia (CML), Philadelphia chromosome positive, developed a non-T cell, non-B cell, acute lymphocytic leukemia (ALL) during her blast cell crisis. The diagnosis was suggested by light microscopy and supported by histochemical stains and transmission electron microscopy. Immunologic studies showed the presence of a non-T, non-B leukemic blast population--indistinguishable from the most common form of ALL (null cell type). Markedly elevated terminal deoxynucleotidyl transferase (TdT) activity was found. The findings support the hypothesis that the primary cell involved in CML is a stem cell with pluripotential characteristics; frequently the blast cell proliferative phase terminates in acute myeloblastic leukemia, but it may also terminate in ALL. The TdT activity may be evidence of leukemic transformation and not necessarily related to the thymic origin of the lymphocytes.
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PMID:Chronic myelocytic leukemia terminating in blast cell crisis with lymphoblastic characteristics. 28 67

A man received a cadaver renal allograft for end-stage renal failure. After 35 months of immunosuppressive therapy with azathioprine and prednisone, he developed septicemia and a high leukocyte count. In spite of successful treatment of the infection, the leukocyte count continued to rise and a diagnosis of Philadelphia chromosome positive chronic granulocytic leukemia was made. An increased incidence of malignant disease, especially lymphoreticular malignancy, is well described in immunosuppressed patients with allografts. However, the association of chronic granulocytic leukemia and immunosuppressive therapy previously has not been reported. An additional etiological factor in this patient may have been the extensive diagnostic radiological investigations undertaken in childhood. The recent addition of allopurinol to the immunosuppressive therapy has normalized the platelet and leukocyte counts, probably by potentiating mercaptopurine.
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PMID:Chronic granulocytic leukemia in a patient with a renal allograft. 35 95

Peripheral blood from a child with adult-type (Philadelphia chromosome positive) chronic granulocytic leukemia was found to contain large numbers of cells capable of colony formation in tissue culture. The majority of the colonies contained granulocytic cells. The source of these granulocytic colonies was found in a population of myeloblasts, promyelocytes, and myelocytes which could be separated from the more mature granulocytic cells of the peripheral blood by sedimentation of the buffy coat on Ficoll-Hypaque. The predominance of granulocytic colonies is in contrast to our observations previously made on the peripheral blood of children with "juvenile" type(Ph1 chromosome negative)CGL in which large numbers of exclusively monocytic colonies were produced in tissue culture. These current studies, when interpreted in light of relevant clinical data, suggest that the "juvenile" and "adult" types of CGL represent two very different forms of chronic leukemia in childhood. The Ph1 chromosome negative form may be classified as a monocytic leukemia with a granulocytic component but the Ph1 chromosome positive adult form, even when it occurs in a child, appears to be a true granulocytic leukemia.
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PMID:In vitro colony-forming characteristics of chronic granulocytic leukemia in childhood. 105 30

24 patients with Philadelphia chromosome positive chronic myeloid leukaemia (CML) in blast crisis were treated with intensive chemotherapy. 16 patients showed either partial or complete response to this treatment, but median survival remained short (13 weeks), and much of this time was spent in hospital. These results were not significantly better than those obtained by others using vincristine and prednisolone alone, and this combination of drugs can often be given on an outpatient basis. It is concluded that until more effective intensive therapy becomes available patients in CML blast crisis should be managed in such a way that the quality of life is not impaired; and that at present vincristine and prednisolone appears to be the most impaired; and that at present vincristine and prednisolone appears to be the most appropriate initial treatment, though even this is far from satisfactory.
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PMID:Blast crisis of chronic myeloid leukaemia: the effect of intensive chemotherapy. 106 6

We investigated the marrows of 19 patients with advanced Philadelphia chromosome positive (Ph+) chronic myeloid leukemia (CML) in long-term marrow culture (LTMC) to determine the frequency of loss of clonogenic leukemic cells in vitro. Sixteen patients were in first chronic phase at a median of 24 months from diagnosis and had received prior therapy with busulphan and/or hydroxyurea. The effect of interferon therapy on loss of Ph+ clonogenic cells in LTMC was also investigated. Of 16 patients who had not previously received interferon, complete loss of Ph+ progenitors was documented by 4-5 weeks in the LTMCs from two (12.5%). Ph+ progenitors persisted at 4-5 weeks in the LTMC derived from 12 patients. Marrows from nine patients treated with interferon were also established in LTMC. Cultures from four patients did not yield colonies with detectable metaphases at 3-5 weeks, while Ph+ clones were present in the cultures initiated with marrows from five patients. Mean hematopoietic colony yields from the adherent layer at 2-4 weeks, and from the supernatant layer at 1-3 weeks, of cultures derived from interferon-treated patients were significantly lower than in LTMCs of patients not treated with interferon (p less than 0.05). The results indicate that in previously treated patients with late chronic phase CML there is a low frequency of conversion of Ph-negative hematopoiesis in long-term culture. Interferon therapy is associated with impaired progenitor yields in LTMC and does not improve selective loss of Ph+ progenitors.
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PMID:Maintenance of Philadelphia-chromosome-positive progenitors in long-term marrow cultures from patients with advanced chronic myeloid leukemia. 137 77

Interferon-alpha (INF-alpha) induces cytogenetic remissions in 20% of chronic myelogenous leukemia (CML) patients. To clarify the mechanisms through which this antiproliferative action of IFN is mediated in the CML cell, a modification of the mobility-shift assay was used to follow the formation of complexes between nuclear proteins and IFN-inducible transcriptional enhancers involved in mediating the cellular effects of IFN-alpha. These studies identified a complex that was present in the myeloid cells of 18/24 (75%) of chronic-phase CML patients tested whose cells contained 100% Philadelphia chromosome positive (Ph+) cells, while the proteins of none of the samples tested from normal peripheral blood samples and only 22% (2/9) of the CML patients in an IFN-induced major cytogenetic remission (less than 30% Ph+ cells) contained these complexes. These studies suggest that the mobility-shift assay detects changes in the CML myeloid cell that distinguish it from the normal myeloid cell.
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PMID:Identification of a complex formed between nuclear proteins and the transcriptional enhancer of interferon-inducible genes that is present in the peripheral blood myeloid cells of CML but not normal individuals. 143 11

Abnormalities of chromosome 16, including inv(16)(p13q22), del(16)(q22), and t(16;16)(p13;q22), have been reported almost exclusively in association with acute myelomonocytic leukemia and are characteristically accompanied by abnormal eosinophils with dysplastic granules in the bone marrow. We observed an inv(16)(p13q22) in two patients with typical Philadelphia chromosome positive chronic myeloid leukemia (CML). The appearance of the abnormality of chromosome 16 was associated with acceleration of disease or onset of blast crisis and with the appearance in the bone marrow of abnormal eosinophils. In both cases the marrow karyotypes were 46,XY,t(9;22)(q34;q11)/46,XY,inv(16)(p13q22),t(9;22)(q34;q11). In these two patients the temporal association of the acquisition of the inversion 16 and the appearance of monocytoid cells and dysplastic eosinophils in the bone marrow further supports the relationship of this karyotypic abnormality with leukemic monocytoid and eosinophilic evolution. This secondary cytogenetic change appears to be an infrequent manifestation of specific phenotypic disease progression in CML.
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PMID:Inversion of chromosome 16 and dysplastic eosinophils in accelerated phase of chronic myeloid leukemia. 159 3

A 52 year old male presenting chronic myeloid leukemia (CML) Philadelphia chromosome positive (Ph) four years after the diagnosis of a non Hodgkin's lymphoma is described. The patient had received high total doses of alkylating drugs (cyclophosphamide and chlorambucil) as part of chemotherapy treatment for a diffuse mixed lymphoma. At four years of diagnosis of the lymphoma the appearance of hepatosplenomegaly, leukocytosis with myeloma and basophilia and thrombocytosis were observed. These alterations augmented progressively until a cytogenetic study of the bone marrow two years late established the diagnosis of CML upon demonstrating the presence of the Ph chromosome with no other karyotypic anomalies being observed. The explorations carried out at that time confirmed that the lymphoma continued to be in remission. The CML initially responded to treatment with busulphan. However, following a year and a half the disease evolved to a phase of acceleration and the patient died a few weeks later due to pneumonia with no signs indicative of lymphoma activity having been detected since the diagnosis of the CML.
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PMID:[Chronic myeloid leukemia after chemotherapy treatment for non-Hodgkin's lymphoma]. 163 10


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