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)

A 58-yr-old male patient presented in the blastic phase of chronic myelogenous leukemia (CML). Cytogenetic studies revealed a 45 XO Ph1 chromosome pattern in bone marrow cells during a short remission and again in the blastic phase of the disease. The patient expired 8 mo following diagnosis. The blastic phase of CML can stimulate acute myelogenous leukemia (AML) clinically and hematologically; CML can be differentiated by the presence of the Ph1 chromosome and the stigmata of CML. Absence of the Y chromosome from the bone marrow in CML is a recently described finding. Previous reports indicating the prevention of the blastic phase in patients with this karyotype could not be confirmed by our or other recently reported cases.
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PMID:Chronic myelogenous leukemia presenting in the blastic phase and its association with a 45 XO Ph1 karyotype. 106 Apr 74

Folic acid binding protein was estimated in the serum of 94 control subjects and a normal range was established. Raised levels were found in folate deficiency and chronic myeloid leukaemia. Considerably raised levels were found in untreated acute myeloid leukaemia, most often in cases with a marked monocytic element.
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PMID:Folic acid binding protein in acute myeloid leukaemia. 106 12

A patient with Ph1 positive chronic myeloid leukemia (CML) developed blastic transformation which by morphologic criteria appeared to be localized to the lymphatic system. Chromosome analysis at this time, however, revealed new chromosomal abnormalities in addition to the existing Ph1 in all tissues studied (lymph node, blood, and bone marrow) consisting primarily of extra chromosome numbers 19 and 9 and a second Ph1. Therapy resulted in clinical remission with significant decrease in the aneuploid cell lines. However, these reappeared with recurrence of the blast crisis. Colony formation in semisolid culture of blood and marrow cells at the time of initial blast crisis yielded growth patterns characteristic of CML. On recurrence of the blast crisis after therapy, growth patterns were characteristic of CML in blast crisis or acute myeloblastic leukemia even though blood and marrow still showed relatively low levels of myeloblasts and promyelocytes. Possible explanations are discussed for the disparity in distribution between morphologic and chromosomal abnormalities in this patient.
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PMID:Discordant patterns of chromosome changes and myeloblast proliferation during the terminal phase of chronic myeloid leukemia. 106 22

A consistent chromosome abnormality of C-G translocation, t(8;21)(q22;q22), was found in 15 acute myelocytic leukemia (AML) patients with low neutrophil alkaline phosphatase (N-AP) activity. Granulocytes of these patients also had specific morphologic abnormalities. The bone marrow showed a tendency to relatively good maturation of leukemic cells for the disease AML. Clinical courses of the patients were mild and median survival was longer than that of patients with normal or high N-AP activity (p = 0.065, suggestive difference). Three out of six male patients with these type of AML had missing Y chromosome in addition to C-G translocation. The results suggest that specific cytogenetic abnormality of C-G translocation would be significantly associated with AML. Contrasting with low N-AP activity and the Philadelphia chromosome in chronic myelocytic leukemia, the findings in AML may offer additional evidence towards the possible relations between alkaline phosphatase activity and C or G chromosome.
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PMID:C-G translocation in acute myelocytic leukemia with low neutrophil alkaline phosphatase activity. 106 58

In a group of 172 cases of polycythemia vera treated with radioactive phosphorus acute granulocytic leukemia developed in 3 and chronic granulocytic leukemia in 6 cases. The author believes that development of acute granulocytic leukemia during this treatment may be considered with some probability as a result of the leukemia-inducing action of ionizing radiation. Transition of polycythemia vera into chronic granulocytic leukemia seems to be a natural outcome of this complex myeloproliferative syndrome in patients with survival prolonged by treatment with 32P.
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PMID:Observations on polycythemia vera turning into acute or chronic granulocytic leukemia during treatment with radioactive phosphorus 32P. 106 85

Leukocyte kinetic studies using chromium-51 were performed in four patients with acute myelocytic leukemia (AML). Intravascular leukocyte survival was prolonged in comparision with granulocyte survival in normal subjects. Significant splenic pooling occurred in three patients, none of whom had splenomegaly. In one patient studied, circulating leukemic cells were shown to return to the bone marrow. The prolongation of intravascular leukocyte survival in AML in relapse, as in chronic myelocytic leukemia, probably depends on several factors including the presence of immature leukemic cells and the recycling of these cells from the spleen and bone marrow.
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PMID:Study of leukocyte kinetics in acute myelocytic leukemia utilizing chromium-51. 106 22

In a consecutive series of 841 patients whose bone marrows were cytogenetically investigated because of verified or suspected haematological disease, 11 patients were found to have at least 10% polyploid bone marrow mitoses. The chromosome numbers varied greatly between the cells of the same patients and between the patients. In 4 cases, the number was nearly or exactly tetraploid and in 1 patient a prevalent octaploid line was seen. Structurally abnormal marker chromosomes were seen in 8 of the patients. A total of 31 bone marrow chromosome counts were performed on a young woman with acute myelomonocytic leukaemia who had had several drug-induced remissions during the 3 1/2 years of disease. The results were related to the clinical findings. On several occasions a clear-cut correlation was noted between high proportions (nearly 100%) of polyploid cells and relapse on the one hand and low proportions (as low as 0%) of polyploids and remission on the other. Of the 11 patients, 2 had chronic myeloid leukaemia, 3 acute myelomonocytic leukaemia, 3 acute myeloid leukaemia and a further 3 some other malignant haematological disorders. We conclude that polyploidy is a feature associated with rare cases of leukaemia and other malignant diseases. It is often a sign of a poor prognosis.
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PMID:Polyploidy of the bone marrow. 106 55

Three male patients with leukemia were found with banding techniques to have unusual cytogenetic pictures in the cells of their marrow, spleen or blood. Case No. 1 (78 yr old) was that of a Ph1-negative CML with a missing Y in the blood (cultured without PHA) and marrow cells. The patient is still alive and responding to therapy. Case No 2 (54 yr old) was considered prior to admission to have either CML or AML, but was shown, in fact, to be in the blastic phase of CML; all the cells in his marrow and spleen were Ph1-positive, but with no evidence of a translocation. Other karyotypic findings (+8, +11, +13, +21) frequently encountered in the blastic phase of CML were present in the cells of this patient. Case No. 3 (50 yr old) with AML was shown to have a Ph1 resulting from a standard translocation, i.e., [t(9;22) (q34;q11)], in a substantial number of the cells in the marrrow and blood (cultured without PHA). The implications of these unusual findings are discussed in relation to the chromosomal pictures usually encountered in these states.
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PMID:Chromosomes and causation of human cancer and leukemia. XXI. Cytogenetically unusual cases of leukemia. 106 75

The occurrence of a missing Y chromosome was investigated in the bone marrow cells of male individuals, i.e., 255 controls, 73 with acute myelocytic leukemia (AML) and 59 with Ph1-positive chronic myelocytic leukemia (CML). The incidence in controls of individuals with 45,X cells increased with age, particularly after the age of 60. In AML, 45,X metaphases were detected in two patients over 70 years of age, but the leukemia seemed to have involved the 46,XY cells rather than the 45,X cells. Four of the six patients with No. 8-No. 21 translocation and two of the 16 with major karyotypic abnormalities (MAKA) exhibited a missing Y in the leukemic cells in addition to other karyotypic aberrations. Four of the Ph1-positive CML patients exhibited a missing Y in all or nearly all the cells in the bone marrow along with the Ph1. In one patient, additional chromosome abnormalities involved the 46,XY,Ph1 rather than the 45,X,Ph1 cells. The genesis of the missing Y in CML cells may be related to the presence of the Ph1, though apparently the patient's age also plays a role. It is our hypothesis that 45,X or 45,X,Ph1 cells are resistant to the development of further chromosomal abnormalities and, thus, reflect their resistance to being involved in an acute leukemic process.
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PMID:The chromosomes and causation of human cancer and leukemia. XVIII. The missing Y in acute myeloblastic leukemia (AML) and Ph1-positive chronic myelocytic leukemia (CML). 106 92

Blast crisis terminates the life of the majority (approximately 80%) of patients with CML. The time of its onset appears to be a random phenomenon, varying from a probable coincidence occurrence with the onset of CML to more than a decade after onset of the chronic phase. In most patients the diagnosis is obvious as very immature cells are found to be the predominant cell in blood and marrow. However, in some, the onset is fairly subtle and the diagnosis of the syndrome will be dependent upon ancillary clinical and laboratory clues supplementing morphologic appearance of the blood and bone marrow. The same spectrum of morphological cell types is observed in blast crisis as is observed in acute myeloid leukemia. The predominant cells usually are myeloblasts and promyelocytes but may be immature monocytes, myelomonocytes, proerythroblasts, or immature megakaryocytes. These and other findings imply that the defect resides in the pluripotent hematopoietic stem cell. It is possible, but by no means proven, that lymphoblastic conversion also may occur. Therapy of blast crisis is quite unsatisfactory but clearly is of benefit in some patients.
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PMID:The pathogenesis and clinical patterns of blastic crisis of chronic myeloid leukemia. 106 30


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