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

Certain human hemopoietic disorders (the clonal hemopathies) originate in pluripotent stem cells. These include acute myeloblastic leukemia (AML), chronic myelocytic leukemia (CML), polycythemia vera (P vera), and idiopathic myelofibrosis. In each affected individual a single abnormal clone becomes dominant, occupying all hematologic spaces. An understanding of the cellular basis of normal hemopoiesis and these diseases requires consideration of stem cell properties, clonal expansion, and the differentiation programs of various myelopoietic lineages. The blast cells of AML provide a test of hypotheses about normal and leukemic hemopoiesis. The suggestion is advanced that these blasts do not develop because normal programs are blocked or aborted, but rather follow novel programs, assembled abnormally from normal components. The finding of individual blast cells expressing markers of more than one lineage simultaneously is advanced as support for this model.
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PMID:Cellular lineages in normal and leukemic hemopoiesis. 658 19

Megakaryoblastic transformation, with cells showing characteristic morphology and ultrastructural cytochemistry, developed in two patients with agnogenic myeloid metaplasia or myelofibrosis, and in one with chronic granulocytic leukemia. From the onset of the leukemic phase, all three have followed a relatively benign clinical course, surviving for 48, 29, and 24 months, respectively; only hydroxyurea has been necessary to control thrombocytosis. This experience emphasizes that it is possible for a patient to have an improved quality of life with minimum chemotherapy. In contrast, megakaryoblastic leukemia or acute myelofibrosis, where splenomegaly and a leukoerythroblastic blood picture are typically absent, responds poorly to any form of chemotherapy, and survival is short.
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PMID:Megakaryoblastic transformation in myeloproliferative disorders. 658 78

On the basis of the trephine marrow histology at presentation, 52 Ph1 positive cases of chronic myeloid leukaemia were divided into two subgroups, classical chronic granulocytic leukaemia (CGL) and chronic megakaryocytic granulocytic myelosis (CMGM). In 24 cases in which conventional therapy had preceded trephine biopsy, the distribution of cases between the two groups was found to have been significantly altered. Subsequent analysis was therefore confined to the remaining 28 untreated cases; of these 15 were classified as CGL and 13 as CMGM; no statistically significant difference was found between the two groups in respect of patient's age, leucocyte counts, platelet counts, NAP scores or of occurrence of 'blast' crisis. The differential diagnosis between idiopathic myelofibrosis (IMF) and CMGM subgroup is discussed. It was concluded that classification of chronic myeloid leukaemia on the basis of marrow histology should be restricted to Ph1 positive cases in order to obviate the possible inclusion of cases of IMF within the CMGM subgroup.
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PMID:Histological classification of chronic granulocytic leukaemia. 659 44

Morphometry was employed on different entities of chronic myeloproliferative diseases (CMPD) and reactive lesions in addition to normal control specimens. The entities studied included: (1) inflammatory reactions of the bone marrow (so-called myelitis in chronic rheumatoid arthritis), (2) chronic granulocytic leukemia (CGL), (3) agnogenic myeloid metaplasia in an early hypercellular stage (so-called chronic megakaryocytic-granulocytic myelosis, CMGM), (4) agnogenic myeloid metaplasia in an advanced fibrosclerotic stage or osteomyelofibrosis/sclerosis (MF/OMS), (5) polycythemia vera (P. vera), (6) reactive thrombocytosis (TH, as a sequel of miscellaneous conditions) and (7) primary (idiopathic, essential) thrombocythemia (PTH). Evaluation was done on plastic-embedded semithin sections with a constant thickness of 3 micron in approximately 20 cases of each group of CMPD. The following parameters were determined: (1) density distributions of the megakaryocyte and non-megakaryocyte compartments, (2) arrangement of megakaryopoiesis in the bone marrow space (i.e., inhomogeneity or clustering) and (3) the fine structure of megakaryocytes in PTH, with a quantitative analysis of the nuclear morphology by circular deviation and contour factors. The megakaryocyte morphology was closely related to a facultative or obligatory increase of the platelet count in these various entities of CMPD and was separable into two major categories: (1) controls, CGL and myelitis versus (2) CMGM, MF/OMS, P. vera, TH and PTH. These two categories were distinguishable by the prominence of megakaryopoiesis in the bone marrow as well as the elevated platelet counts in the periphery. Moreover, in comparison with CMGM and MF/OMS, PTH was characterized by an apparently normal maturation and a conspicuous polyploidization of megakaryocytes according to the nuclear morphology, which was similar to that of P. vera. Our results suggest that PTH presents a monolinear growth of the megakaryopoiesis in the same way as CGL exhibits a monolinear proliferation of the neutrophilic granulopoiesis. This is in contrast to the mixed cellularity of both the megakaryocyte and granulocyte lineage in CMGM and MF/OMS.
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PMID:Megakaryopoiesis in chronic myeloproliferative diseases. A morphometric evaluation with special emphasis on primary thrombocythemia. 659 64

Isozymes of amino acid naphthylamidase (called B and C) with deviating electrophoretic mobilities were found in peripheral blood leukocytes of 25 out 25 untreated acute and chronic myeloid leukemias (AML and CML) and in 2 out of 2 cases of idiopathic myelofibrosis, while a normal pattern was found in 3 control groups and 5 cases of polycythemia vera. In the AML group, a correlation between electrophoretic mobility and the number of blast cells was found, and on remission, the B isozyme mobility was nearly normalized. Thus, deviating electrophoretic mobility of the B isozyme seemed to be valuable for diagnosis of myeloid leukemias, and in the AML group, the change in mobility might indicate the size of the leukemic clone.
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PMID:Discriminative value of isozymes of amino acid naphthylamidase in the diagnosis of myeloid leukemias. 693 Mar 22

Over a period of 22 years, 4844 pleural and peritoneal fluids from 3279 patients were examined cytologically. Megakaryocytes were found in the fluids from five patients. The clinical diagnoses in the five patients were agnogenic myeloid metaplasia, chronic myeloid leukaemia, and lymphocytic lymphoma. All of these patients had persistent serous effusions. Megakaryocytes in serous fluids occurred in three forms: (1) a large type with abundant cytoplasm and multilobed nuclei, (2) a smaller type with a high nucleocytoplasmic ratio and unlobed nuclei, and (3) anucleate cytoplasmic masses. Foci of agnogenic myeloid metaplasia found on the serous surfaces at necropsy of two patients contained megakaryocytes similar to those in the corresponding effusions. The clinical course of our patients confirmed that the presence of megakaryocytes in serous fluids signifies an advanced haematopoietic malignancy.
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PMID:Megakaryocytes in pleural and peritoneal fluids: prevalence, significance, morphology, and cytohistological correlation. 693 44

The Authors have studied bone marrow CFUc and CLFC of 8 cases affected by idiopathic myelofibrosis, 7 by chronic granulocytic leukemia, 6 by polycythemia, and 3 by sideroblastic anemia. The authors studied also C.S.F. activity in peripheral blood of 8 cases. The method of Pike and Robinson for in agar culture was utilized. The results indicated a correlation between increase of clusters/colonies fraction, growth of blasts-like clusters, reduction of C.S.F. activity in peripheral blood and transformation in acute leukemia of preleukemic syndromes.
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PMID:[Evaluation of the proliferative activity of hematopoietic cells in preleukemic syndromes]. 693 4

An FBP has been purified from the spleen (FBP-S) of a patient with agnogenic myeloid metaplasia and myelofibrosis. This binder is similar to a previously purified protein from CML cells (FBP-L) in its molecular weight and affinity for folate analogues. However, each protein has very little cross-reactivity in specific RIAs for each binder, indicating that there are structural differences which can be detected by the immune system. THe concentration of FBP-L in the serum from normal subjects was 2.0 +/- 0.39 ng/ml (mean +/- S.E.M.) and was significantly elevated in the serum from some patients with CML, uremia, hepatitis, and cancer. The concentration of FBP-S, on the other hand, was 8.31 +/- 0.51 ng/ml in normal serum and remained in this range in the same serum that contained the elevated concentration of FBP-L. In contrast, the concentration of FBP-L was only 13% to 30% of the concentration of FBP-S measured in the homogenates of normal and adjacent cancerous tissue from lungs and colons. These studies indicate that some FBP(s) in human tissues have immunologic specificity even though they are functionally similar.
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PMID:Immunologic heterogeneity of the folate-binding proteins from chronic myelogenous leukemia cells and myelofibrosis spleen. 694 34

Blood flow in hematopoietic bone marrow and in nonhematopoietic bone has been measured with a Xe-133 washout method in 20 patients with chronic granulocytic leukemia (CGL) and in seven with primary myelofibrosis. Age-matched healthy persons served as controls. Bone-marrow blood flow in CGL was dependent upon the phase of the disease. In the metamorphosis phase, bone-marrow blood flow was high compared with that in the well-controlled phase. Apart from the initial phase, the mean values for bone blood flow in CGL were increased compared with the values of the healthy controls. In myelofibrosis the bone blood flow was also increased. Bone-marrow blood flow in these diseases was dependent upon the cellularity of bone marrow as measured morphometrically.
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PMID:Bone and bone-marrow blood flow in chronic granulocytic leukemia and primary myelofibrosis. 695 31

76 cases of CML were divided according to clinical parameters (duration of illness prior to diagnosis, size of spleen, leucocyte and platelet counts, ALP index, bone marrow cytology and others) into groups showing a classical or an atypical course of the disease. All patients were submitted to bone marrow biopsy, using the method of Jamshidi and Swaim. The histological subtypes of CML, i.e. chronic granulocytic leukaemia and chronic megakaryocytic granulocytic myelosis were correlated with the two clinical types of disease. The classical form of CML was histologically inhomogeneous and was subdivided into 40% cases of chronic granulocytic leukaemia and 60% cases of chronic megakaryocytic granulocytic myelosis. At the time of bone marrow biopsy 20% of patients with classical leukaemia were already found to have myelofibrosis. The atypical myeloses consisted of chronic megakaryocytic granulocytic myelosis only and myelofibrosis was present initially in 50% of patients. In view of these findings agnogenic myeloid metaplasia is considered to be merely a variant of chronic myeloid leukaemia and the term "atypical myelosis" is preferred.
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PMID:[Comparative clinical and histological investigations in chronic myeloid leukaemias ]. 695 71


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