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

In a prospective study of 32 patients with chronic myeloid leukemia the frequency of chromosome abnormalities in addition to the Philadelphia chromosome (Ph) increased when the disease progressed. Before metamorphosis, 10 patients (31%) had developed additional abnormalities. Such abnormalities were present in three of them at the time of diagnosis; in the other seven, they were detected late in the chronic phase. New clonal abnormalities heralded or accompanied a more malignant phase of the disorder, usually a blastic leukemia. During metamorphosis, 78% of the patients had additional abnormalities, which in 68% of these cases comprised at least one of +8, +22q- or i(17q). Clones with additional abnormalities disappeared in eight cases, either spontaneously or in association with cytostatic therapy during the chronic or blastic phase. Involvement of chromosome #8, usually in the form of a trisomy, was found in 7 of 12 patients treated with busulfan, but was not found in any of the 10 hydroxyurea-treated patients, of whom 8 were splenectomized early during the chronic phase. Cells from the spleen, obtained by fine needle aspiration or splenectomy were cytogenetically examined in 18 cases during the chronic phase, but abnormalities in addition to the Ph were noted in only one patient, who was examined in the late chronic phase. The same abnormalities were present in bone marrow cells of this patient.
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PMID:Karyotypic evolution in Ph-positive chronic myeloid leukemia in relation to management and disease progression. 386 Dec 36

Tetraploid populations have been observed in various types of leukemia, but relatively few reports exist of triploid cell populations in acute or chronic leukemia. We report two cases of Ph-positive leukemia with a modal triploid cell population. Examination of peripheral blood from a 3-year-old boy with Ph-positive acute lymphoblastic leukemia (ALL) and a 68-year-old male with Ph-positive chronic myelocytic leukemia (CML) in blastic crisis revealed modal populations of 72 and 63 chromosomes, respectively. G-banding analysis of both cases revealed the following: karyotypic instability (no clonality), dominant trisomy, and the random association of the Ph chromosome with gains and losses of chromosomes involved in this translocation. The cytogenetic evidence obtained suggests that the triploid cell populations were not derived from a duplication of a hypodiploid cell population, but resulted from random loss of chromosomes from tetraploid cell populations derived from duplication of pseudodiploid cells.
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PMID:Near-triploid Ph-positive leukemia. 386 95

A 59-year-old woman was treated with surgery followed by monthly injections of the alkylating agent thiotepa for a granulosa cell tumor of the left ovary. Chemotherapy was continued for 22 years. At the age of 84, chronic myelogenous leukemia (CML) developed. Cytogenetic studies revealed incomplete trisomy of the long arm of chromosome No. 1 as the only karyotypic abnormality. No Philadelphia chromosome was detected. The significance of trisomy 1q as an isolated cytogenetic abnormality in CML and the occurrence of CML following treatment of ovarian cancer are discussed.
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PMID:Philadelphia-chromosome-negative chronic myelogenous leukemia with incomplete trisomy 1q following chemotherapy for ovarian carcinoma. 393 61

The gene for erythrocyte glutathione reductase (E-GR) activity has been assigned to chromosome #8. In the present series, we examined the E-GR activity in 14 cases with chronic myelodysplastic syndrome (CMS, preleukemia), atypical acute myelogenous leukemia (AML), or chronic myelogenous leukemia (CML), with and without acquired trisomy #8. No difference in the incidence of high levels of this enzyme was found between two groups, i.e., those with and without trisomy #8 suggesting the existence of a complex regulatory system in addition to chromosome #8.
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PMID:Erythrocyte glutathione reductase activity and acquired trisomy #8 in various hematologic disorders. 672 65

The chromosomal involvement in the development of malignancy in chronic myeloid leukemia is not a random event. A second Ph1, a trisomy 8, an isochromosome 17q, a trisomy 17 are the main abnormalities. These aberrations use to occur as a karyotypic evolution, either simple or complicated. An extra-medullary development of blastic transformation was demonstrated by chromosomal analysis. It is difficult to demonstrate a correlation between chromosomal abnormalities and clinical evolution in the acute phase of chronic myeloid leukemia.
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PMID:[Chromosomal abnormalities of the blastic phase of chronic myeloid leukemia]. 676 78

Previous reports emphasize that trisomy 8 is the most common, single chromosomal abnormality in both Philadelphia (Ph1) chromosome-positive and Ph1-negative chronic myelogenous leukemia (CML). Karyotype analysis on a 78-year-old man with Ph1-negative CML showed trisomy D, confirmed on banding studies to be an extra No. 14 chromosome. Although the abnormality is likely to be related to the leukemic clone, the importance of this chromosomal deviation is not known.
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PMID:Philadelphia chromosome-negative chronic myelogenous leukemia with trisomy D. 693 Sep 38

One case of a patient with Chronic Granulocytic Leukemia showing a double Ph' together with trisomy 17 during blastic crisis is reported. The Ph' chromosome resulting from a standard translocation of the chromosomes 9 and 22 was present in all the 16 mitoses observed, while the trisomy 17 was found in 15. This case is an additional contribution which demonstrates the presence of the alterations of the chromosome group E during the blastic crisis.
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PMID:[Karyotype in chronic myeloid leukemia in a blastic crisis. II. Trisomy 17]. 694 Jun 6

In routine analyses, abnormalities of chromosome No. 17 were found in the bone marrow cells of 28 patients with Ph1-positive and three patients with Ph1-negative chronic myeloid leukemia (CML), 4 patients with acute nonlymphocytic leukemia (ANLL), and 4 patients with preleukemia. With three exceptions, all patients were in the blastic (CML) or the terminal phase. In 28 patients, the aberrant chromosome No. 17 arose by clonal evolution from the karyotype found at diagnosis or before the terminal phase. The abnormalities encountered were an isochromosome for the long arm, i(17q), (26 cases), translocations involving No. 17 (12 cases), trisomy 17 (three cases), and ring 17 (one case). In 35 patients, there was an unbalanced structural aberration of at least one of the No. 17 chromosomes. In every case (35/35), detailed analysis of the structurally abnormal No. 17 revealed loss of the distal part of the short arm (or possibly most of the short arm). Gain of the long arm (or at least its proximal part) was also common, but not invariably present (26/35). It is suggested that loss of 17p is a highly nonrandom event related to blastic crisis in CML and the terminal phase in other myeloid leukemias.
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PMID:Abnormalities of chromosome No. 17 in myeloproliferative disorders. 695 Aug 7

A chromosomally abnormal clone is demonstrable in the bone marrow of a significant number of patients with hemic disorders that carry an increased risk for the subsequent development of leukemia. These "preleukemia" states include a variety of cytopenias, myeloproliferative disorders, and childhood syndromes. The cytogenetic alterations that occur nonrandomly in these dyscrasias are often similar to those observed in acute nonlymphocytic leukemia and in the accelerated phase of chronic granulocytic leukemia: monosomy for chromosome 7; trisomy for 8,9,21, and the long arm of 1(1q); deletions of 5 and 20 (5q-, 20q-); and an isochromosome derived from 17 (iso 17q). These findings support the view that despite clinical differences, these various preleukemic disorders are all characterized by the presence in the hematopoietic tissues of a clone of cells derived from an altered hemic stem cell. Furthermore, the data suggest that preleukemia, chronic leukemia, and acute leukemia may be fundamentally similar diseases, differing primarily in the rate at which the aberrant clone is expanding. Chromosome studies may be of prognostic value in the cytopenic preleukemias. Patients with abnormalities show a decreased survival and are at increased risk for progression to acute nonlymphocytic leukemia. In the myeloproliferative disorders and the preleukemic childhood disorders, cytogenetic alterations are not clearly predictive, and aberrant clones may persist for years without clinical progression.
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PMID:Preleukemias. 727 93

Clonal chromosome disorders occurring or acquired at any postnatal age are often closely related with the origin of tumours. In man the Ph1-chromosome (9; 22) anomaly in CML or the 8; 14 translocation in the African malignant Burkitt Non-Hodgkin lymphoma are, among other cases, prominent examples. On the other hand, constitutive, inherited or novel chromosome anomalies conveyed from the zygote to all tissues of the organism may cause a higher risk for the origin of tumours. Rarely, inheritable minor structural chromosome mutations are known to determine the occurrence of dysontogenetic tumours, as e.g., nephroblastoma, but it is assumed that more such cases will become elucidated in the future. As a special phenomenon, true hydatiform mole is a tumour of the placental tissue due to a disorder of intragenome regulation. Constitutive or numerical structural chromosome anomalies of man are a frequent cause of early or late abortion or of abnormal development and malformation. Despite the predominating principle of selective fetal elimination, a few anomalies such as Down's syndrome, may escape to longer survival due to the relatively mild effects of chromosome 21 triplication. Trisomies which represent in man the most frequent type of chromosome disorders, can be induced, and systematically studied in an experimental model of the mouse. This allows the elaboration of the developmental profiles of all trisomies (and monosomies) of the mouse. Also, the above mentioned principle of selective elimination of abnormal implants can be analysed experimentally. Although the developmental span of a trisomic zygote is limited, there is evidence that cells and tissues isolated from the chromosomally abnormal organism can survive much longer. Thus, haemopoietic stem cells, at least in Ts 12 and 19 of the mouse, can be rescued from trisomic fetuses by transferring them to lethally irradiated adult mice, whose blood forming organs may eventually become permanently repopulated by the trisomic cell lineage. This type of experiments is suited for closer analyses of potential functions vs. defects of chromosomally abnormal cellular systems, e.g., with regard to growth and development.
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PMID:[Chromosome abnormalities, tumours and developmental disorders (author's transl)]. 728 43


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