Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0023467 (acute myeloid leukemia)
 35,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Bone marrow from each of 8 untreated patients with myeloproliferative disorders was grown in diffusion chambers in 760 rad total body irradiated rats. Rats were then exposed to 11.5, 57.5, or 108.5 rad daily for 14-2l d and cell growth compared to that detected in unirradiated chambers. Cells from acute myelogenous leukaemia patients exposed to 11.5 rad per d grew for 11-21 d and there was no consistent stimulation of differentiation of immature granulocytic cells to mature granulocytes that was attributable to irradiation. Cells from a chronic myeloid leukaemia patient in chronic phase or blast crisis, and a polycythaemia vera patient with myeloid metaplasia showed significant morphologic differentiation from immature to mature granulocytes in control chambers with no additional effect of daily irradiation. Marrow specimens from 2 AML patients exposed to each of 3 daily dose fractions over 14 d revealed a dose-dependent decrease in immature granulocytes with no persistent increase in mature granulocytes. In both irradiated and control chambers, macrophages increased over 21 d. Thus, cells from patients with myeloproliferative disorders may not necessarily differentiate to mature granulocytes following in vivo exposure to ionizing irradiation.
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PMID:The effect of daily low dose gamma irradiation on growth and differentiation of human myeloid leukaemic bone marrow in diffusion chambers. 695 39

Studies during the past five decades have failed to demonstrate myelogenous leukemia in laboratory animals exposed to benzene despite epidemiologic evidence linking such exposure to myelogenous leukemia in man. We report four cases of myeloproliferative disease among rodents exposed to benzene, 6 h a day, 5 days weekly, for life. There was one case of chronic myelogenous leukemia, one of acute myeloblastic leukemia, and one of granulocytic hyperplasia among 40 CD-1 mice exposed to 300 ppm benzene; and one case of chronic myelogenous leukemia among 40 rats exposed to 100 ppm benzene. Although not statistically significant as compared to the respective control groups, the fact that myelogenous leukemia has not been reported in control animals of these two strains is suggestive of a causative role for benzene.
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PMID:Myelogenous leukemia in rodents inhaling benzene. 695 83

Monosomy 7 is frequent in acute myeloid leukaemia (AML) and in preleukaemic dysmyelopoietic syndromes but often it is not the only chromosome anomaly associated with these conditions. We report 14 patients with "pure" monosomy 7 and their clinical and haematological data are analysed in order to clarify the possible implications of this chromosome anomaly. The following points are considered: 1) In spite of the apparent variability of clinical forms in which monosomy 7 is found, several characteristics are common to all monosomy 7 patients, i.e. the presence of a preleukaemic phase and blood and marrow features suggesting the early involvement in the disease of all marrow cell lines. The different diagnoses associated with monosomy 7 are correlated with different steps of a unique myeloproliferative disease whose typical course can be reconstructed. 2) Monosomy 7 has a negative prognostic value. When it is found in a preleukaemic disorder it indicates a high risk of progression to AML, while in AML it implies recurrent infections, poor response to therapy and short survival. 3) The significance of the lack of Colton blood group antigens in monosomy 7 patients is discussed, with particular regard to the fact that the patients in whom this lack was found are the only ones who had not received transfusions in the months before the tests were done. 4) The finding of defective neutrophil chemotaxis in monosomy 7 patients is confirmed and the clinical importance of this fact is emphasized. 5) The data on the 14 patients support the opinion that AML, in general, is heterogeneous in origin. It is postulated that monosomy 7 is a marker of a specific pathogenetic pathway of AML, which implies the beginning of the malignancy in a pluripotent stem cell.
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PMID:Pathogenetic significance of "pure" monosomy 7 in myeloproliferative disorders. Analysis of 14 cases. 696 Oct 98

Granulocytic sarcoma is an uncommon tumor composed of granulocytic precursor cells. Because it occurs in a variety of clinical settings and because the tumor cells are primitive it is frequently unrecognized during life. This presentation details the authors' experience with 61 biopsy-proven granulocytic sarcomas. The patient age range was from 2 to 81 years (mean 48 years). In eight patients the tumors were multiple. Most common sites of involvement were bone, periosteum, soft tissue, lymph node and skin. Twenty-two tumors occurred in 15 patients with no known disease, 26 occurred in 24 patients with a known myeloproliferative disorder, and 13 occurred in 11 patients with proven acute myeloid leukemia. Thirteen of the 15 patients with no known disease developed acute leukemia in from one to 49 months after the biopsy of their tumors (mean 10 months). Most tumors occurring in patients with a known myeloproliferative disorder were associated with blast crisis. The authors' cases displayed a morphologic range from well-differentiated to those tumors that displayed virtually no evidence of differentiation by conventional microscopy. It was therefore not surprising that most tumors were originally diagnosed as lymphoma. Chloro-acetate esterase (CAE) stains were performed on 56 tumors and 47 were studied with antilysozyme immunoperoxidase technique. Fifty-six of the 57 specimens studied by either technique were positive. Antilysozyme immunoperoxidase stains were particularly useful in confirming the diagnosis.
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PMID:Granulocytic sarcoma: a clinicopathologic study of 61 biopsied cases. 702 56

Membrane extracts of human acute myelogenous leukemia cells were passed over immunoadsorbent columns containing antibodies directed to equivalent preparations of pooled normal peripheral blood leukocytes. This material, when compared to equivalent normal cell preparations on nonreducing polyacrylamide gels, demonstrated the presence of four unique bands, not found in normal cell preparations. With the use of a previously described leukemia-specific heteroantiserum, these bands, after elution, were tested for reactivity with the antiserum. The eluted material containing reactive antigen was used to immunize rabbits. The resulting antiserum showed strong reactivity with myelogenous leukemic cells extracts and none with normal materials. A series of bone marrow samples from patients with a variety of lymphoproliferative and myeloproliferative disorders were tested with this antiserum in the fluorescence-activated cell sorter. In every instance, bone marrow cells from patients with acute myelogenous leukemia and chronic myelogenous leukemia showed strong positive fluorescence with this antiserum. However, no bone marrow cells from patients with lymphoproliferative disorders or patients with other leukemias showed any fluorescence above background with this antiserum.
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PMID:Detection of a tumor-associated antigen on the surface of human myelogenous leukemia cells. 704 42

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

Karyotypes were analyzed from 14 patients with various myeloproliferative disorders who had marrow samples processed directly and cultured in various ways. Eleven patients had acute nonlymphocytic leukemia (ANLL) (seven patients) or a dysmyelopoietic syndrome (four patients). All of these patients were known to have an abnormal karyotype, and in each case, two samples of a bone marrow aspirate were available: one processed directly and another cultured for 24 hr. Five of the 11 patients had essentially the same proportion of abnormal cells in the direct and 24-hr samples; in five other patients, the percentage of aneuploid cells in the sample cultured for 24 hr was higher than that in the direct preparation. A higher percentage of aneuploid cells was observed in the direct preparation in only one case. In three other cases of ANLL, a marrow aspirate was cultured with methotrexate in addition to samples processed directly and after 24-hr culture; only two of these had an abnormal clone in any sample. The results of karyotype analysis differed in these two patients. The proportion of aneuploid cells was substantially higher in the methotrexate culture than in the 24-hr culture in one patient; in the other patient, the 24-hr culture contained aneuploid cells, whereas the methotrexate culture showed none. Three of the 13 aneuploid patients would have been incorrectly classified as being karyotypically normal on the basis of the initial analysis of the direct preparation, since only a single abnormal cell was detected in each case. The karyotypic pattern in untreated patients with ANLL has prognostic significance; therefore, the method of processing marrow aspirates may substantially influence the degree of correlation between the karyotype and survival reported by different laboratories.
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PMID:Methods of processing marrow samples may affect the frequency of detectable aneuploid cells. 733 95

Out of 151 patients with preleukemic syndrome, bone marrow chromosome studies were carried out in 88 during the preleukemic phase and in 10 after blastic transformation. Out of 54 cases studied without banding techniques, 13 (24%) were abnormal, while 17 (50%) out of 34 banded cases showed abnormalities. This highly significant increase in yield of aberrations was not restricted to structural abnormalities. During the preleukemic phase of the disease, only 5 of the abnormal patients had no normal metaphases in their bone marrow. Four types of chromosome aberrations were observed more than once: -Y, +8, del 5q and del F or del 20q. They are all frequently observed in myeloproliferative disorders. After blastic transformation, 15 out of 19 patients were abnormal and the abnormalities were more complex. It seems, therefore, that a qualitative and quantitative difference exists between this group of patients and the published series of patients with ANLL. Small abnormal cell lines with the same chromosome abnormalities as in the bone marrow were observed in PHA-stimulated blood cultures of 9 patients. Unstimulated cultures of the same blood sample did not show any mitosis. It is suggested that small subpopulations of lymphocytes arose from the same pluripotent stem cell as the leukemic myelogenous cells, although there may be other explanations.
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PMID:The preleukemic syndrome. II. Cytogenetic findings. 742 63

Granulocytic sarcoma is rare extramedullary tumor composed of myeloblasts and other granulocytic precursors. The majority of cases have been reported in association with acute myeloid leukemia (AML) or myeloproliferative disorders. Granulocytic sarcoma may occur in patients with myelodysplastic syndromes. Reports are very rare, especially in the brain. We report an unusual case of granulocytic sarcoma of the parenchyma of the brain, occurring in a patient with myelodysplastic syndrome, diagnosed by cerebro-spinal fluid cytology and magnetic resonance imaging brain scan.
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PMID:A case of granulocytic sarcoma of the brain in a patient with myelodysplastic syndrome. 749 77

Research in oncogenetics has led to the identification of two major classes of tumor-associated genes, oncogenes and tumor suppressor genes. In a wide variety of solid tumor types, mutations of both groups of genes have been implicated in the tumorigenic process. In hematologic neoplasms, on the other hand, most attention has focused on illegitimate activation of oncogenes, e.g., deregulation leading to disturbed transcriptional activity and structural rearrangements resulting in hybrid genes. Whether loss or mutational inactivation of tumor suppressor genes also plays an essential role in the genesis of tumors of the hematopoietic system has received less attention. Because such inactivation can be the result of karyotypically detectable loss of chromosomal material, cytogenetic studies may prove helpful in pinpointing genomic sites that harbor tumor suppressor genes. The present study is based on a total of 12,473 cytogenetically abnormal hematologic neoplasms reported in the literature to date. Among these, we selected the 6,422 cases with sole clonal chromosomal abnormalities in order to include only aberrations of importance in the genesis, rather than in the progression, of these neoplasms. All tumors with monosomies or structural abnormalities resulting in loss of chromosomal material were compiled, and for every such structural aberration, i.e., deletion, unbalanced translocation, isochromosome, and ring chromosome, the chromosome bands lost were ascertained. This cytogenetic deletion mapping revealed that the most commonly lost chromosomes were Y and 7 in acute myeloid leukemia (AML), myelodysplastic syndromes (MDS), and chronic myeloproliferative disorders (MPD); X, Y, 7, 20, and 21 in acute lymphocytic leukemia (ALL); X, Y, and 17 in chronic lymphoproliferative disorders (LPD); and X and Y in non-Hodgkin's lymphoma (NHL). Chromosome segments/bands lost due to unbalanced structural abnormalities in at least 5% of the cases were 5q13-33, 7q22-36, 9q13-31, 11q23-25, 12p12-13, 17p11-13, and 20q11-13 in AML; 5q13-35 and 20q11-13 in MDS; 5q22-23, 7q22, 13q12-22, 17p11-13, and 20q11-13 in MPD; 6q15-27, 9p11-24, 12p12-13, and 19p13 in ALL; 6q16-27, 11q21-25, 13q13-14, and 14q32 in LPD; and 6q21-27, 11q13-25, and 14q24-32 in NHL. Based on these findings, three conclusions can be drawn. First, there is no good correspondence between total and partial monosomies, the only exception being -7 and 7q-, both of which are common in myeloid neoplasms. This indicates different pathogenetic effects of total and partial losses.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Cytogenetic deletion maps of hematologic neoplasms: circumstantial evidence for tumor suppressor loci. 751 63


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