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

Normal cross-reacting antigen, a glycoprotein that shares some antigenic determinants with carcinoembryonic antigen, was consistently demonstrated by tissue immunoperoxidase staining in the cytoplasm of both non-neoplastic and neoplastic neutrophilic granulocytes. It was absent in lymphoid cells, but occasional cells of the macrophage/histiocyte series showed variable staining. Malignant cells from patients who had non-Hodgkin or Hodgkin lymphomas were negative for normal cross-reacting antigen. These findings were in contrast to the findings of specific normal cross-reacting antigen positivity in neoplastic granulocytes from three patients who had acute granulocytic leukemia, three who had chronic granulocytic leukemia, and one who had a granulocytic sarcoma. Similar normal cross-reacting antigen positivity was also seen in granulocytes from two patients who had granulocyte dysplasia. It is suggested that direct tissue visualization of normal cross-reacting antigen using immunoperoxidase technics may be of value in the classification and diagnosis of hematologic malignancies, and may provide an additional marker for cells of the granulocytic series.
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PMID:Direct tissue visualization of normal cross-reacting antigen in neoplastic granulocytes. 698 61

We report here two cases of a previously undescribed myeloproliferative disorder. Both were young adult males who presented with generalized lymphadenopathy, splenomegaly, leukocytosis, polycythemia, and persistent thrombocytopenia. The leukocyte alkaline phosphatase (LAP) score was low in both cases, and the bone marrow was hypercellular without dysplasia or fibrosis, but lacked the Philadelphia chromosome, BCR gene rearrangement, or other karyotypic abnormalities. The clinical course was indolent in each case. One patient died from an unusual "blast crisis" after 12 years, while the second patient remains in a complete hematologic remission on hydroxyurea and alpha interferon 4 years from diagnosis. Interestingly, changes in therapy in this patient have consistently resulted in precise and concerted fluctuations in his blood counts, with the red and white cells cycling together and the platelets and mean corpuscular volume (MCV) changing concomitantly but in the opposite direction. This unique myeloproliferative disorder is distinguishable from all previously described forms of chronic myeloid leukemia and other myeloproliferative syndromes.
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PMID:A new myeloproliferative syndrome. 786 27

We have reviewed our experience with four of the entities that are included under the generic term chronic myeloid leukaemia (CML), namely the classic Ph+ CGL, both BCR+ and BCR-, aCML and CMML. We have developed a statistical model that confirms that CGL, aCML and CMML can be distinguished from each other with reasonable success employing five quantitative parameters (WBC, percentage immature granulocytes, percentage monocytes, percentage basophils, percentage erythroid precursors in bone marrow) and one qualitative parameter (granulocytic dysplasia). It is hoped that these detailed recommendations will enable investigators to improve their diagnostic accuracy. This should permit more uniform comparisons of molecular biologic and clinical studies.
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PMID:The chronic myeloid leukaemias: guidelines for distinguishing chronic granulocytic, atypical chronic myeloid, and chronic myelomonocytic leukaemia. Proposals by the French-American-British Cooperative Leukaemia Group. 787

Chronic myelomonocytic leukaemia (CMML), a disorder belonging to the group of myelodysplastic syndromes, has a number of peculiar features which raise the question as to whether it should be considered a distinct entity in its own right. The problems associated with its classification and diagnosis are discussed in this report using all currently available tools from clinical data to molecular genetics, including morphology, histology, cellular biology and cytogenetics. Three groups of patients can be identified (isolated monocytosis with a mild degree of dysplasia, severe cytopenia and the most frequent type with proliferative symptoms dominating the clinical picture). The latter group is close to atypical chronic myeloid leukaemia and perhaps these two entities should be regarded as a single one. Classification of the disease is further complicated by the possibility of evolution from one subgroup into another one and by the finding that CMML can also arise as a disorder secondary to other myeloproliferative (MPS) or myelodysplastic (MDS) syndromes. No specific marker of the disease has been identified by cytogenetics or molecular biology. Due to all these facts, we believe that CMML should perhaps be viewed more pragmatically by considering the use of prognostic factors that could at least help to define different groups of patients who may require different therapeutic strategies. We conclude that CMML is a heterogeneous syndrome with features of both MPS and MDS, encompassing primary and secondary stem cell disorders and varying widely in its clinical presentation. This heterogeneity should stimulate the search for reliable predictors of evolution which would allow a better definition of CMML subtypes based on prognostic factors.
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PMID:Chronic myelomonocytic leukaemia (CMML)--a myelodysplastic or myeloproliferative syndrome? 847 99

We have identified a new recurrent reciprocal translocation between chromosome 3 and 12 with breakpoints at bands 3q26 and 12p13, t(3;12)(q26;p13) in the malignant cells from five patients with acute transformation of myelodysplastic syndrome or blast crisis of chronic myelogenous leukemia. t(3;12)(q26;p13) appears as a rare but nonrandom event present in various myeloid leukemia subtypes, which is frequently associated with dysplasia of megakaryocytes, multilineage involvement, short duration of any blastic phase, and a very poor prognosis. Here, we report the molecular cytogenetic analysis of the t(3;12). Fluorescence in situ hybridization results indicate that the 3q26 breakpoints are quite heterogeneous and occur 5' of MDS1, 3' of EVI1, or between MDS1 and EVI1. Our results are very similar to those observed in other 3q26 rearrangements in which breakpoints were shown to occur over considerable distances 5' and 3' of EVI1. Fluorescence in situ hybridization investigations proved that, in three myelodysplastic syndrome cases with t(3;12)(q26;p13), the 12p 13 breakpoint occurred within the TEL gene.
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PMID:Fluorescence in situ hybridization analysis of t(3; 12)(q26; p13): a recurring chromosomal abnormality involving the TEL gene (ETV6) in myelodysplastic syndromes. 869 16

The CD56 antigen is normally expressed on natural-killer cells but has additionally been shown to be present on a variety of hematologic malignancies, including a subset of acute myelogenous leukemia (AML). There is disagreement, however, about its prognostic significance and its association with specific cytogenetic abnormalities. All clinical samples from June 1994, through September 1995, with increased myeloblasts were analyzed by multiparameter flow cytometry for anomalous expression of CD56. Patients with CD56+ blast cells were selected, and morphologic review was performed. Clinical information was obtained, and cytogenetic data were reviewed. Southern blot analysis to detect rearrangement of the mixed lineage leukemia (MLL) gene was performed when possible. The samples from 23 of 114 patients studied demonstrated anomalous expression of CD56 on myeloblasts, including patients with AML, myelodysplastic syndromes (MDS), and chronic myelogenous leukemia in blast crisis. The samples from 10 of 15 patients with CD56+ AML demonstrated at least partial monocytic differentiation. Dysplastic features were displayed in the samples of 12 patients. Correlation with specific cytogenetic abnormalities was not found. The MLL gene was rearranged in five of 18 patients. Seventeen patients have died, with a median survival of 4.6 months for patients with AML. Three have sustained a complete remission. One has findings of high-grade myelodysplastic syndrome. Two were unavailable for follow-up. Expression of CD56 was found in 20% of patients with increased myeloblasts, including patients with high-grade MDS, chronic myelogenous leukemia in blast crisis, and AML. This phenotype was associated with dysplasia, monocytic differentiation, and rearrangement of the MLL gene.
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PMID:Neural cell adhesion molecule (CD56)-positive acute myelogenous leukemia and myelodysplastic and myeloproliferative syndromes. 916 61

We have identified ten patients with acute myeloid leukemia (AML) and one patient with chronic myeloid leukemia with megakaryocytic crisis who displayed an inv(3)(q21q26). Seven of them had an additional monosomy 7. Most of them had a myelodysplastic syndrome (MDS) preceding AML, normal or increased platelet counts, increased number of megakaryocyte, megakaryocytic dysplasia, and erythroid dysplasia. There was a high incidence of resistance to induction chemotherapy, short remission time, and early relapse. Seven patients were immunologically analyzed. The main immunophenotypes were as follow: CD7+, CD34+, HLA-DR+, CD38+, CD13+, CD33+, CDw65+, CD2-, CD3-, CD4-, CD8-, CD19+, CD20-, CD11b-. Our results suggest that the leukemia with inv(3)(q21q26) represents a new cytogenetic-clinicopathologic subtype, characterized by 1) abnormal megakaryopoiesis and multiple hematopoietic lineage involvement; 2) an antecedent MDS; 3) poor response to conventional chemotherapy; and 4) expression of CD7, CD34, CD38, HLA-DR, CD13, and CD33 antigens. We propose that the malignant transformation in patients with inv(3)(q21q26) occurs in an early stem cell prior to lineage commitment.
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PMID:Chromosomal abnormality inv(3)(q21q26) associated with multilineage hematopoietic progenitor cells in hematopoietic malignancies. 920 72

The axl tyrosine kinase receptor is aberrantly expressed on myeloid cells of many individuals afflicted with chronic myelogenous leukemia (CML) and other myeloid leukemias. Although previous studies demonstrated this kinase to have oncogenic potential, it is not known whether axl actively participates in the onset and/or progression of CML. We addressed this question by generating transgenic mice possessing constitutive ectopic expression of human axl throughout cells of the myeloid hematopoietic lineage through the use of the granulocyte colony-stimulating factor (GCSF) receptor promoter. The transgenics did not exhibit hematopoietic malignancies, but did exhibit phenotypic characteristics associated with noninsulin-dependent diabetes mellitus (NIDDM) including hyperglycemia and hyperinsulinemia, severe insulin resistance, progressive obesity, hepatic lipidosis, and pancreatic islet dysplasia. The obese-diabetes phenotype was similar to that observed in the agouti and melanocortin-4(-/-) mutants, however the axl transgenics were not hyperphagic. Axl transgenic animals expressed elevated serum tumor necrosis factor (TNF)-alpha levels that were further enhanced upon in vitro lipopolysaccharide (LPS) stimulation of peripheral blood. Administration of the axl ligand, gas6, to peripheral transgenic blood samples eliminated excessive TNF-alpha production in response to LPS stimulation. As a means to better understand axl-gas6 biology, transgenic animals were produced which systemically expressed the gas6-binding axl proteolytic cleavage product. A more severe NIDDM phenotype occurred in these mice. The observed phenotypes may be related to the axl receptor or proteolytic cleavage product competing with related axl family receptors for binding of the gas6 ligand. We conclude that axl expression in myeloid cells in itself does not lead to the onset or progression of leukemia and suggest that ectopic axl expression affects endogenous modulation of TNF-alpha production indirectly resulting in the NIDDM phenotype.
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PMID:Noninsulin-dependent diabetes mellitus occurs in mice ectopically expressing the human Axl tyrosine kinase receptor. 1052 29

Chronic myeloid disorders (CMD) are collectively characterized by monoclonal myeloproliferation that involves multiple lineages, retains a variable degree of cellular maturation, and has the potential to undergo clonal evolution. However, monoclonal hematopoiesis is neither essential nor specific to CMD. Morphologic and cytogenetic characteristics allow a working classification of these disorders that is clinically useful. There are four major divisions: chronic myeloid leukemia (CML), which is easily identified by the presence of the Philadelphia chromosome (or its molecular equivalent); the myelodysplastic syndromes (MDS), which are characterized by trilineage dysplasia; chronic myeloproliferative diseases (CMPD), which include essential thrombocythemia, polycythemia vera, and agnogenic myeloid metaplasia (AMM); and atypical CMD, which includes chronic neutrophilic leukemia, chronic eosinophilic leukemia, mast cell disease, and myeloid processes that display overlapping features of MDS and CMPD (hybrid CMD). In CMPD, a diagnosis of polycythemia vera requires evidence of an erythropoietin-independent increase in red blood cell mass; the diagnosis of both AMM and essential thrombocythemia requires the exclusion of reactive causes of bone marrow fibrosis and thrombocytosis, respectively. In addition, the Philadelphia chromosome, increased red blood cell mass, and dyserythropoiesis should also be absent. Semin Hematol 38(suppl 2):1-4.
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PMID:Chronic myeloid disorders: Classification and treatment overview. 1124 95

Certain chemotherapeutic agents can induce bizarre epithelial atypia. The lower respiratory tract is a frequently targeted site, but similar changes have not been described adequately in the sinonasal tract. Unfamiliarity with these changes could potentially cause confusion with an infectious or neoplastic process. All biopsies of the sinonasal tract at The Johns Hopkins Hospital were reviewed prospectively over a 54-month period. Eleven cases with bizarre atypia of the respiratory epithelium formed the basis of this study. The medical records of these patients were reviewed. The specimens were from 11 patients who had previously undergone chemotherapy and bone marrow transplantation for acute myelocytic leukemia (n = 5), multiple myeloma (n = 3), acute lymphocytic leukemia (n = 2), and chronic myelocytic leukemia (n = 1). Although the chemotherapy regimens were highly variable, all included one or more of the alkylating agents (cyclophosphamide, n = 11; busulfan, n = 5; melphalan, n = 1). In all 11 patients, biopsies were acquired to rule out invasive fungal sinusitis. The atypical epithelial changes included striking nuclear enlargement, hyperchromasia, and pleomorphism. Sometimes these changes were full thickness and were associated with squamous metaplasia. Two of eight cases evaluated by frozen section were misinterpreted initially as high-grade epithelial dysplasia. Certain chemotherapeutic agents can induce striking epithelial atypia in the sinonasal tract. These changes should not be interpreted as neoplastic in nature, a potential pitfall in the frozen section evaluation of a destructive nasal process in oncology patients.
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PMID:Bizarre epithelial atypia of the sinonasal tract after chemotherapy. 1134 78


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