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)

The technical performances of the Coulter S+II counter was evaluated for lymphocyte counts and the data obtained were compared to those supplied by the ELT 800 analyzer to the results for manual and Hemalog D counting methods. We assessed accuracy of three types of information supplied by the S+II model in the following conditions: erythrocyte indices in anemia, white cell histograms in chronic myeloid leukemia, chronic lymphoid leukemia, acute leukemia and eosinophilia, and the reliability of the analyzer in showing the degree of thrombopenia and hyperthrombocytosis.
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PMID:[Evaluation of the performance of Coulter S+II]. 670 97

Clinical and laboratory findings at the time of diagnosis were correlated with the survival of 242 patients with chronic myelocytic leukemia. Twelve patients with the blastic stage of the disease (blasts greater than or equal to 29%) had a median survival of eight months. Of the nonblastic patients, 28 without the Philadelphia chromosome had a relatively constant mortality averaging 43% per year and a median survival of 13 months, markedly worse than the Ph1-positive group (mortality, 6% in the first year, 17% in the second year, and the 25% per year, with a median survival of 43 months; P less than 0.001). In the latter group of 202 patients, features reflecting the "quantity" of leukemia (leukocyte count, marrow cellularity, and M:E serum B12, different degrees of splenomegaly, presence or absence of symptoms) had weaker or short-term correlations with mortality, while "qualitative" abnormalities (e.g., increased percentage of circulating blast, extramedullary leukemic tumors, major abnormalities of erythropoiesis or platelet production, marked basophilia or eosinophilia) had strong and persistent correlations with mortality. Chromosome abnormalities in addition to the Ph appeared to have a delayed though significant effect on survival. Serum alkaline phosphatase and SGOT levels did not correlate significantly with survival, but major elevations of serum LDH were associated with increased mortality throughout the course of the disease.
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PMID:Prognostic features at diagnosis of chronic myelocytic leukemia. 694 41

Increased numbers of bone marrow mast cells were found in 45 (2.2%) of 2,000 bone marrow specimens obtained from patients who had hematologic disorders. Mast cells were most frequently seen in the marrows of patients who had preleukemic syndromes, lymphoproliferative disorders, and acute leukemia. The 16 patients who had preleukemic syndromes included those with refractory sideroblastic and megaloblastic anemia (with or without an excess of blasts), idiopathic pancytopenia or pure erythrocytic aplasia, paroxysmal nocturnal hemoglobinuria, idiopathic refractory neutropenia, agranulocytosis or thrombocytopenia, and persistent eosinophilia. Five of the seven patients who had acute leukemia had nonlymphoblastic leukemia; two had blastic crisis of chronic granulocytic leukemia. Of the 13 patients who had lymphoproliferative disorders, eight had chronic lymphocytic leukemia, three had macroglobulinemia, and two had non-Hodgkin's lymphoma. Three patients who had chronic renal failure associated with severe anemia and two who had chronic liver disease, splenomegaly, or hypersplenism were also encountered. In this study there appeared to be a consistent relationship between the presence of increased numbers of mast cells and the lymphocyte and plasma cell counts in the bone marrow. The significance of the presence of secondary mastocytosis in premalignant lesions, neoplasia, and, in particular, lympho- and myeloproliferative disorders, is still unclear.
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PMID:Increased bone marrow mast cells in preleukemic syndromes, acute leukemia, and lymphoproliferative disorders. 745 27

A patient with chronic myeloid leukaemia developed bone marrow granulomas during treatment with interferon alpha-2b. Some granulomas had necrotic centres and giant cells and there was marked eosinophilia surrounding them. The granulomas disappeared when the interferon treatment was discontinued. Mycobacteriosis was ruled out. The most likely explanation for the granuloma formation was drug hypersensitivity.
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PMID:Granulomatous bone marrow inflammation during treatment of chronic myeloid leukaemia with interferon alpha-2b. 749 Mar 29

Analysis of most hematologic neoplasms indicates the involvement of one or more cell lineages in the bone marrow and/or the blood but rules out the involvement of all lineages in any one neoplasm. It is important to detect lineage involvement in order to clarify which stem cells are involved in leukemia, to predict prognosis, and to select appropriate treatment. Our aim was to study the cell lineage involvement of some of the recurrent chromosomal abnormalities seen in hematological neoplasms. The direct morphology-antibody-chromosomes (MAC) method was used. The deletion 20q in myeloproliferative diseases (MPD), the deletion of 5q and t(1;7) in myelodysplastic syndromes (MDS), and t(3;3) in acute myeloid leukemia subtype M7 (AML-M7) were seen in all or at least in two myeloid lineages. These were interpreted as stem cell abnormalities. Deletion 13q in MPD, t(8;21) in AML-M2 and t(15;17) in AML-M3 were seen in granulocytic lineages only; t(14;18) in non-Hodgkin's lymphoma and trisomy 12 as the sole abnormality in chronic lymphocytic leukemia (B-CLL) were seen only in immunoglobulin light chain clonal B cells; inversion 14 in T-CLL was seen only in T cells, whereas t(15;14) in acute lymphocytic leukemia with eosinophilia (ALL-EO) was seen in lymphoid stem cells but not in mature granulocytes or lymphocytes. Additional abnormalities (in addition to the Philadelphia chromosome) in chronic myeloid leukemia (CML) were seen in all myeloid cell lineages and also in mature granulocytes, B cells, and large granular lymphocytes. Abnormalities in Hodgkin's disease were restricted to CD30-positive Reed-Sternberg cells. Trisomy 8 and monosomy 7 are abnormalities that may be present in either stem cells or any of the single cell lineages.
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PMID:Cell lineage involvement of recurrent chromosomal abnormalities in hematologic neoplasms. 752 Feb 72

We describe a patient with acute nonlymphocytic leukemia (ANLL) and isochromosome 17q as the sole cytogenetic abnormality. ANNL with i(17q) may represent a distinct entity with certain clinical features, such as male sex, hepatosplenomegaly, and characteristic findings in bone marrow (BM) cytology, including hypercellularity, marked basophilia and eosinophilia, and massive increase in abnormal megakaryocytes. Molecular studies of peripheral blood (PB) cells of our patient, by polymerase chain reaction (PCR) analysis, showed expression of the GCSF gene, which is located on 17q. Southern blots hybridized with a GCSF probe showed no rearrangement of this gene as has been described in some patients with i(17q) positive chronic myeloid leukemia (CML).
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PMID:GCSF gene is expressed but not rearranged in a patient with isochromosome 17q positive acute nonlymphocytic leukemia. 768 96

Cytogenetic analysis of bone marrow cells from a patient with anemia, marked leukocytosis with eosinophilia, and thrombocytopenia showed monosomy 7 in all metaphases examined. The patient has refractory anemia (RA) according to FAB classification. Because of the hypereosinophilia of the patient, PCR technique was performed and no bcr-abl mRNA, specific for chronic myelogenous leukemia, was detected. Monosomy 7 has not been previously described in cases with hypereosinophilia. We assume, according to previous reports, that multiple genetic lesions can be involved in the pathogenesis of hypereosinophilia in this patient.
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PMID:Hypereosinophilia associated with monosomy 7. 769 37

An 82-year-old female was diagnosed as having 5q- syndrome accompanied by basophilia, eosinophilia and thrombocytosis. Since cytogenetic abnormalities other than 5q- were also detected, she was considered to be type B of 5q- syndrome. According to the FAB classification a diagnosis of refractory anemia with excess of blasts (RAEB) was made. She was treated with recombinant interferon alpha 2b, because peripheral blood findings resembled those of chronic myelogenous leukemia. Interferon was effective, and resulted in disappearance of peripheral blasts, normalization of platelet numbers, and improvement of basophilia. These changes were interferon-dependent. After 1 year, cytogenetic studies revealed that about 2/3 of metaphases showed normal karyotype. Twenty months after diagnosis, myeloid blastic crisis occurred and eventually the patient died. However, treatment with interferon in this case might support the usefulness of the drugs for this kind of disease.
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PMID:[Hematologic improvement by alpha-interferon in a case of the 5q- syndrome with basophilia and eosinophilia]. 771 73

The safety, tolerance, and clinical effects of combined therapy with recombinant interferon-alpha (IFN-alpha) and interleukin-2 (rIL-2) administered subcutaneously for 2 courses of 4 weeks each, with 4 weeks interval between courses, given as outpatient therapy have been assessed in 10 patients with Philadelphia chromosome (Ph1)-positive chronic myelogenous leukemia (CML). All patients were previously treated with conventional chemotherapy and 3 failed to respond to IFN-alpha administered prior to our study. Median duration of disease from diagnosis was 36 months. Seven patients were in first chronic phase and the other 3 were in blast crisis, second chronic phase, and relapse post-bone marrow transplantation (BMT), respectively. Hematological response (median follow-up 16 months) was observed in 9 patients, with a decline in number of white blood cells and platelets. Elimination of Ph1 was observed in the patient who relapsed post-BMT with complete elimination bcr/abl RNA by polymerase chain reaction. Rebound lymphocytosis and eosinophilia were observed in most of the patients. Toxicity was acceptable. The main adverse effects were fever, chills, fatigue, anorexia, nausea, and vomiting. The side effects were reversible and no interruption of treatment was required. There was no treatment-related hospitalization or deaths. These data suggest that simultaneous subcutaneous IFN-alpha and rIL-2 home therapy is feasible, reasonably well tolerated, and potentially beneficial in CML patients. These observations may have important implications for the treatment of minimal residual disease following allogeneic and autologous marrow transplantation.
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PMID:Treatment of chronic myelogenous leukemia with recombinant human interleukin-2 and interferon-alpha 2a. 792 12

Eosinophil leukaemia is a rare and poorly defined entity characterized by neoplastic proliferation of eosinophil cell line. This form of the hypereosinophilic state is considered to be a variant form of CML, although as a diseases entity is not generally accepted. A history of a patients is reported, whose clinical course is thought to fulfill the requirements of eosinophil leukaemia. On the basis of the initial results (pathological lymphogram, eosinophilia, Ph-negativity) lymphogranulomatosis was suspected and explorative laparotomy was performed. However, only marked eosinophilic infiltration of the spleen was detected. After splenectomy his disease was stable without treatment for six months when his leukocytosis and eosinophilia increased. Despite the administration of hydroxyurea the leukocyte count exceeded 100 x 10(9)/l (eosinophil cells 70%), and the bone marrow revealed massive (80%) eosinophilic infiltration. Neither Ph-chromosome, nor cabl and bcr gen rearrangement were demonstrated, but the expression and amplification of c-myc oncogene indicated disease progression. Interferon therapy produced long-term clinical and haematological improvement, but blastic transformation was developed in the second year of his disease. Autopsy showed multiple organ involvement characteristic of CML, but no marked eosinophilic infiltration was found. The feature of this case suggest that eosinophil leukaemia might represent an uncommon form of Ph-negative CML.
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PMID:[Eosinophilic leukemia: a rare form of Philadelphia chromosome negative chronic myeloid leukemia?]. 805 96


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