Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0023473 (chronic myeloid leukemia)
 18,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Seven cases of miliary tuberculosis in patients with hematologic disease were analyzed clinicopathologically. Mean age of the patients was 65 years, and the hematologic diseases were CML, AML, ALL, MDS and malignant lymphoma. Diabetes mellitus was present as a complication in three patients. Miliary tuberculosis was found in 5 cases during the first admission to our hospital owing to hematologic problems. In 4 of 6 cases, fever had started more than two months before admission, consequently, the tuberculosis probably began about that time. After admission, chemotherapy was administered in 5 cases, and steroid in 6 cases for hematologic disease. The mean total quantity of steroid administered was 2,134 mg of prednisolone and average treatment duration was 69 days. The chest roentgenographic shadow was so atypical that miliary tuberculosis was suspected in only one case. The initial chest roentgenogram showed hilar and mediastinal lymph node swelling as well as the shadow of pulmonary tuberculosis in two cases. It was thought that the hilar and mediastinal lymph node swelling could be explained by primary complex, although the patients were of advanced age, or by "secondary complex" reported by Terplan, K in 1940. The diagnosis of tuberculosis was made in two patients before their death by smear of aspirated fluid of cervical lymph node and by bone marrow cell block in one patients, and by pathological examination of mediastinal lymph node biopsy in the other patients. Tubercles were found from bone marrow cell block in 2 out of 5 patients and from bone marrow biopsy in 1 out of 3 patients, but the positive results were reported in 2 patients following death. Smears of sputum, gastric juice, urine, spinal fluid and pleural effusion were negative in all cases. One patient diagnosed as miliary tuberculosis also had pneumocystis carinii pneumonia. This case was treated with antituberculosis drugs for 20 days without improvement. Another patient diagnosed as miliary tuberculosis improved under treatment with antituberculosis drugs, but died of cytomegalovirus pneumonia. Autopsy in 5 cases revealed non-reactive miliary tuberculosis, and pulmonary hemorrhage probably due to DIC was present as a complication in two cases. In these cases, severe immunosuppression, which is a major precipitating factor of miliary tuberculosis, is thought to be induced by hematologic disease itself, chemotherapy, steroid or other underlying disease such as diabetes mellitus. Miliary tuberculosis in such compromised host is cryptic and progresses rapidly. Consequently, early diagnosis is very important. Retrospectively, the unexplained pyrexia was most important to suspect tuberculosis.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Clinicopathological study of miliary tuberculosis in patients with hematologic disease]. 237 32

Using the megakaryocytic leukemia cell lines, K-562 and CMK established from a Down's patient with acute megakaryoblastic leukemia, we studied the changes of antigen expression, cytosolic Ca2+ mobilization, thromboxane (TX) A2 formation and gene expression during megakaryocyte differentiation. We found that thrombospondin synthesis and platelet factor (PF)-4 gene expression were specific for mature megakaryoblasts, whereas collagen unresponsiveness and prostaglandin E1-induced Ca2+ mobilization were noted in immature megakaryoblasts alone. This experiment shows that functional and genetic analysis are useful for characterizing the leukemic megakaryoblastic cells. We analyzed the clinical, hematologic and genetic features of 4 patients with M7, and acute megakaryoblastic transformation of CML, MDS and essential thrombocythemia. In two patients, prednisolone and 6-MP were effective in cytoreduction. In 3 patients with increased platelet counts, normal CFU-Meg formation, the megakaryoblasts with platelet production, or the coexistence of immature megakaryoblasts with mature megakaryocytes were observed, thus indicating that some megakaryoblastic leukemia cells still have the capacity of differentiation. One patient had megakaryoblastic cells with PF-4 gene expression. These clinical findings suggest that the megakaryoblastic leukemia could not be characterized as usual leukemia and a more sensitive marker is required to differentiate leukemic megakaryoblasts from normal megakaryoblasts.
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PMID:[Megakaryocytic leukemia cell lines and megakaryocytic leukemia]. 238 Oct 77

The expression of the multidrug resistance (mdr) phenotype is connected with the overexpression of the P-glycoprotein. By applying the immunocytochemical assay, we have demonstrated that in myeloproliferative diseases (AML, ALL, MDS, CGL) in single cases in smear preparations from the peripheral blood as well as from the bone marrow P-glycoprotein-positive cells, respectively, cells with mdr-positive phenotype can be detected in the material obtained from patients before therapy and without clinically and anamnestically known exposure to cytotoxic or immunosuppressive drugs. In the control group of probands without hematologic disorders and also without clinically or anamnestically confirmed contact with cytotoxic or immunosuppressive drugs, we have found P-glycoprotein-positive subpopulations of cells with positive mdr phenotype in a few cases as well. The uniqueness of our results lies in the fact that this finding demonstrates the presence of subpopulations of mdr-positive cells in leukemias and myelodysplastic syndromes before therapy, and furthermore makes evident that a positive mdr phenotype is not necessarily associated with a malignant phenotype or a malignant cell transformation.
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PMID:Detection of cells with multidrug-resistant phenotype in myeloproliferative disorders before therapy. 257 Jul 76

A total of 165 patients were entered into this study and 140 were evaluate for effects and 165 for toxicities. Of 39 patients with chronic myelogenous leukemia (CML) 21 achieved complete remission (CR), 6 achieved partial remission (PR) with a response rate of 69.2%. In MDS, of 11 patients with chronic myelomonocytic leukemia (CMMoL), one good partial response and 4 partial response were observed (CR + PR:45.5%); of 14 patients with RAEB, one complete response, 4 partial response (CR + PR: 35.7%); of 11 patients with RAEB in T, 3 partial response were observed (response rate: 27.3%). Of 13 patients with polycythemia vera, 4 excellent effect and 7 moderate effect (84.6%) were observed. Seven of 30 patients with acute myelocytic leukemia achieved partial response (23.3%). Mean dosages of SM-108 until remission were 400-500 mg/m2/day on CMMoL, RAEB in MDS, polycythemia vera and CML, and 600-800 mg/m2/day on RAEB in T and AML. In the analysis of adverse effects of SM-108, a subjective side effects including mainly gastrointestinal toxicities were observed in 38 cases (23.0%) of the patients : 26 patients (15.8%) showed objective side effects including liver dysfunction, but these symptoms were transient and not serious. Our study indicates that SM-108 is useful agent against MDS, especially CMMoL, RAEB, RAEB in T, polycythemia vera and CML.
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PMID:[Phase II study of SM-108 (4-carbamoylimidazolium-5-olate) in hematological malignancies]. 264 92

Evaluation of anti-HLA antibody (HLA-Ab) by lymphocytotoxicity test (LCT) was reviewed in 69 patients with hematopoietic diseases. Twenty-five (36.2%) of these 69 patients developed HLA-Ab at some time during their treatment course. In patient characteristics, eleven of 32 patients with ANLL (34.4%), one of ten patients with ALL (10%), four of nine patients with CML-BC (44.4%), six of seven patients with AA (85.7%), two of four patients with MDS (50%), and one of seven patients with other types (14.3%), who had random-donor transfusion, developed HLA-Ab. Transfused leukocytes count during two months from initial transfusion were compared between LCT positive group and LCT negative group. There were no significant differences between leukocytes count (13.8 x 10(9] of LCT positive group and that (14.2 x 10(9] of LCT negative group. As the result, we can enumerate the following factors, which are important to develop HLA-Ab. The HLA phenotype and immunity of patients may have a more important role than total transfusion volume. The longterm and continuous transfusion may increase the possibility to develop HLA-Ab. The transfusion purging leukocytes may diminish the occasions of alloimmunization. HLA-matched platelet transfusions were best against the patients who developed HLA-Ab and became refractory to platelet transfusion.
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PMID:[Measurement of anti-HLA antibody by lymphocytotoxicity test in patients with hematopoietic diseases]. 279 92

This thesis is a survey of nine previously published articles on MPO deficient PMN. The incidences in leukaemia and allied disorders of the presence of this abnormal subpopulation of mature neutrophils and the relationship to clinical course in AML, susceptibility to infections in AML, FAB classification in AML and MDS, cytogenetically defined aberrations in MDS and morphometrical characteristics were investigated. The aims of the studies were to examine the diagnostic as well as the prognostic value of the parameter, to examine the usefulness of the parameter as an predictive indicator of CR and relapse in AML and to examine the concept that MPO deficient PMN may originate from leukaemic precursors. MPO deficient PMN were found to occur in a minor number (less than 4% of the total number of PMN) in normal humans and the incidences of an abnormal number (greater than 4%) were found to be about 40% in AML (I, II, III, IV, VIII), 60% in CML (I, VII), 30% in MPD other than CML (VII) and 30% in MDS (V). The highest incidences in AML were found in the FAB subtypes possessing the most myeloid differentiation potential i.e. FAB M2 and FAB M4 (IV). In ALL, CLL, HCL, Hodgkin's disease, anaemia not related to leukaemia and leukaemoid reactions the incidences all were 0% (I, unpublished data). The abnormal MPO deficient PMN subpopulation, if present, disappeared when CR was achieved and reappeared when relapse eventually was developed (II, VIII). In both situations serial determinations showed that the change occurred before the usual routine blood examinations predicted CR and relapse; several days and several months prior, respectively (VIII). The probability of obtaining CR was lower in the AML patients with the abnormal subpopulation and the risk of developing relapse higher than in AML patients without the anomaly (II, VIII). These differences were not statistically significant, however. AML patients, showing an increased number of MPO deficient PMN, revealed a statistically significant increased susceptibility to infections (P less than 0.01) during the preremission phase accounting for 18% to 67% of the total number of infections in this period (III). This increase was positively correlated to the extent of the anomaly (P less than 0.002). The spontaneous occurrence of a subpopulation of MPO deficient PMN in MDS went together with a simultaneous progression in cytogenetically determined clonal chromosomal aberrations and were related to progression in FAB subtype as well (VI). Morphometrically MPO deficient PMN were characterized by a decreased total cell size and an increased nucleus size of the projected images (IX).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Myeloperoxidase deficient polymorphonuclear leucocytes in leukaemia and allied disorders. 285 15

We treated 11 patients who had Philadelphia-chromosome-positive chronic myelogenous leukemia with natural interferon alpha (human lymphoblastoid interferon; HLBI). HLBI was given at 6-12 X 10(6) u/day i.m. or i.s.c. during induction therapy. Nine patients responded to the treatment, of whom 7 had hematologic remission and 2 had partial remission. Six patients with MDS or hypoplastic leukemia, and 3 patients with overt leukemia from MDS were treated with recombinant interferon gamma (GI-3). GI-3 was given at 0.4 X 10(6) u/m2 of body-surface area per day i.s.c. or i.v. for 4-6 weeks. In 2 patients with RAEB and hypoplastic leukemia, the blast cell count in bone marrow decreased from 8-16% to 2-3% after 4 weeks of administration. In another patient with hypoplastic leukemia, blast cells in the marrow did not decrease, but anemia was improved without transfusion, increasing the bone marrow NCC and erythroblast count. In patients with overt leukemia and CMML, no clinical effect was obtained. Interferons can therefore be offered to patients in a preleukemic state.
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PMID:[Clinical investigation of interferons in the preleukemic state (CML and MDS)]. 313 93

There is compelling evidence that leukemia arises via a multistep process. Molecular analysis of human leukemias, which are typically clonal, commonly shows multiple genetic lesions in a single leukemia including chromosomal translocations, gene amplification, and point mutations, and in several cases the mutational activation of an oncogene and the loss of a tumor suppressor gene have been found in the same leukemic cell. Accumulative evidences suggest that a number of oncogenes and tumor suppressor genes are involved in the hematopoietic tumorigenesis. These mutations can be utilized for molecular diagnosis of human hematopoietic tumors. Among them, detection of chimeric gene generated by chromosomal translocation is especially useful for molecular diagnosis. The t(3;21) (q26;q22) translocation is found usually in blastic crisis of CML and leukemias developed from MDS or hematopoietic proliferative diseases, but never in de novo acute myelocytic leukemia. This raises the possibility that the molecular event underlying the t(3;21) translocation has a critical role in progression from a preleukemic state to a leukemic state. The generation of AML1/EVI-1 chimeric gene has been demonstrated to be consistent in t(3;21)-carrying leukemias. Although target genes remain to be elucidated for both AML1 and EVI-1 as transcription factors, the AML1/EVI-1 fusion protein could work on different set of genes critical to the process of proliferation and differentiation of hematopoietic cells.
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PMID:[Diagnosis of hematological disorders by mutational analysis of oncogenes]. 760 95

The aim of the present study was to evaluate the significance of immunomorphometric assessment of megakaryocyte size and number in normal and pathologic human bone marrow. Thus, we compared morphometric characteristics of megakaryocytes in 56 bone marrow trephine biopsies stained by immunohistochemical and conventional techniques. Morphometric results showed that precise megakaryocyte size in normal and pathologic samples can be calculated even by using conventional staining technique, but only employing specific stereological corrections. Immunomorphometric evaluation revealed populations of "small" megakaryocytes (< 14 microns), "morphologically unrecognized" by conventional staining technique (promegakaryoblasts in normal and stimulated as well as micromegakaryocytes in pathologic bone marrow). In patients with normal and stimulated megakaryocytopoises percentage of "small" megakaryocytes was generally low (10.6% and 14%, respect.); so, megakaryocyte number was similar in immunohistochemically and conventionally stained sections. In contrast, percentages of "small" megakaryocytes were significantly higher in patients with stem cell disorders (namely, myelodisplastic syndrome and chronic granulocytic leukaemia), as compared to controls (35.3% in MDS; 22.9% in CML and 10.6% in controls). In those patients megakaryocyte numbers were more sensitively detected by immunohistochemistry than by conventional staining.
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PMID:[Importance of immunomorphometric evaluation of the size and number of megakaryocytes in normal and pathologic bone marrow]. 771 37

Allogeneic bone marrow transplantation is the treatment of choice for many childhood leukemias. The donor of choice-an HLA matched sibling-is only available about 30% of the time. Unrelated donors are an alternative choice. In this report, we describe the results of unrelated donor bone marrow transplants (BMT) in 50 children with leukemia (25 acute lymphoblastic leukemia [ALL], 3 acute myeloid leukemia [AML], 3 juvenile chronic myelogenous leukemia [JCML], 10 chronic myeloid leukemia [CML]) or myelodysplastic syndrome (MDS; 9). The median age of the 31 male and 19 female patients was 9 years (range 2 to 18). Only 13 patients were serologically matched at HLA-A, B, DR, and DQ with their donors; 6 of these were reactive in mixed lymphocyte culture. The other 37 patients were mismatched for one (36 patients) or more (1 patient) HLA antigens. Pretransplant conditioning included cytosine arabinoside, cyclophosphamide, fractionated total body irradiation (TBI) (with lung, liver, and more recently, kidney shielding), and methylprednisolone. High-risk patients also received busulfan. Graft-versus-host disease (GVHD) prophylaxis consisted of T-cell depletion with IgM monoclonal antibody T10B9 plus complement and posttransplant cyclosporine-A. Forty-nine patients (98%) engrafted. Median times to greater than 500 polymorphonuclear leukocytes (PMN)/microL and greater than 25,000 platelets/microL were 18 and 20 days, respectively. Acute GVHD > or = grade II occurred in 16 patients (33%); 13 (81%) of these died. Chronic GVHD developed in 30 of 40 patients at risk, but was extensive in only 5. Event-free survival (EFS) for all patients was 44% +/- 7% (median follow-up was 49 months), and overall survival was 50 +/- 7%. Patients with low-risk disease (ALL or AML in first or second remission and CML in chronic phase) had a better EFS than children with high-risk disease (60% v 34%, P = .07). There was no significant difference in EFS between patients who were serologically matched with their donors (46%) and those who were partially mismatched (43%) (P = .97). These data compare favorably with published reports for children transplanted with HLA-matched sibling donors and should encourage earlier consideration of unrelated donor BMT in children with leukemia or myelodysplasia.
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PMID:Unrelated bone marrow donor transplants for children with leukemia or myelodysplasia. 772 69


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