Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: KEGG:D03343 (MDS)
 2,225 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Epidemiological studies indicating that exposure to organic solvents is a risk factor for haematological malignancies are reviewed. Exposure to benzene is a risk factor for ANLL. A preleukaemic phase with pancytopenia is common and may be associated with a normo- or hypercellular marrow with morphological characteristics suggesting MDS. There are indications that other organic solvents than benzene may be leukaemogenic. Certain chromosome aberrations are characteristic in leukaemic cells from solvent exposed ANLL patients. The average latency time from start of occupational exposure until diagnosis is about 10-11 years. There is epidemiological evidence that exposure to organic solvents may also increase the risk of lymphoproliferative malignancies, i.e. ALL, NHL, HD and myeloma.
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PMID:Exposure to organic solvents and risk of haematological malignancies. 173 76

This is a review of preleukaemic states in children. In a prospective series of 109 children with AML the overt disease was preceded by MDS in 22 cases. Ten of these patients had Down's syndrome. Advanced FAB groups were represented in the series. An important subgroup is the bone marrow monosomy 7 syndrome. Cytogenetic anomalies are common in MDS, and multiple and complicated abnormalities develop in nearly all patients with progressing disease. Some children die before transformation to overt ANLL. Transformation usually occurs, few children survive. With cytostatic treatment the risk of irreversible aplasia is great. The choice of schedule should therefore be carefully considered. Bone marrow transplantation has proved beneficial in a number of cases, but these are still quite few. The dysfunction of the bone marrow preceding ALL is due to transient aplastic anaemia--spontaneous remission--overt ALL, often FAB type L1, immunophenotype CALLA. The ALL reacts to the same treatment as de novo ALL of the same type and the prognosis is the same.
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PMID:Bone marrow dysfunctions preceding acute leukemia in children: a clinical study. 173 77

The expression of the multidrug resistance (MDR) phenotype is connected with the overexpression of 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 and bone marrow the 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. This finding has demonstrated the presence of subpopulations of MDR-positive cells in leukemias and myelodysplastic syndromes already before therapy, and, furthermore, has evidenced that a positive MDR phenotype is not necessarily associated with a malignant phenotype of a malignant cell transformation.
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PMID:[Detection of cells with phenotype of multiple drug resistance in myeloproliferative disorders before the treatment]. 197 May 42

We studied the activity of serum adenosine deaminase (ADA) and its isozyme in 36 leukemic patients (16 ANLL, 11 ALL, and 9 CML) and 8 MDS. Isozyme was measured by erythro-9-(2-hydroxy-3-nonyl) adenine (EHNA) inhibitory assay. This assay was simple and reliable. The appearance rate of abnormally high ADA value were 81.24% for ANLL, 100% for ALL, 77.8% for CML and 37.5% for MDS. The ADA level became high when MDS turned into overt leukemia. In isozyme pattern, there was a clear difference between ANLL and ALL. The isozyme I/II ratio was significantly higher (p less than 0.001) in ALL than ANLL. Lymphoblastic crisis of CML also had a high isozyme I/II ratio. There was a correlation between isozyme I and absolute number of peripheral blasts in ALL (r = 0.768). When observed time sequentially, ADA and isozyme changed correlatively with the number of blasts counts. Serum ADA and its isozyme are useful parameters both for leukemic diagnosis and treatment.
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PMID:[Serum adenosine deaminase and its isozyme activity in leukemia and MDS]. 223 54

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

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

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

The main purpose of this review is to emphasize the critical role that chromosome analysis can play in the diagnosis, prognosis and management of blood malignancies. Table 3 shows that most patients with AML, MDS and ALL can be placed into one of three major prognostic categories. When chromosome analysis is combined with a cytological study in AML and MDS and with a cytological and immunophenotypic study in ALL, the clinical value of such analysis is further enhanced. Because of critical prognostic information that may be obtained primarily from refined chromosome analysis, we recommend that a major effort be undertaken to develop capability for such analysis in all large institutions so that the information derived can be used routinely in the assessment of haematological malignancies. In particular, it is now necessary to reassess the value of current treatments taking into consideration refined chromosome studies. We believe that patients within specific chromosomal categories should be treated with specific types of therapy in an attempt to improve overall survival.
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PMID:Prognostic significance of chromosomal abnormalities in acute leukaemias and myelodysplastic syndromes. 353 36

A deletion of the long arm of chromosome #5 (5q-) occurs nonrandomly in human malignancies. As a rule, the deletion is interstitial; the distal breakpoint by conventional techniques is usually in band q32, the proximal breakpoints in q12 or q14. Variant breakpoints occur in less than 10% of all cases. As the sole anomaly, 5q- is characteristically found in refractory anemia with or without excess of blasts. It can occur as the sole anomaly in de novo or secondary acute nonlymphocytic leukemia, but is usually accompanied in those disorders by other chromosome changes that are also nonrandomly distributed. In addition, it can be found in lymphoproliferative disorders, and occasionally, also in solid tumors. The 5q- myelodysplastic syndrome typically occurs in older age groups, particularly in females. Characteristic features are macrocytic anemia, normal or elevated platelets in the presence of megakaryocytic anomalies, and a mild clinical course. In cases with 5q- only, transformation into ANLL occurs rarely. Additional chromosome anomalies and male sex are prognostically unfavorable signs. Sex ratio is also at the disadvantage of females in de novo 5q- ANLL, and the latter disorder can occur without being preceded by a myelodysplastic phase. A myelodysplastic phase usually precedes 5q- secondary leukemia, in males as well as in females, and additional chromosome anomalies, especially of chromosome #7, are almost invariably present in those cases. We conclude that 5q- is the most frequently occurring single chromosome anomaly in secondary leukemia. Furthermore, the resemblance between de novo and secondary 5q- MDS and ANLL is striking; clinically, as well as cytogenetically, they are indistinguishable, suggesting that all de novo cases may be due to environmental (chemical) carcinogens. Response to treatment and prognosis are very poor with current therapeutic regimens in de novo as well as in secondary 5q- ANLL. Morphologically, these ANLLs fall into all FAB categories. There is considerable evidence to show that the 5q- anomaly occurs in a myeloid precursor stem cell. The occasional occurrence in lymphoid malignancies, of B cell as well as T cell type, suggests that, as in Ph-positive disorders, a common progenitor stem cell may be affected in 5q- also. The 5q- lymphoid malignancies, however, are much more rare; it is not clear at the present time whether or not a 5q- counterpart of Ph-positive ALL exists, and mixed lymphoid-myeloid 5q- disorders have not yet been documented.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The 5q-anomaly. 389 Oct 74


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