Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026986 (myelodysplastic syndrome)
 14,926 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clonal composition of each cell population was determined from the characteristic methylation pattern of DNA and the restriction fragment length polymorphism (RFLP) of the hypoxanthine phosphoribosyltransferase (HPRT) and phosphoglycerate kinase (PGK) genes, both located on the X chromosome. About 71% of Japanese females are heterozygous in terms of the RFLP of either HPRT or PGK genes, which was demonstrated by using 5' genomic DNA or cDNA probes for these genes. All 3 cases of chronic myeloproliferative disorders showed monoclonal patterns. AML or ALL cases demonstrated either monoclonal or polyclonal patterns depending upon the percentage of blastic cells. Monoclonal patterns were seen in 3 of 4 cases of myelodysplastic syndromes and both PNH cases.
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PMID:Molecular genetic approach to the analysis of clonal proliferation in hematologic disorders. 257 94

Systematic clinical and laboratory observations of 64 cases of myelodysplastic syndrome (MDS) were made. The results showed that malignant clone already exists in the bone marrow of patients with MDS. Eighteen cases of them have transformed into AML. The rates of transforming into AML in RAEB, RAEB-T and CMML were markedly higher than that in RA. The courses of MDS which transformed into AML from the various types were different. The transformation in RA was obviously longer than those in RAEB and RAEB-T. Two cases transformed into myelofibrosis. Diagnosis of CMML according to the FAB classification criteria revealed that it has two forms. One shows only increase of mature monocytes and it has no relation with the types of acute leukemia to be transformed. It is considered as a reactive monocytosis. The other form, in addition to increase of mature monocytes, also has increase of a few monoblasts and promonocytes. These are considered as true CMML and usually quickly developed into M4 or M5 which are related with monocytes.
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PMID:[A clinical study on myelodysplastic syndrome. Report of 64 cases]. 259 Dec 61

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

Recent advances of cytogenetics in human hematological malignancies and solid tumors were reviewed. In leukemia and lymphoma, many non-random chromosome aberrations have been found in the last decade. Further specific chromosome aberrations, which existed usually in less than five percent of acute leukemia cases, were recently found, including t (1 ; 3) in MDS or AML M4, +der (1) t (1 ; 7) in MDS, t (1 ; 11) in AML M4 or M5 and +4 in AML M2 or M4. Recurrent chromosome deletions of 17p-, 9q- and 2p- were also found as secondary aberrations in association with tumor development. Accumulation of the data from variant translocation for the 9 ; 22, 8 ; 21 and 15 ; 17 gave us important informations of critical sites of the chromosome in leukemia development. A new trial for the simultaneous analysis of morphology, immunologic phenotype and karyotype on the same metaphase clearly demonstrated stem cell origin of leukemia in some cases, specializing the affected cell lineage. Progress in non-radioactive in situ hybridization techniques now allows approaches to the recognition of particular chromosome abnormality in metaphase and also in interphase cell by means of specific repetitive probes for each chromosome. Though a hypothesis that fragile sites may act as factors predisposing to chromosomal rearrangements have attracted attention in past few years, recent results appear to be conflicting without any direct proof. Cytogenetic studies in solid tumor have been remarkably progressed with advances of methodology. Recurrent chromosome aberrations in solid tumor were found, such as t (X ; 18) in synovial sarcoma, t (12 ; 16) in liposarcoma, and i (12p) in seminoma. Studies on the correlation between specific chromosome changes and histologic subtypes resulted in an useful orientation to the diagnosis and the therapy. Advance in cytogenetics may serve as new concepts for patho-physiology of malignant tumors and contribute to further understandings of molecular genetics in human solid tumors.
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PMID:[Cancer and chromosomes]. 268 17

Intensive antileukemia treatment was evaluated in 22 patients with untreated secondary acute myelogenous leukemia (sAML) and 14 patients with bad prognosis myelodysplastic syndrome (MDS). Results of combination remission-induction chemotherapy were compared with 126 patients treated for primary AML. The duration of hypoplasia tended to be longer in the sAML and MDS patients when compared to de novo AML, but reached significance only for the duration of thrombocytopenia: 26 days versus 18 days (p less than 0.01). The complete remission (CR) rates were similar in primary AML: 67%, sAML: 62%, and MDS: 64%. The CR rates of patients younger than 45 years were 75% for de novo AML, 75% for sAML, and 71% for MDS. The number of hypoplastic deaths during remission-induction chemotherapy of patients with sAML and MDS was low. Four of the 36 patients treated for sAML or MDS died during subsequent hypoplastic phases induced by remission-induction chemotherapy. The remission duration without bone marrow transplantation (BMT) was significantly shorter (p less than 0.03) in MDS and sAML, when compared with primary AML. Longlasting complete remissions in MDS and sAML were only obtained in 3 of the 6 patients treated with allogeneic BMT. Intensive antileukemic therapy should be considered in young patients with MDS and life-threatening cytopenias or patients with sAML or RAEBt.
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PMID:Intensive chemotherapy for patients with myelodysplastic syndromes and acute myelogenous leukaemia younger than 65 years. 269 96

This retrospective survey of the EBMT Leukaemia Working Parking describes 78 patients with myelodysplasia (MDS) or secondary acute myelogenous leukaemia (sAML) who were given an allogeneic bone marrow transplant (BMT). The status of underlying disease at the time of transplantation was prognostic for the two-year disease-free survival which was 60% for patients transplanted in complete remission. Similar results were obtained for those with less advanced MDS (50-64%) who had not received any prior intensive chemotherapy. The results were significantly less favourable for those with more advanced disease who only partially responded to prior intensive chemotherapy (18%) while none of those who either relapsed or were resistant to chemotherapy survived. Allogeneic BMT can therefore be considered as curative treatment for patients with MDS. Patients with sAML who have a histocompatible donor should be given chemotherapy intensive enough to induce complete remission. If this is achieved these individuals have a prognosis comparable to those with de novo AML in first remission after BMT.
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PMID:Allogeneic bone marrow transplantation for secondary leukaemia and myelodysplastic syndromes. Leukaemia Working Party of the European Bone Marrow Transplantation Group (EBMTG). 269 98

We tried to treat 13 patients with myelodysplastic syndromes (MDS), leukemias and myeloproliferative disorders, with alfacalcidol for their hematological improvement. Eight of them had MDS, 2 acute leukemia (M3, M4), 1 chronic myelogenous leukemia and 2 primary myelofibrosis. All patients were untreated except for 3 patients (PASA, RAEB, AML-M4) who had been treated with mepitiostane, prednisolone and BH.AC-AMP regimen, respectively, prior to alfacalcidol therapy. All patients received alfacalcidol orally for at least one month. The dosage of alfacalcidol ranged from 0.25 to 10 micrograms/day, and the medicine was administrated intermittently when the dosage exceeded 6 micrograms/day to prevent hypercalcemia. The therapeutic effectiveness of alfacalcidol was evaluated according to a criteria by Koeffler (Cancer Treat Rep 69: 1399, 1985) with minor modifications. Three patients (PASA, RAEB, CMML) showed partial response, 3 (RAEB, RAEB in T, AML-M4) minor response and rest of the patients did not respond. The hematological improvement of 6 responders was transient (from 1 to 2 months), however, one patient (PASA) is still responding to alfacalcidol therapy (0.25 microgram/day) for over 12 months. The dysplastic features of hemopoietic cells in the bone marrow showed no noticeable change during the hematological improvement in these responders, suggesting the improvement was obtained as a result of alteration in the proliferation or differentiation of neoplastic clone. None of 13 patients developed hypercalcemia. One patient (AML-M4) became excitable on high dose alfacalcidol (10 micrograms/day). In conclusion, alfacalcidol therapy is effective in some patients with MDS or leukemias and appears worthy especially in the clinical state in which chemotherapy is not indicated.
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PMID:[Therapeutic effectiveness of vitamin D3 in patients with myelodysplastic syndromes, leukemias and myeloproliferative disorders]. 271 94

A case of AML (M 4) with t(6; 11) showed recovery to myelodysplastic syndrome (MDS)-like bone marrow after one course of DCMP regimen. Dysplastic changes of three cell-lineages were observed and micromegakaryocytes were markedly increased in number. Recovering hematopoiesis was incomplete. During MDS-like phase, t(6; 11) disappeared, reverting to normal karyotypes. Low dose ara-C regimen did not show any effect. AML soon relapsed with reappearance of t(6; 11). MDS-like abnormal hematopoiesis has recently been reported to occur after remission induction therapy or at the time of relapse. G-6PD isozyme study revealed in a remission case of AML that hematopoiesis still consisted of abnormal clone in spite of karyotypic normalization. The abnormal hematopoiesis observed in our case can be referred to such a clonal disorder predominating after disappearance of blastic component of AML. It seems important to reveal what proportion of de novo AMLs shows such an abnormal hematopoiesis and to establish suitable therapeutic approach.
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PMID:[Marked dysmyelopoiesis after induction chemotherapy in a case of acute myelomonocytic leukemia (M 4) with t(6; 11)]. 274 77

Survival, causes of death and hospitalization have been studied in 99 patients with the myelodysplastic syndrome. The median survival of the patients was 702 days, and the 10 year actuarial survival only 10 per cent, which is not significantly better than the corresponding figures in the remission stage of AML. Although MDS-patients who developed acute leukemia had significantly (p less than 0.05) more platelets, they also had significantly (p less than 0.05) more major bleeding as a contributory cause of death than patients who did not develop leukemia. Bleeding seems to be diagnosed only in 12 per cent in vivo, whereas major bleeding is found at autopsy in 38 per cent of the patients. The patients who did not develop leukemia died significantly (p = 0.018) more often of cardiovascular causes. MDS patients spend one sixth of their remaining life in hospital, on an average. This is true both for those who develop leukemia and for those who do not. The terminal hospital stay lasts an average of 24 days, which is comparable to the figure for myeloma.
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PMID:Survival, hospitalization and cause of death in 99 patients with the myelodysplastic syndrome. 281 15

It is important to make the correct diagnosis of MDS and to exclude very carefully all other disorders that may induce dysplastic features in the bone marrow. In patients without excess of bone marrow blasts, cytogenetics and in vitro bone marrow cultures may aid in making the correct diagnosis. MDS patients without excess of bone marrow blasts or symptomatic cytopenia or cytogenetic abnormalities associated with poor prognosis should be followed on a regular basis with sequential examinations of blood counts and bone marrow specimens. In the absence of obvious disease progression, ie, increasing cytopenia or increasing percentage of marrow blasts, patients should only receive supportive care. An increase in RBC requirements alone is insufficient reason to start cytotoxic therapy. Once progression of the disease has been well documented, cytotoxic treatment is indicated. There is no reason to delay treatment until these patients have progressed to overt AML. In patients over the age of 50, the best available therapy is low-dose cytarabine with a 30% probability of a good response; this therapy requires careful supervision and the availability of intensive supportive care. In patients under 50 years with progressive disease, or with clear evidence of a poor prognosis, allogeneic BMT is the therapy of choice if a HLA-identical sibling can be identified. In those patients who lack a HLA-identical sibling, intensive combination therapy is the treatment of choice and should preferably include high-dose cytarabine. Intensive consolidation therapy will be necessary for a durable remission. Trials with inducers of differentiation remain experimental. Results to date have been disappointing.
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PMID:Management of the myelodysplastic syndromes. 282 13


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