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 occurrence of Myelodysplastic Syndrome (MDS) and Acute Myeloblastic Leukaemia (AML) following cytotoxic therapy for neoplastic disease is well recognised. RAS mutations are common in patients with MDS and AML. To determine whether these lesions are found as early markers of secondary disease, we have studied the incidence of RAS mutations in the peripheral blood of 70 patients in complete remission from lymphoma. Patients were treated by standard chemotherapy regimes and/or localised radiotherapy. Treatment had been given 6 months to 14 1/2 years previously and no patient showed any sign of residual disease. Genomic DNA from peripheral blood leukocytes was amplified in vitro at target codons of N, K and H RAS genes, and mutations detected by hybridisation with oligonucleotide probes. RAS mutations were detected in 9 subjects. One patient with an N12 valine (Val) substitution had been in complete remission from Hodgkin's disease (HD) for 9 years. DNA from this patient registered in a nude mouse tumorigenicity assay (NMT). The N12 Val mutation was not detected in the original tumour tissue from the same patient. A second patient in remission from HD showed evidence of co-existent N12 cysteine (Cys) and N13 valine (Val) substitutions which were not detected in presentation material or unaffected tissues. All patients are currently haematologically normal, indicating that clones of mutant RAS bearing cells may be detected prior to any overt sign of disease.
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PMID:RAS mutations in patients following cytotoxic therapy for lymphoma. 217 19

Two hundred fifty-seven eligible patients with stage I, IIA "high risk" ovarian carcinoma and IIB, IIIO (disease confined to pelvis), were randomized to either total abdominal radiotherapy (arm A) 2,250 rad in 20 fractions (107 patients), melphalan (arm B) 8 mg/m2/d X 4 every 4 weeks X 18 courses (106 patients), or intraperitoneal chromic phosphate (arm C) 10 to 20 mCi (44 patients). All patients were initially treated with pelvic radiotherapy; arm A, 2,250 rad in ten fractions; and arms B and C, 4,500 rad in 20 fractions. Entry to arm C was discontinued early because of toxicity. In a multifactor analysis using proportional hazards models, no significant difference in survival was observed although there was a marginally significant difference in disease-free survival (P = .015) with arm B being superior to arm A. Stage (P less than .0001), grade (P less than .0001), and histology (P less than .008) were predictors of survival in the multifactor analysis. Performance status, age, and residual disease were significant predictors in the single factor analysis but were not predictive when correction was made for the effects of stage, grade, and histology. Five-year survival rates are 62% for arm A, 61% for arm B, and 66% for arm C. Median duration of follow-up is 8 years. Long-term complications of radiotherapy were seen in 19 patients on arm A, 11 on arm B, and 11 on arm C. Four patients who had received melphalan developed either a myelodysplastic syndrome or acute leukemia. Violations in covering the whole abdominal target volume were correlated with survival.
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PMID:Early stage ovarian cancer: a randomized clinical trial comparing whole abdominal radiotherapy, melphalan, and intraperitoneal chromic phosphate: a National Cancer Institute of Canada Clinical Trials Group report. 304 64

Between March 1983 and December 1992, we performed 178 allogeneic BMTs for patients with hematopoietic stem cell disorders: 48 acute myelogenous leukemia (AML), 27 acute lymphoblastic leukemia (ALL), 40 chronic myelogenous leukemia (CML), 55 severe aplastic anemia (SAA), 6 myelodysplastic syndrome (MDS), 1 non-Hodgkin's lymphoma and 1 hybrid leukemia. Twenty-five of 48 AML are in disease-free survival (DFS). Fifteen of 27 ALL are in unmaintained remission. Twenty-four of 40 CML are in DFS. Forty-four out of 55 SAA patients are alive and well. Comparing the survival between standard (< or = CR1: 21 of 31 (68%)) and high risk (> or = CR2: 4 of 17 (24%)) AML, our data suggest that the preparative regimen for high risk AML was not potent enough to eradicate the residual disease in advanced AML. Although our cases are limited and the follow-up period is short, the result of ALL (overall: 56%, standard risk (adult < or = CR1, children < or = CR2: 10 of 14 (71%) and high risk (adult > or = CR2, children > CR2): 5 of 13 (38%)) and CML (overall: 60%; CP: 19 of 27 (70%), AP or BC: 5 of 13 (38%)) are promising. The probability of 5 year survival of SAA was 80 +/- 4 years.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Allogeneic bone marrow transplantation in Korea: 1983-92. 792 Mar 1

Paranasal and nasal neoplasms often elude early diagnosis in the pediatric population. This report examines 3 cases of nasal and paranasal sinus lymphomas out of 29 lymphomas and lymphoproliferative disorders seen from 1983 to 1990. Diagnostic delays are common. The development of orbital signs and symptoms often leads to diagnosis. Computed tomography and magnetic resonance imaging are important in delineating the extent of disease and allow appropriate staging. Transnasal biopsy yields the definitive diagnosis, with low associated morbidity. Aggressive chemotherapy and irradiation prolongs survival; with this regimen all of our patients have remained alive, although 1 has residual disease. B-cell lymphomas are more common than T-cell varieties in children. One patient demonstrated B-cell immunodeficiency and preleukemia prior to developing primary paranasal sinus non-Hodgkin's lymphoma; this case reiterates the systemic nature of lymphoma, Key differences between children and adults in the manifestations of nasal and sinus lymphomas are emphasized.
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PMID:Non-Hodgkin's lymphomas of the nose and paranasal sinuses in the pediatric population. 815 71

The recognition of distinct cytoimmunological subsets of pre-leukaemia and overt AML has been accomplished by morphological, immunological and ultrastructural studies. In many cases, a strong association has been documented between distinctive cytological features and specific chromosome changes. The primary genetic event underlying malignant transformation was also elucidated in a number of acute leukaemias and, as a matter of fact, assessment of these biological parameters has now an established role in the diagnostic work-up and in the monitoring of residual disease. On a more general basis, biological research in MDS is gradually clarifying the fundamental pathophysiological mechanisms of altered cell growth, and differentiation and therapeutic decision making in leukaemia is becoming increasingly dependent on the precise characterization of blast cells. Further refinement of the cytoimmunological classification of acute leukaemias and MDS is warranted in order to provide the physician with an updated framework of reference for the categorization of these heterogeneous haematological disorders and to improve the reproducibility of current morphological diagnosis among different centres (Castoldi et al, 1993).
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PMID:Special cytological subtypes of acute myeloid leukaemias and myelodysplastic syndromes. 873 May 49

Samples of peripheral blood were taken from 11 patients (blood group A, B and O), suffering from acute myeloblastic leukemia (AML), acute lymphoblastic leukemia (ALL), myelodysplastic syndrome (MDS), before and after chemotherapy, compared to normal control samples. The RBC's typing was done by standard agglutination technique (with conventional human and murine anti-sera) and flow cytometry. While using different reagent dilutions, a lower expression of the A or B antigen was noticed in all patients, even if direct typing of the RBC's revealed an apparently normal pattern. The most important depletion of antigenic expression was found to correspond to the highest concentration of myeloblasts in the bone marrow, with hypoplastic erythrocytic series. The modified H reactivity, detected at admission, was still present after complete remission, as an expression of the residual disease. Studies of the H expression could eventually become a parameter of evaluating the moment of relapse of the myeloproliferative disease.
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PMID:[Temporary changes and permanent changes in the erythrocyte blood-group antigens in malignant hemopathies]. 922 Oct 50

Interleukin-3 (IL-3) is a pleiotropic cytokine which has stimulatory effects on a broad range of hematopoietic progenitor cells. These effects have led to the use of IL-3 in clinical trials for the treatment of aplastic anemia and myelodysplastic syndrome as well as to stimulate bone marrow recovery in patients who have received high-dose therapy and bone marrow/stem cell transplantation. However, because one study suggested that IL-3 may also stimulate the growth of follicular small cleaved cell lymphoma (FSCCL) cells in vitro, it was concerning that the use of IL-3 after bone marrow transplantation in patients with FSCCL may stimulate the growth of undetectable minimal residual tumor cells resulting in early relapsed disease. In contrast to these observations, our own in vitro studies demonstrated that IL-3 inhibited FSCCL cells in short-term culture in a dose-dependent manner. Subsequently, we conducted a phase II clinical trial using single agent IL-3 for the treatment of patients with follicular low grade lymphoma. Our clinical data did not support the hypothesis that IL-3 is a growth stimulator of FSCCL.
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PMID:In vitro and in vivo biologic effects of interleukin-3 (IL-3) in follicular low-grade lymphoma. 925 Jul 83

Traditionally, acute myeloid leukemia (AML) has been diagnosed and classified based on the morphologic and cytochemical criteria of the French-American-British (FAB) classification system. However, more recent studies have demonstrated that the cytogenetic and molecular genetic abnormalities consistently associated with distinct forms of AML confer the most important prognostic information. Each broad category of de novo AML that arises in infants and children, young adults, and the elderly, or, AML arising secondary to antecedent myelodysplasia (MDS) or prior exposure to chemotherapy, radiotherapy, or environmental agents is characterized by distinct cytogenetic and molecular genetic abnormalities. Over the past 15 years, a number of these recurrent cytogenetic abnormalities have been cloned and characterized, yielding valuable insights into the mechanisms of leukemogenesis and providing powerful molecular tools for precise diagnosis and monitoring of minimal residual disease. As cytogenetic and molecular genetic characterization of AML cells is now considered crucial for both diagnostic and therapeutic decision-making, it is essential to have a working knowledge of the molecular basis of AML. This chapter reviews the molecular genetic features of different forms of AML and the new automated molecular technologies for residual disease assessment; the emerging molecular paradigms in this disease that are being exploited for therapeutic decision-making are presented.
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PMID:Molecular evaluation of acute myeloid leukemias. 1053 Jul 20

Wilms' tumor gene WT1 mRNA is a new marker of leukemic blast cells for AML, ALL, and CML. Minimal residual disease(MRD) of leukemia can be detected at frequencies as low as 1 in 10(3) to 10(4) normal bone marrow cells and 1 in 10(5) normal peripheral blood mononuclear cells by means of the quantitation of WT1 mRNA(WT1 assay) using reverse transcriptase-polymerase chain reaction. Thus, the WT1 assay makes it possible to rapidly assess the effectiveness of treatment and to evaluate the degree of eradication of leukemic cell in individual leukemia patients. Furthermore, WT1 assay can continuously assess the disease progression of myelodysplastic syndromes(MDS) and predict the evolution of MDS to overt AML within 6 months.
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PMID:[Genetic diagnosis of leukemia: diagnosis of relapse and complete remission, and prediction of leukemia onset]. 1080 19

The use of all-trans retinoic acid (ATRA) in combination with chemotherapy has markedly improved the prognosis for patients with acute promyelocytic leukemia (APL); the higher complete remission (CR) and survival rates now reported in this disease almost approach those obtained for other highly curable hematologic malignancies. Of 77 patients with APL who were consecutively treated at a single institution and who achieved CR after induction and consolidation therapy, 5 (6.5%) acquired therapy-related myelodysplasia (tMDS), acute myelogenous leukemia (AML), or both (tMDS-AML). Of these, 3 of 46 (6.5%) patients received front-line chemotherapy with or without ATRA and acquired tMDS-AML while in first remission of APL. Two underwent repeated chemotherapy cycles with ATRA because of APL relapse and acquired tMDS-AML while in the second or third remission of APL. In 2 patients, clinical and biologic characteristics of tMDS-AML were as expected for postalkylating forms (long latency, MDS phase preceding AML, karyotypic aberrations involving chromosomes 5 or 7), even though one of them had not previously received alkylating drugs. Three of the 5 patients died shortly after tMDS-AML diagnosis, one is alive with tMDS, and one is alive and in CR after allogeneic bone marrow transplantation. The occurrence of tMDS-AML after successful therapy for APL is an emerging problem. The availability of prognostic score systems at initial diagnosis and monitoring of residual disease by polymerase chain reaction might allow better tailoring of treatment intensity in APL to spare unnecessary toxicity and to minimize the risk for tMDS-AML in patients who are presumably cured.
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PMID:Therapy-related myelodysplastic syndrome-acute myelogenous leukemia in patients treated for acute promyelocytic leukemia: an emerging problem. 1221 Nov 97


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