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)

Ten patients with a hematologic disorder and a clone of cells with trisomy 9 in the bone marrow were studied in order to investigate the clinical significance of this chromosome anomaly. In five of the patients, trisomy 9 was the only anomaly; in four, there was also trisomy 8; and in one, a Y chromosome was also lacking. Four patients had a myelodysplastic syndrome, and six had a myeloproliferative disorder. Interestingly, four patients had primary thrombocytosis.
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PMID:Trisomy 9 in hematologic disorders: possible association with primary thrombocytosis. 347 49

Cytogenetic analysis was performed in 86 cases of hematologic malignancy, using conventional cytogenetic analysis and fluorescence in situ hybridization (FISH) analysis at two university hospitals in Korea between 1993 and 1995. In addition to well-known anomalies, some unusual abnormalities were found, such as t(17;22), trisomy 9 combined with t(14;17), (2;7) and Philadelphia chromosome in CML; t(1;12), t(11;22), t(9;17), and t(12;21) in AML; trisomy 11 in MDS; t(2;9) and complex t(8;8;13;14) in ALL. The results of FISH analysis in interphase nuclei using a translocation probe for CML and APL showed more than 85% positive cells in CML, and 75% positive cells in APL.
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PMID:Cytogenetic and fluorescence in situ hybridization analyses of hematologic malignancies in Korea. 946 Apr 92

We report 4 unusual cases of myelodysplastic syndrome with distinct persistent nodular lesions noted on serial bone marrow examinations, even during remission. The lesions were predominantly composed of immature monocytes that stained positively for CD68. Trisomy 9 and 11 were demonstrated in the cells of the nodular lesions and surrounding marrow of 1 patient, indicating the same clonal origin. Evaluation of p53 glycoprotein, retinoblastoma protein (pRb), proliferation-related protein (Ki-67), multiple drug-resistant enzyme glutathione-S-transferase pi, and topoisomerase IIalpha (Topo IIalpha) revealed decreased topoisomerase expression within the nodular lesions compared with the surrounding marrow and absence of Ki-67 antigen within nodular lesions. Most cells in the lesion were not in a proliferative cycle, with very low expression of Topo IIalpha, which may explain the apparent drug resistance of these nodular lesions.
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PMID:Nodular lesions of monocytic component in myelodysplastic syndrome. 1019 82

Long-term survivors of acquired aplastic anemia (AA) have an increased risk of developing myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML) after immunosuppressive therapy (IST). It is uncertain whether the increased survival time simply discloses the natural history of AA as a premalignant disease or whether secondary disease is related to the therapy itself. Between November 1992 and September 1997, 113 AA children with normal cytogenetics at diagnosis were treated with IST using antithymocyte globulin, cyclosporin, and danazol with or without granulocyte colony-stimulating factor (G-CSF). We assessed risk factors for developing MDS/AML by Cox proportional hazards models. Twelve of 113 patients developed MDS between 9 and 81 months following the time of diagnosis, giving a cumulative incidence of 13.7 +/- 3.9%. The following cytogenetic abnormalities were observed at the time of diagnosis of MDS: monosomy 7 (6 patients), monosomy7/trisomy21 (1 patient), trisomy 11 (1 patient), del (11) (9?:14) (1 patient), add (9q) (1 patient), add 7 (q 32) (1 patient), and trisomy 9 (1 patient). The number of days of G-CSF therapy and nonresponse to therapy at 6 months were statistically significant risk factors by multivariate analysis. The present study suggests a close relationship between long-term use of G-CSF and secondary MDS in nonresponders to IST.
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PMID:Risk factors for evolution of acquired aplastic anemia into myelodysplastic syndrome and acute myeloid leukemia after immunosuppressive therapy in children. 1213 Apr 87

A minority of patients with newly diagnosed polycythemia vera (PV) have an abnormal karyotype in their myeloid cells but no invariant chromosomal aberration has been found. The most frequent visible alteration is a 20q deletion, also characterized in other myeloproliferative diseases (MPD) and myeloid malignancies; among other chromosomal changes, trisomy 9 appears more common in PV than in other MPDs. When a myelofibrosis complicates the course of the disease, cytogenetic anomalies become quite common with a striking frequency of partial duplication 1q; an evolution towards myelodysplasia or acute leukemia is almost always associated with nonspecific chromosomal aberrations. Modern cytogenetic methods have disclosed cryptic anomalies and pointed out the high frequency of 9p alterations affecting a restricted region, thus stimulating an active search for candidate genes or specific mutations.
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PMID:Karyotype and molecular cytogenetic studies in polycythemia vera. 1586 76