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

A new human myeloid leukemia cell line (OIH-1), with alterations in chromosome 18 and the deleted in the colorectal carcinoma (DCC) gene and its product, was established from the peripheral blood (PB) of a patient with acute myeloblastic leukemia (AML) after myelodysplastic syndrome (MDS). Serial cytogenetics showed the presence of two clones, one with i(18)(q11) and another with trisomy 18. Southern blot analysis of OIH-1 cells with i(18)(q11) showed an extremely reduced intensity of 20- and 14-kb EcoRI fragments, suggesting the allelic loss of the DCC gene. Immunoprecipitation (IP) analysis by the murine monoclonal antibody (MoAb) AF5, specific for the DCC extracellular domain, failed to detect normal 180-kDa DCC protein, however extra 85-kDa protein was detected. However, Southern blot analysis of the latter clone of OIH-1 with trisomy 18 showed normal structure of the DCC gene. IP analysis with AF5 or G92-13 (specific for the extracellular domain) did not detect the DCC protein, but a 150-kDa protein other than the DCC-specific 180-kDa protein was detected with G97-449, specific for the cytoplasmic domain of the DCC protein. RT-PCR analysis showed the expression of the DCC mRNA in OIH-1 cells carrying each type of chromosome 18 abnormalities. These alterations in the DCC gene and protein may contribute to progression of malignancy for OIH-1 cells. The OIH-1 cell line may be useful for studying the role of the DCC gene in leukemogenesis of MDS or AML.
 ...
PMID:Alterations in the colorectal carcinoma gene and protein in a novel human myeloid leukemia cell line with trisomy 18 established from overt leukemia after myelodysplastic syndrome. 963 82

We report two cases of acute myeloid leukemia (AML) with tetrasomy 8 detected in patients' bone marrow samples using chromosome GTG-banding, fluorescence in situ hybridization (FISH) and primed in situ labeling (PRINS) techniques. Case 1 was a myelodysplastic syndrome (MDS) in transition to AML-M4 and case 2 was an AML-M2. In case 1, the tetrasomy 8 was found in 40% of metaphase cells and constituted the only chromosome abnormality. In case 2, it was accompanied by a double Ph, trisomy 18 and disomy Y and was found in 68% of metaphase cells. However, FISH and PRINS techniques revealed the coexistence of tetrasomy 8 and trisomy 8 in interphase nuclei of both cases. When the proportion of cells with tetrasomy 8 was compared between metaphases and interphase nuclei, it showed a much higher percentage of cells with tetrasomy 8 in metaphases than in interphase nuclei. Moreover, in case 2, although multi-PRINS and FISH-PRINS techniques showed other populations of interphase nuclei with different combinations of chromosome anomalies with respect to the copy numbers for chromosomes 8, 18, Y and Ph, only cells that contained either a single Ph or tetrasomy 8 plus trisomy 18, disomy Y, and double Ph could be seen in metaphases. This strongly suggests that tetrasomy 8 confers a higher proliferative advantage to cells. Our cases also show that the tetrasomy 8 is associated with a poor prognosis.
 ...
PMID:Tetrasomy 8 is associated with a major cellular proliferative advantage and a poor prognosis. two cases of myeloid hematologic disorders and review of the literature. 1129 62