Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.7.49 (reverse transcriptase)
 31,746 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Inactivation of the deleted in colorectal carcinoma (DCC) tumor suppressor gene has been reported not only in colorectal carcinoma but also in other human malignancies. In order to evaluate the role of the DCC gene in leukemogenesis, we examined DCC expression using the reverse transcriptase-polymerase chain reaction (RT-PCR) method. Expression of the DCC gene was reduced or absent in 10 of 39 (26%) patients with acute myelogenous leukemia (AML), three of 14 (29%) patients with acute lymphocytic leukemia (ALL), seven of 33 (21%) patients with chronic myelogenous leukemia (CML), three of 39 (8%) patients with myelodysplastic syndromes (MDS), and five of nine (56%) patients with overt leukemia progressed from MDS. These findings suggest that inactivation of the DCC gene contributes to some instances of leukemogenesis.
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PMID:Expression of the DCC gene in human hematological malignancies. 769 19

The putative tumor suppressor gene deleted in colorectal carcinoma (DCC), located on human chromosome band 18q21, is deleted or inactivated in many solid tumors. Its role in the pathogenesis of non-Hodgkin's lymphoma (NHL) has not been studied. Recently, inactivation of this gene was reported in cases of leukemia with monosomy 18. As monosomy 18 is frequently observed in low-grade NHL, we investigated the incidence of altered DCC gene expression in patients with NHL, and correlated it with the number of copies of chromosome 18. Fifteen unselected cases of NHL were studied for evidence of DCC gene expression by reverse transcriptase-polymerase chain reaction. The results were correlated with Southern blot analysis of the DCC gene and with the number of copies of chromosome 18 determined by fluorescent in situ hybridization (FISH). The controls were tissues from normal colon mucosa and normal tonsils. Eight of 15 (53%) NHL cases lacked DCC mRNA, and one expressed substantially less than normal. Southern blot analysis showed normal configuration of the DCC gene in all samples. Two copies of chromosome 18 were found in 9 of 11 samples studied by FISH: one case had a subpopulation of cells with monosomy 18 and one had trisomy 18. All controls expressed DCC. We conclude that DCC gene expression is frequently absent or decreased in NHL and may be involved in the pathogenesis of NHL. Monosomy 18 was not required for DCC inactivation.
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PMID:Decreased expression of the deleted in colorectal carcinoma gene in non-Hodgkin's lymphoma. 774 42

To evaluate the role of the deleted in colorectal carcinoma (DCC) gene in leukemogenesis, we examined loss of heterozygosity (LOH) in the DCC gene in 64 primary human leukemias using Southern blot analysis and examined the expression of the DCC gene using reverse transcriptase-polymerase chain reaction (RT-PCR) analysis. Allelic loss in the DCC gene was observed in two patients (6%, 2 of 35 informative cases), and expression of the DCC gene was reduced or absent in 8 of 26 (31%) patients with acute myelogenous leukemia (AML), 3 of 9 (33%) patients with acute lymphocytic leukemia (ALL), and 7 of 29 (24%) patients with chronic myelogenous leukemia (CML). Moreover, in one ALL patient with absent DCC expression at diagnosis, its expression became normal after performing chemotherapy and achieving remission. These findings suggest that inactivation of the DCC gene contributes to some instances of leukemogenesis.
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PMID:Alterations in the deleted in colorectal carcinoma gene in human primary leukemia. 833 56

To evaluate the molecular events in the genome that are associated with myelodysplastic syndromes (MDS) and the development of leukemia, we investigated the expression of the deleted in colorectal carcinoma (DCC) gene by the reverse transcriptase-polymerase chain reaction (RTPCR) method in 24 MDS cases and in 7 overt leukemia cases that progressed from MDS. Expression of the DCC gene was absent or extremely reduced in 2 of the 24 MDS cases, and those 2 cases developed overt leukemia within 6 months. Moreover, in 5 of the 7 cases of overt leukemia that developed from MDS, expression of the DCC gene was absent or extremely reduced. These findings suggest that inactivation of the DCC gene may be the late event that triggers the progression of MDS to leukemia.
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PMID:Expression of the DCC gene in myelodysplastic syndromes and overt leukemia. 837 79

The deleted in colorectal carcinoma (DCC) gene, a candidate tumour suppressor, might be inactivated in a number of human cancers. In order to evaluate the possible role of DCC alterations in the pathogenesis of neuroblastoma, we examined 25 neuroblastoma cell lines and 16 primary tumours, including 6 samples with loss of heterozygosity (LOH) at the DCC locus for DCC mRNA expression, by using the reverse transcriptase-polymerase chain reaction (RT-PCR) technique. The level of DCC expression was significantly reduced or undetectable in 12 of 25 (48%) cell lines and 7 of 16 (44%) primary tumours, suggesting that inactivation of the DCC gene is involved in the development of neuroblastoma. Three of the 6 tumours with LOH at the DCC locus revealed reduced DCC mRNA expression, indicating that LOH at the DCC locus might have affected the levels of DCC mRNA. We also screened for mutations in 4 exons of the DCC gene in 12 cell lines by using PCR-single strand conformation polymorphism (PCR-SSCP) analysis. Point mutations were not found except a polymorphic change at codon 201. The mechanism for inactivation of the DCC gene will be further investigated.
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PMID:Alterations of the tumour suppressor gene DCC in neuroblastoma. 951 33