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Aplasia Ras Homologous Member I Gene and Development of Glial Tumors
The ARHI (aplasia Ras homologue member I, also known as DIRAS3) gene shows 60.0% sequence homology to the Ras proto-oncogene and was the first mater-nally-imprinted tumor suppressor gene identified in the Ras family. It is constitutively expressed from the paternal allele in normal breast, ovary, he...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Macedonian Science of Sciences and Arts
2011
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3776691/ https://www.ncbi.nlm.nih.gov/pubmed/24052701 http://dx.doi.org/10.2478/v10034-011-0016-1 |
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author | Yakut, S Tuncer, MR Berker, M Goksu, E Gurer, I Ozes, ON Luleci, G Karauzum, SB |
author_facet | Yakut, S Tuncer, MR Berker, M Goksu, E Gurer, I Ozes, ON Luleci, G Karauzum, SB |
author_sort | Yakut, S |
collection | PubMed |
description | The ARHI (aplasia Ras homologue member I, also known as DIRAS3) gene shows 60.0% sequence homology to the Ras proto-oncogene and was the first mater-nally-imprinted tumor suppressor gene identified in the Ras family. It is constitutively expressed from the paternal allele in normal breast, ovary, heart, liver, pancreas, thyroid and brain tissues, and is lost or markedly down-regulated primarily in breast, ovarian, pancreas and thyroid tumor tissues. We have investigated the expression, LOH (loss of heterozygosity) and methylation status of this gene in glial tumors and peripheral blood samples of 21 patients, and in seven normal brain tissue samples. Gene expression by real time reverse transcriptase polymerase chain reaction (RT-PCR) was found to be increased in 14 and decreased in seven of the 21 tumors. The LOH was detected by fragment analysis, using five labeled polymorphic markers specific for the 1p31 region, in two of the tumors. Methylation status of the CpG island I, II and III was evaluated using COBRA (combined bisulfite restriction analysis) and RFLP (restriction fragment length polymorphism) in 21 tumors and also a hypermethylated healthy volunteer as a positive control, revealed that only two tumors had hypermethylation in CpG island I (of which one also had LOH). These results suggest that LOH and hypermethylation may be one mechanism of silencing the ARHI gene expression and development of glial tumor development. |
format | Online Article Text |
id | pubmed-3776691 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2011 |
publisher | Macedonian Science of Sciences and Arts |
record_format | MEDLINE/PubMed |
spelling | pubmed-37766912013-09-19 Aplasia Ras Homologous Member I Gene and Development of Glial Tumors Yakut, S Tuncer, MR Berker, M Goksu, E Gurer, I Ozes, ON Luleci, G Karauzum, SB Balkan J Med Genet Original Article The ARHI (aplasia Ras homologue member I, also known as DIRAS3) gene shows 60.0% sequence homology to the Ras proto-oncogene and was the first mater-nally-imprinted tumor suppressor gene identified in the Ras family. It is constitutively expressed from the paternal allele in normal breast, ovary, heart, liver, pancreas, thyroid and brain tissues, and is lost or markedly down-regulated primarily in breast, ovarian, pancreas and thyroid tumor tissues. We have investigated the expression, LOH (loss of heterozygosity) and methylation status of this gene in glial tumors and peripheral blood samples of 21 patients, and in seven normal brain tissue samples. Gene expression by real time reverse transcriptase polymerase chain reaction (RT-PCR) was found to be increased in 14 and decreased in seven of the 21 tumors. The LOH was detected by fragment analysis, using five labeled polymorphic markers specific for the 1p31 region, in two of the tumors. Methylation status of the CpG island I, II and III was evaluated using COBRA (combined bisulfite restriction analysis) and RFLP (restriction fragment length polymorphism) in 21 tumors and also a hypermethylated healthy volunteer as a positive control, revealed that only two tumors had hypermethylation in CpG island I (of which one also had LOH). These results suggest that LOH and hypermethylation may be one mechanism of silencing the ARHI gene expression and development of glial tumor development. Macedonian Science of Sciences and Arts 2011-06 2011-07-25 /pmc/articles/PMC3776691/ /pubmed/24052701 http://dx.doi.org/10.2478/v10034-011-0016-1 Text en © Macedonian Academy of Sciences and Arts This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivs license (http://creativecommons.org/licenses/by-nc-nd/3.0/), which means that the text may be used for non-commercial purposes, provided credit is given to the author. |
spellingShingle | Original Article Yakut, S Tuncer, MR Berker, M Goksu, E Gurer, I Ozes, ON Luleci, G Karauzum, SB Aplasia Ras Homologous Member I Gene and Development of Glial Tumors |
title | Aplasia Ras Homologous Member I Gene and Development of Glial Tumors |
title_full | Aplasia Ras Homologous Member I Gene and Development of Glial Tumors |
title_fullStr | Aplasia Ras Homologous Member I Gene and Development of Glial Tumors |
title_full_unstemmed | Aplasia Ras Homologous Member I Gene and Development of Glial Tumors |
title_short | Aplasia Ras Homologous Member I Gene and Development of Glial Tumors |
title_sort | aplasia ras homologous member i gene and development of glial tumors |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3776691/ https://www.ncbi.nlm.nih.gov/pubmed/24052701 http://dx.doi.org/10.2478/v10034-011-0016-1 |
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