A cluster of genes located in 1p36 are down-regulated in neuroblastomas with poor prognosis, but not due to CpG island methylation
<p>Abstract</p> <p>Background</p> <p>A common feature of neuroblastoma tumours are partial deletions of the short arm of chromosome 1 (1p-deletions). This is indicative of a neuroblastoma tumour suppressor gene being located in the region. Several groups including our h...
| Main Authors: | , , , , , , , |
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| Format: | Article |
| Language: | English |
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BMC
2005-03-01
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| Series: | Molecular Cancer |
| Online Access: | http://www.molecular-cancer.com/content/4/1/10 |
| _version_ | 1819181178655080448 |
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| author | Krona Cecilia Sjöberg Rose-Marie Latif Farida Hesson Luke Fransson Susanne Ejeskär Katarina Carén Helena Martinsson Tommy |
| author_facet | Krona Cecilia Sjöberg Rose-Marie Latif Farida Hesson Luke Fransson Susanne Ejeskär Katarina Carén Helena Martinsson Tommy |
| author_sort | Krona Cecilia |
| collection | DOAJ |
| description | <p>Abstract</p> <p>Background</p> <p>A common feature of neuroblastoma tumours are partial deletions of the short arm of chromosome 1 (1p-deletions). This is indicative of a neuroblastoma tumour suppressor gene being located in the region. Several groups including our have been studying candidate neuroblastoma genes in the region, but no gene/genes have yet been found that fulfil the criteria for being a neuroblastoma tumour suppressor. Since frequent mutations have not been detected, we have now analyzed the expression and promoter CpG island methylation status of the genes <it>UBE4B</it>, <it>KIF1B</it>, <it>PGD</it>, <it>APITD1</it>, <it>DFFA </it>and <it>PEX14 </it>in the 1p36.22 region in order to find an explanation for a possible down-regulation of this region.</p> <p>Results</p> <p>The current study shows that gene transcripts in high stage neuroblastoma tumours are significantly down-regulated compared to those in low stage tumours in the 1p36.22 region. CpG island methylation does not seem to be the mechanism of down-regulation for most of the genes tested, since no methylation was detected in the fragments analyzed. One exception is the CpG island of <it>APITD1</it>. Methylation of this gene is also seen in blood from control individuals and is therefore not believed to participate in tumour development.</p> <p>Conclusion</p> <p>The genes <it>UBE4B</it>, <it>KIF1B</it>, <it>PGD</it>, <it>APITD1</it>, <it>DFFA </it>and <it>PEX14 </it>are down-regulated in high stage NB tumours, a feature that can not be explained by CpG island methylation.</p> |
| first_indexed | 2024-12-22T22:26:06Z |
| format | Article |
| id | doaj.art-328aaefc2ffc4f18839f5991dc366f0c |
| institution | Directory Open Access Journal |
| issn | 1476-4598 |
| language | English |
| last_indexed | 2024-12-22T22:26:06Z |
| publishDate | 2005-03-01 |
| publisher | BMC |
| record_format | Article |
| series | Molecular Cancer |
| spelling | doaj.art-328aaefc2ffc4f18839f5991dc366f0c2022-12-21T18:10:33ZengBMCMolecular Cancer1476-45982005-03-01411010.1186/1476-4598-4-10A cluster of genes located in 1p36 are down-regulated in neuroblastomas with poor prognosis, but not due to CpG island methylationKrona CeciliaSjöberg Rose-MarieLatif FaridaHesson LukeFransson SusanneEjeskär KatarinaCarén HelenaMartinsson Tommy<p>Abstract</p> <p>Background</p> <p>A common feature of neuroblastoma tumours are partial deletions of the short arm of chromosome 1 (1p-deletions). This is indicative of a neuroblastoma tumour suppressor gene being located in the region. Several groups including our have been studying candidate neuroblastoma genes in the region, but no gene/genes have yet been found that fulfil the criteria for being a neuroblastoma tumour suppressor. Since frequent mutations have not been detected, we have now analyzed the expression and promoter CpG island methylation status of the genes <it>UBE4B</it>, <it>KIF1B</it>, <it>PGD</it>, <it>APITD1</it>, <it>DFFA </it>and <it>PEX14 </it>in the 1p36.22 region in order to find an explanation for a possible down-regulation of this region.</p> <p>Results</p> <p>The current study shows that gene transcripts in high stage neuroblastoma tumours are significantly down-regulated compared to those in low stage tumours in the 1p36.22 region. CpG island methylation does not seem to be the mechanism of down-regulation for most of the genes tested, since no methylation was detected in the fragments analyzed. One exception is the CpG island of <it>APITD1</it>. Methylation of this gene is also seen in blood from control individuals and is therefore not believed to participate in tumour development.</p> <p>Conclusion</p> <p>The genes <it>UBE4B</it>, <it>KIF1B</it>, <it>PGD</it>, <it>APITD1</it>, <it>DFFA </it>and <it>PEX14 </it>are down-regulated in high stage NB tumours, a feature that can not be explained by CpG island methylation.</p>http://www.molecular-cancer.com/content/4/1/10 |
| spellingShingle | Krona Cecilia Sjöberg Rose-Marie Latif Farida Hesson Luke Fransson Susanne Ejeskär Katarina Carén Helena Martinsson Tommy A cluster of genes located in 1p36 are down-regulated in neuroblastomas with poor prognosis, but not due to CpG island methylation Molecular Cancer |
| title | A cluster of genes located in 1p36 are down-regulated in neuroblastomas with poor prognosis, but not due to CpG island methylation |
| title_full | A cluster of genes located in 1p36 are down-regulated in neuroblastomas with poor prognosis, but not due to CpG island methylation |
| title_fullStr | A cluster of genes located in 1p36 are down-regulated in neuroblastomas with poor prognosis, but not due to CpG island methylation |
| title_full_unstemmed | A cluster of genes located in 1p36 are down-regulated in neuroblastomas with poor prognosis, but not due to CpG island methylation |
| title_short | A cluster of genes located in 1p36 are down-regulated in neuroblastomas with poor prognosis, but not due to CpG island methylation |
| title_sort | cluster of genes located in 1p36 are down regulated in neuroblastomas with poor prognosis but not due to cpg island methylation |
| url | http://www.molecular-cancer.com/content/4/1/10 |
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