t(15;21) translocations leading to the concurrent downregulation of RUNX1 and its transcription factor partner genes SIN3A and TCF12 in myeloid disorders
Through a combined approach integrating RNA-Seq, SNP-array, FISH and PCR techniques, we identified two novel t(15;21) translocations leading to the inactivation of RUNX1 and its partners SIN3A and TCF12. One is a complex t(15;21)(q24;q22), with both breakpoints mapped at the nucleotide level, joinin...
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| Veröffentlicht in: | Molecular cancer 2015-12, Vol.14 (9172), p.211-211, Article 211 |
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| creator | L'Abbate, Alberto Tolomeo, Doron De Astis, Francesca Lonoce, Angelo Lo Cunsolo, Crocifissa Mühlematter, Dominique Schoumans, Jacqueline Vandenberghe, Peter Van Hoof, Achilles Palumbo, Orazio Carella, Massimo Mazza, Tommaso Storlazzi, Clelia Tiziana |
| description | Through a combined approach integrating RNA-Seq, SNP-array, FISH and PCR techniques, we identified two novel t(15;21) translocations leading to the inactivation of RUNX1 and its partners SIN3A and TCF12. One is a complex t(15;21)(q24;q22), with both breakpoints mapped at the nucleotide level, joining RUNX1 to SIN3A and UBL7-AS1 in a patient with myelodysplasia. The other is a recurrent t(15;21)(q21;q22), juxtaposing RUNX1 and TCF12, with an opposite transcriptional orientation, in three myeloid leukemia cases. Since our transcriptome analysis indicated a significant number of differentially expressed genes associated with both translocations, we speculate an important pathogenetic role for these alterations involving RUNX1. |
| doi_str_mv | 10.1186/s12943-015-0484-0 |
| format | Article |
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One is a complex t(15;21)(q24;q22), with both breakpoints mapped at the nucleotide level, joining RUNX1 to SIN3A and UBL7-AS1 in a patient with myelodysplasia. The other is a recurrent t(15;21)(q21;q22), juxtaposing RUNX1 and TCF12, with an opposite transcriptional orientation, in three myeloid leukemia cases. Since our transcriptome analysis indicated a significant number of differentially expressed genes associated with both translocations, we speculate an important pathogenetic role for these alterations involving RUNX1.</description><identifier>ISSN: 1476-4598</identifier><identifier>EISSN: 1476-4598</identifier><identifier>DOI: 10.1186/s12943-015-0484-0</identifier><identifier>PMID: 26671595</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Analysis ; Base Sequence ; Basic Helix-Loop-Helix Transcription Factors - genetics ; Basic Helix-Loop-Helix Transcription Factors - metabolism ; Care and treatment ; Complications and side effects ; Core Binding Factor Alpha 2 Subunit - genetics ; Core Binding Factor Alpha 2 Subunit - metabolism ; Down-Regulation ; Genetic aspects ; Humans ; Influence ; Letter to the Editor ; Leukemia, Myeloid - genetics ; Myelocytic leukemia ; Nonlymphoid leukemia ; Repressor Proteins - genetics ; Repressor Proteins - metabolism ; Sequence Analysis, DNA ; Transcription factors ; Translocation (Genetics) ; Translocation, Genetic</subject><ispartof>Molecular cancer, 2015-12, Vol.14 (9172), p.211-211, Article 211</ispartof><rights>COPYRIGHT 2015 BioMed Central Ltd.</rights><rights>Copyright BioMed Central 2015</rights><rights>L’Abbate et al. 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c522t-3b7f1412d45b08a90f393fd710d254f6f90bae6480d8b57c4f528c8eecf8b4593</citedby><cites>FETCH-LOGICAL-c522t-3b7f1412d45b08a90f393fd710d254f6f90bae6480d8b57c4f528c8eecf8b4593</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4681058/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4681058/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26671595$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>L'Abbate, Alberto</creatorcontrib><creatorcontrib>Tolomeo, Doron</creatorcontrib><creatorcontrib>De Astis, Francesca</creatorcontrib><creatorcontrib>Lonoce, Angelo</creatorcontrib><creatorcontrib>Lo Cunsolo, Crocifissa</creatorcontrib><creatorcontrib>Mühlematter, Dominique</creatorcontrib><creatorcontrib>Schoumans, Jacqueline</creatorcontrib><creatorcontrib>Vandenberghe, Peter</creatorcontrib><creatorcontrib>Van Hoof, Achilles</creatorcontrib><creatorcontrib>Palumbo, Orazio</creatorcontrib><creatorcontrib>Carella, Massimo</creatorcontrib><creatorcontrib>Mazza, Tommaso</creatorcontrib><creatorcontrib>Storlazzi, Clelia Tiziana</creatorcontrib><title>t(15;21) translocations leading to the concurrent downregulation of RUNX1 and its transcription factor partner genes SIN3A and TCF12 in myeloid disorders</title><title>Molecular cancer</title><addtitle>Mol Cancer</addtitle><description>Through a combined approach integrating RNA-Seq, SNP-array, FISH and PCR techniques, we identified two novel t(15;21) translocations leading to the inactivation of RUNX1 and its partners SIN3A and TCF12. One is a complex t(15;21)(q24;q22), with both breakpoints mapped at the nucleotide level, joining RUNX1 to SIN3A and UBL7-AS1 in a patient with myelodysplasia. The other is a recurrent t(15;21)(q21;q22), juxtaposing RUNX1 and TCF12, with an opposite transcriptional orientation, in three myeloid leukemia cases. Since our transcriptome analysis indicated a significant number of differentially expressed genes associated with both translocations, we speculate an important pathogenetic role for these alterations involving RUNX1.</description><subject>Analysis</subject><subject>Base Sequence</subject><subject>Basic Helix-Loop-Helix Transcription Factors - genetics</subject><subject>Basic Helix-Loop-Helix Transcription Factors - metabolism</subject><subject>Care and treatment</subject><subject>Complications and side effects</subject><subject>Core Binding Factor Alpha 2 Subunit - genetics</subject><subject>Core Binding Factor Alpha 2 Subunit - metabolism</subject><subject>Down-Regulation</subject><subject>Genetic aspects</subject><subject>Humans</subject><subject>Influence</subject><subject>Letter to the Editor</subject><subject>Leukemia, Myeloid - genetics</subject><subject>Myelocytic leukemia</subject><subject>Nonlymphoid leukemia</subject><subject>Repressor Proteins - genetics</subject><subject>Repressor Proteins - metabolism</subject><subject>Sequence Analysis, DNA</subject><subject>Transcription factors</subject><subject>Translocation (Genetics)</subject><subject>Translocation, Genetic</subject><issn>1476-4598</issn><issn>1476-4598</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNptktFqFDEUhgdRbK0-gDcS8KZeTE0yySSDICyL1UKpoC14FzLJyTZlNlmTjNJH8W3NdmttRXKRkPP9fzgnf9O8JPiIENm_zYQOrGsx4S1mkrX4UbNPmOhbxgf5-N55r3mW8xXGREjBnjZ7tO8F4QPfb36VQ8LfUfIGlaRDnqLRxceQ0QTa-rBCJaJyCcjEYOaUIBRk48-QYDVPNySKDn25OPtGkA4W-ZJ3Rib5zU3ZaVNiQhudSoCEVhAgo68nZ93iRnC-PCYU-YDW1zBFb5H1OSYLKT9vnjg9ZXhxux80F8cfzpef2tPPH0-Wi9PWcEpL243CEUaoZXzEUg_YdUPnrCDYUs5c7wY8auiZxFaOXBjmOJVGAhgnxzqb7qB5v_PdzOMarKktJj2pTfJrna5V1F49rAR_qVbxh2K9JJjLanB4a5Di9xlyUWufDUyTDhDnrIjgdfK0411FX_-DXsU5hdpepcTQ02Fg4i-10hMoH1ys75qtqVowTnqBO7mljv5D1WVh7et3gfP1_oGA7AQmxZwTuLseCVbbPKldnlTNk9rmSeGqeXV_OHeKPwHqfgP1jMXT</recordid><startdate>20151216</startdate><enddate>20151216</enddate><creator>L'Abbate, Alberto</creator><creator>Tolomeo, Doron</creator><creator>De Astis, Francesca</creator><creator>Lonoce, Angelo</creator><creator>Lo Cunsolo, Crocifissa</creator><creator>Mühlematter, Dominique</creator><creator>Schoumans, Jacqueline</creator><creator>Vandenberghe, Peter</creator><creator>Van Hoof, Achilles</creator><creator>Palumbo, Orazio</creator><creator>Carella, Massimo</creator><creator>Mazza, Tommaso</creator><creator>Storlazzi, Clelia Tiziana</creator><general>BioMed Central Ltd</general><general>BioMed Central</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20151216</creationdate><title>t(15;21) translocations leading to the concurrent downregulation of RUNX1 and its transcription factor partner genes SIN3A and TCF12 in myeloid disorders</title><author>L'Abbate, Alberto ; Tolomeo, Doron ; De Astis, Francesca ; Lonoce, Angelo ; Lo Cunsolo, Crocifissa ; Mühlematter, Dominique ; Schoumans, Jacqueline ; Vandenberghe, Peter ; Van Hoof, Achilles ; Palumbo, Orazio ; Carella, Massimo ; Mazza, Tommaso ; Storlazzi, Clelia Tiziana</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c522t-3b7f1412d45b08a90f393fd710d254f6f90bae6480d8b57c4f528c8eecf8b4593</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Analysis</topic><topic>Base Sequence</topic><topic>Basic Helix-Loop-Helix Transcription Factors - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Molecular cancer</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>L'Abbate, Alberto</au><au>Tolomeo, Doron</au><au>De Astis, Francesca</au><au>Lonoce, Angelo</au><au>Lo Cunsolo, Crocifissa</au><au>Mühlematter, Dominique</au><au>Schoumans, Jacqueline</au><au>Vandenberghe, Peter</au><au>Van Hoof, Achilles</au><au>Palumbo, Orazio</au><au>Carella, Massimo</au><au>Mazza, Tommaso</au><au>Storlazzi, Clelia Tiziana</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>t(15;21) translocations leading to the concurrent downregulation of RUNX1 and its transcription factor partner genes SIN3A and TCF12 in myeloid disorders</atitle><jtitle>Molecular cancer</jtitle><addtitle>Mol Cancer</addtitle><date>2015-12-16</date><risdate>2015</risdate><volume>14</volume><issue>9172</issue><spage>211</spage><epage>211</epage><pages>211-211</pages><artnum>211</artnum><issn>1476-4598</issn><eissn>1476-4598</eissn><abstract>Through a combined approach integrating RNA-Seq, SNP-array, FISH and PCR techniques, we identified two novel t(15;21) translocations leading to the inactivation of RUNX1 and its partners SIN3A and TCF12. One is a complex t(15;21)(q24;q22), with both breakpoints mapped at the nucleotide level, joining RUNX1 to SIN3A and UBL7-AS1 in a patient with myelodysplasia. The other is a recurrent t(15;21)(q21;q22), juxtaposing RUNX1 and TCF12, with an opposite transcriptional orientation, in three myeloid leukemia cases. Since our transcriptome analysis indicated a significant number of differentially expressed genes associated with both translocations, we speculate an important pathogenetic role for these alterations involving RUNX1.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>26671595</pmid><doi>10.1186/s12943-015-0484-0</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Analysis Base Sequence Basic Helix-Loop-Helix Transcription Factors - genetics Basic Helix-Loop-Helix Transcription Factors - metabolism Care and treatment Complications and side effects Core Binding Factor Alpha 2 Subunit - genetics Core Binding Factor Alpha 2 Subunit - metabolism Down-Regulation Genetic aspects Humans Influence Letter to the Editor Leukemia, Myeloid - genetics Myelocytic leukemia Nonlymphoid leukemia Repressor Proteins - genetics Repressor Proteins - metabolism Sequence Analysis, DNA Transcription factors Translocation (Genetics) Translocation, Genetic |
| title | t(15;21) translocations leading to the concurrent downregulation of RUNX1 and its transcription factor partner genes SIN3A and TCF12 in myeloid disorders |
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