SEPT2 is a new fusion partner of MLL in acute myeloid leukemia with t(2;11)(q37;q23)
We have identified a new mixed lineage leukemia ( MLL ) gene fusion partner in a patient with treatment-related acute myeloid leukemia (AML) presenting a t(2;11)(q37;q23) as the only cytogenetic abnormality. Fluorescence in situ hybridization demonstrated a rearrangement of the MLL gene and molecula...
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| Veröffentlicht in: | Oncogene 2006-10, Vol.25 (45), p.6147-6152 |
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| creator | Cerveira, N Correia, C Bizarro, S Pinto, C Lisboa, S Mariz, J M Marques, M Teixeira, M R |
| description | We have identified a new mixed lineage leukemia (
MLL
) gene fusion partner in a patient with treatment-related acute myeloid leukemia (AML) presenting a t(2;11)(q37;q23) as the only cytogenetic abnormality. Fluorescence
in situ
hybridization demonstrated a rearrangement of the
MLL
gene and molecular genetic analyses identified a septin family gene,
SEPT2
, located on chromosome 2q37, as the fusion partner of
MLL
. RNA and DNA analyses showed the existence of an in-frame fusion of
MLL
exon 7 with
SEPT2
exon 3, with the genomic breakpoints located in intron 7 and 2 of
MLL
and
SEPT2
, respectively. Search for DNA sequence motifs revealed the existence of two sequences with 94.4% homology with the topoisomerase II consensus cleavage site in
MLL
intron 7 and
SEPT2
intron 2.
SEPT2
is the fifth septin family gene fused with
MLL
, making this gene family the most frequently involved in
MLL
-related AML (about 10% of all known fusion partners). The protein encoded by
SEPT2
is highly homologous to septins 1, 4 and 5 and is involved in the coordination of several key steps of mitosis. Further studies are warranted to understand why the septin protein family is particularly involved in the pathogenesis of
MLL
-associated leukemia. |
| doi_str_mv | 10.1038/sj.onc.1209626 |
| format | Article |
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MLL
) gene fusion partner in a patient with treatment-related acute myeloid leukemia (AML) presenting a t(2;11)(q37;q23) as the only cytogenetic abnormality. Fluorescence
in situ
hybridization demonstrated a rearrangement of the
MLL
gene and molecular genetic analyses identified a septin family gene,
SEPT2
, located on chromosome 2q37, as the fusion partner of
MLL
. RNA and DNA analyses showed the existence of an in-frame fusion of
MLL
exon 7 with
SEPT2
exon 3, with the genomic breakpoints located in intron 7 and 2 of
MLL
and
SEPT2
, respectively. Search for DNA sequence motifs revealed the existence of two sequences with 94.4% homology with the topoisomerase II consensus cleavage site in
MLL
intron 7 and
SEPT2
intron 2.
SEPT2
is the fifth septin family gene fused with
MLL
, making this gene family the most frequently involved in
MLL
-related AML (about 10% of all known fusion partners). The protein encoded by
SEPT2
is highly homologous to septins 1, 4 and 5 and is involved in the coordination of several key steps of mitosis. Further studies are warranted to understand why the septin protein family is particularly involved in the pathogenesis of
MLL
-associated leukemia.</description><identifier>ISSN: 0950-9232</identifier><identifier>EISSN: 1476-5594</identifier><identifier>DOI: 10.1038/sj.onc.1209626</identifier><identifier>PMID: 16682951</identifier><identifier>CODEN: ONCNES</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Acute myeloid leukemia ; Amino Acid Sequence ; Apoptosis ; Base Sequence ; Biological and medical sciences ; Breakpoints ; Cell Biology ; Cell physiology ; Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes ; Chromosome 2 ; Chromosomes, Human, Pair 11 ; Chromosomes, Human, Pair 2 ; Cytogenetics ; Deoxyribonucleic acid ; DNA ; DNA topoisomerase (ATP-hydrolysing) ; DNA, Neoplasm ; Exons ; Female ; Fluorescence ; Fluorescence in situ hybridization ; Fundamental and applied biological sciences. Psychology ; Fusion protein ; Gene fusion ; Gene rearrangement ; Genes ; Genetic analysis ; Genetics ; Hematologic and hematopoietic diseases ; Histone-Lysine N-Methyltransferase ; Homology ; Human Genetics ; Humans ; Hybridization ; In Situ Hybridization, Fluorescence ; Internal Medicine ; Karyotyping ; Leukemia ; Leukemia, Myeloid - chemically induced ; Leukemia, Myeloid - genetics ; Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis ; Medical sciences ; Medical treatment ; Medicine ; Medicine & Public Health ; Middle Aged ; Mitosis ; MLL protein ; Molecular and cellular biology ; Molecular Sequence Data ; Myeloid-Lymphoid Leukemia Protein - genetics ; Nucleotide sequence ; oncogenomics ; Oncology ; Phosphoric Monoester Hydrolases - genetics ; Reverse Transcriptase Polymerase Chain Reaction ; Septin ; Sequence Homology, Nucleic Acid ; Translocation, Genetic</subject><ispartof>Oncogene, 2006-10, Vol.25 (45), p.6147-6152</ispartof><rights>Springer Nature Limited 2006</rights><rights>2006 INIST-CNRS</rights><rights>COPYRIGHT 2006 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Oct 5, 2006</rights><rights>Nature Publishing Group 2006.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c587t-a3c07b0a5d7335b6fc419dbe53633e2032fe8178b28a8ac569e20aef17f555173</citedby><cites>FETCH-LOGICAL-c587t-a3c07b0a5d7335b6fc419dbe53633e2032fe8178b28a8ac569e20aef17f555173</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/sj.onc.1209626$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/sj.onc.1209626$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18171737$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16682951$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Cerveira, N</creatorcontrib><creatorcontrib>Correia, C</creatorcontrib><creatorcontrib>Bizarro, S</creatorcontrib><creatorcontrib>Pinto, C</creatorcontrib><creatorcontrib>Lisboa, S</creatorcontrib><creatorcontrib>Mariz, J M</creatorcontrib><creatorcontrib>Marques, M</creatorcontrib><creatorcontrib>Teixeira, M R</creatorcontrib><title>SEPT2 is a new fusion partner of MLL in acute myeloid leukemia with t(2;11)(q37;q23)</title><title>Oncogene</title><addtitle>Oncogene</addtitle><addtitle>Oncogene</addtitle><description>We have identified a new mixed lineage leukemia (
MLL
) gene fusion partner in a patient with treatment-related acute myeloid leukemia (AML) presenting a t(2;11)(q37;q23) as the only cytogenetic abnormality. Fluorescence
in situ
hybridization demonstrated a rearrangement of the
MLL
gene and molecular genetic analyses identified a septin family gene,
SEPT2
, located on chromosome 2q37, as the fusion partner of
MLL
. RNA and DNA analyses showed the existence of an in-frame fusion of
MLL
exon 7 with
SEPT2
exon 3, with the genomic breakpoints located in intron 7 and 2 of
MLL
and
SEPT2
, respectively. Search for DNA sequence motifs revealed the existence of two sequences with 94.4% homology with the topoisomerase II consensus cleavage site in
MLL
intron 7 and
SEPT2
intron 2.
SEPT2
is the fifth septin family gene fused with
MLL
, making this gene family the most frequently involved in
MLL
-related AML (about 10% of all known fusion partners). The protein encoded by
SEPT2
is highly homologous to septins 1, 4 and 5 and is involved in the coordination of several key steps of mitosis. Further studies are warranted to understand why the septin protein family is particularly involved in the pathogenesis of
MLL
-associated leukemia.</description><subject>Acute myeloid leukemia</subject><subject>Amino Acid Sequence</subject><subject>Apoptosis</subject><subject>Base Sequence</subject><subject>Biological and medical sciences</subject><subject>Breakpoints</subject><subject>Cell Biology</subject><subject>Cell physiology</subject><subject>Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes</subject><subject>Chromosome 2</subject><subject>Chromosomes, Human, Pair 11</subject><subject>Chromosomes, Human, Pair 2</subject><subject>Cytogenetics</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>DNA topoisomerase (ATP-hydrolysing)</subject><subject>DNA, Neoplasm</subject><subject>Exons</subject><subject>Female</subject><subject>Fluorescence</subject><subject>Fluorescence in situ hybridization</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Fusion protein</subject><subject>Gene fusion</subject><subject>Gene rearrangement</subject><subject>Genes</subject><subject>Genetic analysis</subject><subject>Genetics</subject><subject>Hematologic and hematopoietic diseases</subject><subject>Histone-Lysine N-Methyltransferase</subject><subject>Homology</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Hybridization</subject><subject>In Situ Hybridization, Fluorescence</subject><subject>Internal Medicine</subject><subject>Karyotyping</subject><subject>Leukemia</subject><subject>Leukemia, Myeloid - chemically induced</subject><subject>Leukemia, Myeloid - genetics</subject><subject>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</subject><subject>Medical sciences</subject><subject>Medical treatment</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Middle Aged</subject><subject>Mitosis</subject><subject>MLL protein</subject><subject>Molecular and cellular biology</subject><subject>Molecular Sequence Data</subject><subject>Myeloid-Lymphoid Leukemia Protein - genetics</subject><subject>Nucleotide sequence</subject><subject>oncogenomics</subject><subject>Oncology</subject><subject>Phosphoric Monoester Hydrolases - genetics</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>Septin</subject><subject>Sequence Homology, Nucleic Acid</subject><subject>Translocation, Genetic</subject><issn>0950-9232</issn><issn>1476-5594</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqFks1rFDEYxoModq1ePUqwKO1htvmYJBN6KqVVYUXB9RwymaRmnUl2kxlK_3uzdGChtEgOgTe_9-vJA8B7jJYY0eY8b5YxmCUmSHLCX4AFrgWvGJP1S7BAkqFKEkqOwJucNwghIRF5DY4w5w2RDC_A-tf1zzWBPkMNg72Dbso-BrjVaQw2wejg99UK-gC1mUYLh3vbR9_B3k5_7eA1vPPjHziekguMz053VFzsCD17C1453Wf7br6Pwe-b6_XV12r148u3q8tVZVgjxkpTg0SLNOsEpazlztRYdq1llFNqCaLE2QaLpiWNbrRhXJagtg4LxxjDgh6Dzw91tynuJptHNfhsbN_rYOOUFcGU1kLI_4NIUIZqXsCTR-AmTimUJRThNaaCkJoV6uOzFCmVqGT0UOpW91b54OKYtNn3VZe4kYjVrCaFWj5BldMVeU0M1vkSfyrBpJhzsk5tkx90ulcYqb0lVN6oYgk1W6IkfJiHndrBdgd89kABPs2Azkb3LulgfD5w5QuK1nu1zx-4XJ7CrU2HrZ9p_Q9b4cff</recordid><startdate>20061005</startdate><enddate>20061005</enddate><creator>Cerveira, N</creator><creator>Correia, C</creator><creator>Bizarro, S</creator><creator>Pinto, C</creator><creator>Lisboa, S</creator><creator>Mariz, J M</creator><creator>Marques, M</creator><creator>Teixeira, M R</creator><general>Nature Publishing Group UK</general><general>Nature Publishing</general><general>Nature Publishing Group</general><scope>IQODW</scope><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>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7T5</scope></search><sort><creationdate>20061005</creationdate><title>SEPT2 is a new fusion partner of MLL in acute myeloid leukemia with t(2;11)(q37;q23)</title><author>Cerveira, N ; Correia, C ; Bizarro, S ; Pinto, C ; Lisboa, S ; Mariz, J M ; Marques, M ; Teixeira, M R</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c587t-a3c07b0a5d7335b6fc419dbe53633e2032fe8178b28a8ac569e20aef17f555173</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Acute myeloid leukemia</topic><topic>Amino Acid Sequence</topic><topic>Apoptosis</topic><topic>Base Sequence</topic><topic>Biological and medical sciences</topic><topic>Breakpoints</topic><topic>Cell Biology</topic><topic>Cell physiology</topic><topic>Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes</topic><topic>Chromosome 2</topic><topic>Chromosomes, Human, Pair 11</topic><topic>Chromosomes, Human, Pair 2</topic><topic>Cytogenetics</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>DNA topoisomerase (ATP-hydrolysing)</topic><topic>DNA, Neoplasm</topic><topic>Exons</topic><topic>Female</topic><topic>Fluorescence</topic><topic>Fluorescence in situ hybridization</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Fusion protein</topic><topic>Gene fusion</topic><topic>Gene rearrangement</topic><topic>Genes</topic><topic>Genetic analysis</topic><topic>Genetics</topic><topic>Hematologic and hematopoietic diseases</topic><topic>Histone-Lysine N-Methyltransferase</topic><topic>Homology</topic><topic>Human Genetics</topic><topic>Humans</topic><topic>Hybridization</topic><topic>In Situ Hybridization, Fluorescence</topic><topic>Internal Medicine</topic><topic>Karyotyping</topic><topic>Leukemia</topic><topic>Leukemia, Myeloid - chemically induced</topic><topic>Leukemia, Myeloid - genetics</topic><topic>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</topic><topic>Medical sciences</topic><topic>Medical treatment</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Middle Aged</topic><topic>Mitosis</topic><topic>MLL protein</topic><topic>Molecular and cellular biology</topic><topic>Molecular Sequence Data</topic><topic>Myeloid-Lymphoid Leukemia Protein - genetics</topic><topic>Nucleotide sequence</topic><topic>oncogenomics</topic><topic>Oncology</topic><topic>Phosphoric Monoester Hydrolases - genetics</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>Septin</topic><topic>Sequence Homology, Nucleic Acid</topic><topic>Translocation, Genetic</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Cerveira, N</creatorcontrib><creatorcontrib>Correia, C</creatorcontrib><creatorcontrib>Bizarro, S</creatorcontrib><creatorcontrib>Pinto, C</creatorcontrib><creatorcontrib>Lisboa, S</creatorcontrib><creatorcontrib>Mariz, J M</creatorcontrib><creatorcontrib>Marques, M</creatorcontrib><creatorcontrib>Teixeira, M R</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>Immunology Abstracts</collection><jtitle>Oncogene</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Cerveira, N</au><au>Correia, C</au><au>Bizarro, S</au><au>Pinto, C</au><au>Lisboa, S</au><au>Mariz, J M</au><au>Marques, M</au><au>Teixeira, M R</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>SEPT2 is a new fusion partner of MLL in acute myeloid leukemia with t(2;11)(q37;q23)</atitle><jtitle>Oncogene</jtitle><stitle>Oncogene</stitle><addtitle>Oncogene</addtitle><date>2006-10-05</date><risdate>2006</risdate><volume>25</volume><issue>45</issue><spage>6147</spage><epage>6152</epage><pages>6147-6152</pages><issn>0950-9232</issn><eissn>1476-5594</eissn><coden>ONCNES</coden><abstract>We have identified a new mixed lineage leukemia (
MLL
) gene fusion partner in a patient with treatment-related acute myeloid leukemia (AML) presenting a t(2;11)(q37;q23) as the only cytogenetic abnormality. Fluorescence
in situ
hybridization demonstrated a rearrangement of the
MLL
gene and molecular genetic analyses identified a septin family gene,
SEPT2
, located on chromosome 2q37, as the fusion partner of
MLL
. RNA and DNA analyses showed the existence of an in-frame fusion of
MLL
exon 7 with
SEPT2
exon 3, with the genomic breakpoints located in intron 7 and 2 of
MLL
and
SEPT2
, respectively. Search for DNA sequence motifs revealed the existence of two sequences with 94.4% homology with the topoisomerase II consensus cleavage site in
MLL
intron 7 and
SEPT2
intron 2.
SEPT2
is the fifth septin family gene fused with
MLL
, making this gene family the most frequently involved in
MLL
-related AML (about 10% of all known fusion partners). The protein encoded by
SEPT2
is highly homologous to septins 1, 4 and 5 and is involved in the coordination of several key steps of mitosis. Further studies are warranted to understand why the septin protein family is particularly involved in the pathogenesis of
MLL
-associated leukemia.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>16682951</pmid><doi>10.1038/sj.onc.1209626</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0950-9232 |
| ispartof | Oncogene, 2006-10, Vol.25 (45), p.6147-6152 |
| issn | 0950-9232 1476-5594 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_21334779 |
| source | MEDLINE; Springer Nature - Complete Springer Journals; Nature Journals Online; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals |
| subjects | Acute myeloid leukemia Amino Acid Sequence Apoptosis Base Sequence Biological and medical sciences Breakpoints Cell Biology Cell physiology Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes Chromosome 2 Chromosomes, Human, Pair 11 Chromosomes, Human, Pair 2 Cytogenetics Deoxyribonucleic acid DNA DNA topoisomerase (ATP-hydrolysing) DNA, Neoplasm Exons Female Fluorescence Fluorescence in situ hybridization Fundamental and applied biological sciences. Psychology Fusion protein Gene fusion Gene rearrangement Genes Genetic analysis Genetics Hematologic and hematopoietic diseases Histone-Lysine N-Methyltransferase Homology Human Genetics Humans Hybridization In Situ Hybridization, Fluorescence Internal Medicine Karyotyping Leukemia Leukemia, Myeloid - chemically induced Leukemia, Myeloid - genetics Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis Medical sciences Medical treatment Medicine Medicine & Public Health Middle Aged Mitosis MLL protein Molecular and cellular biology Molecular Sequence Data Myeloid-Lymphoid Leukemia Protein - genetics Nucleotide sequence oncogenomics Oncology Phosphoric Monoester Hydrolases - genetics Reverse Transcriptase Polymerase Chain Reaction Septin Sequence Homology, Nucleic Acid Translocation, Genetic |
| title | SEPT2 is a new fusion partner of MLL in acute myeloid leukemia with t(2;11)(q37;q23) |
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