Identification of a common microdeletion cluster in 7q21.3 subband among patients with myeloid leukemia and myelodysplastic syndrome
Monosomy 7 and interstitial deletions in the long arm of chromosome 7 (−7/7q−) is a common nonrandom chromosomal abnormality found frequently in myeloid disorders including acute myeloid leukemia (AML), myelodysplastic syndrome (MDS), and juvenile myelomonocytic leukemia (JMML). Using a short probe-...
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Veröffentlicht in: | Biochemical and biophysical research communications 2009-05, Vol.383 (2), p.245-251 |
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description | Monosomy 7 and interstitial deletions in the long arm of chromosome 7 (−7/7q−) is a common nonrandom chromosomal abnormality found frequently in myeloid disorders including acute myeloid leukemia (AML), myelodysplastic syndrome (MDS), and juvenile myelomonocytic leukemia (JMML). Using a short probe-based microarray comparative genomic hybridization (mCGH) technology, we identified a common microdeletion cluster in 7q21.3 subband, which is adjacent to ‘hot deletion region’ thus far identified by conventional methods. This common microdeletion cluster contains three poorly characterized genes;
Samd9,
Samd9L, and a putative gene
LOC253012, which we named
Miki. Gene copy number assessment of three genes by real-time PCR revealed heterozygous deletion of these three genes in adult patients with AML and MDS at high frequency, in addition to JMML patients. Miki locates to mitotic spindles and centrosomes and downregulation of Miki by RNA interference induced abnormalities in mitosis and nuclear morphology, similar to myelodysplasia. In addition, a recent report indicated Samd9 as a tumor suppressor. These findings indicate the usefulness of the short probe-based CGH to detect microdeletions. The three genes located to 7q21.3 would be candidates for myeloid tumor-suppressor genes on 7q. |
doi_str_mv | 10.1016/j.bbrc.2009.04.004 |
format | Article |
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Samd9,
Samd9L, and a putative gene
LOC253012, which we named
Miki. Gene copy number assessment of three genes by real-time PCR revealed heterozygous deletion of these three genes in adult patients with AML and MDS at high frequency, in addition to JMML patients. Miki locates to mitotic spindles and centrosomes and downregulation of Miki by RNA interference induced abnormalities in mitosis and nuclear morphology, similar to myelodysplasia. In addition, a recent report indicated Samd9 as a tumor suppressor. These findings indicate the usefulness of the short probe-based CGH to detect microdeletions. The three genes located to 7q21.3 would be candidates for myeloid tumor-suppressor genes on 7q.</description><identifier>ISSN: 0006-291X</identifier><identifier>EISSN: 1090-2104</identifier><identifier>DOI: 10.1016/j.bbrc.2009.04.004</identifier><identifier>PMID: 19358830</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>60 APPLIED LIFE SCIENCES ; Base Sequence ; Cell Line, Tumor ; Cell Nucleus - ultrastructure ; Chromosome Aberrations ; CHROMOSOMES ; Chromosomes, Human, Pair 7 - genetics ; GENES ; Genes, Tumor Suppressor ; Humans ; Leukemia, Myeloid - genetics ; MITOSIS ; Mitosis - genetics ; Monosomy 7 ; MORPHOLOGY ; Multigene Family ; Myelodysplastic Syndromes - genetics ; MYELOID LEUKEMIA ; Myeloid malignancy ; PATIENTS ; POLYMERASE CHAIN REACTION ; Proteins - genetics ; RNA ; Sequence Deletion ; Tumor suppressor</subject><ispartof>Biochemical and biophysical research communications, 2009-05, Vol.383 (2), p.245-251</ispartof><rights>2009 Elsevier Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c457t-9156fc5460944048ac7cf1b6e130862b336d25cf0c94945cc3af0c7fe536ef703</citedby><cites>FETCH-LOGICAL-c457t-9156fc5460944048ac7cf1b6e130862b336d25cf0c94945cc3af0c7fe536ef703</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0006291X09006779$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,776,780,881,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19358830$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://www.osti.gov/biblio/22199707$$D View this record in Osti.gov$$Hfree_for_read</backlink></links><search><creatorcontrib>Asou, Hiroya</creatorcontrib><creatorcontrib>Matsui, Hirotaka</creatorcontrib><creatorcontrib>Ozaki, Yuko</creatorcontrib><creatorcontrib>Nagamachi, Akiko</creatorcontrib><creatorcontrib>Nakamura, Megumi</creatorcontrib><creatorcontrib>Aki, Daisuke</creatorcontrib><creatorcontrib>Inaba, Toshiya</creatorcontrib><title>Identification of a common microdeletion cluster in 7q21.3 subband among patients with myeloid leukemia and myelodysplastic syndrome</title><title>Biochemical and biophysical research communications</title><addtitle>Biochem Biophys Res Commun</addtitle><description>Monosomy 7 and interstitial deletions in the long arm of chromosome 7 (−7/7q−) is a common nonrandom chromosomal abnormality found frequently in myeloid disorders including acute myeloid leukemia (AML), myelodysplastic syndrome (MDS), and juvenile myelomonocytic leukemia (JMML). Using a short probe-based microarray comparative genomic hybridization (mCGH) technology, we identified a common microdeletion cluster in 7q21.3 subband, which is adjacent to ‘hot deletion region’ thus far identified by conventional methods. This common microdeletion cluster contains three poorly characterized genes;
Samd9,
Samd9L, and a putative gene
LOC253012, which we named
Miki. Gene copy number assessment of three genes by real-time PCR revealed heterozygous deletion of these three genes in adult patients with AML and MDS at high frequency, in addition to JMML patients. Miki locates to mitotic spindles and centrosomes and downregulation of Miki by RNA interference induced abnormalities in mitosis and nuclear morphology, similar to myelodysplasia. In addition, a recent report indicated Samd9 as a tumor suppressor. These findings indicate the usefulness of the short probe-based CGH to detect microdeletions. The three genes located to 7q21.3 would be candidates for myeloid tumor-suppressor genes on 7q.</description><subject>60 APPLIED LIFE SCIENCES</subject><subject>Base Sequence</subject><subject>Cell Line, Tumor</subject><subject>Cell Nucleus - ultrastructure</subject><subject>Chromosome Aberrations</subject><subject>CHROMOSOMES</subject><subject>Chromosomes, Human, Pair 7 - genetics</subject><subject>GENES</subject><subject>Genes, Tumor Suppressor</subject><subject>Humans</subject><subject>Leukemia, Myeloid - genetics</subject><subject>MITOSIS</subject><subject>Mitosis - genetics</subject><subject>Monosomy 7</subject><subject>MORPHOLOGY</subject><subject>Multigene Family</subject><subject>Myelodysplastic Syndromes - genetics</subject><subject>MYELOID LEUKEMIA</subject><subject>Myeloid malignancy</subject><subject>PATIENTS</subject><subject>POLYMERASE CHAIN REACTION</subject><subject>Proteins - genetics</subject><subject>RNA</subject><subject>Sequence Deletion</subject><subject>Tumor suppressor</subject><issn>0006-291X</issn><issn>1090-2104</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU2L1TAUhoMoznX0D7iQgOCu9SRNkwbcyODHwIAbBXchTU6dXNvmTtKO3L0_3HTuBXe6yiF5zhPOeQl5yaBmwOTbfd33ydUcQNcgagDxiOwYaKg4A_GY7ABAVlyz7xfkWc57AMaE1E_JBdNN23UN7Mjva4_zEobg7BLiTONALXVxmko9BZeixxEfXty45gUTDTNVd5zVDc1r39vZU1vgH_RQBEWV6a-w3NLpiGMMno64_sQpWLqBD5f-mA-jzUtwNB9nn-KEz8mTwY4ZX5zPS_Lt44evV5-rmy-frq_e31ROtGqpNGvl4FohQQsBorNOuYH1ElkDneR900jPWzeA00KL1rnGlloN2DYSBwXNJXl98sbyvckuLOhuXZxndIvhnGmtQBXqzYk6pHi3Yl7MFLLDcbQzxjUbqZiSXQf_BTm0kqmWF5CfwLLPnBMO5pDCZNPRMDBblGZvtijNFqUBYUqUpenV2b72E_q_LefsCvDuBGBZ2X3AtE2Es0Mf0jaQj-Ff_j_MjLC8</recordid><startdate>20090529</startdate><enddate>20090529</enddate><creator>Asou, Hiroya</creator><creator>Matsui, Hirotaka</creator><creator>Ozaki, Yuko</creator><creator>Nagamachi, Akiko</creator><creator>Nakamura, Megumi</creator><creator>Aki, Daisuke</creator><creator>Inaba, Toshiya</creator><general>Elsevier Inc</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>7QR</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>OTOTI</scope></search><sort><creationdate>20090529</creationdate><title>Identification of a common microdeletion cluster in 7q21.3 subband among patients with myeloid leukemia and myelodysplastic syndrome</title><author>Asou, Hiroya ; Matsui, Hirotaka ; Ozaki, Yuko ; Nagamachi, Akiko ; Nakamura, Megumi ; Aki, Daisuke ; Inaba, Toshiya</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c457t-9156fc5460944048ac7cf1b6e130862b336d25cf0c94945cc3af0c7fe536ef703</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>60 APPLIED LIFE SCIENCES</topic><topic>Base Sequence</topic><topic>Cell Line, Tumor</topic><topic>Cell Nucleus - ultrastructure</topic><topic>Chromosome Aberrations</topic><topic>CHROMOSOMES</topic><topic>Chromosomes, Human, Pair 7 - genetics</topic><topic>GENES</topic><topic>Genes, Tumor Suppressor</topic><topic>Humans</topic><topic>Leukemia, Myeloid - genetics</topic><topic>MITOSIS</topic><topic>Mitosis - genetics</topic><topic>Monosomy 7</topic><topic>MORPHOLOGY</topic><topic>Multigene Family</topic><topic>Myelodysplastic Syndromes - genetics</topic><topic>MYELOID LEUKEMIA</topic><topic>Myeloid malignancy</topic><topic>PATIENTS</topic><topic>POLYMERASE CHAIN REACTION</topic><topic>Proteins - genetics</topic><topic>RNA</topic><topic>Sequence Deletion</topic><topic>Tumor suppressor</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Asou, Hiroya</creatorcontrib><creatorcontrib>Matsui, Hirotaka</creatorcontrib><creatorcontrib>Ozaki, Yuko</creatorcontrib><creatorcontrib>Nagamachi, Akiko</creatorcontrib><creatorcontrib>Nakamura, Megumi</creatorcontrib><creatorcontrib>Aki, Daisuke</creatorcontrib><creatorcontrib>Inaba, Toshiya</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Chemoreception Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>OSTI.GOV</collection><jtitle>Biochemical and biophysical research communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Asou, Hiroya</au><au>Matsui, Hirotaka</au><au>Ozaki, Yuko</au><au>Nagamachi, Akiko</au><au>Nakamura, Megumi</au><au>Aki, Daisuke</au><au>Inaba, Toshiya</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Identification of a common microdeletion cluster in 7q21.3 subband among patients with myeloid leukemia and myelodysplastic syndrome</atitle><jtitle>Biochemical and biophysical research communications</jtitle><addtitle>Biochem Biophys Res Commun</addtitle><date>2009-05-29</date><risdate>2009</risdate><volume>383</volume><issue>2</issue><spage>245</spage><epage>251</epage><pages>245-251</pages><issn>0006-291X</issn><eissn>1090-2104</eissn><abstract>Monosomy 7 and interstitial deletions in the long arm of chromosome 7 (−7/7q−) is a common nonrandom chromosomal abnormality found frequently in myeloid disorders including acute myeloid leukemia (AML), myelodysplastic syndrome (MDS), and juvenile myelomonocytic leukemia (JMML). Using a short probe-based microarray comparative genomic hybridization (mCGH) technology, we identified a common microdeletion cluster in 7q21.3 subband, which is adjacent to ‘hot deletion region’ thus far identified by conventional methods. This common microdeletion cluster contains three poorly characterized genes;
Samd9,
Samd9L, and a putative gene
LOC253012, which we named
Miki. Gene copy number assessment of three genes by real-time PCR revealed heterozygous deletion of these three genes in adult patients with AML and MDS at high frequency, in addition to JMML patients. Miki locates to mitotic spindles and centrosomes and downregulation of Miki by RNA interference induced abnormalities in mitosis and nuclear morphology, similar to myelodysplasia. In addition, a recent report indicated Samd9 as a tumor suppressor. These findings indicate the usefulness of the short probe-based CGH to detect microdeletions. The three genes located to 7q21.3 would be candidates for myeloid tumor-suppressor genes on 7q.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>19358830</pmid><doi>10.1016/j.bbrc.2009.04.004</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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subjects | 60 APPLIED LIFE SCIENCES Base Sequence Cell Line, Tumor Cell Nucleus - ultrastructure Chromosome Aberrations CHROMOSOMES Chromosomes, Human, Pair 7 - genetics GENES Genes, Tumor Suppressor Humans Leukemia, Myeloid - genetics MITOSIS Mitosis - genetics Monosomy 7 MORPHOLOGY Multigene Family Myelodysplastic Syndromes - genetics MYELOID LEUKEMIA Myeloid malignancy PATIENTS POLYMERASE CHAIN REACTION Proteins - genetics RNA Sequence Deletion Tumor suppressor |
title | Identification of a common microdeletion cluster in 7q21.3 subband among patients with myeloid leukemia and myelodysplastic syndrome |
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