PPP1R7 Is a Novel Translocation Partner of CBFB via t(2;16)(q37;q22) in Acute Myeloid Leukemia
In a subset of acute myeloid leukemia (AML) cases, the core binding factor beta subunit gene (CBFB) was rearranged via inv(16)(p13.1q22) or t(16;16)(p13.1;q22), in which the smooth muscle myosin heavy chain 11 gene (MYH11) was the partner (CBFB::MYH11). Rare variants of CBFB rearrangement occurring...
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| Veröffentlicht in: | Genes 2022-07, Vol.13 (8), p.1367 |
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| creator | Wang, Lulu Wang, Wei Beird, Hannah Cheng, Xueqian Fang, Hong Tang, Guilin Toruner, Gokce Yin, C. You, M. Issa, Ghayas Borthakur, Gautam Peng, Guang Khoury, Joseph Medeiros, L. Tang, Zhenya |
| description | In a subset of acute myeloid leukemia (AML) cases, the core binding factor beta subunit gene (CBFB) was rearranged via inv(16)(p13.1q22) or t(16;16)(p13.1;q22), in which the smooth muscle myosin heavy chain 11 gene (MYH11) was the partner (CBFB::MYH11). Rare variants of CBFB rearrangement occurring via non-classic chromosomal aberrations have been reported, such as t(1;16), t(2;16), t(3;16), t(5;16), and t(16;19), but the partners of CBFB have not been characterized. We report a case of AML with a complex karyotype, including t(2;16)(q37;q22), in which the protein phosphatase 1 regulatory subunit 7 gene (PPP1R7) at chromosome 2q37 was rearranged with CBFB (CBFB::PPP1R7). This abnormality was inconspicuous by conventional karyotype and interphase fluorescence in situ hybridization (FISH), thus leading to an initial interpretation of inv(16)(p13.1q22); however, metaphase FISH showed that the CBFB rearrangement involved chromosome 2. Using whole genome and Sanger sequencing, the breakpoints were identified as being located in intron 5 of CBFB and intron 7 of PPP1R7. A microhomology of CAG was found in the break and reconnection sites of CBFB and PPP1R7, thus supporting the formation of CBFB::PPP1R7 by microhomology-mediated end joining. |
| doi_str_mv | 10.3390/genes13081367 |
| format | Article |
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Rare variants of CBFB rearrangement occurring via non-classic chromosomal aberrations have been reported, such as t(1;16), t(2;16), t(3;16), t(5;16), and t(16;19), but the partners of CBFB have not been characterized. We report a case of AML with a complex karyotype, including t(2;16)(q37;q22), in which the protein phosphatase 1 regulatory subunit 7 gene (PPP1R7) at chromosome 2q37 was rearranged with CBFB (CBFB::PPP1R7). This abnormality was inconspicuous by conventional karyotype and interphase fluorescence in situ hybridization (FISH), thus leading to an initial interpretation of inv(16)(p13.1q22); however, metaphase FISH showed that the CBFB rearrangement involved chromosome 2. Using whole genome and Sanger sequencing, the breakpoints were identified as being located in intron 5 of CBFB and intron 7 of PPP1R7. A microhomology of CAG was found in the break and reconnection sites of CBFB and PPP1R7, thus supporting the formation of CBFB::PPP1R7 by microhomology-mediated end joining.</description><identifier>ISSN: 2073-4425</identifier><identifier>EISSN: 2073-4425</identifier><identifier>DOI: 10.3390/genes13081367</identifier><identifier>PMID: 36011278</identifier><language>eng</language><publisher>Basel: MDPI AG</publisher><subject>Acute myeloid leukemia ; Blood ; Bone marrow ; Breakpoints ; Case reports ; Chemotherapy ; Chromosome 2 ; Chromosome aberrations ; Chromosomes ; Cytogenetics ; Fluorescence in situ hybridization ; Gene rearrangement ; Genomes ; Karyotypes ; Laboratories ; Leukemia ; Metaphase ; Myosin ; Phosphoprotein phosphatase ; Protein phosphatase ; Remission (Medicine) ; Smooth muscle ; Trinucleotide repeats</subject><ispartof>Genes, 2022-07, Vol.13 (8), p.1367</ispartof><rights>2022 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2022 by the authors. 2022</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c348t-4b5f4bdd489611a04eac9996ff679936af1ca3aa7acf15c15878eaa58b3025f03</cites><orcidid>0000-0003-2621-3584 ; 0000-0001-6577-8006 ; 0000-0002-5078-534X ; 0000-0002-8079-9945 ; 0000-0002-5305-6337 ; 0000-0002-4339-8683 ; 0000-0001-8454-1071</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9407081/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9407081/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,725,778,782,883,27907,27908,53774,53776</link.rule.ids></links><search><creatorcontrib>Wang, Lulu</creatorcontrib><creatorcontrib>Wang, Wei</creatorcontrib><creatorcontrib>Beird, Hannah</creatorcontrib><creatorcontrib>Cheng, Xueqian</creatorcontrib><creatorcontrib>Fang, Hong</creatorcontrib><creatorcontrib>Tang, Guilin</creatorcontrib><creatorcontrib>Toruner, Gokce</creatorcontrib><creatorcontrib>Yin, C.</creatorcontrib><creatorcontrib>You, M.</creatorcontrib><creatorcontrib>Issa, Ghayas</creatorcontrib><creatorcontrib>Borthakur, Gautam</creatorcontrib><creatorcontrib>Peng, Guang</creatorcontrib><creatorcontrib>Khoury, Joseph</creatorcontrib><creatorcontrib>Medeiros, L.</creatorcontrib><creatorcontrib>Tang, Zhenya</creatorcontrib><title>PPP1R7 Is a Novel Translocation Partner of CBFB via t(2;16)(q37;q22) in Acute Myeloid Leukemia</title><title>Genes</title><description>In a subset of acute myeloid leukemia (AML) cases, the core binding factor beta subunit gene (CBFB) was rearranged via inv(16)(p13.1q22) or t(16;16)(p13.1;q22), in which the smooth muscle myosin heavy chain 11 gene (MYH11) was the partner (CBFB::MYH11). Rare variants of CBFB rearrangement occurring via non-classic chromosomal aberrations have been reported, such as t(1;16), t(2;16), t(3;16), t(5;16), and t(16;19), but the partners of CBFB have not been characterized. We report a case of AML with a complex karyotype, including t(2;16)(q37;q22), in which the protein phosphatase 1 regulatory subunit 7 gene (PPP1R7) at chromosome 2q37 was rearranged with CBFB (CBFB::PPP1R7). This abnormality was inconspicuous by conventional karyotype and interphase fluorescence in situ hybridization (FISH), thus leading to an initial interpretation of inv(16)(p13.1q22); however, metaphase FISH showed that the CBFB rearrangement involved chromosome 2. Using whole genome and Sanger sequencing, the breakpoints were identified as being located in intron 5 of CBFB and intron 7 of PPP1R7. A microhomology of CAG was found in the break and reconnection sites of CBFB and PPP1R7, thus supporting the formation of CBFB::PPP1R7 by microhomology-mediated end joining.</description><subject>Acute myeloid leukemia</subject><subject>Blood</subject><subject>Bone marrow</subject><subject>Breakpoints</subject><subject>Case reports</subject><subject>Chemotherapy</subject><subject>Chromosome 2</subject><subject>Chromosome aberrations</subject><subject>Chromosomes</subject><subject>Cytogenetics</subject><subject>Fluorescence in situ hybridization</subject><subject>Gene rearrangement</subject><subject>Genomes</subject><subject>Karyotypes</subject><subject>Laboratories</subject><subject>Leukemia</subject><subject>Metaphase</subject><subject>Myosin</subject><subject>Phosphoprotein phosphatase</subject><subject>Protein phosphatase</subject><subject>Remission (Medicine)</subject><subject>Smooth muscle</subject><subject>Trinucleotide repeats</subject><issn>2073-4425</issn><issn>2073-4425</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNpdkc1rGzEQxUVpaIKbY--CXpzDtvpaaUWgkJikDTiJKem1YiyPUqVrKZZ2Dfnva5NQms5lBubHY948Qj5w9klKyz7fY8LKJeu41OYNORLMyEYp0b79Zz4kx7U-sF0pJhhr35FDqRnnwnRH5OdiseDfDb2qFOhN3mJP7wqk2mcPQ8yJLqAMCQvNgc7OL8_pNgIdpuKU65PpRprTjRAnNCZ65scB6fUT9jmu6BzH37iO8J4cBOgrHr_0CflxeXE3-9bMb79ezc7mjZeqGxq1bINarlaqs5pzYArBW2t1CNpYKzUE7kECGPCBt563nekQoO2Wkok2MDkhX551H8flGlce01Cgd48lrqE8uQzRvd6k-Mvd562zipn9-yZk-iJQ8mbEOrh1rB77HhLmsTphmNGcWaN26Mf_0Ic8lrSzt6c0t0oos6OaZ8qXXGvB8PcYztw-PPcqPPkHTzaIYw</recordid><startdate>20220729</startdate><enddate>20220729</enddate><creator>Wang, Lulu</creator><creator>Wang, Wei</creator><creator>Beird, Hannah</creator><creator>Cheng, Xueqian</creator><creator>Fang, Hong</creator><creator>Tang, Guilin</creator><creator>Toruner, Gokce</creator><creator>Yin, C.</creator><creator>You, M.</creator><creator>Issa, Ghayas</creator><creator>Borthakur, Gautam</creator><creator>Peng, Guang</creator><creator>Khoury, Joseph</creator><creator>Medeiros, L.</creator><creator>Tang, Zhenya</creator><general>MDPI AG</general><general>MDPI</general><scope>AAYXX</scope><scope>CITATION</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</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>GNUQQ</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M7P</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0003-2621-3584</orcidid><orcidid>https://orcid.org/0000-0001-6577-8006</orcidid><orcidid>https://orcid.org/0000-0002-5078-534X</orcidid><orcidid>https://orcid.org/0000-0002-8079-9945</orcidid><orcidid>https://orcid.org/0000-0002-5305-6337</orcidid><orcidid>https://orcid.org/0000-0002-4339-8683</orcidid><orcidid>https://orcid.org/0000-0001-8454-1071</orcidid></search><sort><creationdate>20220729</creationdate><title>PPP1R7 Is a Novel Translocation Partner of CBFB via t(2;16)(q37;q22) in Acute Myeloid Leukemia</title><author>Wang, Lulu ; Wang, Wei ; Beird, Hannah ; Cheng, Xueqian ; Fang, Hong ; Tang, Guilin ; Toruner, Gokce ; Yin, C. ; You, M. ; Issa, Ghayas ; Borthakur, Gautam ; Peng, Guang ; Khoury, Joseph ; Medeiros, L. ; Tang, Zhenya</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c348t-4b5f4bdd489611a04eac9996ff679936af1ca3aa7acf15c15878eaa58b3025f03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Acute myeloid leukemia</topic><topic>Blood</topic><topic>Bone marrow</topic><topic>Breakpoints</topic><topic>Case reports</topic><topic>Chemotherapy</topic><topic>Chromosome 2</topic><topic>Chromosome aberrations</topic><topic>Chromosomes</topic><topic>Cytogenetics</topic><topic>Fluorescence in situ hybridization</topic><topic>Gene rearrangement</topic><topic>Genomes</topic><topic>Karyotypes</topic><topic>Laboratories</topic><topic>Leukemia</topic><topic>Metaphase</topic><topic>Myosin</topic><topic>Phosphoprotein phosphatase</topic><topic>Protein phosphatase</topic><topic>Remission (Medicine)</topic><topic>Smooth muscle</topic><topic>Trinucleotide repeats</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Lulu</creatorcontrib><creatorcontrib>Wang, Wei</creatorcontrib><creatorcontrib>Beird, Hannah</creatorcontrib><creatorcontrib>Cheng, Xueqian</creatorcontrib><creatorcontrib>Fang, Hong</creatorcontrib><creatorcontrib>Tang, Guilin</creatorcontrib><creatorcontrib>Toruner, Gokce</creatorcontrib><creatorcontrib>Yin, C.</creatorcontrib><creatorcontrib>You, M.</creatorcontrib><creatorcontrib>Issa, Ghayas</creatorcontrib><creatorcontrib>Borthakur, Gautam</creatorcontrib><creatorcontrib>Peng, Guang</creatorcontrib><creatorcontrib>Khoury, Joseph</creatorcontrib><creatorcontrib>Medeiros, L.</creatorcontrib><creatorcontrib>Tang, Zhenya</creatorcontrib><collection>CrossRef</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</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 (ProQuest)</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Publicly Available Content Database</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>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Genes</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Lulu</au><au>Wang, Wei</au><au>Beird, Hannah</au><au>Cheng, Xueqian</au><au>Fang, Hong</au><au>Tang, Guilin</au><au>Toruner, Gokce</au><au>Yin, C.</au><au>You, M.</au><au>Issa, Ghayas</au><au>Borthakur, Gautam</au><au>Peng, Guang</au><au>Khoury, Joseph</au><au>Medeiros, L.</au><au>Tang, Zhenya</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>PPP1R7 Is a Novel Translocation Partner of CBFB via t(2;16)(q37;q22) in Acute Myeloid Leukemia</atitle><jtitle>Genes</jtitle><date>2022-07-29</date><risdate>2022</risdate><volume>13</volume><issue>8</issue><spage>1367</spage><pages>1367-</pages><issn>2073-4425</issn><eissn>2073-4425</eissn><abstract>In a subset of acute myeloid leukemia (AML) cases, the core binding factor beta subunit gene (CBFB) was rearranged via inv(16)(p13.1q22) or t(16;16)(p13.1;q22), in which the smooth muscle myosin heavy chain 11 gene (MYH11) was the partner (CBFB::MYH11). Rare variants of CBFB rearrangement occurring via non-classic chromosomal aberrations have been reported, such as t(1;16), t(2;16), t(3;16), t(5;16), and t(16;19), but the partners of CBFB have not been characterized. We report a case of AML with a complex karyotype, including t(2;16)(q37;q22), in which the protein phosphatase 1 regulatory subunit 7 gene (PPP1R7) at chromosome 2q37 was rearranged with CBFB (CBFB::PPP1R7). This abnormality was inconspicuous by conventional karyotype and interphase fluorescence in situ hybridization (FISH), thus leading to an initial interpretation of inv(16)(p13.1q22); however, metaphase FISH showed that the CBFB rearrangement involved chromosome 2. Using whole genome and Sanger sequencing, the breakpoints were identified as being located in intron 5 of CBFB and intron 7 of PPP1R7. A microhomology of CAG was found in the break and reconnection sites of CBFB and PPP1R7, thus supporting the formation of CBFB::PPP1R7 by microhomology-mediated end joining.</abstract><cop>Basel</cop><pub>MDPI AG</pub><pmid>36011278</pmid><doi>10.3390/genes13081367</doi><orcidid>https://orcid.org/0000-0003-2621-3584</orcidid><orcidid>https://orcid.org/0000-0001-6577-8006</orcidid><orcidid>https://orcid.org/0000-0002-5078-534X</orcidid><orcidid>https://orcid.org/0000-0002-8079-9945</orcidid><orcidid>https://orcid.org/0000-0002-5305-6337</orcidid><orcidid>https://orcid.org/0000-0002-4339-8683</orcidid><orcidid>https://orcid.org/0000-0001-8454-1071</orcidid><oa>free_for_read</oa></addata></record> |
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| source | Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central Open Access; MDPI - Multidisciplinary Digital Publishing Institute; PubMed Central |
| subjects | Acute myeloid leukemia Blood Bone marrow Breakpoints Case reports Chemotherapy Chromosome 2 Chromosome aberrations Chromosomes Cytogenetics Fluorescence in situ hybridization Gene rearrangement Genomes Karyotypes Laboratories Leukemia Metaphase Myosin Phosphoprotein phosphatase Protein phosphatase Remission (Medicine) Smooth muscle Trinucleotide repeats |
| title | PPP1R7 Is a Novel Translocation Partner of CBFB via t(2;16)(q37;q22) in Acute Myeloid Leukemia |
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