Sensitive detection of GATA1 mutations using complementary DNA‐based analysis for transient abnormal myelopoiesis associated with the Down syndrome
Introduction GATA1 mutation plays an important role in initiating transient abnormal myelopoiesis (TAM) and in the clonal evolution towards acute megakaryoblastic leukaemia (AMKL) associated with Down syndrome (DS). This study aimed to develop and validate the clinical utility of a complementary DNA...
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| Veröffentlicht in: | International journal of laboratory hematology 2022-04, Vol.44 (2), p.349-355 |
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| creator | Mizuta, Shumpei Yamane, Noriko Mononobe, Saya Watanabe, Asami Kitamura, Ritsuko Takahara, Tadamori Matsushima, Chieko Yoshida, Atushi Okamoto, Seiji Tanaka, Kuniaki Iwai, Atsushi Ikegawa, Atsuko Wada, Takahito Usami, Ikuya Maihara, Toshiro Komai, Takao Heike, Toshio Nishida, Yoshinobu Kobayashi, Kenichiro |
| description | Introduction
GATA1 mutation plays an important role in initiating transient abnormal myelopoiesis (TAM) and in the clonal evolution towards acute megakaryoblastic leukaemia (AMKL) associated with Down syndrome (DS). This study aimed to develop and validate the clinical utility of a complementary DNA (cDNA) analysis in parallel with the conventional genomic DNA (gDNA) Sanger sequencing (Ss), as an initial screening test for GATA1 mutations.
Methods
GATA1 mutations were evaluated using both gDNA and cDNA in 14 DS patients using Ss and fragment analysis (FA), respectively.
Results
The detection sensitivity of conventional gDNA sequencing was limited in low blast percentage TAM (LBP‐TAM); however, cDNA‐based Ss readily detected all the pathognomonic GATA1 mutations. The cDNA‐based FA readily detected GATA1 frameshift mutation with a reliable sensitivity ranging from 0.005% to 0.01% of clonal cells.
Conclusions
GATA1 mutations are heterogeneous; therefore, we would like to propose a dual cDNA and gDNA analysis as a standard diagnostic approach, especially for LBP‐TAM. cDNA‐based FA promises an excellent sensitivity for detecting frameshift GATA1 mutations in the longitudinal clonal evolution towards AMKL without using a patient specific primer. |
| doi_str_mv | 10.1111/ijlh.13756 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2596456102</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2640943631</sourcerecordid><originalsourceid>FETCH-LOGICAL-c3576-f7d7410553b9f337e536508d08ed56750ccf129d4f9c05e9f2c1676f6266b8253</originalsourceid><addsrcrecordid>eNp90U9vFCEYBnBiNLa2XvwAhsRLY7ItDAPsHDet_WM29WCbeJswzIvLhoEVGDdz60fw4hf0k8i6tQcPcoGQH0_y8iD0hpJTWtaZXbvVKWWSi2fokEpOZ5yzL8-fzhU9QK9SWhPCZU2al-iA1VJQXslD9PMz-GSz_Q64hww62-BxMPhqcbegeBiz2t0kPCbrv2Idho2DAXxWccIXt4tfDz86laDHyis3JZuwCRHnqEpoUVh1PsRBOTxM4MImWNgZlVLQVuXybmvzCucV4Iuw9ThNvo9hgGP0wiiX4PXjfoTuLz_cnV_Plp-ubs4Xy5lmXIqZkb2sKSnTdo1hTAJngpN5T-bQcyE50drQqulr02jCoTGVpkIKIyohunnF2RE62eduYvg2QsrtYJMG55SHMKa24o2ouaCkKvTdP3QdxlimLkqUX62ZYLSo93ulY0gpgmk30Q7ls1pK2l1Z7a6s9k9ZBb99jBy7Afon-redAugebK2D6T9R7c3H5fU-9DesS6Hf</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2640943631</pqid></control><display><type>article</type><title>Sensitive detection of GATA1 mutations using complementary DNA‐based analysis for transient abnormal myelopoiesis associated with the Down syndrome</title><source>MEDLINE</source><source>Wiley Online Library Journals Frontfile Complete</source><creator>Mizuta, Shumpei ; Yamane, Noriko ; Mononobe, Saya ; Watanabe, Asami ; Kitamura, Ritsuko ; Takahara, Tadamori ; Matsushima, Chieko ; Yoshida, Atushi ; Okamoto, Seiji ; Tanaka, Kuniaki ; Iwai, Atsushi ; Ikegawa, Atsuko ; Wada, Takahito ; Usami, Ikuya ; Maihara, Toshiro ; Komai, Takao ; Heike, Toshio ; Nishida, Yoshinobu ; Kobayashi, Kenichiro</creator><creatorcontrib>Mizuta, Shumpei ; Yamane, Noriko ; Mononobe, Saya ; Watanabe, Asami ; Kitamura, Ritsuko ; Takahara, Tadamori ; Matsushima, Chieko ; Yoshida, Atushi ; Okamoto, Seiji ; Tanaka, Kuniaki ; Iwai, Atsushi ; Ikegawa, Atsuko ; Wada, Takahito ; Usami, Ikuya ; Maihara, Toshiro ; Komai, Takao ; Heike, Toshio ; Nishida, Yoshinobu ; Kobayashi, Kenichiro</creatorcontrib><description>Introduction
GATA1 mutation plays an important role in initiating transient abnormal myelopoiesis (TAM) and in the clonal evolution towards acute megakaryoblastic leukaemia (AMKL) associated with Down syndrome (DS). This study aimed to develop and validate the clinical utility of a complementary DNA (cDNA) analysis in parallel with the conventional genomic DNA (gDNA) Sanger sequencing (Ss), as an initial screening test for GATA1 mutations.
Methods
GATA1 mutations were evaluated using both gDNA and cDNA in 14 DS patients using Ss and fragment analysis (FA), respectively.
Results
The detection sensitivity of conventional gDNA sequencing was limited in low blast percentage TAM (LBP‐TAM); however, cDNA‐based Ss readily detected all the pathognomonic GATA1 mutations. The cDNA‐based FA readily detected GATA1 frameshift mutation with a reliable sensitivity ranging from 0.005% to 0.01% of clonal cells.
Conclusions
GATA1 mutations are heterogeneous; therefore, we would like to propose a dual cDNA and gDNA analysis as a standard diagnostic approach, especially for LBP‐TAM. cDNA‐based FA promises an excellent sensitivity for detecting frameshift GATA1 mutations in the longitudinal clonal evolution towards AMKL without using a patient specific primer.</description><identifier>ISSN: 1751-5521</identifier><identifier>EISSN: 1751-553X</identifier><identifier>DOI: 10.1111/ijlh.13756</identifier><identifier>PMID: 34761527</identifier><language>eng</language><publisher>England: Wiley Subscription Services, Inc</publisher><subject>Complementary DNA ; DNA sequencing ; DNA, Complementary ; Down syndrome ; Down Syndrome - complications ; Down Syndrome - diagnosis ; Down Syndrome - genetics ; Down's syndrome ; fragment analysis ; Frameshift mutation ; GATA-1 protein ; GATA1 mutation ; GATA1 Transcription Factor - genetics ; Humans ; Leukemia ; Leukemia, Megakaryoblastic, Acute - complications ; Leukemia, Megakaryoblastic, Acute - diagnosis ; Leukemia, Megakaryoblastic, Acute - genetics ; Leukemoid Reaction - diagnosis ; Leukemoid Reaction - genetics ; Mutation ; Myelopoiesis ; Patients ; Prenatal diagnosis ; transient abnormal myelopoiesis</subject><ispartof>International journal of laboratory hematology, 2022-04, Vol.44 (2), p.349-355</ispartof><rights>2021 John Wiley & Sons Ltd</rights><rights>2021 John Wiley & Sons Ltd.</rights><rights>Copyright © 2022 John Wiley & Sons Ltd</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3576-f7d7410553b9f337e536508d08ed56750ccf129d4f9c05e9f2c1676f6266b8253</citedby><cites>FETCH-LOGICAL-c3576-f7d7410553b9f337e536508d08ed56750ccf129d4f9c05e9f2c1676f6266b8253</cites><orcidid>0000-0003-2688-8522</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fijlh.13756$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fijlh.13756$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34761527$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Mizuta, Shumpei</creatorcontrib><creatorcontrib>Yamane, Noriko</creatorcontrib><creatorcontrib>Mononobe, Saya</creatorcontrib><creatorcontrib>Watanabe, Asami</creatorcontrib><creatorcontrib>Kitamura, Ritsuko</creatorcontrib><creatorcontrib>Takahara, Tadamori</creatorcontrib><creatorcontrib>Matsushima, Chieko</creatorcontrib><creatorcontrib>Yoshida, Atushi</creatorcontrib><creatorcontrib>Okamoto, Seiji</creatorcontrib><creatorcontrib>Tanaka, Kuniaki</creatorcontrib><creatorcontrib>Iwai, Atsushi</creatorcontrib><creatorcontrib>Ikegawa, Atsuko</creatorcontrib><creatorcontrib>Wada, Takahito</creatorcontrib><creatorcontrib>Usami, Ikuya</creatorcontrib><creatorcontrib>Maihara, Toshiro</creatorcontrib><creatorcontrib>Komai, Takao</creatorcontrib><creatorcontrib>Heike, Toshio</creatorcontrib><creatorcontrib>Nishida, Yoshinobu</creatorcontrib><creatorcontrib>Kobayashi, Kenichiro</creatorcontrib><title>Sensitive detection of GATA1 mutations using complementary DNA‐based analysis for transient abnormal myelopoiesis associated with the Down syndrome</title><title>International journal of laboratory hematology</title><addtitle>Int J Lab Hematol</addtitle><description>Introduction
GATA1 mutation plays an important role in initiating transient abnormal myelopoiesis (TAM) and in the clonal evolution towards acute megakaryoblastic leukaemia (AMKL) associated with Down syndrome (DS). This study aimed to develop and validate the clinical utility of a complementary DNA (cDNA) analysis in parallel with the conventional genomic DNA (gDNA) Sanger sequencing (Ss), as an initial screening test for GATA1 mutations.
Methods
GATA1 mutations were evaluated using both gDNA and cDNA in 14 DS patients using Ss and fragment analysis (FA), respectively.
Results
The detection sensitivity of conventional gDNA sequencing was limited in low blast percentage TAM (LBP‐TAM); however, cDNA‐based Ss readily detected all the pathognomonic GATA1 mutations. The cDNA‐based FA readily detected GATA1 frameshift mutation with a reliable sensitivity ranging from 0.005% to 0.01% of clonal cells.
Conclusions
GATA1 mutations are heterogeneous; therefore, we would like to propose a dual cDNA and gDNA analysis as a standard diagnostic approach, especially for LBP‐TAM. cDNA‐based FA promises an excellent sensitivity for detecting frameshift GATA1 mutations in the longitudinal clonal evolution towards AMKL without using a patient specific primer.</description><subject>Complementary DNA</subject><subject>DNA sequencing</subject><subject>DNA, Complementary</subject><subject>Down syndrome</subject><subject>Down Syndrome - complications</subject><subject>Down Syndrome - diagnosis</subject><subject>Down Syndrome - genetics</subject><subject>Down's syndrome</subject><subject>fragment analysis</subject><subject>Frameshift mutation</subject><subject>GATA-1 protein</subject><subject>GATA1 mutation</subject><subject>GATA1 Transcription Factor - genetics</subject><subject>Humans</subject><subject>Leukemia</subject><subject>Leukemia, Megakaryoblastic, Acute - complications</subject><subject>Leukemia, Megakaryoblastic, Acute - diagnosis</subject><subject>Leukemia, Megakaryoblastic, Acute - genetics</subject><subject>Leukemoid Reaction - diagnosis</subject><subject>Leukemoid Reaction - genetics</subject><subject>Mutation</subject><subject>Myelopoiesis</subject><subject>Patients</subject><subject>Prenatal diagnosis</subject><subject>transient abnormal myelopoiesis</subject><issn>1751-5521</issn><issn>1751-553X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp90U9vFCEYBnBiNLa2XvwAhsRLY7ItDAPsHDet_WM29WCbeJswzIvLhoEVGDdz60fw4hf0k8i6tQcPcoGQH0_y8iD0hpJTWtaZXbvVKWWSi2fokEpOZ5yzL8-fzhU9QK9SWhPCZU2al-iA1VJQXslD9PMz-GSz_Q64hww62-BxMPhqcbegeBiz2t0kPCbrv2Idho2DAXxWccIXt4tfDz86laDHyis3JZuwCRHnqEpoUVh1PsRBOTxM4MImWNgZlVLQVuXybmvzCucV4Iuw9ThNvo9hgGP0wiiX4PXjfoTuLz_cnV_Plp-ubs4Xy5lmXIqZkb2sKSnTdo1hTAJngpN5T-bQcyE50drQqulr02jCoTGVpkIKIyohunnF2RE62eduYvg2QsrtYJMG55SHMKa24o2ouaCkKvTdP3QdxlimLkqUX62ZYLSo93ulY0gpgmk30Q7ls1pK2l1Z7a6s9k9ZBb99jBy7Afon-redAugebK2D6T9R7c3H5fU-9DesS6Hf</recordid><startdate>202204</startdate><enddate>202204</enddate><creator>Mizuta, Shumpei</creator><creator>Yamane, Noriko</creator><creator>Mononobe, Saya</creator><creator>Watanabe, Asami</creator><creator>Kitamura, Ritsuko</creator><creator>Takahara, Tadamori</creator><creator>Matsushima, Chieko</creator><creator>Yoshida, Atushi</creator><creator>Okamoto, Seiji</creator><creator>Tanaka, Kuniaki</creator><creator>Iwai, Atsushi</creator><creator>Ikegawa, Atsuko</creator><creator>Wada, Takahito</creator><creator>Usami, Ikuya</creator><creator>Maihara, Toshiro</creator><creator>Komai, Takao</creator><creator>Heike, Toshio</creator><creator>Nishida, Yoshinobu</creator><creator>Kobayashi, Kenichiro</creator><general>Wiley Subscription Services, 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>7T5</scope><scope>H94</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0003-2688-8522</orcidid></search><sort><creationdate>202204</creationdate><title>Sensitive detection of GATA1 mutations using complementary DNA‐based analysis for transient abnormal myelopoiesis associated with the Down syndrome</title><author>Mizuta, Shumpei ; Yamane, Noriko ; Mononobe, Saya ; Watanabe, Asami ; Kitamura, Ritsuko ; Takahara, Tadamori ; Matsushima, Chieko ; Yoshida, Atushi ; Okamoto, Seiji ; Tanaka, Kuniaki ; Iwai, Atsushi ; Ikegawa, Atsuko ; Wada, Takahito ; Usami, Ikuya ; Maihara, Toshiro ; Komai, Takao ; Heike, Toshio ; Nishida, Yoshinobu ; Kobayashi, Kenichiro</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3576-f7d7410553b9f337e536508d08ed56750ccf129d4f9c05e9f2c1676f6266b8253</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Complementary DNA</topic><topic>DNA sequencing</topic><topic>DNA, Complementary</topic><topic>Down syndrome</topic><topic>Down Syndrome - complications</topic><topic>Down Syndrome - diagnosis</topic><topic>Down Syndrome - genetics</topic><topic>Down's syndrome</topic><topic>fragment analysis</topic><topic>Frameshift mutation</topic><topic>GATA-1 protein</topic><topic>GATA1 mutation</topic><topic>GATA1 Transcription Factor - genetics</topic><topic>Humans</topic><topic>Leukemia</topic><topic>Leukemia, Megakaryoblastic, Acute - complications</topic><topic>Leukemia, Megakaryoblastic, Acute - diagnosis</topic><topic>Leukemia, Megakaryoblastic, Acute - genetics</topic><topic>Leukemoid Reaction - diagnosis</topic><topic>Leukemoid Reaction - genetics</topic><topic>Mutation</topic><topic>Myelopoiesis</topic><topic>Patients</topic><topic>Prenatal diagnosis</topic><topic>transient abnormal myelopoiesis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Mizuta, Shumpei</creatorcontrib><creatorcontrib>Yamane, Noriko</creatorcontrib><creatorcontrib>Mononobe, Saya</creatorcontrib><creatorcontrib>Watanabe, Asami</creatorcontrib><creatorcontrib>Kitamura, Ritsuko</creatorcontrib><creatorcontrib>Takahara, Tadamori</creatorcontrib><creatorcontrib>Matsushima, Chieko</creatorcontrib><creatorcontrib>Yoshida, Atushi</creatorcontrib><creatorcontrib>Okamoto, Seiji</creatorcontrib><creatorcontrib>Tanaka, Kuniaki</creatorcontrib><creatorcontrib>Iwai, Atsushi</creatorcontrib><creatorcontrib>Ikegawa, Atsuko</creatorcontrib><creatorcontrib>Wada, Takahito</creatorcontrib><creatorcontrib>Usami, Ikuya</creatorcontrib><creatorcontrib>Maihara, Toshiro</creatorcontrib><creatorcontrib>Komai, Takao</creatorcontrib><creatorcontrib>Heike, Toshio</creatorcontrib><creatorcontrib>Nishida, Yoshinobu</creatorcontrib><creatorcontrib>Kobayashi, Kenichiro</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>International journal of laboratory hematology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Mizuta, Shumpei</au><au>Yamane, Noriko</au><au>Mononobe, Saya</au><au>Watanabe, Asami</au><au>Kitamura, Ritsuko</au><au>Takahara, Tadamori</au><au>Matsushima, Chieko</au><au>Yoshida, Atushi</au><au>Okamoto, Seiji</au><au>Tanaka, Kuniaki</au><au>Iwai, Atsushi</au><au>Ikegawa, Atsuko</au><au>Wada, Takahito</au><au>Usami, Ikuya</au><au>Maihara, Toshiro</au><au>Komai, Takao</au><au>Heike, Toshio</au><au>Nishida, Yoshinobu</au><au>Kobayashi, Kenichiro</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Sensitive detection of GATA1 mutations using complementary DNA‐based analysis for transient abnormal myelopoiesis associated with the Down syndrome</atitle><jtitle>International journal of laboratory hematology</jtitle><addtitle>Int J Lab Hematol</addtitle><date>2022-04</date><risdate>2022</risdate><volume>44</volume><issue>2</issue><spage>349</spage><epage>355</epage><pages>349-355</pages><issn>1751-5521</issn><eissn>1751-553X</eissn><abstract>Introduction
GATA1 mutation plays an important role in initiating transient abnormal myelopoiesis (TAM) and in the clonal evolution towards acute megakaryoblastic leukaemia (AMKL) associated with Down syndrome (DS). This study aimed to develop and validate the clinical utility of a complementary DNA (cDNA) analysis in parallel with the conventional genomic DNA (gDNA) Sanger sequencing (Ss), as an initial screening test for GATA1 mutations.
Methods
GATA1 mutations were evaluated using both gDNA and cDNA in 14 DS patients using Ss and fragment analysis (FA), respectively.
Results
The detection sensitivity of conventional gDNA sequencing was limited in low blast percentage TAM (LBP‐TAM); however, cDNA‐based Ss readily detected all the pathognomonic GATA1 mutations. The cDNA‐based FA readily detected GATA1 frameshift mutation with a reliable sensitivity ranging from 0.005% to 0.01% of clonal cells.
Conclusions
GATA1 mutations are heterogeneous; therefore, we would like to propose a dual cDNA and gDNA analysis as a standard diagnostic approach, especially for LBP‐TAM. cDNA‐based FA promises an excellent sensitivity for detecting frameshift GATA1 mutations in the longitudinal clonal evolution towards AMKL without using a patient specific primer.</abstract><cop>England</cop><pub>Wiley Subscription Services, Inc</pub><pmid>34761527</pmid><doi>10.1111/ijlh.13756</doi><tpages>7</tpages><orcidid>https://orcid.org/0000-0003-2688-8522</orcidid></addata></record> |
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| subjects | Complementary DNA DNA sequencing DNA, Complementary Down syndrome Down Syndrome - complications Down Syndrome - diagnosis Down Syndrome - genetics Down's syndrome fragment analysis Frameshift mutation GATA-1 protein GATA1 mutation GATA1 Transcription Factor - genetics Humans Leukemia Leukemia, Megakaryoblastic, Acute - complications Leukemia, Megakaryoblastic, Acute - diagnosis Leukemia, Megakaryoblastic, Acute - genetics Leukemoid Reaction - diagnosis Leukemoid Reaction - genetics Mutation Myelopoiesis Patients Prenatal diagnosis transient abnormal myelopoiesis |
| title | Sensitive detection of GATA1 mutations using complementary DNA‐based analysis for transient abnormal myelopoiesis associated with the Down syndrome |
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