Detection of KMT2A Partial Tandem Duplication by Optical Genome Mapping in Myeloid Neoplasms: Associated Cytogenetics, Gene Mutations, Treatment Responses, and Patient Outcomes
partial tandem duplication (PTD) involves intragenic duplications and has been associated with poorer prognosis. In this study, we evaluated PTD in 1277 patients with hematological malignancies using optical genome mapping (OGM). PTD was detected in 35 patients with acute myeloid leukemia (AML) (7%)...
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| Veröffentlicht in: | Cancers 2024-12, Vol.16 (24), p.4193 |
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| creator | Wei, Qing Hu, Shimin Xu, Jie Loghavi, Sanam Daver, Naval Toruner, Gokce A Wang, Wei Medeiros, L Jeffrey Tang, Guilin |
| description | partial tandem duplication (PTD) involves intragenic
duplications and has been associated with poorer prognosis. In this study, we evaluated
PTD in 1277 patients with hematological malignancies using optical genome mapping (OGM).
PTD was detected in 35 patients with acute myeloid leukemia (AML) (7%), 5 patients with myelodysplastic syndrome (MDS) (2.2%), and 5 patients with chronic myelomonocytic leukemia (CMML) (7.1%). The PTDs varied in size, region, and copy number. An Archer RNA fusion assay confirmed
PTD in all 25 patients tested: 15 spanning exons 2 to 8 and 10 spanning exons 2 to 10. Most patients exhibited a normal (
= 21) or non-complex (
= 20) karyotype. The most common chromosomal abnormalities included loss of 20q or 7q and trisomy 11/gain of 11q. All patients had gene mutations, with
ITD and
prevalent in AML and
and
common in MDS and CMML. Among patients who received treatment and had at least one follow-up bone marrow evaluation, 82% of those with de novo AML achieved complete remission after initial induction chemotherapy, whereas 90% of patients with secondary or refractory/relapsed AML showed refractory or partial responses. All but one patient with MDS and CMML were refractory to therapy. We conclude that OGM is an effective tool for detecting
PTD. Neoplasms with
PTD frequently harbor gene mutations and display normal or non-complex karyotypes. Patients with
PTD are generally refractory to conventional therapy, except for de novo AML. |
| doi_str_mv | 10.3390/cancers16244193 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_11674272</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A821761455</galeid><sourcerecordid>A821761455</sourcerecordid><originalsourceid>FETCH-LOGICAL-c332t-f2fa6edc5e9194b55cc7c20523276c7bce13d6f407b0b37a89541df46802dace3</originalsourceid><addsrcrecordid>eNptUk1v1DAQjRCIVqVnbsgSFw5sG3_E3nBBqy0URJdFaDlbjjNZXCV2ajtI-6_4icy2pbQV9sGe8XtvZjxTFC9pecJ5XZ5a4y3ERCUTgtb8SXHISsVmUtbi6b37QXGc0mWJi3OqpHpeHPBaSVnW7LD4fQYZbHbBk9CRL6sNW5BvJmZnerIxvoWBnE1j76y5xjQ7sh4zWj05Bx8GICszjs5vifNktYM-uJZ8hTD2Jg3pHVmkFKwzGVqy3OWwBQ_ITm_3bORO-VoW7U0EkwfwmXyHNKIL0InxMZns9u71lC3GSy-KZ53pExzfnkfFj48fNstPs4v1-efl4mJmOWd51rHOSGhtBTWtRVNV1irLyopxpqRVjQXKW9mJUjVlw5WZ15WgbSfkvGStscCPivc3uuPUDCiEOUTT6zG6wcSdDsbphy_e_dTb8EtTKpVgiqHCm1uFGK4mSFkPLlnoe-MhTElzWvH5Pl6N0NePoJdhih7rQ5TA1JSo5D_U1vSgne8CBrZ7Ub2YM2wtFVWFqJP_oHBjL50NHjqH_geE0xuCjSGlCN1dkbTU-0HTjwYNGa_u_80d_u9Y8T9rRtFY</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>3149547456</pqid></control><display><type>article</type><title>Detection of KMT2A Partial Tandem Duplication by Optical Genome Mapping in Myeloid Neoplasms: Associated Cytogenetics, Gene Mutations, Treatment Responses, and Patient Outcomes</title><source>MDPI - Multidisciplinary Digital Publishing Institute</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>PubMed Central</source><source>PubMed Central Open Access</source><creator>Wei, Qing ; Hu, Shimin ; Xu, Jie ; Loghavi, Sanam ; Daver, Naval ; Toruner, Gokce A ; Wang, Wei ; Medeiros, L Jeffrey ; Tang, Guilin</creator><creatorcontrib>Wei, Qing ; Hu, Shimin ; Xu, Jie ; Loghavi, Sanam ; Daver, Naval ; Toruner, Gokce A ; Wang, Wei ; Medeiros, L Jeffrey ; Tang, Guilin</creatorcontrib><description>partial tandem duplication (PTD) involves intragenic
duplications and has been associated with poorer prognosis. In this study, we evaluated
PTD in 1277 patients with hematological malignancies using optical genome mapping (OGM).
PTD was detected in 35 patients with acute myeloid leukemia (AML) (7%), 5 patients with myelodysplastic syndrome (MDS) (2.2%), and 5 patients with chronic myelomonocytic leukemia (CMML) (7.1%). The PTDs varied in size, region, and copy number. An Archer RNA fusion assay confirmed
PTD in all 25 patients tested: 15 spanning exons 2 to 8 and 10 spanning exons 2 to 10. Most patients exhibited a normal (
= 21) or non-complex (
= 20) karyotype. The most common chromosomal abnormalities included loss of 20q or 7q and trisomy 11/gain of 11q. All patients had gene mutations, with
ITD and
prevalent in AML and
and
common in MDS and CMML. Among patients who received treatment and had at least one follow-up bone marrow evaluation, 82% of those with de novo AML achieved complete remission after initial induction chemotherapy, whereas 90% of patients with secondary or refractory/relapsed AML showed refractory or partial responses. All but one patient with MDS and CMML were refractory to therapy. We conclude that OGM is an effective tool for detecting
PTD. Neoplasms with
PTD frequently harbor gene mutations and display normal or non-complex karyotypes. Patients with
PTD are generally refractory to conventional therapy, except for de novo AML.</description><identifier>ISSN: 2072-6694</identifier><identifier>EISSN: 2072-6694</identifier><identifier>DOI: 10.3390/cancers16244193</identifier><identifier>PMID: 39766092</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Acute myeloid leukemia ; Bone marrow ; Cancer ; Chemotherapy ; Chromosomes ; Chronic myelomonocytic leukemia ; Cytogenetics ; Development and progression ; DNA binding proteins ; Epigenetic inheritance ; Epigenetics ; Fluorescence in situ hybridization ; Gene mapping ; Gene mutations ; Genes ; Genetic aspects ; Genetic transcription ; Genomes ; Genomics ; Hematology ; Karyotypes ; Kinases ; Leukemia ; Medical prognosis ; MLL protein ; Mutation ; Myelodysplastic syndrome ; Myelomonocytic leukemia ; Patient outcomes ; Point mutation ; Remission ; Signal transduction ; Transcription factors ; Tumors</subject><ispartof>Cancers, 2024-12, Vol.16 (24), p.4193</ispartof><rights>COPYRIGHT 2024 MDPI AG</rights><rights>2024 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>2024 by the authors. 2024</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c332t-f2fa6edc5e9194b55cc7c20523276c7bce13d6f407b0b37a89541df46802dace3</cites><orcidid>0000-0001-8980-3202 ; 0000-0001-7110-3814 ; 0000-0002-9482-4806 ; 0000-0002-5305-6337 ; 0000-0003-0141-9682 ; 0000-0001-6577-8006</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/PMC11674272/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11674272/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/39766092$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wei, Qing</creatorcontrib><creatorcontrib>Hu, Shimin</creatorcontrib><creatorcontrib>Xu, Jie</creatorcontrib><creatorcontrib>Loghavi, Sanam</creatorcontrib><creatorcontrib>Daver, Naval</creatorcontrib><creatorcontrib>Toruner, Gokce A</creatorcontrib><creatorcontrib>Wang, Wei</creatorcontrib><creatorcontrib>Medeiros, L Jeffrey</creatorcontrib><creatorcontrib>Tang, Guilin</creatorcontrib><title>Detection of KMT2A Partial Tandem Duplication by Optical Genome Mapping in Myeloid Neoplasms: Associated Cytogenetics, Gene Mutations, Treatment Responses, and Patient Outcomes</title><title>Cancers</title><addtitle>Cancers (Basel)</addtitle><description>partial tandem duplication (PTD) involves intragenic
duplications and has been associated with poorer prognosis. In this study, we evaluated
PTD in 1277 patients with hematological malignancies using optical genome mapping (OGM).
PTD was detected in 35 patients with acute myeloid leukemia (AML) (7%), 5 patients with myelodysplastic syndrome (MDS) (2.2%), and 5 patients with chronic myelomonocytic leukemia (CMML) (7.1%). The PTDs varied in size, region, and copy number. An Archer RNA fusion assay confirmed
PTD in all 25 patients tested: 15 spanning exons 2 to 8 and 10 spanning exons 2 to 10. Most patients exhibited a normal (
= 21) or non-complex (
= 20) karyotype. The most common chromosomal abnormalities included loss of 20q or 7q and trisomy 11/gain of 11q. All patients had gene mutations, with
ITD and
prevalent in AML and
and
common in MDS and CMML. Among patients who received treatment and had at least one follow-up bone marrow evaluation, 82% of those with de novo AML achieved complete remission after initial induction chemotherapy, whereas 90% of patients with secondary or refractory/relapsed AML showed refractory or partial responses. All but one patient with MDS and CMML were refractory to therapy. We conclude that OGM is an effective tool for detecting
PTD. Neoplasms with
PTD frequently harbor gene mutations and display normal or non-complex karyotypes. Patients with
PTD are generally refractory to conventional therapy, except for de novo AML.</description><subject>Acute myeloid leukemia</subject><subject>Bone marrow</subject><subject>Cancer</subject><subject>Chemotherapy</subject><subject>Chromosomes</subject><subject>Chronic myelomonocytic leukemia</subject><subject>Cytogenetics</subject><subject>Development and progression</subject><subject>DNA binding proteins</subject><subject>Epigenetic inheritance</subject><subject>Epigenetics</subject><subject>Fluorescence in situ hybridization</subject><subject>Gene mapping</subject><subject>Gene mutations</subject><subject>Genes</subject><subject>Genetic aspects</subject><subject>Genetic transcription</subject><subject>Genomes</subject><subject>Genomics</subject><subject>Hematology</subject><subject>Karyotypes</subject><subject>Kinases</subject><subject>Leukemia</subject><subject>Medical prognosis</subject><subject>MLL protein</subject><subject>Mutation</subject><subject>Myelodysplastic syndrome</subject><subject>Myelomonocytic leukemia</subject><subject>Patient outcomes</subject><subject>Point mutation</subject><subject>Remission</subject><subject>Signal transduction</subject><subject>Transcription factors</subject><subject>Tumors</subject><issn>2072-6694</issn><issn>2072-6694</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNptUk1v1DAQjRCIVqVnbsgSFw5sG3_E3nBBqy0URJdFaDlbjjNZXCV2ajtI-6_4icy2pbQV9sGe8XtvZjxTFC9pecJ5XZ5a4y3ERCUTgtb8SXHISsVmUtbi6b37QXGc0mWJi3OqpHpeHPBaSVnW7LD4fQYZbHbBk9CRL6sNW5BvJmZnerIxvoWBnE1j76y5xjQ7sh4zWj05Bx8GICszjs5vifNktYM-uJZ8hTD2Jg3pHVmkFKwzGVqy3OWwBQ_ITm_3bORO-VoW7U0EkwfwmXyHNKIL0InxMZns9u71lC3GSy-KZ53pExzfnkfFj48fNstPs4v1-efl4mJmOWd51rHOSGhtBTWtRVNV1irLyopxpqRVjQXKW9mJUjVlw5WZ15WgbSfkvGStscCPivc3uuPUDCiEOUTT6zG6wcSdDsbphy_e_dTb8EtTKpVgiqHCm1uFGK4mSFkPLlnoe-MhTElzWvH5Pl6N0NePoJdhih7rQ5TA1JSo5D_U1vSgne8CBrZ7Ub2YM2wtFVWFqJP_oHBjL50NHjqH_geE0xuCjSGlCN1dkbTU-0HTjwYNGa_u_80d_u9Y8T9rRtFY</recordid><startdate>20241216</startdate><enddate>20241216</enddate><creator>Wei, Qing</creator><creator>Hu, Shimin</creator><creator>Xu, Jie</creator><creator>Loghavi, Sanam</creator><creator>Daver, Naval</creator><creator>Toruner, Gokce A</creator><creator>Wang, Wei</creator><creator>Medeiros, L Jeffrey</creator><creator>Tang, Guilin</creator><general>MDPI AG</general><general>MDPI</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7T5</scope><scope>7TO</scope><scope>7XB</scope><scope>8FE</scope><scope>8FH</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>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-8980-3202</orcidid><orcidid>https://orcid.org/0000-0001-7110-3814</orcidid><orcidid>https://orcid.org/0000-0002-9482-4806</orcidid><orcidid>https://orcid.org/0000-0002-5305-6337</orcidid><orcidid>https://orcid.org/0000-0003-0141-9682</orcidid><orcidid>https://orcid.org/0000-0001-6577-8006</orcidid></search><sort><creationdate>20241216</creationdate><title>Detection of KMT2A Partial Tandem Duplication by Optical Genome Mapping in Myeloid Neoplasms: Associated Cytogenetics, Gene Mutations, Treatment Responses, and Patient Outcomes</title><author>Wei, Qing ; Hu, Shimin ; Xu, Jie ; Loghavi, Sanam ; Daver, Naval ; Toruner, Gokce A ; Wang, Wei ; Medeiros, L Jeffrey ; Tang, Guilin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c332t-f2fa6edc5e9194b55cc7c20523276c7bce13d6f407b0b37a89541df46802dace3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Acute myeloid leukemia</topic><topic>Bone marrow</topic><topic>Cancer</topic><topic>Chemotherapy</topic><topic>Chromosomes</topic><topic>Chronic myelomonocytic leukemia</topic><topic>Cytogenetics</topic><topic>Development and progression</topic><topic>DNA binding proteins</topic><topic>Epigenetic inheritance</topic><topic>Epigenetics</topic><topic>Fluorescence in situ hybridization</topic><topic>Gene mapping</topic><topic>Gene mutations</topic><topic>Genes</topic><topic>Genetic aspects</topic><topic>Genetic transcription</topic><topic>Genomes</topic><topic>Genomics</topic><topic>Hematology</topic><topic>Karyotypes</topic><topic>Kinases</topic><topic>Leukemia</topic><topic>Medical prognosis</topic><topic>MLL protein</topic><topic>Mutation</topic><topic>Myelodysplastic syndrome</topic><topic>Myelomonocytic leukemia</topic><topic>Patient outcomes</topic><topic>Point mutation</topic><topic>Remission</topic><topic>Signal transduction</topic><topic>Transcription factors</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wei, Qing</creatorcontrib><creatorcontrib>Hu, Shimin</creatorcontrib><creatorcontrib>Xu, Jie</creatorcontrib><creatorcontrib>Loghavi, Sanam</creatorcontrib><creatorcontrib>Daver, Naval</creatorcontrib><creatorcontrib>Toruner, Gokce A</creatorcontrib><creatorcontrib>Wang, Wei</creatorcontrib><creatorcontrib>Medeiros, L Jeffrey</creatorcontrib><creatorcontrib>Tang, Guilin</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</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>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Research Library</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</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>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cancers</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wei, Qing</au><au>Hu, Shimin</au><au>Xu, Jie</au><au>Loghavi, Sanam</au><au>Daver, Naval</au><au>Toruner, Gokce A</au><au>Wang, Wei</au><au>Medeiros, L Jeffrey</au><au>Tang, Guilin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Detection of KMT2A Partial Tandem Duplication by Optical Genome Mapping in Myeloid Neoplasms: Associated Cytogenetics, Gene Mutations, Treatment Responses, and Patient Outcomes</atitle><jtitle>Cancers</jtitle><addtitle>Cancers (Basel)</addtitle><date>2024-12-16</date><risdate>2024</risdate><volume>16</volume><issue>24</issue><spage>4193</spage><pages>4193-</pages><issn>2072-6694</issn><eissn>2072-6694</eissn><abstract>partial tandem duplication (PTD) involves intragenic
duplications and has been associated with poorer prognosis. In this study, we evaluated
PTD in 1277 patients with hematological malignancies using optical genome mapping (OGM).
PTD was detected in 35 patients with acute myeloid leukemia (AML) (7%), 5 patients with myelodysplastic syndrome (MDS) (2.2%), and 5 patients with chronic myelomonocytic leukemia (CMML) (7.1%). The PTDs varied in size, region, and copy number. An Archer RNA fusion assay confirmed
PTD in all 25 patients tested: 15 spanning exons 2 to 8 and 10 spanning exons 2 to 10. Most patients exhibited a normal (
= 21) or non-complex (
= 20) karyotype. The most common chromosomal abnormalities included loss of 20q or 7q and trisomy 11/gain of 11q. All patients had gene mutations, with
ITD and
prevalent in AML and
and
common in MDS and CMML. Among patients who received treatment and had at least one follow-up bone marrow evaluation, 82% of those with de novo AML achieved complete remission after initial induction chemotherapy, whereas 90% of patients with secondary or refractory/relapsed AML showed refractory or partial responses. All but one patient with MDS and CMML were refractory to therapy. We conclude that OGM is an effective tool for detecting
PTD. Neoplasms with
PTD frequently harbor gene mutations and display normal or non-complex karyotypes. Patients with
PTD are generally refractory to conventional therapy, except for de novo AML.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>39766092</pmid><doi>10.3390/cancers16244193</doi><orcidid>https://orcid.org/0000-0001-8980-3202</orcidid><orcidid>https://orcid.org/0000-0001-7110-3814</orcidid><orcidid>https://orcid.org/0000-0002-9482-4806</orcidid><orcidid>https://orcid.org/0000-0002-5305-6337</orcidid><orcidid>https://orcid.org/0000-0003-0141-9682</orcidid><orcidid>https://orcid.org/0000-0001-6577-8006</orcidid><oa>free_for_read</oa></addata></record> |
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| source | MDPI - Multidisciplinary Digital Publishing Institute; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; PubMed Central Open Access |
| subjects | Acute myeloid leukemia Bone marrow Cancer Chemotherapy Chromosomes Chronic myelomonocytic leukemia Cytogenetics Development and progression DNA binding proteins Epigenetic inheritance Epigenetics Fluorescence in situ hybridization Gene mapping Gene mutations Genes Genetic aspects Genetic transcription Genomes Genomics Hematology Karyotypes Kinases Leukemia Medical prognosis MLL protein Mutation Myelodysplastic syndrome Myelomonocytic leukemia Patient outcomes Point mutation Remission Signal transduction Transcription factors Tumors |
| title | Detection of KMT2A Partial Tandem Duplication by Optical Genome Mapping in Myeloid Neoplasms: Associated Cytogenetics, Gene Mutations, Treatment Responses, and Patient Outcomes |
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