Genome-Wide Somatic Alterations in Multiple Myeloma Reveal a Superior Outcome Group
Multiple myeloma (MM) is accompanied by heterogeneous somatic alterations. The overall goal of this study was to describe the genomic landscape of myeloma using deep whole-genome sequencing (WGS) and develop a model that identifies patients with long survival. We analyzed deep WGS data from 183 newl...
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| Veröffentlicht in: | Journal of clinical oncology 2020-09, Vol.38 (27), p.3107-3118 |
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| creator | Samur, Mehmet Kemal Aktas Samur, Anil Fulciniti, Mariateresa Szalat, Raphael Han, Tessa Shammas, Masood Richardson, Paul Magrangeas, Florence Minvielle, Stephane Corre, Jill Moreau, Philippe Thakurta, Anjan Anderson, Kenneth C Parmigiani, Giovanni Avet-Loiseau, Hervé Munshi, Nikhil C |
| description | Multiple myeloma (MM) is accompanied by heterogeneous somatic alterations. The overall goal of this study was to describe the genomic landscape of myeloma using deep whole-genome sequencing (WGS) and develop a model that identifies patients with long survival.
We analyzed deep WGS data from 183 newly diagnosed patients with MM treated with lenalidomide, bortezomib, and dexamethasone (RVD) alone or RVD + autologous stem cell transplant (ASCT) in the IFM/DFCI 2009 study (ClinicalTrials.gov identifier: NCT01191060). We integrated genomic markers with clinical data.
We report significant variability in mutational load and processes within MM subgroups. The timeline of observed activation of mutational processes provides the basis for 2 distinct models of acquisition of mutational changes detected at the time of diagnosis of myeloma. Virtually all MM subgroups have activated DNA repair-associated signature as a prominent late mutational process, whereas APOBEC signature targeting C>G is activated in the intermediate phase of disease progression in high-risk MM. Importantly, we identify a genomically defined MM subgroup (17% of newly diagnosed patients) with low DNA damage (low genomic scar score with chromosome 9 gain) and a superior outcome (100% overall survival at 69 months), which was validated in a large independent cohort. This subgroup allowed us to distinguish patients with low- and high-risk hyperdiploid MM and identify patients with prolongation of progression-free survival. Genomic characteristics of this subgroup included lower mutational load with significant contribution from age-related mutations as well as frequent
mutation. Surprisingly, their overall survival was independent of International Staging System and minimal residual disease status.
This is a comprehensive study identifying genomic markers of a good-risk group with prolonged survival. Identification of this patient subgroup will affect future therapeutic algorithms and research planning. |
| doi_str_mv | 10.1200/jco.20.00461 |
| format | Article |
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We analyzed deep WGS data from 183 newly diagnosed patients with MM treated with lenalidomide, bortezomib, and dexamethasone (RVD) alone or RVD + autologous stem cell transplant (ASCT) in the IFM/DFCI 2009 study (ClinicalTrials.gov identifier: NCT01191060). We integrated genomic markers with clinical data.
We report significant variability in mutational load and processes within MM subgroups. The timeline of observed activation of mutational processes provides the basis for 2 distinct models of acquisition of mutational changes detected at the time of diagnosis of myeloma. Virtually all MM subgroups have activated DNA repair-associated signature as a prominent late mutational process, whereas APOBEC signature targeting C>G is activated in the intermediate phase of disease progression in high-risk MM. Importantly, we identify a genomically defined MM subgroup (17% of newly diagnosed patients) with low DNA damage (low genomic scar score with chromosome 9 gain) and a superior outcome (100% overall survival at 69 months), which was validated in a large independent cohort. This subgroup allowed us to distinguish patients with low- and high-risk hyperdiploid MM and identify patients with prolongation of progression-free survival. Genomic characteristics of this subgroup included lower mutational load with significant contribution from age-related mutations as well as frequent
mutation. Surprisingly, their overall survival was independent of International Staging System and minimal residual disease status.
This is a comprehensive study identifying genomic markers of a good-risk group with prolonged survival. Identification of this patient subgroup will affect future therapeutic algorithms and research planning.</description><identifier>ISSN: 0732-183X</identifier><identifier>ISSN: 1527-7755</identifier><identifier>EISSN: 1527-7755</identifier><identifier>DOI: 10.1200/jco.20.00461</identifier><identifier>PMID: 32687451</identifier><language>eng</language><publisher>United States: American Society of Clinical Oncology</publisher><subject>Adult ; Aged ; Antineoplastic Combined Chemotherapy Protocols - therapeutic use ; Biomarkers, Tumor - genetics ; Bortezomib - administration & dosage ; Cancer ; Combined Modality Therapy ; Dexamethasone ; DNA Mutational Analysis ; DNA, Neoplasm ; Female ; GTP Phosphohydrolases - genetics ; Humans ; INDEL Mutation ; Lenalidomide - administration & dosage ; Life Sciences ; Male ; Membrane Proteins - genetics ; Middle Aged ; Multiple Myeloma - genetics ; Multiple Myeloma - therapy ; ORIGINAL REPORTS ; Progression-Free Survival ; Stem Cell Transplantation ; Survival Rate ; Treatment Outcome ; Whole Genome Sequencing</subject><ispartof>Journal of clinical oncology, 2020-09, Vol.38 (27), p.3107-3118</ispartof><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><rights>2020 by American Society of Clinical Oncology 2020 American Society of Clinical Oncology</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c487t-ffcbf1d9fb514ead0d2cb0f0e262c00a2a4165e58a9cc3949b3e7d14d33b2f983</citedby><cites>FETCH-LOGICAL-c487t-ffcbf1d9fb514ead0d2cb0f0e262c00a2a4165e58a9cc3949b3e7d14d33b2f983</cites><orcidid>0000-0003-1389-312X ; 0000-0003-1580-6106 ; 0000-0002-3050-0140 ; 0000-0003-1780-8746</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,3729,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32687451$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://inserm.hal.science/inserm-02913784$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Samur, Mehmet Kemal</creatorcontrib><creatorcontrib>Aktas Samur, Anil</creatorcontrib><creatorcontrib>Fulciniti, Mariateresa</creatorcontrib><creatorcontrib>Szalat, Raphael</creatorcontrib><creatorcontrib>Han, Tessa</creatorcontrib><creatorcontrib>Shammas, Masood</creatorcontrib><creatorcontrib>Richardson, Paul</creatorcontrib><creatorcontrib>Magrangeas, Florence</creatorcontrib><creatorcontrib>Minvielle, Stephane</creatorcontrib><creatorcontrib>Corre, Jill</creatorcontrib><creatorcontrib>Moreau, Philippe</creatorcontrib><creatorcontrib>Thakurta, Anjan</creatorcontrib><creatorcontrib>Anderson, Kenneth C</creatorcontrib><creatorcontrib>Parmigiani, Giovanni</creatorcontrib><creatorcontrib>Avet-Loiseau, Hervé</creatorcontrib><creatorcontrib>Munshi, Nikhil C</creatorcontrib><title>Genome-Wide Somatic Alterations in Multiple Myeloma Reveal a Superior Outcome Group</title><title>Journal of clinical oncology</title><addtitle>J Clin Oncol</addtitle><description>Multiple myeloma (MM) is accompanied by heterogeneous somatic alterations. The overall goal of this study was to describe the genomic landscape of myeloma using deep whole-genome sequencing (WGS) and develop a model that identifies patients with long survival.
We analyzed deep WGS data from 183 newly diagnosed patients with MM treated with lenalidomide, bortezomib, and dexamethasone (RVD) alone or RVD + autologous stem cell transplant (ASCT) in the IFM/DFCI 2009 study (ClinicalTrials.gov identifier: NCT01191060). We integrated genomic markers with clinical data.
We report significant variability in mutational load and processes within MM subgroups. The timeline of observed activation of mutational processes provides the basis for 2 distinct models of acquisition of mutational changes detected at the time of diagnosis of myeloma. Virtually all MM subgroups have activated DNA repair-associated signature as a prominent late mutational process, whereas APOBEC signature targeting C>G is activated in the intermediate phase of disease progression in high-risk MM. Importantly, we identify a genomically defined MM subgroup (17% of newly diagnosed patients) with low DNA damage (low genomic scar score with chromosome 9 gain) and a superior outcome (100% overall survival at 69 months), which was validated in a large independent cohort. This subgroup allowed us to distinguish patients with low- and high-risk hyperdiploid MM and identify patients with prolongation of progression-free survival. Genomic characteristics of this subgroup included lower mutational load with significant contribution from age-related mutations as well as frequent
mutation. Surprisingly, their overall survival was independent of International Staging System and minimal residual disease status.
This is a comprehensive study identifying genomic markers of a good-risk group with prolonged survival. Identification of this patient subgroup will affect future therapeutic algorithms and research planning.</description><subject>Adult</subject><subject>Aged</subject><subject>Antineoplastic Combined Chemotherapy Protocols - therapeutic use</subject><subject>Biomarkers, Tumor - genetics</subject><subject>Bortezomib - administration & dosage</subject><subject>Cancer</subject><subject>Combined Modality Therapy</subject><subject>Dexamethasone</subject><subject>DNA Mutational Analysis</subject><subject>DNA, Neoplasm</subject><subject>Female</subject><subject>GTP Phosphohydrolases - genetics</subject><subject>Humans</subject><subject>INDEL Mutation</subject><subject>Lenalidomide - administration & dosage</subject><subject>Life Sciences</subject><subject>Male</subject><subject>Membrane Proteins - genetics</subject><subject>Middle Aged</subject><subject>Multiple Myeloma - genetics</subject><subject>Multiple Myeloma - therapy</subject><subject>ORIGINAL REPORTS</subject><subject>Progression-Free Survival</subject><subject>Stem Cell Transplantation</subject><subject>Survival Rate</subject><subject>Treatment Outcome</subject><subject>Whole Genome Sequencing</subject><issn>0732-183X</issn><issn>1527-7755</issn><issn>1527-7755</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkU1v1DAQhi0Eokvhxhn5yIEs4684uSCtVrAFbbUSC4Kb5TgT6sqJg52s1H9PoKV8nGakeeYZjV5CnjNYMw7w-trFNYc1gCzZA7JiiutCa6UekhVowQtWia9n5EnO1wBMVkI9JmeCl5WWiq3IcYdD7LH44lukx9jbyTu6CROmpYtDpn6gl3OY_BiQXt5gWBD6EU9oA7X0OI-YfEz0ME9u0dBdivP4lDzqbMj47K6ek8_v3n7aXhT7w-79drMvnKz0VHSdazrW1l2jmETbQstdAx0gL7kDsNxKVipUla2dE7WsG4G6ZbIVouFdXYlz8ubWO85Nj63DYUo2mDH53qYbE603_04Gf2W-xZPRsq5LJhbBq1vB1X9rF5u98UPG1BvgNRO6kie24C_v7qX4fcY8md5nhyHYAeOcDZdcVbUCrf6YXYo5J-zu9QzMz9jMh-3BcDC_YlvwF39_cg__zkn8AL91lFo</recordid><startdate>20200920</startdate><enddate>20200920</enddate><creator>Samur, Mehmet Kemal</creator><creator>Aktas Samur, Anil</creator><creator>Fulciniti, Mariateresa</creator><creator>Szalat, Raphael</creator><creator>Han, Tessa</creator><creator>Shammas, Masood</creator><creator>Richardson, Paul</creator><creator>Magrangeas, Florence</creator><creator>Minvielle, Stephane</creator><creator>Corre, Jill</creator><creator>Moreau, Philippe</creator><creator>Thakurta, Anjan</creator><creator>Anderson, Kenneth C</creator><creator>Parmigiani, Giovanni</creator><creator>Avet-Loiseau, Hervé</creator><creator>Munshi, Nikhil C</creator><general>American Society of Clinical Oncology</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>7X8</scope><scope>1XC</scope><scope>VOOES</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0003-1389-312X</orcidid><orcidid>https://orcid.org/0000-0003-1580-6106</orcidid><orcidid>https://orcid.org/0000-0002-3050-0140</orcidid><orcidid>https://orcid.org/0000-0003-1780-8746</orcidid></search><sort><creationdate>20200920</creationdate><title>Genome-Wide Somatic Alterations in Multiple Myeloma Reveal a Superior Outcome Group</title><author>Samur, Mehmet Kemal ; 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The overall goal of this study was to describe the genomic landscape of myeloma using deep whole-genome sequencing (WGS) and develop a model that identifies patients with long survival.
We analyzed deep WGS data from 183 newly diagnosed patients with MM treated with lenalidomide, bortezomib, and dexamethasone (RVD) alone or RVD + autologous stem cell transplant (ASCT) in the IFM/DFCI 2009 study (ClinicalTrials.gov identifier: NCT01191060). We integrated genomic markers with clinical data.
We report significant variability in mutational load and processes within MM subgroups. The timeline of observed activation of mutational processes provides the basis for 2 distinct models of acquisition of mutational changes detected at the time of diagnosis of myeloma. Virtually all MM subgroups have activated DNA repair-associated signature as a prominent late mutational process, whereas APOBEC signature targeting C>G is activated in the intermediate phase of disease progression in high-risk MM. Importantly, we identify a genomically defined MM subgroup (17% of newly diagnosed patients) with low DNA damage (low genomic scar score with chromosome 9 gain) and a superior outcome (100% overall survival at 69 months), which was validated in a large independent cohort. This subgroup allowed us to distinguish patients with low- and high-risk hyperdiploid MM and identify patients with prolongation of progression-free survival. Genomic characteristics of this subgroup included lower mutational load with significant contribution from age-related mutations as well as frequent
mutation. Surprisingly, their overall survival was independent of International Staging System and minimal residual disease status.
This is a comprehensive study identifying genomic markers of a good-risk group with prolonged survival. Identification of this patient subgroup will affect future therapeutic algorithms and research planning.</abstract><cop>United States</cop><pub>American Society of Clinical Oncology</pub><pmid>32687451</pmid><doi>10.1200/jco.20.00461</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0003-1389-312X</orcidid><orcidid>https://orcid.org/0000-0003-1580-6106</orcidid><orcidid>https://orcid.org/0000-0002-3050-0140</orcidid><orcidid>https://orcid.org/0000-0003-1780-8746</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | Journal of clinical oncology, 2020-09, Vol.38 (27), p.3107-3118 |
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| source | MEDLINE; American Society of Clinical Oncology Online Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Adult Aged Antineoplastic Combined Chemotherapy Protocols - therapeutic use Biomarkers, Tumor - genetics Bortezomib - administration & dosage Cancer Combined Modality Therapy Dexamethasone DNA Mutational Analysis DNA, Neoplasm Female GTP Phosphohydrolases - genetics Humans INDEL Mutation Lenalidomide - administration & dosage Life Sciences Male Membrane Proteins - genetics Middle Aged Multiple Myeloma - genetics Multiple Myeloma - therapy ORIGINAL REPORTS Progression-Free Survival Stem Cell Transplantation Survival Rate Treatment Outcome Whole Genome Sequencing |
| title | Genome-Wide Somatic Alterations in Multiple Myeloma Reveal a Superior Outcome Group |
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