Rapid, ultra low coverage copy number profiling of cell-free DNA as a precision oncology screening strategy
Current cell-free DNA (cfDNA) next generation sequencing (NGS) precision oncology workflows are typically limited to targeted and/or disease-specific applications. In advanced cancer, disease burden and cfDNA tumor content are often elevated, yielding unique precision oncology opportunities. We soug...
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| creator | Hovelson, Daniel H Liu, Chia-Jen Wang, Yugang Kang, Qing Henderson, James Gursky, Amy Brockman, Scott Ramnath, Nithya Krauss, John C Talpaz, Moshe Kandarpa, Malathi Chugh, Rashmi Tuck, Missy Herman, Kirk Grasso, Catherine S Quist, Michael J Feng, Felix Y Haakenson, Christine Langmore, John Kamberov, Emmanuel Tesmer, Tim Husain, Hatim Lonigro, Robert J Robinson, Dan Smith, David C Alva, Ajjai S Hussain, Maha H Chinnaiyan, Arul M Tewari, Muneesh Mills, Ryan E Morgan, Todd M Tomlins, Scott A |
| description | Current cell-free DNA (cfDNA) next generation sequencing (NGS) precision oncology workflows are typically limited to targeted and/or disease-specific applications. In advanced cancer, disease burden and cfDNA tumor content are often elevated, yielding unique precision oncology opportunities. We sought to demonstrate the utility of a pan-cancer, rapid, inexpensive, whole genome NGS of cfDNA approach (PRINCe) as a precision oncology screening strategy via ultra-low coverage (~0.01x) tumor content determination through genome-wide copy number alteration (CNA) profiling. We applied PRINCe to a retrospective cohort of 124 cfDNA samples from 100 patients with advanced cancers, including 76 men with metastatic castration-resistant prostate cancer (mCRPC), enabling cfDNA tumor content approximation and actionable focal CNA detection, while facilitating concordance analyses between cfDNA and tissue-based NGS profiles and assessment of cfDNA alteration associations with mCRPC treatment outcomes. Therapeutically relevant focal CNAs were present in 42 (34%) cfDNA samples, including 36 of 93 (39%) mCRPC patient samples harboring AR amplification. PRINCe identified pre-treatment cfDNA CNA profiles facilitating disease monitoring. Combining PRINCe with routine targeted NGS of cfDNA enabled mutation and CNA assessment with coverages tuned to cfDNA tumor content. In mCRPC, genome-wide PRINCe cfDNA and matched tissue CNA profiles showed high concordance (median Pearson correlation = 0.87), and PRINCe detectable
amplifications predicted reduced time on therapy, independent of therapy type (Kaplan-Meier log-rank test, chi-square = 24.9,
< 0.0001). Our screening approach enables robust, broadly applicable cfDNA-based precision oncology for patients with advanced cancer through scalable identification of therapeutically relevant CNAs and pre-/post-treatment genomic profiles, enabling cfDNA- or tissue-based precision oncology workflow optimization. |
| doi_str_mv | 10.18632/oncotarget.21163 |
| format | Article |
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amplifications predicted reduced time on therapy, independent of therapy type (Kaplan-Meier log-rank test, chi-square = 24.9,
< 0.0001). Our screening approach enables robust, broadly applicable cfDNA-based precision oncology for patients with advanced cancer through scalable identification of therapeutically relevant CNAs and pre-/post-treatment genomic profiles, enabling cfDNA- or tissue-based precision oncology workflow optimization.</description><identifier>ISSN: 1949-2553</identifier><identifier>EISSN: 1949-2553</identifier><identifier>DOI: 10.18632/oncotarget.21163</identifier><identifier>PMID: 29163793</identifier><language>eng</language><publisher>United States: Impact Journals LLC</publisher><subject>Research Paper</subject><ispartof>Oncotarget, 2017-10, Vol.8 (52), p.89848-89866</ispartof><rights>Copyright: © 2017 Hovelson et al. 2017</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c399t-4273d32354dc6237f18e262dbed63164df0f4cfe53f9d5573c82eecbeccacad73</citedby><cites>FETCH-LOGICAL-c399t-4273d32354dc6237f18e262dbed63164df0f4cfe53f9d5573c82eecbeccacad73</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5685714/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5685714/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29163793$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hovelson, Daniel H</creatorcontrib><creatorcontrib>Liu, Chia-Jen</creatorcontrib><creatorcontrib>Wang, Yugang</creatorcontrib><creatorcontrib>Kang, Qing</creatorcontrib><creatorcontrib>Henderson, James</creatorcontrib><creatorcontrib>Gursky, Amy</creatorcontrib><creatorcontrib>Brockman, Scott</creatorcontrib><creatorcontrib>Ramnath, Nithya</creatorcontrib><creatorcontrib>Krauss, John C</creatorcontrib><creatorcontrib>Talpaz, Moshe</creatorcontrib><creatorcontrib>Kandarpa, Malathi</creatorcontrib><creatorcontrib>Chugh, Rashmi</creatorcontrib><creatorcontrib>Tuck, Missy</creatorcontrib><creatorcontrib>Herman, Kirk</creatorcontrib><creatorcontrib>Grasso, Catherine S</creatorcontrib><creatorcontrib>Quist, Michael J</creatorcontrib><creatorcontrib>Feng, Felix Y</creatorcontrib><creatorcontrib>Haakenson, Christine</creatorcontrib><creatorcontrib>Langmore, John</creatorcontrib><creatorcontrib>Kamberov, Emmanuel</creatorcontrib><creatorcontrib>Tesmer, Tim</creatorcontrib><creatorcontrib>Husain, Hatim</creatorcontrib><creatorcontrib>Lonigro, Robert J</creatorcontrib><creatorcontrib>Robinson, Dan</creatorcontrib><creatorcontrib>Smith, David C</creatorcontrib><creatorcontrib>Alva, Ajjai S</creatorcontrib><creatorcontrib>Hussain, Maha H</creatorcontrib><creatorcontrib>Chinnaiyan, Arul M</creatorcontrib><creatorcontrib>Tewari, Muneesh</creatorcontrib><creatorcontrib>Mills, Ryan E</creatorcontrib><creatorcontrib>Morgan, Todd M</creatorcontrib><creatorcontrib>Tomlins, Scott A</creatorcontrib><title>Rapid, ultra low coverage copy number profiling of cell-free DNA as a precision oncology screening strategy</title><title>Oncotarget</title><addtitle>Oncotarget</addtitle><description>Current cell-free DNA (cfDNA) next generation sequencing (NGS) precision oncology workflows are typically limited to targeted and/or disease-specific applications. In advanced cancer, disease burden and cfDNA tumor content are often elevated, yielding unique precision oncology opportunities. We sought to demonstrate the utility of a pan-cancer, rapid, inexpensive, whole genome NGS of cfDNA approach (PRINCe) as a precision oncology screening strategy via ultra-low coverage (~0.01x) tumor content determination through genome-wide copy number alteration (CNA) profiling. We applied PRINCe to a retrospective cohort of 124 cfDNA samples from 100 patients with advanced cancers, including 76 men with metastatic castration-resistant prostate cancer (mCRPC), enabling cfDNA tumor content approximation and actionable focal CNA detection, while facilitating concordance analyses between cfDNA and tissue-based NGS profiles and assessment of cfDNA alteration associations with mCRPC treatment outcomes. Therapeutically relevant focal CNAs were present in 42 (34%) cfDNA samples, including 36 of 93 (39%) mCRPC patient samples harboring AR amplification. PRINCe identified pre-treatment cfDNA CNA profiles facilitating disease monitoring. Combining PRINCe with routine targeted NGS of cfDNA enabled mutation and CNA assessment with coverages tuned to cfDNA tumor content. In mCRPC, genome-wide PRINCe cfDNA and matched tissue CNA profiles showed high concordance (median Pearson correlation = 0.87), and PRINCe detectable
amplifications predicted reduced time on therapy, independent of therapy type (Kaplan-Meier log-rank test, chi-square = 24.9,
< 0.0001). 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In advanced cancer, disease burden and cfDNA tumor content are often elevated, yielding unique precision oncology opportunities. We sought to demonstrate the utility of a pan-cancer, rapid, inexpensive, whole genome NGS of cfDNA approach (PRINCe) as a precision oncology screening strategy via ultra-low coverage (~0.01x) tumor content determination through genome-wide copy number alteration (CNA) profiling. We applied PRINCe to a retrospective cohort of 124 cfDNA samples from 100 patients with advanced cancers, including 76 men with metastatic castration-resistant prostate cancer (mCRPC), enabling cfDNA tumor content approximation and actionable focal CNA detection, while facilitating concordance analyses between cfDNA and tissue-based NGS profiles and assessment of cfDNA alteration associations with mCRPC treatment outcomes. Therapeutically relevant focal CNAs were present in 42 (34%) cfDNA samples, including 36 of 93 (39%) mCRPC patient samples harboring AR amplification. PRINCe identified pre-treatment cfDNA CNA profiles facilitating disease monitoring. Combining PRINCe with routine targeted NGS of cfDNA enabled mutation and CNA assessment with coverages tuned to cfDNA tumor content. In mCRPC, genome-wide PRINCe cfDNA and matched tissue CNA profiles showed high concordance (median Pearson correlation = 0.87), and PRINCe detectable
amplifications predicted reduced time on therapy, independent of therapy type (Kaplan-Meier log-rank test, chi-square = 24.9,
< 0.0001). Our screening approach enables robust, broadly applicable cfDNA-based precision oncology for patients with advanced cancer through scalable identification of therapeutically relevant CNAs and pre-/post-treatment genomic profiles, enabling cfDNA- or tissue-based precision oncology workflow optimization.</abstract><cop>United States</cop><pub>Impact Journals LLC</pub><pmid>29163793</pmid><doi>10.18632/oncotarget.21163</doi><tpages>19</tpages><oa>free_for_read</oa></addata></record> |
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| title | Rapid, ultra low coverage copy number profiling of cell-free DNA as a precision oncology screening strategy |
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