Phylogenetic analyses of melanoma reveal complex patterns of metastatic dissemination
Melanoma is difficult to treat once it becomes metastatic. However, the precise ancestral relationship between primary tumors and their metastases is not well understood. We performed whole-exome sequencing of primary melanomas and multiple matched metastases from eight patients to elucidate their p...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Joe W. Gray [verfasserIn] |
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| Format: |
Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2015 |
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| Rechteinformationen: |
Nutzungsrecht: © COPYRIGHT 2015 National Academy of Sciences |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
Enthalten in: Proceedings of the National Academy of Sciences of the United States of America - Washington, DC : NAS, 1877, 112(2015), 35, Seite 10995-11000 |
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| Übergeordnetes Werk: |
volume:112 ; year:2015 ; number:35 ; pages:10995-11000 |
| Links: |
Volltext |
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| DOI / URN: |
10.1073/pnas.1508074112 |
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OLC1970285060 |
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| 520 | |a Melanoma is difficult to treat once it becomes metastatic. However, the precise ancestral relationship between primary tumors and their metastases is not well understood. We performed whole-exome sequencing of primary melanomas and multiple matched metastases from eight patients to elucidate their phylogenetic relationships. In six of eight patients, we found that genetically distinct cell populations in the primary tumor metastasized in parallel to different anatomic sites, rather than sequentially from one site to the next. In five of these six patients, the metastasizing cells had themselves arisen from a common parental subpopulation in the primary, indicating that the ability to establish metastases is a late-evolving trait. Interestingly, we discovered that individual metastases were sometimes founded by multiple cell populations of the primary that were genetically distinct. Such establishment of metastases by multiple tumor subpopulations could help explain why identical resistance variants are identified in different sites after initial response to systemic therapy. One primary tumor harbored two subclones with different oncogenic mutations in CTNNB1, which were both propagated to the same metastasis, raising the possibility that activation of wingless-type mouse mammary tumor virus integration site (WNT) signaling may be involved, as has been suggested by experimental models. | ||
| 540 | |a Nutzungsrecht: © COPYRIGHT 2015 National Academy of Sciences | ||
| 650 | 4 | |a Melanoma - pathology | |
| 650 | 4 | |a Melanoma - genetics | |
| 650 | 4 | |a Phylogeny | |
| 650 | 4 | |a Observations | |
| 650 | 4 | |a Melanoma | |
| 650 | 4 | |a Genetic aspects | |
| 650 | 4 | |a Metastasis | |
| 650 | 4 | |a Tumors | |
| 650 | 4 | |a Phylogenetics | |
| 650 | 4 | |a genetics | |
| 650 | 4 | |a melanoma | |
| 650 | 4 | |a Biological Sciences | |
| 650 | 4 | |a metastasis | |
| 700 | 0 | |a Elizabeth Purdom |4 oth | |
| 700 | 0 | |a John F. Thompson |4 oth | |
| 700 | 0 | |a Jongsuk Chung |4 oth | |
| 700 | 0 | |a Richard A. Scolyer |4 oth | |
| 700 | 0 | |a Robyn P. M. Saw |4 oth | |
| 700 | 0 | |a J. Zachary Sanborn |4 oth | |
| 700 | 0 | |a Timothy Butler |4 oth | |
| 700 | 0 | |a Boris C. Bastian |4 oth | |
| 700 | 0 | |a Nicholas J. Wang |4 oth | |
| 700 | 0 | |a Joe S. Hur |4 oth | |
| 700 | 0 | |a Lauren E. Haydu |4 oth | |
| 700 | 0 | |a Roger S. Lo |4 oth | |
| 700 | 0 | |a Raymond J. Cho |4 oth | |
| 700 | 0 | |a Rajmohan Murali |4 oth | |
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| 700 | 0 | |a Klaus J. Busam |4 oth | |
| 700 | 0 | |a James E. Cleaver |4 oth | |
| 700 | 0 | |a Eric A. Collisson |4 oth | |
| 700 | 0 | |a James S. Wilmott |4 oth | |
| 700 | 0 | |a Graham J. Mann |4 oth | |
| 700 | 0 | |a Paul T. Spellman |4 oth | |
| 700 | 0 | |a Nam Huh |4 oth | |
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10.1073/pnas.1508074112 doi PQ20160211 (DE-627)OLC1970285060 (DE-599)GBVOLC1970285060 (PRQ)g2667-e55bc499b8852e7e580610191e0b486a1a0fb95a0a5a2db2fd849a33b48894280 (KEY)0583363920150000112003510995phylogeneticanalysesofmelanomarevealcomplexpattern DE-627 ger DE-627 rakwb eng 500 DNB 570 AVZ LING fid BIODIV fid Joe W. Gray verfasserin aut Phylogenetic analyses of melanoma reveal complex patterns of metastatic dissemination 2015 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Melanoma is difficult to treat once it becomes metastatic. However, the precise ancestral relationship between primary tumors and their metastases is not well understood. We performed whole-exome sequencing of primary melanomas and multiple matched metastases from eight patients to elucidate their phylogenetic relationships. In six of eight patients, we found that genetically distinct cell populations in the primary tumor metastasized in parallel to different anatomic sites, rather than sequentially from one site to the next. In five of these six patients, the metastasizing cells had themselves arisen from a common parental subpopulation in the primary, indicating that the ability to establish metastases is a late-evolving trait. Interestingly, we discovered that individual metastases were sometimes founded by multiple cell populations of the primary that were genetically distinct. Such establishment of metastases by multiple tumor subpopulations could help explain why identical resistance variants are identified in different sites after initial response to systemic therapy. One primary tumor harbored two subclones with different oncogenic mutations in CTNNB1, which were both propagated to the same metastasis, raising the possibility that activation of wingless-type mouse mammary tumor virus integration site (WNT) signaling may be involved, as has been suggested by experimental models. Nutzungsrecht: © COPYRIGHT 2015 National Academy of Sciences Melanoma - pathology Melanoma - genetics Phylogeny Observations Melanoma Genetic aspects Metastasis Tumors Phylogenetics genetics melanoma Biological Sciences metastasis Elizabeth Purdom oth John F. Thompson oth Jongsuk Chung oth Richard A. Scolyer oth Robyn P. M. Saw oth J. Zachary Sanborn oth Timothy Butler oth Boris C. Bastian oth Nicholas J. Wang oth Joe S. Hur oth Lauren E. Haydu oth Roger S. Lo oth Raymond J. Cho oth Rajmohan Murali oth Hojabr Kakavand oth Klaus J. Busam oth James E. Cleaver oth Eric A. Collisson oth James S. Wilmott oth Graham J. Mann oth Paul T. Spellman oth Nam Huh oth Enthalten in Proceedings of the National Academy of Sciences of the United States of America Washington, DC : NAS, 1877 112(2015), 35, Seite 10995-11000 (DE-627)129505269 (DE-600)209104-5 (DE-576)014909189 0027-8424 nnns volume:112 year:2015 number:35 pages:10995-11000 http://dx.doi.org/10.1073/pnas.1508074112 Volltext http://www.pnas.org/content/112/35/10995.abstract http://www.ncbi.nlm.nih.gov/pubmed/26286987 http://search.proquest.com/docview/1711093359 http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=4568214&tool=pmcentrez&rendertype=abstract GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-LING FID-BIODIV SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-MAT SSG-OLC-FOR SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-MAT SSG-OPC-FOR GBV_ILN_40 GBV_ILN_59 AR 112 2015 35 10995-11000 |
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10.1073/pnas.1508074112 doi PQ20160211 (DE-627)OLC1970285060 (DE-599)GBVOLC1970285060 (PRQ)g2667-e55bc499b8852e7e580610191e0b486a1a0fb95a0a5a2db2fd849a33b48894280 (KEY)0583363920150000112003510995phylogeneticanalysesofmelanomarevealcomplexpattern DE-627 ger DE-627 rakwb eng 500 DNB 570 AVZ LING fid BIODIV fid Joe W. Gray verfasserin aut Phylogenetic analyses of melanoma reveal complex patterns of metastatic dissemination 2015 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Melanoma is difficult to treat once it becomes metastatic. However, the precise ancestral relationship between primary tumors and their metastases is not well understood. We performed whole-exome sequencing of primary melanomas and multiple matched metastases from eight patients to elucidate their phylogenetic relationships. In six of eight patients, we found that genetically distinct cell populations in the primary tumor metastasized in parallel to different anatomic sites, rather than sequentially from one site to the next. In five of these six patients, the metastasizing cells had themselves arisen from a common parental subpopulation in the primary, indicating that the ability to establish metastases is a late-evolving trait. Interestingly, we discovered that individual metastases were sometimes founded by multiple cell populations of the primary that were genetically distinct. Such establishment of metastases by multiple tumor subpopulations could help explain why identical resistance variants are identified in different sites after initial response to systemic therapy. One primary tumor harbored two subclones with different oncogenic mutations in CTNNB1, which were both propagated to the same metastasis, raising the possibility that activation of wingless-type mouse mammary tumor virus integration site (WNT) signaling may be involved, as has been suggested by experimental models. Nutzungsrecht: © COPYRIGHT 2015 National Academy of Sciences Melanoma - pathology Melanoma - genetics Phylogeny Observations Melanoma Genetic aspects Metastasis Tumors Phylogenetics genetics melanoma Biological Sciences metastasis Elizabeth Purdom oth John F. Thompson oth Jongsuk Chung oth Richard A. Scolyer oth Robyn P. M. Saw oth J. Zachary Sanborn oth Timothy Butler oth Boris C. Bastian oth Nicholas J. Wang oth Joe S. Hur oth Lauren E. Haydu oth Roger S. Lo oth Raymond J. Cho oth Rajmohan Murali oth Hojabr Kakavand oth Klaus J. Busam oth James E. Cleaver oth Eric A. Collisson oth James S. Wilmott oth Graham J. Mann oth Paul T. Spellman oth Nam Huh oth Enthalten in Proceedings of the National Academy of Sciences of the United States of America Washington, DC : NAS, 1877 112(2015), 35, Seite 10995-11000 (DE-627)129505269 (DE-600)209104-5 (DE-576)014909189 0027-8424 nnns volume:112 year:2015 number:35 pages:10995-11000 http://dx.doi.org/10.1073/pnas.1508074112 Volltext http://www.pnas.org/content/112/35/10995.abstract http://www.ncbi.nlm.nih.gov/pubmed/26286987 http://search.proquest.com/docview/1711093359 http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=4568214&tool=pmcentrez&rendertype=abstract GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-LING FID-BIODIV SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-MAT SSG-OLC-FOR SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-MAT SSG-OPC-FOR GBV_ILN_40 GBV_ILN_59 AR 112 2015 35 10995-11000 |
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10.1073/pnas.1508074112 doi PQ20160211 (DE-627)OLC1970285060 (DE-599)GBVOLC1970285060 (PRQ)g2667-e55bc499b8852e7e580610191e0b486a1a0fb95a0a5a2db2fd849a33b48894280 (KEY)0583363920150000112003510995phylogeneticanalysesofmelanomarevealcomplexpattern DE-627 ger DE-627 rakwb eng 500 DNB 570 AVZ LING fid BIODIV fid Joe W. Gray verfasserin aut Phylogenetic analyses of melanoma reveal complex patterns of metastatic dissemination 2015 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Melanoma is difficult to treat once it becomes metastatic. However, the precise ancestral relationship between primary tumors and their metastases is not well understood. We performed whole-exome sequencing of primary melanomas and multiple matched metastases from eight patients to elucidate their phylogenetic relationships. In six of eight patients, we found that genetically distinct cell populations in the primary tumor metastasized in parallel to different anatomic sites, rather than sequentially from one site to the next. In five of these six patients, the metastasizing cells had themselves arisen from a common parental subpopulation in the primary, indicating that the ability to establish metastases is a late-evolving trait. Interestingly, we discovered that individual metastases were sometimes founded by multiple cell populations of the primary that were genetically distinct. Such establishment of metastases by multiple tumor subpopulations could help explain why identical resistance variants are identified in different sites after initial response to systemic therapy. One primary tumor harbored two subclones with different oncogenic mutations in CTNNB1, which were both propagated to the same metastasis, raising the possibility that activation of wingless-type mouse mammary tumor virus integration site (WNT) signaling may be involved, as has been suggested by experimental models. Nutzungsrecht: © COPYRIGHT 2015 National Academy of Sciences Melanoma - pathology Melanoma - genetics Phylogeny Observations Melanoma Genetic aspects Metastasis Tumors Phylogenetics genetics melanoma Biological Sciences metastasis Elizabeth Purdom oth John F. Thompson oth Jongsuk Chung oth Richard A. Scolyer oth Robyn P. M. Saw oth J. Zachary Sanborn oth Timothy Butler oth Boris C. Bastian oth Nicholas J. Wang oth Joe S. Hur oth Lauren E. Haydu oth Roger S. Lo oth Raymond J. Cho oth Rajmohan Murali oth Hojabr Kakavand oth Klaus J. Busam oth James E. Cleaver oth Eric A. Collisson oth James S. Wilmott oth Graham J. Mann oth Paul T. Spellman oth Nam Huh oth Enthalten in Proceedings of the National Academy of Sciences of the United States of America Washington, DC : NAS, 1877 112(2015), 35, Seite 10995-11000 (DE-627)129505269 (DE-600)209104-5 (DE-576)014909189 0027-8424 nnns volume:112 year:2015 number:35 pages:10995-11000 http://dx.doi.org/10.1073/pnas.1508074112 Volltext http://www.pnas.org/content/112/35/10995.abstract http://www.ncbi.nlm.nih.gov/pubmed/26286987 http://search.proquest.com/docview/1711093359 http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=4568214&tool=pmcentrez&rendertype=abstract GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-LING FID-BIODIV SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-MAT SSG-OLC-FOR SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-MAT SSG-OPC-FOR GBV_ILN_40 GBV_ILN_59 AR 112 2015 35 10995-11000 |
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10.1073/pnas.1508074112 doi PQ20160211 (DE-627)OLC1970285060 (DE-599)GBVOLC1970285060 (PRQ)g2667-e55bc499b8852e7e580610191e0b486a1a0fb95a0a5a2db2fd849a33b48894280 (KEY)0583363920150000112003510995phylogeneticanalysesofmelanomarevealcomplexpattern DE-627 ger DE-627 rakwb eng 500 DNB 570 AVZ LING fid BIODIV fid Joe W. Gray verfasserin aut Phylogenetic analyses of melanoma reveal complex patterns of metastatic dissemination 2015 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Melanoma is difficult to treat once it becomes metastatic. However, the precise ancestral relationship between primary tumors and their metastases is not well understood. We performed whole-exome sequencing of primary melanomas and multiple matched metastases from eight patients to elucidate their phylogenetic relationships. In six of eight patients, we found that genetically distinct cell populations in the primary tumor metastasized in parallel to different anatomic sites, rather than sequentially from one site to the next. In five of these six patients, the metastasizing cells had themselves arisen from a common parental subpopulation in the primary, indicating that the ability to establish metastases is a late-evolving trait. Interestingly, we discovered that individual metastases were sometimes founded by multiple cell populations of the primary that were genetically distinct. Such establishment of metastases by multiple tumor subpopulations could help explain why identical resistance variants are identified in different sites after initial response to systemic therapy. One primary tumor harbored two subclones with different oncogenic mutations in CTNNB1, which were both propagated to the same metastasis, raising the possibility that activation of wingless-type mouse mammary tumor virus integration site (WNT) signaling may be involved, as has been suggested by experimental models. Nutzungsrecht: © COPYRIGHT 2015 National Academy of Sciences Melanoma - pathology Melanoma - genetics Phylogeny Observations Melanoma Genetic aspects Metastasis Tumors Phylogenetics genetics melanoma Biological Sciences metastasis Elizabeth Purdom oth John F. Thompson oth Jongsuk Chung oth Richard A. Scolyer oth Robyn P. M. Saw oth J. Zachary Sanborn oth Timothy Butler oth Boris C. Bastian oth Nicholas J. Wang oth Joe S. Hur oth Lauren E. Haydu oth Roger S. Lo oth Raymond J. Cho oth Rajmohan Murali oth Hojabr Kakavand oth Klaus J. Busam oth James E. Cleaver oth Eric A. Collisson oth James S. Wilmott oth Graham J. Mann oth Paul T. Spellman oth Nam Huh oth Enthalten in Proceedings of the National Academy of Sciences of the United States of America Washington, DC : NAS, 1877 112(2015), 35, Seite 10995-11000 (DE-627)129505269 (DE-600)209104-5 (DE-576)014909189 0027-8424 nnns volume:112 year:2015 number:35 pages:10995-11000 http://dx.doi.org/10.1073/pnas.1508074112 Volltext http://www.pnas.org/content/112/35/10995.abstract http://www.ncbi.nlm.nih.gov/pubmed/26286987 http://search.proquest.com/docview/1711093359 http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=4568214&tool=pmcentrez&rendertype=abstract GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-LING FID-BIODIV SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-MAT SSG-OLC-FOR SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-MAT SSG-OPC-FOR GBV_ILN_40 GBV_ILN_59 AR 112 2015 35 10995-11000 |
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10.1073/pnas.1508074112 doi PQ20160211 (DE-627)OLC1970285060 (DE-599)GBVOLC1970285060 (PRQ)g2667-e55bc499b8852e7e580610191e0b486a1a0fb95a0a5a2db2fd849a33b48894280 (KEY)0583363920150000112003510995phylogeneticanalysesofmelanomarevealcomplexpattern DE-627 ger DE-627 rakwb eng 500 DNB 570 AVZ LING fid BIODIV fid Joe W. Gray verfasserin aut Phylogenetic analyses of melanoma reveal complex patterns of metastatic dissemination 2015 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Melanoma is difficult to treat once it becomes metastatic. However, the precise ancestral relationship between primary tumors and their metastases is not well understood. We performed whole-exome sequencing of primary melanomas and multiple matched metastases from eight patients to elucidate their phylogenetic relationships. In six of eight patients, we found that genetically distinct cell populations in the primary tumor metastasized in parallel to different anatomic sites, rather than sequentially from one site to the next. In five of these six patients, the metastasizing cells had themselves arisen from a common parental subpopulation in the primary, indicating that the ability to establish metastases is a late-evolving trait. Interestingly, we discovered that individual metastases were sometimes founded by multiple cell populations of the primary that were genetically distinct. Such establishment of metastases by multiple tumor subpopulations could help explain why identical resistance variants are identified in different sites after initial response to systemic therapy. One primary tumor harbored two subclones with different oncogenic mutations in CTNNB1, which were both propagated to the same metastasis, raising the possibility that activation of wingless-type mouse mammary tumor virus integration site (WNT) signaling may be involved, as has been suggested by experimental models. Nutzungsrecht: © COPYRIGHT 2015 National Academy of Sciences Melanoma - pathology Melanoma - genetics Phylogeny Observations Melanoma Genetic aspects Metastasis Tumors Phylogenetics genetics melanoma Biological Sciences metastasis Elizabeth Purdom oth John F. Thompson oth Jongsuk Chung oth Richard A. Scolyer oth Robyn P. M. Saw oth J. Zachary Sanborn oth Timothy Butler oth Boris C. Bastian oth Nicholas J. Wang oth Joe S. Hur oth Lauren E. Haydu oth Roger S. Lo oth Raymond J. Cho oth Rajmohan Murali oth Hojabr Kakavand oth Klaus J. Busam oth James E. Cleaver oth Eric A. Collisson oth James S. Wilmott oth Graham J. Mann oth Paul T. Spellman oth Nam Huh oth Enthalten in Proceedings of the National Academy of Sciences of the United States of America Washington, DC : NAS, 1877 112(2015), 35, Seite 10995-11000 (DE-627)129505269 (DE-600)209104-5 (DE-576)014909189 0027-8424 nnns volume:112 year:2015 number:35 pages:10995-11000 http://dx.doi.org/10.1073/pnas.1508074112 Volltext http://www.pnas.org/content/112/35/10995.abstract http://www.ncbi.nlm.nih.gov/pubmed/26286987 http://search.proquest.com/docview/1711093359 http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=4568214&tool=pmcentrez&rendertype=abstract GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-LING FID-BIODIV SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-MAT SSG-OLC-FOR SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-MAT SSG-OPC-FOR GBV_ILN_40 GBV_ILN_59 AR 112 2015 35 10995-11000 |
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Phylogenetic analyses of melanoma reveal complex patterns of metastatic dissemination |
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Melanoma is difficult to treat once it becomes metastatic. However, the precise ancestral relationship between primary tumors and their metastases is not well understood. We performed whole-exome sequencing of primary melanomas and multiple matched metastases from eight patients to elucidate their phylogenetic relationships. In six of eight patients, we found that genetically distinct cell populations in the primary tumor metastasized in parallel to different anatomic sites, rather than sequentially from one site to the next. In five of these six patients, the metastasizing cells had themselves arisen from a common parental subpopulation in the primary, indicating that the ability to establish metastases is a late-evolving trait. Interestingly, we discovered that individual metastases were sometimes founded by multiple cell populations of the primary that were genetically distinct. Such establishment of metastases by multiple tumor subpopulations could help explain why identical resistance variants are identified in different sites after initial response to systemic therapy. One primary tumor harbored two subclones with different oncogenic mutations in CTNNB1, which were both propagated to the same metastasis, raising the possibility that activation of wingless-type mouse mammary tumor virus integration site (WNT) signaling may be involved, as has been suggested by experimental models. |
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Melanoma is difficult to treat once it becomes metastatic. However, the precise ancestral relationship between primary tumors and their metastases is not well understood. We performed whole-exome sequencing of primary melanomas and multiple matched metastases from eight patients to elucidate their phylogenetic relationships. In six of eight patients, we found that genetically distinct cell populations in the primary tumor metastasized in parallel to different anatomic sites, rather than sequentially from one site to the next. In five of these six patients, the metastasizing cells had themselves arisen from a common parental subpopulation in the primary, indicating that the ability to establish metastases is a late-evolving trait. Interestingly, we discovered that individual metastases were sometimes founded by multiple cell populations of the primary that were genetically distinct. Such establishment of metastases by multiple tumor subpopulations could help explain why identical resistance variants are identified in different sites after initial response to systemic therapy. One primary tumor harbored two subclones with different oncogenic mutations in CTNNB1, which were both propagated to the same metastasis, raising the possibility that activation of wingless-type mouse mammary tumor virus integration site (WNT) signaling may be involved, as has been suggested by experimental models. |
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Melanoma is difficult to treat once it becomes metastatic. However, the precise ancestral relationship between primary tumors and their metastases is not well understood. We performed whole-exome sequencing of primary melanomas and multiple matched metastases from eight patients to elucidate their phylogenetic relationships. In six of eight patients, we found that genetically distinct cell populations in the primary tumor metastasized in parallel to different anatomic sites, rather than sequentially from one site to the next. In five of these six patients, the metastasizing cells had themselves arisen from a common parental subpopulation in the primary, indicating that the ability to establish metastases is a late-evolving trait. Interestingly, we discovered that individual metastases were sometimes founded by multiple cell populations of the primary that were genetically distinct. Such establishment of metastases by multiple tumor subpopulations could help explain why identical resistance variants are identified in different sites after initial response to systemic therapy. One primary tumor harbored two subclones with different oncogenic mutations in CTNNB1, which were both propagated to the same metastasis, raising the possibility that activation of wingless-type mouse mammary tumor virus integration site (WNT) signaling may be involved, as has been suggested by experimental models. |
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However, the precise ancestral relationship between primary tumors and their metastases is not well understood. We performed whole-exome sequencing of primary melanomas and multiple matched metastases from eight patients to elucidate their phylogenetic relationships. In six of eight patients, we found that genetically distinct cell populations in the primary tumor metastasized in parallel to different anatomic sites, rather than sequentially from one site to the next. In five of these six patients, the metastasizing cells had themselves arisen from a common parental subpopulation in the primary, indicating that the ability to establish metastases is a late-evolving trait. Interestingly, we discovered that individual metastases were sometimes founded by multiple cell populations of the primary that were genetically distinct. Such establishment of metastases by multiple tumor subpopulations could help explain why identical resistance variants are identified in different sites after initial response to systemic therapy. One primary tumor harbored two subclones with different oncogenic mutations in CTNNB1, which were both propagated to the same metastasis, raising the possibility that activation of wingless-type mouse mammary tumor virus integration site (WNT) signaling may be involved, as has been suggested by experimental models.</subfield></datafield><datafield tag="540" ind1=" " ind2=" "><subfield code="a">Nutzungsrecht: © COPYRIGHT 2015 National Academy of Sciences</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Melanoma - pathology</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Melanoma - genetics</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Phylogeny</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Observations</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Melanoma</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Genetic aspects</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Metastasis</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Tumors</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Phylogenetics</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">genetics</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">melanoma</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Biological Sciences</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">metastasis</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Elizabeth Purdom</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">John F. 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