The Genetic Evolution of Treatment-Resistant Cutaneous, Acral, and Uveal Melanomas

Melanoma is a biologically heterogeneous disease composed of distinct clinicopathologic subtypes that frequently resist treatment. To explore the evolution of treatment resistance and metastasis, we used a combination of temporal and multilesional tumor sampling in conjunction with whole-exome seque...

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Veröffentlicht in:Clinical cancer research Jg. 27; H. 5; S. 1516
Hauptverfasser: Makohon-Moore, Alvin P, Lipson, Evan J, Hooper, Jody E, Zucker, Amanda, Hong, Jungeui, Bielski, Craig M, Hayashi, Akimasa, Tokheim, Collin, Baez, Priscilla, Kappagantula, Rajya, Kohutek, Zachary, Makarov, Vladimir, Riaz, Nadeem, Postow, Michael A, Chapman, Paul B, Karchin, Rachel, Socci, Nicholas D, Solit, David B, Chan, Timothy A, Taylor, Barry S, Topalian, Suzanne L, Iacobuzio-Donahue, Christine A
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Sprache:Englisch
Veröffentlicht: United States 01.03.2021
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ISSN:1557-3265, 1557-3265
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Abstract Melanoma is a biologically heterogeneous disease composed of distinct clinicopathologic subtypes that frequently resist treatment. To explore the evolution of treatment resistance and metastasis, we used a combination of temporal and multilesional tumor sampling in conjunction with whole-exome sequencing of 110 tumors collected from 7 patients with cutaneous ( = 3), uveal ( = 2), and acral ( = 2) melanoma subtypes. Primary tumors, metastases collected longitudinally, and autopsy tissues were interrogated. All but 1 patient died because of melanoma progression. For each patient, we generated phylogenies and quantified the extent of genetic diversity among tumors, specifically among putative somatic alterations affecting therapeutic resistance. In 4 patients who received immunotherapy, we found 1-3 putative acquired and intrinsic resistance mechanisms coexisting in the same patient, including mechanisms that were shared by all tumors within each patient, suggesting that future therapies directed at overcoming intrinsic resistance mechanisms may be broadly effective.
AbstractList Melanoma is a biologically heterogeneous disease composed of distinct clinicopathologic subtypes that frequently resist treatment. To explore the evolution of treatment resistance and metastasis, we used a combination of temporal and multilesional tumor sampling in conjunction with whole-exome sequencing of 110 tumors collected from 7 patients with cutaneous (n = 3), uveal (n = 2), and acral (n = 2) melanoma subtypes.PURPOSEMelanoma is a biologically heterogeneous disease composed of distinct clinicopathologic subtypes that frequently resist treatment. To explore the evolution of treatment resistance and metastasis, we used a combination of temporal and multilesional tumor sampling in conjunction with whole-exome sequencing of 110 tumors collected from 7 patients with cutaneous (n = 3), uveal (n = 2), and acral (n = 2) melanoma subtypes.Primary tumors, metastases collected longitudinally, and autopsy tissues were interrogated. All but 1 patient died because of melanoma progression.EXPERIMENTAL DESIGNPrimary tumors, metastases collected longitudinally, and autopsy tissues were interrogated. All but 1 patient died because of melanoma progression.For each patient, we generated phylogenies and quantified the extent of genetic diversity among tumors, specifically among putative somatic alterations affecting therapeutic resistance.RESULTSFor each patient, we generated phylogenies and quantified the extent of genetic diversity among tumors, specifically among putative somatic alterations affecting therapeutic resistance.In 4 patients who received immunotherapy, we found 1-3 putative acquired and intrinsic resistance mechanisms coexisting in the same patient, including mechanisms that were shared by all tumors within each patient, suggesting that future therapies directed at overcoming intrinsic resistance mechanisms may be broadly effective.CONCLUSIONSIn 4 patients who received immunotherapy, we found 1-3 putative acquired and intrinsic resistance mechanisms coexisting in the same patient, including mechanisms that were shared by all tumors within each patient, suggesting that future therapies directed at overcoming intrinsic resistance mechanisms may be broadly effective.
Melanoma is a biologically heterogeneous disease composed of distinct clinicopathologic subtypes that frequently resist treatment. To explore the evolution of treatment resistance and metastasis, we used a combination of temporal and multilesional tumor sampling in conjunction with whole-exome sequencing of 110 tumors collected from 7 patients with cutaneous ( = 3), uveal ( = 2), and acral ( = 2) melanoma subtypes. Primary tumors, metastases collected longitudinally, and autopsy tissues were interrogated. All but 1 patient died because of melanoma progression. For each patient, we generated phylogenies and quantified the extent of genetic diversity among tumors, specifically among putative somatic alterations affecting therapeutic resistance. In 4 patients who received immunotherapy, we found 1-3 putative acquired and intrinsic resistance mechanisms coexisting in the same patient, including mechanisms that were shared by all tumors within each patient, suggesting that future therapies directed at overcoming intrinsic resistance mechanisms may be broadly effective.
Author Riaz, Nadeem
Tokheim, Collin
Solit, David B
Topalian, Suzanne L
Chapman, Paul B
Hong, Jungeui
Hooper, Jody E
Baez, Priscilla
Karchin, Rachel
Zucker, Amanda
Postow, Michael A
Socci, Nicholas D
Lipson, Evan J
Kohutek, Zachary
Makarov, Vladimir
Makohon-Moore, Alvin P
Bielski, Craig M
Taylor, Barry S
Chan, Timothy A
Hayashi, Akimasa
Kappagantula, Rajya
Iacobuzio-Donahue, Christine A
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  organization: Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, New York
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  givenname: Evan J
  orcidid: 0000-0003-2976-0911
  surname: Lipson
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  organization: Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, Maryland
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  givenname: Jody E
  surname: Hooper
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  organization: Department of Pathology, Johns Hopkins University School of Medicine and Sidney Kimmel Comprehensive Cancer Center, Baltimore, Maryland
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  fullname: Hayashi, Akimasa
  organization: Department of Pathology, Kyorin University, Mitaka City, Tokyo, Japan
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  givenname: Collin
  orcidid: 0000-0003-1395-5378
  surname: Tokheim
  fullname: Tokheim, Collin
  organization: Department of Biostatistics, Harvard T.H. Chan School of Public Health, Boston, Massachusetts
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  fullname: Baez, Priscilla
  organization: Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, New York
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  organization: Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, New York
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  organization: Department of Radiation Oncology, Vanderbilt University Medical Center, Nashville, Tennessee
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  organization: Radiation Oncology, Memorial Sloan Kettering Cancer Center, New York, New York
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  organization: Weill Cornell Medical College, New York, New York
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  organization: Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York
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  surname: Karchin
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  organization: Department of Biomedical Engineering, Institute for Computational Medicine, Johns Hopkins University, Baltimore, Maryland
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  givenname: Nicholas D
  orcidid: 0000-0002-8254-6925
  surname: Socci
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  surname: Solit
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  organization: Center for Molecular Oncology, Memorial Sloan Kettering Cancer Center, New York, New York
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  surname: Chan
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  organization: Center for Immunotherapy and Precision Immuno-Oncology, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio
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  givenname: Barry S
  surname: Taylor
  fullname: Taylor, Barry S
  organization: Department of Epidemiology and Biostatistics, Memorial Sloan Kettering Cancer Center, New York, New York
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  givenname: Suzanne L
  orcidid: 0000-0002-0821-8587
  surname: Topalian
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  email: iacobuzc@mskcc.org, stopali1@jhmi.edu
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  email: iacobuzc@mskcc.org, stopali1@jhmi.edu
  organization: Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, New York
BackLink https://www.ncbi.nlm.nih.gov/pubmed/33323400$$D View this record in MEDLINE/PubMed
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Snippet Melanoma is a biologically heterogeneous disease composed of distinct clinicopathologic subtypes that frequently resist treatment. To explore the evolution of...
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SubjectTerms Biomarkers, Tumor
Drug Resistance, Neoplasm - genetics
Evolution, Molecular
Humans
Immunotherapy - methods
Melanoma - drug therapy
Melanoma - genetics
Melanoma - immunology
Melanoma - pathology
Mutation
Prognosis
Skin Neoplasms - drug therapy
Skin Neoplasms - genetics
Skin Neoplasms - immunology
Skin Neoplasms - pathology
Uveal Neoplasms - drug therapy
Uveal Neoplasms - genetics
Uveal Neoplasms - immunology
Uveal Neoplasms - pathology
Title The Genetic Evolution of Treatment-Resistant Cutaneous, Acral, and Uveal Melanomas
URI https://www.ncbi.nlm.nih.gov/pubmed/33323400
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Volume 27
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