Histological Transformation and Progression in Follicular Lymphoma: A Clonal Evolution Study
Follicular lymphoma (FL) is an indolent, yet incurable B cell malignancy. A subset of patients experience an increased mortality rate driven by two distinct clinical end points: histological transformation and early progression after immunochemotherapy. The nature of tumor clonal dynamics leading to...
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| Published in: | PLoS medicine Vol. 13; no. 12; p. e1002197 |
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| Main Authors: | , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , |
| Format: | Journal Article |
| Language: | English |
| Published: |
United States
Public Library of Science
13.12.2016
Public Library of Science (PLoS) |
| Subjects: | |
| ISSN: | 1549-1676, 1549-1277, 1549-1676 |
| Online Access: | Get full text |
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| Abstract | Follicular lymphoma (FL) is an indolent, yet incurable B cell malignancy. A subset of patients experience an increased mortality rate driven by two distinct clinical end points: histological transformation and early progression after immunochemotherapy. The nature of tumor clonal dynamics leading to these clinical end points is poorly understood, and previously determined genetic alterations do not explain the majority of transformed cases or accurately predict early progressive disease. We contend that detailed knowledge of the expansion patterns of specific cell populations plus their associated mutations would provide insight into therapeutic strategies and disease biology over the time course of FL clinical histories.
Using a combination of whole genome sequencing, targeted deep sequencing, and digital droplet PCR on matched diagnostic and relapse specimens, we deciphered the constituent clonal populations in 15 transformation cases and 6 progression cases, and measured the change in clonal population abundance over time. We observed widely divergent patterns of clonal dynamics in transformed cases relative to progressed cases. Transformation specimens were generally composed of clones that were rare or absent in diagnostic specimens, consistent with dramatic clonal expansions that came to dominate the transformation specimens. This pattern was independent of time to transformation and treatment modality. By contrast, early progression specimens were composed of clones that were already present in the diagnostic specimens and exhibited only moderate clonal dynamics, even in the presence of immunochemotherapy. Analysis of somatic mutations impacting 94 genes was undertaken in an extension cohort consisting of 395 samples from 277 patients in order to decipher disrupted biology in the two clinical end points. We found 12 genes that were more commonly mutated in transformed samples than in the preceding FL tumors, including TP53, B2M, CCND3, GNA13, S1PR2, and P2RY8. Moreover, ten genes were more commonly mutated in diagnostic specimens of patients with early progression, including TP53, BTG1, MKI67, and XBP1.
Our results illuminate contrasting modes of evolution shaping the clinical histories of transformation and progression. They have implications for interpretation of evolutionary dynamics in the context of treatment-induced selective pressures, and indicate that transformation and progression will require different clinical management strategies. |
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| AbstractList |
Background
Follicular lymphoma (FL) is an indolent, yet incurable B cell malignancy. A subset of patients experience an increased mortality rate driven by two distinct clinical end points: histological transformation and early progression after immunochemotherapy. The nature of tumor clonal dynamics leading to these clinical end points is poorly understood, and previously determined genetic alterations do not explain the majority of transformed cases or accurately predict early progressive disease. We contend that detailed knowledge of the expansion patterns of specific cell populations plus their associated mutations would provide insight into therapeutic strategies and disease biology over the time course of FL clinical histories.
Methods and Findings
Using a combination of whole genome sequencing, targeted deep sequencing, and digital droplet PCR on matched diagnostic and relapse specimens, we deciphered the constituent clonal populations in 15 transformation cases and 6 progression cases, and measured the change in clonal population abundance over time. We observed widely divergent patterns of clonal dynamics in transformed cases relative to progressed cases. Transformation specimens were generally composed of clones that were rare or absent in diagnostic specimens, consistent with dramatic clonal expansions that came to dominate the transformation specimens. This pattern was independent of time to transformation and treatment modality. By contrast, early progression specimens were composed of clones that were already present in the diagnostic specimens and exhibited only moderate clonal dynamics, even in the presence of immunochemotherapy. Analysis of somatic mutations impacting 94 genes was undertaken in an extension cohort consisting of 395 samples from 277 patients in order to decipher disrupted biology in the two clinical end points. We found 12 genes that were more commonly mutated in transformed samples than in the preceding FL tumors, including TP53, B2M, CCND3, GNA13, S1PR2, and P2RY8. Moreover, ten genes were more commonly mutated in diagnostic specimens of patients with early progression, including TP53, BTG1, MKI67, and XBP1.
Conclusions
Our results illuminate contrasting modes of evolution shaping the clinical histories of transformation and progression. They have implications for interpretation of evolutionary dynamics in the context of treatment-induced selective pressures, and indicate that transformation and progression will require different clinical management strategies. Background Follicular lymphoma (FL) is an indolent, yet incurable B cell malignancy. A subset of patients experience an increased mortality rate driven by two distinct clinical end points: histological transformation and early progression after immunochemotherapy. The nature of tumor clonal dynamics leading to these clinical end points is poorly understood, and previously determined genetic alterations do not explain the majority of transformed cases or accurately predict early progressive disease. We contend that detailed knowledge of the expansion patterns of specific cell populations plus their associated mutations would provide insight into therapeutic strategies and disease biology over the time course of FL clinical histories. Methods and Findings Using a combination of whole genome sequencing, targeted deep sequencing, and digital droplet PCR on matched diagnostic and relapse specimens, we deciphered the constituent clonal populations in 15 transformation cases and 6 progression cases, and measured the change in clonal population abundance over time. We observed widely divergent patterns of clonal dynamics in transformed cases relative to progressed cases. Transformation specimens were generally composed of clones that were rare or absent in diagnostic specimens, consistent with dramatic clonal expansions that came to dominate the transformation specimens. This pattern was independent of time to transformation and treatment modality. By contrast, early progression specimens were composed of clones that were already present in the diagnostic specimens and exhibited only moderate clonal dynamics, even in the presence of immunochemotherapy. Analysis of somatic mutations impacting 94 genes was undertaken in an extension cohort consisting of 395 samples from 277 patients in order to decipher disrupted biology in the two clinical end points. We found 12 genes that were more commonly mutated in transformed samples than in the preceding FL tumors, including TP53, B2M, CCND3, GNA13, S1PR2, and P2RY8. Moreover, ten genes were more commonly mutated in diagnostic specimens of patients with early progression, including TP53, BTG1, MKI67, and XBP1. Conclusions Our results illuminate contrasting modes of evolution shaping the clinical histories of transformation and progression. They have implications for interpretation of evolutionary dynamics in the context of treatment-induced selective pressures, and indicate that transformation and progression will require different clinical management strategies. Follicular lymphoma (FL) is an indolent, yet incurable B cell malignancy. A subset of patients experience an increased mortality rate driven by two distinct clinical end points: histological transformation and early progression after immunochemotherapy. The nature of tumor clonal dynamics leading to these clinical end points is poorly understood, and previously determined genetic alterations do not explain the majority of transformed cases or accurately predict early progressive disease. We contend that detailed knowledge of the expansion patterns of specific cell populations plus their associated mutations would provide insight into therapeutic strategies and disease biology over the time course of FL clinical histories.BACKGROUNDFollicular lymphoma (FL) is an indolent, yet incurable B cell malignancy. A subset of patients experience an increased mortality rate driven by two distinct clinical end points: histological transformation and early progression after immunochemotherapy. The nature of tumor clonal dynamics leading to these clinical end points is poorly understood, and previously determined genetic alterations do not explain the majority of transformed cases or accurately predict early progressive disease. We contend that detailed knowledge of the expansion patterns of specific cell populations plus their associated mutations would provide insight into therapeutic strategies and disease biology over the time course of FL clinical histories.Using a combination of whole genome sequencing, targeted deep sequencing, and digital droplet PCR on matched diagnostic and relapse specimens, we deciphered the constituent clonal populations in 15 transformation cases and 6 progression cases, and measured the change in clonal population abundance over time. We observed widely divergent patterns of clonal dynamics in transformed cases relative to progressed cases. Transformation specimens were generally composed of clones that were rare or absent in diagnostic specimens, consistent with dramatic clonal expansions that came to dominate the transformation specimens. This pattern was independent of time to transformation and treatment modality. By contrast, early progression specimens were composed of clones that were already present in the diagnostic specimens and exhibited only moderate clonal dynamics, even in the presence of immunochemotherapy. Analysis of somatic mutations impacting 94 genes was undertaken in an extension cohort consisting of 395 samples from 277 patients in order to decipher disrupted biology in the two clinical end points. We found 12 genes that were more commonly mutated in transformed samples than in the preceding FL tumors, including TP53, B2M, CCND3, GNA13, S1PR2, and P2RY8. Moreover, ten genes were more commonly mutated in diagnostic specimens of patients with early progression, including TP53, BTG1, MKI67, and XBP1.METHODS AND FINDINGSUsing a combination of whole genome sequencing, targeted deep sequencing, and digital droplet PCR on matched diagnostic and relapse specimens, we deciphered the constituent clonal populations in 15 transformation cases and 6 progression cases, and measured the change in clonal population abundance over time. We observed widely divergent patterns of clonal dynamics in transformed cases relative to progressed cases. Transformation specimens were generally composed of clones that were rare or absent in diagnostic specimens, consistent with dramatic clonal expansions that came to dominate the transformation specimens. This pattern was independent of time to transformation and treatment modality. By contrast, early progression specimens were composed of clones that were already present in the diagnostic specimens and exhibited only moderate clonal dynamics, even in the presence of immunochemotherapy. Analysis of somatic mutations impacting 94 genes was undertaken in an extension cohort consisting of 395 samples from 277 patients in order to decipher disrupted biology in the two clinical end points. We found 12 genes that were more commonly mutated in transformed samples than in the preceding FL tumors, including TP53, B2M, CCND3, GNA13, S1PR2, and P2RY8. Moreover, ten genes were more commonly mutated in diagnostic specimens of patients with early progression, including TP53, BTG1, MKI67, and XBP1.Our results illuminate contrasting modes of evolution shaping the clinical histories of transformation and progression. They have implications for interpretation of evolutionary dynamics in the context of treatment-induced selective pressures, and indicate that transformation and progression will require different clinical management strategies.CONCLUSIONSOur results illuminate contrasting modes of evolution shaping the clinical histories of transformation and progression. They have implications for interpretation of evolutionary dynamics in the context of treatment-induced selective pressures, and indicate that transformation and progression will require different clinical management strategies. Follicular lymphoma (FL) is an indolent, yet incurable B cell malignancy. A subset of patients experience an increased mortality rate driven by two distinct clinical end points: histological transformation and early progression after immunochemotherapy. The nature of tumor clonal dynamics leading to these clinical end points is poorly understood, and previously determined genetic alterations do not explain the majority of transformed cases or accurately predict early progressive disease. We contend that detailed knowledge of the expansion patterns of specific cell populations plus their associated mutations would provide insight into therapeutic strategies and disease biology over the time course of FL clinical histories. Using a combination of whole genome sequencing, targeted deep sequencing, and digital droplet PCR on matched diagnostic and relapse specimens, we deciphered the constituent clonal populations in 15 transformation cases and 6 progression cases, and measured the change in clonal population abundance over time. We observed widely divergent patterns of clonal dynamics in transformed cases relative to progressed cases. Transformation specimens were generally composed of clones that were rare or absent in diagnostic specimens, consistent with dramatic clonal expansions that came to dominate the transformation specimens. This pattern was independent of time to transformation and treatment modality. By contrast, early progression specimens were composed of clones that were already present in the diagnostic specimens and exhibited only moderate clonal dynamics, even in the presence of immunochemotherapy. Analysis of somatic mutations impacting 94 genes was undertaken in an extension cohort consisting of 395 samples from 277 patients in order to decipher disrupted biology in the two clinical end points. We found 12 genes that were more commonly mutated in transformed samples than in the preceding FL tumors, including TP53, B2M, CCND3, GNA13, S1PR2, and P2RY8. Moreover, ten genes were more commonly mutated in diagnostic specimens of patients with early progression, including TP53, BTG1, MKI67, and XBP1. Our results illuminate contrasting modes of evolution shaping the clinical histories of transformation and progression. They have implications for interpretation of evolutionary dynamics in the context of treatment-induced selective pressures, and indicate that transformation and progression will require different clinical management strategies. Follicular lymphoma (FL) is an indolent, yet incurable B cell malignancy. A subset of patients experience an increased mortality rate driven by two distinct clinical end points: histological transformation and early progression after immunochemotherapy. The nature of tumor clonal dynamics leading to these clinical end points is poorly understood, and previously determined genetic alterations do not explain the majority of transformed cases or accurately predict early progressive disease. We contend that detailed knowledge of the expansion patterns of specific cell populations plus their associated mutations would provide insight into therapeutic strategies and disease biology over the time course of FL clinical histories. Using a combination of whole genome sequencing, targeted deep sequencing, and digital droplet PCR on matched diagnostic and relapse specimens, we deciphered the constituent clonal populations in 15 transformation cases and 6 progression cases, and measured the change in clonal population abundance over time. We observed widely divergent patterns of clonal dynamics in transformed cases relative to progressed cases. Transformation specimens were generally composed of clones that were rare or absent in diagnostic specimens, consistent with dramatic clonal expansions that came to dominate the transformation specimens. This pattern was independent of time to transformation and treatment modality. By contrast, early progression specimens were composed of clones that were already present in the diagnostic specimens and exhibited only moderate clonal dynamics, even in the presence of immunochemotherapy. Analysis of somatic mutations impacting 94 genes was undertaken in an extension cohort consisting of 395 samples from 277 patients in order to decipher disrupted biology in the two clinical end points. We found 12 genes that were more commonly mutated in transformed samples than in the preceding FL tumors, including TP53, B2M, CCND3, GNA13, S1PR2, and P2RY8. Moreover, ten genes were more commonly mutated in diagnostic specimens of patients with early progression, including TP53, BTG1, MKI67, and XBP1. Our results illuminate contrasting modes of evolution shaping the clinical histories of transformation and progression. They have implications for interpretation of evolutionary dynamics in the context of treatment-induced selective pressures, and indicate that transformation and progression will require different clinical management strategies. Sohrab Shah and colleagues explore the evolutionary histories that shape clinical and transformation dynamics in follicular lymphoma BackgroundFollicular lymphoma (FL) is an indolent, yet incurable B cell malignancy. A subset of patients experience an increased mortality rate driven by two distinct clinical end points: histological transformation and early progression after immunochemotherapy. The nature of tumor clonal dynamics leading to these clinical end points is poorly understood, and previously determined genetic alterations do not explain the majority of transformed cases or accurately predict early progressive disease. We contend that detailed knowledge of the expansion patterns of specific cell populations plus their associated mutations would provide insight into therapeutic strategies and disease biology over the time course of FL clinical histories.Methods and findingsUsing a combination of whole genome sequencing, targeted deep sequencing, and digital droplet PCR on matched diagnostic and relapse specimens, we deciphered the constituent clonal populations in 15 transformation cases and 6 progression cases, and measured the change in clonal population abundance over time. We observed widely divergent patterns of clonal dynamics in transformed cases relative to progressed cases. Transformation specimens were generally composed of clones that were rare or absent in diagnostic specimens, consistent with dramatic clonal expansions that came to dominate the transformation specimens. This pattern was independent of time to transformation and treatment modality. By contrast, early progression specimens were composed of clones that were already present in the diagnostic specimens and exhibited only moderate clonal dynamics, even in the presence of immunochemotherapy. Analysis of somatic mutations impacting 94 genes was undertaken in an extension cohort consisting of 395 samples from 277 patients in order to decipher disrupted biology in the two clinical end points. We found 12 genes that were more commonly mutated in transformed samples than in the preceding FL tumors, including TP53, B2M, CCND3, GNA13, S1PR2, and P2RY8. Moreover, ten genes were more commonly mutated in diagnostic specimens of patients with early progression, including TP53, BTG1, MKI67, and XBP1.ConclusionsOur results illuminate contrasting modes of evolution shaping the clinical histories of transformation and progression. They have implications for interpretation of evolutionary dynamics in the context of treatment-induced selective pressures, and indicate that transformation and progression will require different clinical management strategies. |
| Audience | Academic |
| Author | Smith, Maia A. Tan, King Gascoyne, Randy D. Giné, Eva Sehn, Laurie H. Ennishi, Daisuke Mungall, Andrew Kridel, Robert Johnson, Nathalie A. Marra, Marco A. Scott, David W. Moore, Richard Shah, Sohrab P. Bashashati, Ali Connors, Joseph M. Nielsen, Cydney Roth, Andrew Telenius, Adele Chan, Fong Chun Shumansky, Karey Boyle, Merrill Dogan, Ahmet Mottok, Anja McPherson, Andrew Meissner, Barbara Rosner, Jamie Morin, Ryan D. Farinha, Pedro Tousseyn, Thomas Steidl, Christian Yap, Damian Ben-Neriah, Susana |
| AuthorAffiliation | 4 Department of Molecular Oncology, BC Cancer Agency, Vancouver, British Columbia, Canada 9 Department of Pathology, Universitaire Ziekenhuizen Leuven (UZ Leuven), Leuven, Belgium 1 Centre for Lymphoid Cancer, BC Cancer Agency, Vancouver, British Columbia, Canada 10 Department of Laboratory and Pathology, Mayo Clinic, Rochester, Minnesota, United States of America 5 Michael Smith Genome Sciences Centre, BC Cancer Agency, Vancouver, British Columbia, Canada 2 Bioinformatics Graduate Program, University of British Columbia, Vancouver, British Columbia, Canada 11 Departments of Pathology and Laboratory Medicine, Memorial Sloan Kettering Cancer Center, New York, New York, United States of America 7 Jewish General Hospital, Montreal, Quebec, Canada 3 Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, British Columbia, Canada 6 Department of Molecular Biology and Biochemistry, Simon Fraser University, Burnaby, British Columbia, Canada 8 Translational Cell and T |
| AuthorAffiliation_xml | – name: 4 Department of Molecular Oncology, BC Cancer Agency, Vancouver, British Columbia, Canada – name: 5 Michael Smith Genome Sciences Centre, BC Cancer Agency, Vancouver, British Columbia, Canada – name: 10 Department of Laboratory and Pathology, Mayo Clinic, Rochester, Minnesota, United States of America – name: 2 Bioinformatics Graduate Program, University of British Columbia, Vancouver, British Columbia, Canada – name: 6 Department of Molecular Biology and Biochemistry, Simon Fraser University, Burnaby, British Columbia, Canada – name: 8 Translational Cell and Tissue Research Lab, Department for Imaging and Pathology, University of Leuven (KU Leuven), Leuven, Belgium – name: 9 Department of Pathology, Universitaire Ziekenhuizen Leuven (UZ Leuven), Leuven, Belgium – name: Washington University School of Medicine, UNITED STATES – name: 1 Centre for Lymphoid Cancer, BC Cancer Agency, Vancouver, British Columbia, Canada – name: 11 Departments of Pathology and Laboratory Medicine, Memorial Sloan Kettering Cancer Center, New York, New York, United States of America – name: 3 Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, British Columbia, Canada – name: 7 Jewish General Hospital, Montreal, Quebec, Canada |
| Author_xml | – sequence: 1 givenname: Robert orcidid: 0000-0003-0287-7124 surname: Kridel fullname: Kridel, Robert – sequence: 2 givenname: Fong Chun surname: Chan fullname: Chan, Fong Chun – sequence: 3 givenname: Anja surname: Mottok fullname: Mottok, Anja – sequence: 4 givenname: Merrill surname: Boyle fullname: Boyle, Merrill – sequence: 5 givenname: Pedro orcidid: 0000-0001-9364-9391 surname: Farinha fullname: Farinha, Pedro – sequence: 6 givenname: King surname: Tan fullname: Tan, King – sequence: 7 givenname: Barbara surname: Meissner fullname: Meissner, Barbara – sequence: 8 givenname: Ali surname: Bashashati fullname: Bashashati, Ali – sequence: 9 givenname: Andrew orcidid: 0000-0002-5654-5101 surname: McPherson fullname: McPherson, Andrew – sequence: 10 givenname: Andrew surname: Roth fullname: Roth, Andrew – sequence: 11 givenname: Karey surname: Shumansky fullname: Shumansky, Karey – sequence: 12 givenname: Damian orcidid: 0000-0002-5370-4592 surname: Yap fullname: Yap, Damian – sequence: 13 givenname: Susana orcidid: 0000-0002-2867-4037 surname: Ben-Neriah fullname: Ben-Neriah, Susana – sequence: 14 givenname: Jamie orcidid: 0000-0001-8901-7228 surname: Rosner fullname: Rosner, Jamie – sequence: 15 givenname: Maia A. orcidid: 0000-0001-7196-0154 surname: Smith fullname: Smith, Maia A. – sequence: 16 givenname: Cydney surname: Nielsen fullname: Nielsen, Cydney – sequence: 17 givenname: Eva surname: Giné fullname: Giné, Eva – sequence: 18 givenname: Adele orcidid: 0000-0002-6901-5126 surname: Telenius fullname: Telenius, Adele – sequence: 19 givenname: Daisuke orcidid: 0000-0001-5118-9235 surname: Ennishi fullname: Ennishi, Daisuke – sequence: 20 givenname: Andrew orcidid: 0000-0002-0905-2742 surname: Mungall fullname: Mungall, Andrew – sequence: 21 givenname: Richard surname: Moore fullname: Moore, Richard – sequence: 22 givenname: Ryan D. surname: Morin fullname: Morin, Ryan D. – sequence: 23 givenname: Nathalie A. orcidid: 0000-0002-3211-9722 surname: Johnson fullname: Johnson, Nathalie A. – sequence: 24 givenname: Laurie H. surname: Sehn fullname: Sehn, Laurie H. – sequence: 25 givenname: Thomas surname: Tousseyn fullname: Tousseyn, Thomas – sequence: 26 givenname: Ahmet surname: Dogan fullname: Dogan, Ahmet – sequence: 27 givenname: Joseph M. orcidid: 0000-0002-1361-7531 surname: Connors fullname: Connors, Joseph M. – sequence: 28 givenname: David W. surname: Scott fullname: Scott, David W. – sequence: 29 givenname: Christian surname: Steidl fullname: Steidl, Christian – sequence: 30 givenname: Marco A. orcidid: 0000-0001-7146-7175 surname: Marra fullname: Marra, Marco A. – sequence: 31 givenname: Randy D. surname: Gascoyne fullname: Gascoyne, Randy D. – sequence: 32 givenname: Sohrab P. surname: Shah fullname: Shah, Sohrab P. |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/27959929$$D View this record in MEDLINE/PubMed |
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| Snippet | Follicular lymphoma (FL) is an indolent, yet incurable B cell malignancy. A subset of patients experience an increased mortality rate driven by two distinct... Background Follicular lymphoma (FL) is an indolent, yet incurable B cell malignancy. A subset of patients experience an increased mortality rate driven by two... Sohrab Shah and colleagues explore the evolutionary histories that shape clinical and transformation dynamics in follicular lymphoma BackgroundFollicular lymphoma (FL) is an indolent, yet incurable B cell malignancy. A subset of patients experience an increased mortality rate driven by two... Background Follicular lymphoma (FL) is an indolent, yet incurable B cell malignancy. A subset of patients experience an increased mortality rate driven by... |
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| SubjectTerms | Academic libraries Bioinformatics Biology Biology and Life Sciences Cancer Care and treatment Clonal Evolution Clone Cells Cloning Colleges & universities Computer and Information Sciences Development and progression Disease Progression Gene expression Gene mutations Genetic aspects Genomes Health aspects Humans Laboratories Lymphoma Lymphoma, Follicular - genetics Lymphoma, Follicular - physiopathology Lymphomas Medicine Medicine and Health Sciences Mutation Oncology Pathology Research and Analysis Methods |
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| Title | Histological Transformation and Progression in Follicular Lymphoma: A Clonal Evolution Study |
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