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...
Saved in:
| Published in: | PLoS medicine Vol. 13; no. 12; p. e1002197 |
|---|---|
| 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 |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| 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. |
|---|---|
| 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 |
| BookMark | eNqVk11r2zAUhs3oWD-2fzA2Q2FsF8kkW5LlXgxCaNdAWMfa7WogZFl2FGQpk-yy_PspiVviEsaGL2RJz_vq6Byd0-jIWCOj6DUEY5hm8OPSds5wPV41shxDABKYZ8-iE4hRPoIkI0d7_8fRqffLwOQgBy-i4yTLcZ4n-Un081r51mpbK8F1fOe48ZV1DW-VNTE3ZfzV2dpJ7zdzZeIrq7USneYunq-b1cI2_CKexFNtQyzx5b3V3VZ623bl-mX0vOLay1f9eBZ9v7q8m16P5jefZ9PJfCRoCtoRKkhJC1wimFUFAQRyTDMsU8xRSspCJoLjQpI0wRhLAAXOioIImBcUCwkkSs-itzvflbae9YnxDFJMKcEpooGY7YjS8iVbOdVwt2aWK7ZdsK5m3LVKaMlExSkVHJUlwghRyUUBK4plzkmGACyD16f-tK4IuRfStI7rgelwx6gFq-09w6EeGCTB4H1v4OyvTvqWNcoLqTU30nbbuBOSpRCmAT1_gh6-XU_VPFxAmcqGc8XGlE1QRglEWQICNTpA1dLIEGR4W5UKywN-fIAPXykbJQ4KPgwEgWnl77bmnfdsdvvtP9gv_87e_Biy7_bYheS6Xfj-Ufoh-Ga_io_le2iNAKAdIJz13snqEYGAbTrwoRRs04Gs78Agu3giE6rdtlPIntJ_F_8B-c012w |
| CitedBy_id | crossref_primary_10_1016_j_lpm_2019_07_024 crossref_primary_10_1038_s41596_021_00506_4 crossref_primary_10_1038_s42255_019_0098_8 crossref_primary_10_1007_s00277_017_3154_z crossref_primary_10_1016_j_ccell_2024_02_001 crossref_primary_10_1016_S2152_2650_21_01256_8 crossref_primary_10_1182_bloodadvances_2023011299 crossref_primary_10_1016_j_cellsig_2017_08_002 crossref_primary_10_1016_j_jmoldx_2017_11_010 crossref_primary_10_1038_s41375_018_0043_y crossref_primary_10_1097_PAS_0000000000001726 crossref_primary_10_1038_s41588_023_01561_1 crossref_primary_10_1002_hon_2508 crossref_primary_10_3389_fimmu_2023_1307242 crossref_primary_10_1038_s41375_022_01618_w crossref_primary_10_1016_j_hoc_2020_02_002 crossref_primary_10_1111_imr_12745 crossref_primary_10_1002_path_5043 crossref_primary_10_1016_j_ccell_2020_04_004 crossref_primary_10_3390_cancers14051316 crossref_primary_10_1111_imr_12860 crossref_primary_10_1007_s12185_022_03461_2 crossref_primary_10_1016_j_humpath_2024_105679 crossref_primary_10_1134_S1022795424701278 crossref_primary_10_1126_scitranslmed_aak9969 crossref_primary_10_1182_blood_2021011362 crossref_primary_10_1038_s41598_017_14150_0 crossref_primary_10_1182_blood_2017_07_737353 crossref_primary_10_1038_s41408_024_01111_w crossref_primary_10_1002_hon_3282 crossref_primary_10_1016_j_intimp_2022_109235 crossref_primary_10_1038_s42003_019_0291_z crossref_primary_10_1002_jcp_27407 crossref_primary_10_33590_emj_10310543 crossref_primary_10_1002_hon_3205 crossref_primary_10_1016_j_humpath_2021_04_014 crossref_primary_10_1182_bloodadvances_2023010779 crossref_primary_10_1038_s41591_020_0757_z crossref_primary_10_1002_jha2_212 crossref_primary_10_1016_j_biopha_2020_110069 crossref_primary_10_1126_sciimmunol_abg1101 crossref_primary_10_3390_cancers17101602 crossref_primary_10_1007_s00277_022_04947_z crossref_primary_10_1016_j_yamp_2024_07_002 crossref_primary_10_1038_nmeth_4303 crossref_primary_10_1016_j_yexmp_2021_104606 crossref_primary_10_1097_HS9_0000000000000213 crossref_primary_10_1097_HS9_0000000000000579 crossref_primary_10_4132_jptm_2021_09_29 crossref_primary_10_1016_j_esmorc_2025_100040 crossref_primary_10_1007_s12094_023_03307_1 crossref_primary_10_1038_s41467_024_47701_x crossref_primary_10_3390_hemato3040042 crossref_primary_10_1182_blood_2018_08_822148 crossref_primary_10_3390_cancers17182952 crossref_primary_10_1016_j_bneo_2024_100044 crossref_primary_10_1016_j_bbmt_2018_03_022 crossref_primary_10_1080_10428194_2019_1594212 crossref_primary_10_3390_cancers17071219 crossref_primary_10_1111_bjh_17383 crossref_primary_10_1016_j_pathol_2019_09_010 crossref_primary_10_1080_17474086_2020_1850252 crossref_primary_10_3390_ijms252011179 crossref_primary_10_1007_s12185_019_02656_4 crossref_primary_10_1053_j_seminhematol_2023_11_002 crossref_primary_10_1182_blood_2019000258 crossref_primary_10_1016_j_beha_2017_11_002 crossref_primary_10_1038_s41598_017_13338_8 crossref_primary_10_1200_EDBK_349307 crossref_primary_10_1016_j_blre_2019_03_006 crossref_primary_10_1038_s41408_023_00847_1 crossref_primary_10_1182_bloodadvances_2017008854 crossref_primary_10_1007_s12185_025_03939_9 crossref_primary_10_1111_bjh_17251 crossref_primary_10_1002_hem3_50 crossref_primary_10_1053_j_seminhematol_2023_11_006 crossref_primary_10_1038_modpathol_2017_58 crossref_primary_10_1186_s12885_022_10070_z crossref_primary_10_1182_blood_2017_08_737361 crossref_primary_10_1016_S2352_3026_18_30093_0 crossref_primary_10_1016_j_hoc_2020_03_001 crossref_primary_10_1182_blood_2024025603 crossref_primary_10_1182_bloodadvances_2020002546 crossref_primary_10_3390_cancers13040641 crossref_primary_10_1158_1078_0432_CCR_22_1654 crossref_primary_10_1634_theoncologist_2019_0138 crossref_primary_10_1136_jcp_2023_209262 crossref_primary_10_1016_j_ccell_2024_05_011 crossref_primary_10_1016_j_blre_2022_100969 crossref_primary_10_1016_j_path_2023_02_001 crossref_primary_10_3389_fonc_2023_1107171 crossref_primary_10_1182_blood_2017_08_799080 crossref_primary_10_3389_fonc_2021_625257 crossref_primary_10_1080_17474086_2020_1690987 crossref_primary_10_1182_blood_2016_08_733469 crossref_primary_10_1186_s40364_024_00711_9 crossref_primary_10_1200_JCO_2018_79_3083 crossref_primary_10_1038_s41598_024_81693_4 crossref_primary_10_1038_s41586_019_1003_z crossref_primary_10_1002_hon_2674 crossref_primary_10_1016_j_ccell_2020_03_016 crossref_primary_10_1016_j_blre_2023_101099 crossref_primary_10_3390_biomedinformatics2020017 crossref_primary_10_1097_MOH_0000000000000437 crossref_primary_10_1182_blood_2017_03_691345 crossref_primary_10_1111_joim_13674 crossref_primary_10_1111_bjh_17990 crossref_primary_10_1182_bloodadvances_2021004528 crossref_primary_10_1111_bjh_19770 crossref_primary_10_1182_blood_2023020999 crossref_primary_10_1097_PCR_0000000000000330 crossref_primary_10_1182_blood_2017_11_764332 crossref_primary_10_1371_journal_pone_0212813 crossref_primary_10_1016_j_beha_2018_07_008 crossref_primary_10_1038_s41467_024_47012_1 crossref_primary_10_1002_hon_3132 crossref_primary_10_1007_s12253_020_00843_x crossref_primary_10_1080_10428194_2020_1762883 crossref_primary_10_1038_s41408_024_01124_5 crossref_primary_10_1038_s41375_019_0691_6 crossref_primary_10_1007_s00292_021_01011_x crossref_primary_10_1002_hon_3138 crossref_primary_10_1182_bloodadvances_2022009461 crossref_primary_10_1182_blood_2022016095 crossref_primary_10_1136_jcp_2024_209880 crossref_primary_10_1080_10428194_2020_1791857 crossref_primary_10_1182_bloodadvances_2022009467 crossref_primary_10_1371_journal_pone_0233449 crossref_primary_10_1002_eji_202149235 crossref_primary_10_1038_s41590_018_0181_4 crossref_primary_10_3389_fimmu_2021_683597 crossref_primary_10_1038_s41572_019_0132_x crossref_primary_10_1111_his_15344 crossref_primary_10_1200_EDBK_239065 crossref_primary_10_1200_JCO_18_00400 crossref_primary_10_1016_j_beha_2017_10_006 crossref_primary_10_1016_j_beha_2017_10_005 crossref_primary_10_1016_S1470_2045_18_30114_1 crossref_primary_10_1182_blood_2024024251 crossref_primary_10_1182_blood_2022018719 crossref_primary_10_1053_j_seminoncol_2018_07_005 crossref_primary_10_1038_s41467_019_12494_x crossref_primary_10_1053_j_seminhematol_2023_08_001 crossref_primary_10_1016_j_modpat_2024_100516 crossref_primary_10_1038_s41598_018_37389_7 crossref_primary_10_1038_nrc_2017_127 crossref_primary_10_1182_blood_2024026664 crossref_primary_10_3390_cancers17050907 crossref_primary_10_1002_jha2_116 crossref_primary_10_1097_PAP_0000000000000481 crossref_primary_10_3389_fmed_2019_00044 crossref_primary_10_1016_j_hoc_2020_02_009 crossref_primary_10_1002_path_6246 crossref_primary_10_1007_s00428_024_03774_z crossref_primary_10_1016_j_hoc_2020_02_006 crossref_primary_10_1007_s11864_025_01297_6 crossref_primary_10_1182_bloodadvances_2021005284 crossref_primary_10_1111_cas_14176 crossref_primary_10_2217_ijh_2017_0003 crossref_primary_10_1053_j_seminhematol_2023_06_003 crossref_primary_10_1186_s13000_018_0758_0 crossref_primary_10_1038_s41467_022_34408_0 crossref_primary_10_3390_cancers14112710 crossref_primary_10_1016_j_hoc_2020_02_010 crossref_primary_10_1002_hon_3272 crossref_primary_10_1007_s00277_024_05618_x |
| Cites_doi | 10.1158/1078-0432.CCR-13-2175 10.1534/genetics.111.132027 10.1038/nature10738 10.1182/blood-2008-05-154013 10.1038/nature15395 10.1182/blood.V84.4.1043.1043 10.1182/blood.V89.11.3909 10.1182/blood-2013-03-491514 10.1038/nature16478 10.1182/blood-2010-05-282780 10.1182/blood.V80.3.758.758 10.1182/blood-2008-08-174839 10.1073/pnas.132253599 10.1200/JCO.2006.09.3260 10.1182/blood.V82.8.2289.2289 10.1023/A:1008265532487 10.1200/JCO.2012.48.3990 10.3109/10428194.2014.885513 10.1093/bioinformatics/btv003 10.3324/haematol.2012.082412 10.1056/NEJM198701083160204 10.1084/jem.20131448 10.1182/blood.V82.7.1994.1994 10.1038/sj.leu.2404696 10.1111/j.1365-2141.2006.06439.x 10.1200/JCO.2014.59.7534 10.1056/NEJMoa1106968 10.1182/blood-2008-08-174953 10.1182/blood-2015-01-621375 10.1182/blood-2008-02-140616 10.1038/nature13765 10.1007/s00277-015-2303-5 10.1038/ng.2856 10.1016/j.celrep.2013.12.027 10.1158/1078-0432.CCR-08-0752 10.1038/nature10983 10.1038/nmeth.2883 10.1002/gcc.10314 10.1182/blood-2016-05-717355 10.1038/leu.2014.251 10.1016/j.cell.2013.01.019 10.1200/JCO.2008.16.0283 |
| ContentType | Journal Article |
| Copyright | COPYRIGHT 2016 Public Library of Science 2016 Public Library of Science. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited: Kridel R, Chan FC, Mottok A, Boyle M, Farinha P, Tan K, et al. (2016) Histological Transformation and Progression in Follicular Lymphoma: A Clonal Evolution Study. PLoS Med 13(12): e1002197. doi:10.1371/journal.pmed.1002197 2016 Kridel et al 2016 Kridel et al 2016 Public Library of Science. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited: Kridel R, Chan FC, Mottok A, Boyle M, Farinha P, Tan K, et al. (2016) Histological Transformation and Progression in Follicular Lymphoma: A Clonal Evolution Study. PLoS Med 13(12): e1002197. doi:10.1371/journal.pmed.1002197 |
| Copyright_xml | – notice: COPYRIGHT 2016 Public Library of Science – notice: 2016 Public Library of Science. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited: Kridel R, Chan FC, Mottok A, Boyle M, Farinha P, Tan K, et al. (2016) Histological Transformation and Progression in Follicular Lymphoma: A Clonal Evolution Study. PLoS Med 13(12): e1002197. doi:10.1371/journal.pmed.1002197 – notice: 2016 Kridel et al 2016 Kridel et al – notice: 2016 Public Library of Science. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited: Kridel R, Chan FC, Mottok A, Boyle M, Farinha P, Tan K, et al. (2016) Histological Transformation and Progression in Follicular Lymphoma: A Clonal Evolution Study. PLoS Med 13(12): e1002197. doi:10.1371/journal.pmed.1002197 |
| DBID | AAYXX CITATION CGR CUY CVF ECM EIF NPM IOV ISN ISR 3V. 7TK 7X7 7XB 88E 8FI 8FJ 8FK ABUWG AFKRA AZQEC BENPR CCPQU DWQXO FYUFA GHDGH K9. M0S M1P PHGZM PHGZT PIMPY PJZUB PKEHL PPXIY PQEST PQQKQ PQUKI PRINS 7X8 5PM DOA CZK |
| DOI | 10.1371/journal.pmed.1002197 |
| DatabaseName | CrossRef Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed Gale In Context: Opposing Viewpoints Gale In Context: Canada Gale In Context: Science ProQuest Central (Corporate) Neurosciences Abstracts Health Medical collection ProQuest Central (purchase pre-March 2016) Medical Database (Alumni Edition) Hospital Premium Collection Hospital Premium Collection (Alumni Edition) ProQuest Central (Alumni) (purchase pre-March 2016) ProQuest Central (Alumni) ProQuest Central UK/Ireland ProQuest Central Essentials - QC ProQuest Central ProQuest One ProQuest Central ProQuest Health & Medical Collection Health Research Premium Collection (Alumni) ProQuest Health & Medical Complete (Alumni) Health & Medical Collection (Alumni) Medical Database ProQuest ProQuest Central Premium ProQuest One Academic (New) Publicly Available Content Database ProQuest Health & Medical Research Collection ProQuest One Academic Middle East (New) One Health & Nursing ProQuest One Academic Eastern Edition (DO NOT USE) ProQuest One Academic (retired) ProQuest One Academic UKI Edition ProQuest Central China MEDLINE - Academic PubMed Central (Full Participant titles) DOAJ Directory of Open Access Journals PLoS Medicine |
| DatabaseTitle | CrossRef MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) Publicly Available Content Database ProQuest One Academic Middle East (New) ProQuest Central Essentials ProQuest Health & Medical Complete (Alumni) ProQuest Central (Alumni Edition) ProQuest One Community College ProQuest One Health & Nursing ProQuest Central China ProQuest Central ProQuest Health & Medical Research Collection Health Research Premium Collection Health and Medicine Complete (Alumni Edition) ProQuest Central Korea Health & Medical Research Collection ProQuest Central (New) ProQuest Medical Library (Alumni) ProQuest One Academic Eastern Edition ProQuest Hospital Collection Health Research Premium Collection (Alumni) Neurosciences Abstracts ProQuest Hospital Collection (Alumni) ProQuest Health & Medical Complete ProQuest Medical Library ProQuest One Academic UKI Edition ProQuest One Academic ProQuest One Academic (New) ProQuest Central (Alumni) MEDLINE - Academic |
| DatabaseTitleList | MEDLINE - Academic Publicly Available Content Database MEDLINE |
| Database_xml | – sequence: 1 dbid: DOA name: DOAJ Directory of Open Access Journals url: https://www.doaj.org/ sourceTypes: Open Website – sequence: 2 dbid: NPM name: PubMed url: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database – sequence: 3 dbid: PIMPY name: ProQuest Publicly Available Content Database url: http://search.proquest.com/publiccontent sourceTypes: Aggregation Database |
| DeliveryMethod | fulltext_linktorsrc |
| Discipline | Medicine Biology |
| DocumentTitleAlternate | Clonal Dynamics in Follicular Lymphoma |
| EISSN | 1549-1676 |
| ExternalDocumentID | 1858865348 oai_doaj_org_article_cfa88ca4dd45448eacb1f85e9a67401d PMC5154502 4302728981 A478614720 27959929 10_1371_journal_pmed_1002197 |
| Genre | Journal Article |
| GeographicLocations | Vancouver British Columbia Canada Canada |
| GeographicLocations_xml | – name: Canada – name: Vancouver British Columbia Canada |
| GrantInformation_xml | – fundername: ; grantid: 1023 |
| GroupedDBID | --- 123 29O 2WC 53G 5VS 7X7 88E 8FI 8FJ AAFWJ AAUCC AAWOE AAWTL AAYXX ABDBF ABUWG ACCTH ACGFO ACIHN ACPRK ACUHS ADBBV ADRAZ AEAQA AENEX AFFHD AFKRA AFPKN AFRAH AFXKF AHMBA AKRSQ ALMA_UNASSIGNED_HOLDINGS AOIJS B0M BAIFH BAWUL BBTPI BCNDV BENPR BPHCQ BVXVI BWKFM CCPQU CITATION CS3 DIK DU5 E3Z EAP EAS EBD EBS EJD EMK EMOBN ESX F5P FPL FYUFA GROUPED_DOAJ GX1 HMCUK HYE IAO IHR IHW INH INR IOF IOV IPO ISN ISR ITC KQ8 M1P M48 MK0 O5R O5S OK1 OVT P2P PHGZM PHGZT PIMPY PJZUB PPXIY PQQKQ PROAC PSQYO PV9 RNS RPM RZL SV3 TR2 TUS UKHRP WOW XSB YZZ ~8M ALIPV CGR CUY CVF ECM EIF H13 IPNFZ NPM RIG WOQ 3V. 7TK 7XB 8FK AZQEC DWQXO K9. PKEHL PQEST PQUKI PRINS 7X8 5PM - AAPBV ABPTK ADACO BBAFP BCGST CZK ICW M~E |
| ID | FETCH-LOGICAL-c830t-4b6d8b5d417fb6061a5875e35a436dbe2ca5be632555e01c57bb6c19b85ce0e43 |
| IEDL.DBID | 7X7 |
| ISICitedReferencesCount | 197 |
| ISICitedReferencesURI | http://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=Summon&SrcAuth=ProQuest&DestLinkType=CitingArticles&DestApp=WOS_CPL&KeyUT=000392142400010&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D |
| ISSN | 1549-1676 1549-1277 |
| IngestDate | Fri Nov 26 17:52:53 EST 2021 Fri Oct 03 12:41:07 EDT 2025 Tue Nov 04 02:01:31 EST 2025 Sun Nov 09 10:20:48 EST 2025 Sat Nov 29 14:21:38 EST 2025 Tue Nov 11 10:40:15 EST 2025 Sat Nov 29 11:27:39 EST 2025 Tue Nov 04 18:01:58 EST 2025 Thu Nov 13 16:37:41 EST 2025 Thu Nov 13 15:54:01 EST 2025 Thu Nov 13 16:53:33 EST 2025 Thu May 22 21:22:13 EDT 2025 Thu Apr 03 07:07:48 EDT 2025 Sat Nov 29 05:44:41 EST 2025 Tue Nov 18 21:43:14 EST 2025 |
| IsDoiOpenAccess | true |
| IsOpenAccess | true |
| IsPeerReviewed | true |
| IsScholarly | true |
| Issue | 12 |
| Language | English |
| License | This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Creative Commons Attribution License |
| LinkModel | DirectLink |
| MergedId | FETCHMERGED-LOGICAL-c830t-4b6d8b5d417fb6061a5875e35a436dbe2ca5be632555e01c57bb6c19b85ce0e43 |
| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 Conceptualization: RK FCC JMC DWS CS MAM RDG SPS.Data curation: RK FCC AB AMc AR KS JR MAS CN.Formal analysis: RK FCC AB AMc AR KS JR CN SPS.Funding acquisition: JMC DWS CS MAM RDG SPS.Investigation: RK FCC AMo MB PF KT BM AB AMc AR KS DY SBN JR MAS CN EG AT DE AMu RM RDM NAJ LHS TT AD DWS.Methodology: RK FCC AMo AB AMc AR KS DY JR MAS CN.Project administration: AMu RM JMC DWS CS MAM RDG SPS.Resources: AMo KT PF LHS TT AD JMC RDG.Software: RK FCC AB AMc AR KS DY JR MAS CN.Supervision: JMC DWS CS MAM RDG SPS.Validation: RK FCC SPS.Visualization: RK FCC AMo AB AMc AR KS JR MAS CN.Writing – original draft: RK FCC SPS.Writing – review & editing: RK FCC AMo MB PF KT BM AB AMc AR KS DY SBN JR MAS CN EG AT DE AMu RM RDM NAJ LHS TT AD JMC DWS CS MAM RDG SPS. I have read the journal's policy and the authors of this manuscript have the following competing interests: SPS is a founder and shareholder of Contextual Genomics Inc., developer of clinical genomic tests for cancer. Current address: Princess Margaret Cancer Centre, Toronto, Ontario, Canada |
| ORCID | 0000-0002-0905-2742 0000-0002-6901-5126 0000-0002-1361-7531 0000-0002-5370-4592 0000-0001-8901-7228 0000-0001-7196-0154 0000-0002-5654-5101 0000-0003-0287-7124 0000-0001-5118-9235 0000-0001-9364-9391 0000-0002-3211-9722 0000-0001-7146-7175 0000-0002-2867-4037 |
| OpenAccessLink | https://www.proquest.com/docview/1858865348?pq-origsite=%requestingapplication% |
| PMID | 27959929 |
| PQID | 1858865348 |
| PQPubID | 1436338 |
| ParticipantIDs | plos_journals_1858865348 doaj_primary_oai_doaj_org_article_cfa88ca4dd45448eacb1f85e9a67401d pubmedcentral_primary_oai_pubmedcentral_nih_gov_5154502 proquest_miscellaneous_1852673113 proquest_journals_1858865348 gale_infotracmisc_A478614720 gale_infotracgeneralonefile_A478614720 gale_infotracacademiconefile_A478614720 gale_incontextgauss_ISR_A478614720 gale_incontextgauss_ISN_A478614720 gale_incontextgauss_IOV_A478614720 gale_healthsolutions_A478614720 pubmed_primary_27959929 crossref_primary_10_1371_journal_pmed_1002197 crossref_citationtrail_10_1371_journal_pmed_1002197 |
| PublicationCentury | 2000 |
| PublicationDate | 20161213 |
| PublicationDateYYYYMMDD | 2016-12-13 |
| PublicationDate_xml | – month: 12 year: 2016 text: 20161213 day: 13 |
| PublicationDecade | 2010 |
| PublicationPlace | United States |
| PublicationPlace_xml | – name: United States – name: San Francisco – name: San Francisco, CA USA |
| PublicationTitle | PLoS medicine |
| PublicationTitleAlternate | PLoS Med |
| PublicationYear | 2016 |
| Publisher | Public Library of Science Public Library of Science (PLoS) |
| Publisher_xml | – name: Public Library of Science – name: Public Library of Science (PLoS) |
| References | HR Junlen (ref5) 2014; 29 S Schiffels (ref41) 2011; 189 BK Link (ref8) 2013; 31 IS Lossos (ref23) 2002; 99 D O’Shea (ref33) 2008; 112 MR Green (ref43) 2010; 116 JR Anderson (ref2) 1998; 9 L Mozessohn (ref9) 2014; 55 J Fitzgibbon (ref26) 2007; 21 ND Wagner-Johnston (ref12) 2015; 126 D Tan (ref4) 2013; 122 AJ Davies (ref27) 2007; 136 AJ Al-Tourah (ref7) 2008; 26 JR Muppidi (ref40) 2014; 516 D O’Shea (ref29) 2009; 113 Landau Da (ref15) 2013; 152 C Casulo (ref10) 2015; 33 A Alhejaily (ref36) 2014; 20 J Okosun (ref20) 2014; 46 DA Landau (ref16) 2015; 526 T Yano (ref22) 1992; 80 MJ Walter (ref18) 2012; 366 G Fabbri (ref19) 2013; 210 F D’Amore (ref34) 2008; 14 A Pastore (ref37) 2015; 2045 K Lerch (ref11) 2015; 94 E Bachy (ref3) 2013; 98 E Carlotti (ref28) 2009; 113 A Roth (ref38) 2014; 11 (ref1) 1997; 89 JJ Yunis (ref30) 1987; 316 AS Morrissy (ref17) 2016; 529 KJJ Cheung (ref35) 2009; 113 V Jurinovic (ref13) 2016; 128 S Malikic (ref39) 2015; 31 S Montoto (ref6) 2007; 25 F Lo Coco (ref24) 1993; 82 L Ding (ref14) 2012; 481 H Tilly (ref31) 1994; 84 L Pasqualucci (ref21) 2014; 6 CA Sander (ref25) 1993; 82 M Höglund (ref32) 2004; 39 C Curtis (ref42) 2012; 486 24388756 - Cell Rep. 2014 Jan 16;6(1):130-40 24450580 - Leuk Lymphoma. 2014 Nov;55(11):2502-7 24633410 - Nat Methods. 2014 Apr;11(4):396-8 18838711 - J Clin Oncol. 2008 Nov 10;26(32):5165-9 24449825 - Clin Cancer Res. 2014 Mar 15;20(6):1676-86 23897955 - J Clin Oncol. 2013 Sep 10;31(26):3272-8 25151959 - Leukemia. 2015 Mar;29(3):668-76 26760213 - Nature. 2016 Jan 21;529(7586):351-7 8049424 - Blood. 1994 Aug 15;84(4):1043-9 26124482 - J Clin Oncol. 2015 Aug 10;33(23):2516-22 22417201 - N Engl J Med. 2012 Mar 22;366(12):1090-8 9739436 - Ann Oncol. 1998 Jul;9(7):717-20 24127483 - J Exp Med. 2013 Oct 21;210(11):2273-88 8400281 - Blood. 1993 Oct 15;82(8):2289-95 12077300 - Proc Natl Acad Sci U S A. 2002 Jun 25;99(13):8886-91 17278262 - Br J Haematol. 2007 Jan;136(2):286-93 23415222 - Cell. 2013 Feb 14;152(4):714-26 14732921 - Genes Chromosomes Cancer. 2004 Mar;39(3):195-204 21926305 - Genetics. 2011 Dec;189(4):1361-75 25274307 - Nature. 2014 Dec 11;516(7530):254-8 19010834 - Clin Cancer Res. 2008 Nov 15;14(22):7180-7 25645656 - Ann Hematol. 2015 Jun;94(6):981-8 8400252 - Blood. 1993 Oct 1;82(7):1994-2004 22237025 - Nature. 2012 Jan 11;481(7382):506-10 27418643 - Blood. 2016 Aug 25;128(8):1112-20 17485708 - J Clin Oncol. 2007 Jun 10;25(17):2426-33 18628487 - Blood. 2008 Oct 15;112(8):3126-9 20628145 - Blood. 2010 Oct 28;116(17):3268-77 23777769 - Blood. 2013 Aug 8;122(6):981-7 26105149 - Blood. 2015 Aug 13;126(7):851-7 9166827 - Blood. 1997 Jun 1;89(11):3909-18 26466571 - Nature. 2015 Oct 22;526(7574):525-30 24362818 - Nat Genet. 2014 Feb;46(2):176-81 23645690 - Haematologica. 2013 Jul;98(7):1107-14 25568283 - Bioinformatics. 2015 May 1;31(9):1349-56 1638027 - Blood. 1992 Aug 1;80(3):758-67 19202129 - Blood. 2009 Apr 9;113(15):3553-7 26256760 - Lancet Oncol. 2015 Sep;16(9):1111-22 18703704 - Blood. 2009 Jan 1;113(1):137-48 17495976 - Leukemia. 2007 Jul;21(7):1514-20 22522925 - Nature. 2012 Apr 18;486(7403):346-52 3537802 - N Engl J Med. 1987 Jan 8;316(2):79-84 19141865 - Blood. 2009 Mar 5;113(10):2298-301 |
| References_xml | – volume: 20 start-page: 1676 issue: 6 year: 2014 ident: ref36 article-title: Inactivation of the CDKN2A tumor suppressor gene by deletion or methylation is common at diagnosis in follicular lymphoma and associated with poor clinical outcome publication-title: Clin Cancer Res doi: 10.1158/1078-0432.CCR-13-2175 – volume: 2045 start-page: 1 issue: 15 year: 2015 ident: ref37 article-title: Integration of gene mutations in risk prognostication for patients receiving first-line immunochemotherapy for follicular lymphoma: a retrospective analysis of a prospective clinical trial and validation in a population-based registry publication-title: Lancet Oncol – volume: 189 start-page: 1361 issue: 4 year: 2011 ident: ref41 article-title: Emergent neutrality in adaptive asexual evolution publication-title: Genetics doi: 10.1534/genetics.111.132027 – volume: 481 start-page: 506 issue: 7382 year: 2012 ident: ref14 article-title: Clonal evolution in relapsed acute myeloid leukaemia revealed by whole-genome sequencing publication-title: Nature doi: 10.1038/nature10738 – volume: 112 start-page: 3126 issue: 8 year: 2008 ident: ref33 article-title: The presence of TP53 mutation at diagnosis of follicular lymphoma identifies a high-risk group of patients with shortened time to disease progression and poorer overall survival publication-title: Blood doi: 10.1182/blood-2008-05-154013 – volume: 526 start-page: 525 issue: 7574 year: 2015 ident: ref16 article-title: Mutations driving CLL and their evolution in progression and relapse publication-title: Nature doi: 10.1038/nature15395 – volume: 84 start-page: 1043 issue: 4 year: 1994 ident: ref31 article-title: Prognostic value of chromosomal abnormalities in follicular lymphoma publication-title: Blood doi: 10.1182/blood.V84.4.1043.1043 – volume: 89 start-page: 3909 issue: 11 year: 1997 ident: ref1 article-title: A clinical evaluation of the International Lymphoma Study Group classification of non-Hodgkin’s lymphoma. The Non-Hodgkin’s Lymphoma Classification Project publication-title: Blood doi: 10.1182/blood.V89.11.3909 – volume: 122 start-page: 981 issue: 6 year: 2013 ident: ref4 article-title: Improvements in observed and relative survival in follicular grade 1–2 lymphoma during 4 decades: the Stanford University experience publication-title: Blood doi: 10.1182/blood-2013-03-491514 – volume: 529 start-page: 351 issue: 7586 year: 2016 ident: ref17 article-title: Divergent clonal selection dominates medulloblastoma at recurrence publication-title: Nature doi: 10.1038/nature16478 – volume: 116 start-page: 3268 issue: 17 year: 2010 ident: ref43 article-title: Integrative analysis reveals selective 9p24.1 amplification, increased PD-1 ligand expression, and further induction via JAK2 in nodular sclerosing Hodgkin lymphoma and primary mediastinal large B-cell lymphoma publication-title: Blood doi: 10.1182/blood-2010-05-282780 – volume: 80 start-page: 758 issue: 3 year: 1992 ident: ref22 article-title: MYC rearrangements in histologically progressed follicular lymphomas publication-title: Blood doi: 10.1182/blood.V80.3.758.758 – volume: 113 start-page: 3553 issue: 15 year: 2009 ident: ref28 article-title: Transformation of follicular lymphoma to diffuse large B-cell lymphoma may occur by divergent evolution from a common progenitor cell or by direct evolution from the follicular lymphoma clone publication-title: Blood doi: 10.1182/blood-2008-08-174839 – volume: 99 start-page: 8886 issue: 13 year: 2002 ident: ref23 article-title: Transformation of follicular lymphoma to diffuse large-cell lymphoma: alternative patterns with increased or decreased expression of c-myc and its regulated genes publication-title: Proc Natl Acad Sci U S A doi: 10.1073/pnas.132253599 – volume: 25 start-page: 2426 issue: 17 year: 2007 ident: ref6 article-title: Risk and clinical implications of transformation of follicular lymphoma to diffuse large B-cell lymphoma publication-title: J Clin Oncol doi: 10.1200/JCO.2006.09.3260 – volume: 82 start-page: 2289 issue: 8 year: 1993 ident: ref24 article-title: p53 mutations are associated with histologic transformation of follicular lymphoma publication-title: Blood doi: 10.1182/blood.V82.8.2289.2289 – volume: 9 start-page: 717 issue: 7 year: 1998 ident: ref2 article-title: Epidemiology of the non-Hodgkin’s lymphomas: distributions of the major subtypes differ by geographic locations. Non-Hodgkin’s Lymphoma Classification Project publication-title: Ann Oncol doi: 10.1023/A:1008265532487 – volume: 31 start-page: 3272 issue: 26 year: 2013 ident: ref8 article-title: Rates and outcomes of follicular lymphoma transformation in the immunochemotherapy era: a report from the University of Iowa/MayoClinic Specialized Program of Research Excellence Molecular Epidemiology Resource publication-title: J Clin Oncol doi: 10.1200/JCO.2012.48.3990 – volume: 55 start-page: 2502 issue: 11 year: 2014 ident: ref9 article-title: Chemoimmunotherapy resistant follicular lymphoma: predictors of resistance, association with transformation and prognosis publication-title: Leuk Lymphoma doi: 10.3109/10428194.2014.885513 – volume: 31 start-page: 1349 issue: 9 year: 2015 ident: ref39 article-title: Clonality inference in multiple tumor samples using phylogeny publication-title: Bioinformatics doi: 10.1093/bioinformatics/btv003 – volume: 98 start-page: 1107 issue: 7 year: 2013 ident: ref3 article-title: Long-term follow up of the FL2000 study comparing CHVP-interferon to CHVP-interferon plus rituximab in follicular lymphoma publication-title: Haematologica doi: 10.3324/haematol.2012.082412 – volume: 316 start-page: 79 issue: 2 year: 1987 ident: ref30 article-title: Multiple recurrent genomic defects in follicular lymphoma. A possible model for cancer publication-title: N Engl J Med doi: 10.1056/NEJM198701083160204 – volume: 210 start-page: 2273 issue: 11 year: 2013 ident: ref19 article-title: Genetic lesions associated with chronic lymphocytic leukemia transformation to Richter syndrome publication-title: J Exp Med doi: 10.1084/jem.20131448 – volume: 82 start-page: 1994 issue: 7 year: 1993 ident: ref25 article-title: p53 mutation is associated with progression in follicular lymphomas publication-title: Blood doi: 10.1182/blood.V82.7.1994.1994 – volume: 21 start-page: 1514 issue: 7 year: 2007 ident: ref26 article-title: Genome-wide detection of recurring sites of uniparental disomy in follicular and transformed follicular lymphoma publication-title: Leukemia doi: 10.1038/sj.leu.2404696 – volume: 136 start-page: 286 issue: 2 year: 2007 ident: ref27 article-title: Transformation of follicular lymphoma to diffuse large B-cell lymphoma proceeds by distinct oncogenic mechanisms publication-title: Br J Haematol doi: 10.1111/j.1365-2141.2006.06439.x – volume: 33 start-page: 2516 issue: 23 year: 2015 ident: ref10 article-title: Early relapse of follicular lymphoma after rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone defines patients at high risk for death: an analysis from the National LymphoCare Study publication-title: J Clin Oncol doi: 10.1200/JCO.2014.59.7534 – volume: 366 start-page: 1090 issue: 12 year: 2012 ident: ref18 article-title: Clonal architecture of secondary acute myeloid leukemia publication-title: N Engl J Med doi: 10.1056/NEJMoa1106968 – volume: 113 start-page: 2298 issue: 10 year: 2009 ident: ref29 article-title: Regions of acquired uniparental disomy at diagnosis of follicular lymphoma are associated with both overall survival and risk of transformation publication-title: Blood doi: 10.1182/blood-2008-08-174953 – volume: 126 start-page: 851 issue: 7 year: 2015 ident: ref12 article-title: Outcomes of transformed follicular lymphoma in the modern era: a report from the National LymphoCare Study (NLCS) publication-title: Blood doi: 10.1182/blood-2015-01-621375 – volume: 113 start-page: 137 issue: 1 year: 2009 ident: ref35 article-title: Genome-wide profiling of follicular lymphoma by array comparative genomic hybridization reveals prognostically significant DNA copy number imbalances publication-title: Blood doi: 10.1182/blood-2008-02-140616 – volume: 516 start-page: 254 issue: 7530 year: 2014 ident: ref40 article-title: Loss of signalling via Gα13 in germinal centre B-cell-derived lymphoma publication-title: Nature doi: 10.1038/nature13765 – volume: 94 start-page: 981 issue: 6 year: 2015 ident: ref11 article-title: Impact of prior treatment on outcome of transformed follicular lymphoma and relapsed de novo diffuse large B cell lymphoma: a retrospective multicentre analysis publication-title: Ann Hematol doi: 10.1007/s00277-015-2303-5 – volume: 46 start-page: 176 issue: 2 year: 2014 ident: ref20 article-title: Integrated genomic analysis identifies recurrent mutations and evolution patterns driving the initiation and progression of follicular lymphoma publication-title: Nat Genet doi: 10.1038/ng.2856 – volume: 6 start-page: 130 issue: 1 year: 2014 ident: ref21 article-title: Genetics of follicular lymphoma transformation publication-title: Cell Rep doi: 10.1016/j.celrep.2013.12.027 – volume: 14 start-page: 7180 issue: 22 year: 2008 ident: ref34 article-title: Clonal evolution in t(14;18)-positive follicular lymphoma, evidence for multiple common pathways, and frequent parallel clonal evolution publication-title: Clin Cancer Res doi: 10.1158/1078-0432.CCR-08-0752 – volume: 486 start-page: 346 issue: 7403 year: 2012 ident: ref42 article-title: The genomic and transcriptomic architecture of 2,000 breast tumours reveals novel subgroups publication-title: Nature doi: 10.1038/nature10983 – volume: 11 start-page: 396 issue: 4 year: 2014 ident: ref38 article-title: PyClone: statistical inference of clonal population structure in cancer publication-title: Nat Methods doi: 10.1038/nmeth.2883 – volume: 39 start-page: 195 issue: 3 year: 2004 ident: ref32 article-title: Identification of cytogenetic subgroups and karyotypic pathways of clonal evolution in follicular lymphomas publication-title: Genes Chromosomes Cancer doi: 10.1002/gcc.10314 – volume: 128 start-page: 1112 issue: 8 year: 2016 ident: ref13 article-title: Clinicogenetic risk models predict early progression of follicular lymphoma after first-line immunochemotherapy publication-title: Blood doi: 10.1182/blood-2016-05-717355 – volume: 29 start-page: 668 issue: 3 year: 2014 ident: ref5 article-title: Follicular lymphoma in Sweden: nationwide improved survival in the rituximab era, particularly in elderly women—a Swedish Lymphoma Registry study publication-title: Leukemia doi: 10.1038/leu.2014.251 – volume: 152 start-page: 714 issue: 4 year: 2013 ident: ref15 article-title: Evolution and impact of subclonal mutations in chronic lymphocytic leukemia publication-title: Cell doi: 10.1016/j.cell.2013.01.019 – volume: 26 start-page: 5165 issue: 32 year: 2008 ident: ref7 article-title: Population-based analysis of incidence and outcome of transformed non-Hodgkin’s lymphoma publication-title: J Clin Oncol doi: 10.1200/JCO.2008.16.0283 – reference: 9166827 - Blood. 1997 Jun 1;89(11):3909-18 – reference: 24633410 - Nat Methods. 2014 Apr;11(4):396-8 – reference: 20628145 - Blood. 2010 Oct 28;116(17):3268-77 – reference: 24362818 - Nat Genet. 2014 Feb;46(2):176-81 – reference: 21926305 - Genetics. 2011 Dec;189(4):1361-75 – reference: 25645656 - Ann Hematol. 2015 Jun;94(6):981-8 – reference: 25151959 - Leukemia. 2015 Mar;29(3):668-76 – reference: 19202129 - Blood. 2009 Apr 9;113(15):3553-7 – reference: 8400252 - Blood. 1993 Oct 1;82(7):1994-2004 – reference: 17495976 - Leukemia. 2007 Jul;21(7):1514-20 – reference: 9739436 - Ann Oncol. 1998 Jul;9(7):717-20 – reference: 26760213 - Nature. 2016 Jan 21;529(7586):351-7 – reference: 25568283 - Bioinformatics. 2015 May 1;31(9):1349-56 – reference: 24449825 - Clin Cancer Res. 2014 Mar 15;20(6):1676-86 – reference: 23645690 - Haematologica. 2013 Jul;98(7):1107-14 – reference: 17485708 - J Clin Oncol. 2007 Jun 10;25(17):2426-33 – reference: 18838711 - J Clin Oncol. 2008 Nov 10;26(32):5165-9 – reference: 23777769 - Blood. 2013 Aug 8;122(6):981-7 – reference: 24127483 - J Exp Med. 2013 Oct 21;210(11):2273-88 – reference: 8049424 - Blood. 1994 Aug 15;84(4):1043-9 – reference: 24388756 - Cell Rep. 2014 Jan 16;6(1):130-40 – reference: 17278262 - Br J Haematol. 2007 Jan;136(2):286-93 – reference: 26256760 - Lancet Oncol. 2015 Sep;16(9):1111-22 – reference: 26466571 - Nature. 2015 Oct 22;526(7574):525-30 – reference: 23415222 - Cell. 2013 Feb 14;152(4):714-26 – reference: 14732921 - Genes Chromosomes Cancer. 2004 Mar;39(3):195-204 – reference: 22417201 - N Engl J Med. 2012 Mar 22;366(12):1090-8 – reference: 25274307 - Nature. 2014 Dec 11;516(7530):254-8 – reference: 19010834 - Clin Cancer Res. 2008 Nov 15;14(22):7180-7 – reference: 19141865 - Blood. 2009 Mar 5;113(10):2298-301 – reference: 26105149 - Blood. 2015 Aug 13;126(7):851-7 – reference: 22522925 - Nature. 2012 Apr 18;486(7403):346-52 – reference: 27418643 - Blood. 2016 Aug 25;128(8):1112-20 – reference: 26124482 - J Clin Oncol. 2015 Aug 10;33(23):2516-22 – reference: 3537802 - N Engl J Med. 1987 Jan 8;316(2):79-84 – reference: 12077300 - Proc Natl Acad Sci U S A. 2002 Jun 25;99(13):8886-91 – reference: 8400281 - Blood. 1993 Oct 15;82(8):2289-95 – reference: 24450580 - Leuk Lymphoma. 2014 Nov;55(11):2502-7 – reference: 1638027 - Blood. 1992 Aug 1;80(3):758-67 – reference: 22237025 - Nature. 2012 Jan 11;481(7382):506-10 – reference: 23897955 - J Clin Oncol. 2013 Sep 10;31(26):3272-8 – reference: 18703704 - Blood. 2009 Jan 1;113(1):137-48 – reference: 18628487 - Blood. 2008 Oct 15;112(8):3126-9 |
| SSID | ssj0029090 |
| Score | 2.5947099 |
| 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... |
| SourceID | plos doaj pubmedcentral proquest gale pubmed crossref |
| SourceType | Open Website Open Access Repository Aggregation Database Index Database Enrichment Source |
| StartPage | e1002197 |
| 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 |
| SummonAdditionalLinks | – databaseName: DOAJ Directory of Open Access Journals dbid: DOA link: http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV3fb9MwELbQhBAviN8LDDAIwVNYnNixw1uZVoE0ygQD7QEpsh1nq1SSam0n7b_nznGjBlXaHnitv1Tq3fn8XXP-jpC3RSEgimQVM5vImGe5jotKi9gaUXDntHKdZP6RnEzU6WlxvDHqC3vCOnngznD7ttZKWc2rigsoJSBPGFYr4Qqd4zC5CrNvIot1MRVKrSLx_66g_ljMUinDpblMsv3gow9zOG28AClDwaeNQ8lr9_cZemc-axfb6Oe_XZQbx9L4PrkX-CQddb_jAbnlmofkztfwxvwR-e11QEKCoycbNLVtqG4qeowNWp04B502dIwi3b43lR5dgafbP_ojHdGDGTJ2engZIpVi_-HVY_JzfHhy8DkOExViq7JkGXOTV8qIijNZGyhdmBZQr7hMaPBSZVxqtTAuz6DOEC5hVkhjcssKo4R1iePZE7LTtI3bJTThrOaJs0BwNDcWKjcnRMotEETlXFFHJFubtLRBbhynXsxK_w5NQtnRWahER5TBERGJ-6fmndzGNfhP6K0ei2LZ_gMIoTKEUHldCEXkFfq67G6e9lu-HHGpgL3INInIG49AwYwGO3LO9GqxKL98-3UD0I_JTUDfB6D3AVS3YDOrw1UJsDyqdQ2Q7wbIs06rfBtwbwCEJGIHy7sY52sbL0qgcUrlIuMKnlzH_vbl1_0yfin27DWuXXlMmsuMsSwiT7ut0vspxRH3wMwjIgebaODI4UozPffq5wJJf5I--x-ef07uAgH2g6hYtkd2lhcr94LctpfL6eLipU8pfwHdHnuf priority: 102 providerName: Directory of Open Access Journals – databaseName: Public Library of Science (PLoS) Journals Open Access dbid: FPL link: http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwlV1bb9MwFLagXMQLl3FZYIBBCJ4CcWzHNm9lWgVSKRUMtAekyHacUakk1dJO6r_HdtywTJ0Yr_XnKjo3nyMffweAV0JQa0WsiJFOWExwJmNRSBprRQUxRnLTUuaP2WTCj47E9G-heO4GHzP0Lsj07cKeDp4wFAl2FVxLcZa5Yms0HXcFlkhEEp7HXbSzd_x4lv4uFg8W87rZlmie75c8cwCN7vzvp98Ft0OqCYetbdwDV0y1A260wyfXO-Dm53Ctfh_89GQhIQrCwzO5bF1BWRVw6rq4WgYPOKvgyDF5-wZWOF5bc6h_y_dwCPfnLq2HB6fBnKFrUlw_AN9HB4f7H-MwdiHWHCfLmKis4IoWBLFS2foGSWqLGoOptKoslEm1pMpk2BYj1CRIU6ZUppFQnGqTGIIfgkFVV2YXwISgkiRG2yxIEqVteWcoTYm2WSQ3RpQRwBtt5DpwkrvRGPPcX7QxW5u0ssqdCPMgwgjE3a5Fy8nxD_wHp-gO6xi1_Q9WV3lw0FyXknMtSVEQaktWex4pVHJqhMzc0MIiAs-dmeTt89QuLuRDwrhNcViaROClRzhWjcq17RzLVdPkn778uATo2-QyoK890JsAKmsrMy3DeworeUfp1UO-7iGPW0LzbcC9HtBGGt1b3nUuspFxk9tcj_OMYsLtzo3bbF9-0S27P3WNfZWpVx6TZgwjhCPwqPWyTk8pE1TY9D0CrOd_PUX2V6rZL0-RTl1lkKSPL_7iJ-CWzX39DCqE98BgebIyT8F1fbqcNSfPfFz5Axird7o priority: 102 providerName: Public Library of Science |
| Title | Histological Transformation and Progression in Follicular Lymphoma: A Clonal Evolution Study |
| URI | https://www.ncbi.nlm.nih.gov/pubmed/27959929 https://www.proquest.com/docview/1858865348 https://www.proquest.com/docview/1852673113 https://pubmed.ncbi.nlm.nih.gov/PMC5154502 https://doaj.org/article/cfa88ca4dd45448eacb1f85e9a67401d http://dx.doi.org/10.1371/journal.pmed.1002197 |
| Volume | 13 |
| WOSCitedRecordID | wos000392142400010&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D |
| hasFullText | 1 |
| inHoldings | 1 |
| isFullTextHit | |
| isPrint | |
| journalDatabaseRights | – providerCode: PRVAON databaseName: DOAJ Directory of Open Access Journals customDbUrl: eissn: 1549-1676 dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0029090 issn: 1549-1676 databaseCode: DOA dateStart: 20040101 isFulltext: true titleUrlDefault: https://www.doaj.org/ providerName: Directory of Open Access Journals – providerCode: PRVPQU databaseName: Health & Medical Collection customDbUrl: eissn: 1549-1676 dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0029090 issn: 1549-1676 databaseCode: 7X7 dateStart: 20041001 isFulltext: true titleUrlDefault: https://search.proquest.com/healthcomplete providerName: ProQuest – providerCode: PRVPQU databaseName: ProQuest Central customDbUrl: eissn: 1549-1676 dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0029090 issn: 1549-1676 databaseCode: BENPR dateStart: 20041001 isFulltext: true titleUrlDefault: https://www.proquest.com/central providerName: ProQuest – providerCode: PRVPQU databaseName: ProQuest Publicly Available Content Database customDbUrl: eissn: 1549-1676 dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0029090 issn: 1549-1676 databaseCode: PIMPY dateStart: 20041001 isFulltext: true titleUrlDefault: http://search.proquest.com/publiccontent providerName: ProQuest – providerCode: PRVATS databaseName: Public Library of Science (PLoS) Journals Open Access customDbUrl: eissn: 1549-1676 dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0029090 issn: 1549-1676 databaseCode: FPL dateStart: 20040101 isFulltext: true titleUrlDefault: http://www.plos.org/publications/ providerName: Public Library of Science |
| link | http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwpV3db9MwELegA8QLH-NjgVEMQvAUFid27PCCuqkVk7oSjTEVCSlyHKdUKklp1kn977EdN2tQBZN4yUP8S5T4zuc7-_w7AN5EEVFaRDMXCY-6OAi5G2WcuCIlEZaSM1lT5g_paMTG4yi2C26VTatc20RjqLNS6DXyAzWvMBaSALOP81-urhqld1dtCY2bYEeXzdZ6TsdXAVfkmTUWzULmIp9Se3QuoOjASur9XM05hoYUadqnjanJMPg3drozn5XVNif0z1zKjclpcP9_f-sBuGfdUtir9eghuCGLXXC7LlS52gV3TuwW_CPw3RCLWIsJzzb83rKAvMhgrDO-arYPOC3gQLN-m2RXOFwp1Sl_8g-wB49mOgSA_Uur-lAnNK4eg6-D_tnRJ9eWaHAFC7wLF6dhxlKSYUTzVMVCiBMVAMmAcCX2LJW-4CSVYaACFyI9JAhN01CgKGVESE_i4AnoFGUh9wD0MMqxJ4XymDhOhQoFJSE-FsrjZFJGuQOCtXQSYfnLdRmNWWI25aiKY-q-SrRMEytTB7jNU_Oav-Mf-EMt-Aar2bfNjXIxSexgTkTOGRMcZxkmKrxVc1eKckZkxENd4DBzwEutNkl9lLWxIUkPU6bcIep7DnhtEJqBo9ApPhO-rKrk-PP5NUBfRtcBnbZA7ywoL1WfCW7PXqie1_RfLeTbFnJSk59vA-63gMoqiVbznh4y6z6ukitFV0-uh8L25ldNs36pTgIsZLk0GD-kAUKBA57Wo66Rk08jEilX3wG0NR5bgmy3FNMfhk6d6CjC85_9_bOeg7vKVzY1q1CwDzoXi6V8AW6Jy4tptegau2OurAt2Dvuj-LRrlnfUdRAP1b34-CT-9ht9hZGf |
| linkProvider | ProQuest |
| linkToHtml | http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMw1V1bb9MwFLZGub5wGZcVBjOIy1NYnNixg4RQGatWrSsTFNQHpOA4bqlUktLLUP8Uv5FjJ-kaVMFe9sBr_SVKj881Of4OQk_DkIEW8cQhyuUO9QPphIlkjopZSLWWQueU-W3e6YheLzzeQL_KszCmrbL0idZRJ5ky78h3Ia4IETCfijfjH46ZGmW-rpYjNHK1ONSLn1CyTV-33sH-PvO85n5378Appgo4SvjuzKFxkIiYJZTwfgzpO5EMcnbtMwlPmsTaU5LFOvAh12baJYrxOA4UCWPBlHY19eG-F9BF8OPcFHu8d1rgha59p2NYzxzicV4c1fM52S004-UYYpylPSWGZmolFNqJAcu4UBuPsum6pPfP3s2VYNi88b-J8Sa6XqTduJHbyS20odNNdDkfxLnYRFeOihaD2-iLJU4pIgLuruT1WYplmuBj09GWs5ngYYqbhtXcNvPi9gJMI_suX-EG3huZEgfvnxSmjU3D5uIO-nQu__IuqqVZqrcQdinpU1cryAgljRWUupoxjyrIqIXWYb-O_FIbIlXws5sxIaPIfnTkUKflsoqMDkWFDtWRs7xqnPOT_AP_1ijaEmvYxe0P2WQQFc4qUn0phJI0SSiD8h1ic0z6gulQBmaAY1JHO0ZNo_yo7tJHRg3KBaR73HPr6IlFGIaR1LQwDeR8Oo1a7z-fAfSxcxbQhwroRQHqZyAzJYuzJSB5Q29WQT6vIAc5ufs64HYFCF5XVZa3jImWMp5Gp4YFV5amt3758XLZ3NQ0OaY6m1uMF3CfEL-O7uVWvtwnj4cshFKmjnjF_isbWV1Jh98sXTwzVZLr3f_7Y-2gqwfdo3bUbnUOH6BrUBfY-VzE30a12WSuH6JL6mQ2nE4eWZ-H0dfz9g6_Aeq06Ic |
| linkToPdf | http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMw1V1bb9MwFLZGBxMvXMZlgcEM4vIUGid27CAhVLZVVNtKNQYaElJwHGdMGklpu6H-NX4dx4kbGlTBXvbAa_0lSo_PNTn-DkJPooiBFvHUJcrjLg1C6UapZK5KWES1lkJXlPm7vN8Xh4fRYAn9nJ2FMW2VM59YOuq0UOYdeRviihAhC6hoZ7YtYrDVfT387poJUuZL62ycRqUiO3r6A8q38aveFuz1U9_vbh9svnXthAFXicCbuDQJU5GwlBKeJZDKE8kgf9cBk_DUaaJ9JVmiwwDybqY9ohhPklCRKBFMaU_TAO57CS1DSk79Floe9PYGn-pyL_LKNzyGA80lPuf24F7ASdvqyYshRLySBJUY0qm5wFjOD6ijRGt4UowXpcB_dnLOhcbu9f9ZqDfQNZuQ405lQTfRks5X0ZVqROd0Fa3s2eaDW-hzSaliYwU-mMv4ixzLPMUD0-tW8Zzg4xx3Dd952eaLd6dgNMU3-RJ38OaJKX7w9pk1emxaOae30YcL-Zd3UCsvcr2GsEdJRj2tIFeUNFFQBGvGfKog1xZaR5mDgplmxMoyt5sBIidx-TmSQwVXySo2-hRbfXKQW181rJhL_oF_Y5Suxhre8fKHYnQUWzcWq0wKoSRNU8qgsIeonZBMMB3J0Ix2TB20YVQ2rg7x1t4z7lAuIBHkvuegxyXCcI_kRuGO5Ol4HPfefTwH6H3_PKD9Bui5BWUFyExJe-oEJG-IzxrIZw3kUUX7vgi43gCCP1aN5TVjrjMZj-PfRgZXzsxw8fKjetnc1LQ_5ro4LTF-yANCAgfdrSy-3iefRyyCIsdBvOELGhvZXMmPv5ZE8szUT55_7--PtYFWwCnEu73-zn10FQqGcnAXCdZRazI61Q_QZXU2OR6PHloHiNGXi3YPvwDr3_LW |
| openUrl | ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Histological+Transformation+and+Progression+in+Follicular+Lymphoma%3A+A+Clonal+Evolution+Study&rft.jtitle=PLoS+medicine&rft.au=Kridel%2C+Robert&rft.au=Chan%2C+Fong+Chun&rft.au=Mottok%2C+Anja&rft.au=Boyle%2C+Merrill&rft.date=2016-12-13&rft.eissn=1549-1676&rft.volume=13&rft.issue=12&rft.spage=e1002197&rft_id=info:doi/10.1371%2Fjournal.pmed.1002197&rft_id=info%3Apmid%2F27959929&rft.externalDocID=27959929 |
| thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=1549-1676&client=summon |
| thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=1549-1676&client=summon |
| thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=1549-1676&client=summon |