Get 20M+ Full-Text Papers For Less Than $1.50/day. Start a 14-Day Trial for You or Your Team.

Learn More →

Clarification of Definitions of Hyperprogressive Disease During Immunotherapy—Reply

Clarification of Definitions of Hyperprogressive Disease During Immunotherapy—Reply In Reply We thank Matos and Garralda for their interest and insightful comments on our article.1 We agree that hyperprogressive disease (HPD), although believed to be associated with immunotherapy, is a pattern of tumoral behavior that in theory could be encountered with other systemic treatments. The objective of our study did not intend to solve this controversy but to provide the more accurate definition of hyperprogression so that future researches on that topic could be reproducible. We selected studies on hyperprogression in the literature that included a prebaseline assessment to estimate the pretreatment tumor growth rate (TGR); most of them had no control group to test our definition with other systemic treatment. Although we agree that TGR is not a perfect tool, we believe that it gives the most chance to describe tumor kinetics. Neither the Response Evaluation Criteria in Solid Tumors (RECIST), version 1.1 criteria nor iRECIST criteria take into account the time interval between baseline and progression, and we are not aware of other criteria that could help in this purpose.2,3 This is one of the limitations of the work published by Matos et al.4 In their study, a 40% increase of the sum of the target lesion between baseline and the first evaluation and/or an increase of 20% plus the appearance of new lesions in 2 different organs was considered as HPD. The moderate concordance between HPD rate according to RECIST or to tumor growth kinetics highlights the need for a more robust definition. In this regard, we have recently reported that using a 50% or greater increase in the sum of the longest diameters of target lesions from baseline (fast progression) may underestimate HPD phenomenon (2.2%) compared with TGR (13.8%).5 In the same study, fast progression occurred at a similar rate in both immune checkpoint inhibitor–treated and chemotherapy-treated patients with non–small cell lung cancer.5 We also agree that the appearance of new lesions should be considered in progression and hyperprogression. This is one of the limitations of the assessment of HPD with TGR. Assessment of HPD with RECIST has also strong limitations. Indeed, the very definition of RECIST is based on the selection of up to 5 target lesions that will be registered, leaving potential other measurable lesions in the nontarget lesions group. Moreover, RECIST measurements cannot be applied to all existing lesions, such as bone metastases, effusions (eg, pleural, peritoneal), lymphangitis, or meningitis. Moreover, we could not find any unquestionable guiding rule on how these new lesions can be taken into account: how can we state that the appearance of 2 (or 3 or 4) new lesions is worse than 1 or which organs are of worse prognosis. All these questions are still pending. Altogether, these findings suggest that HPD definitions should include a comparison to a prebaseline time period, and we absolutely agree on the importance of pursuing efforts in researching how and to what extent HPD can happen. Prebaseline computed tomography scans should be captured in databases of clinical trials to evaluate HPD during the initiation of immune checkpoint inhibitor therapy or other systemic treatments. Back to top Article Information Corresponding Author: Caroline Caramella, MD, Radiology Department, Gustave Roussy, Université Paris-Saclay, 114 rue Edouard Vaillant, Villejuif 94805, France (caroline.caramella@gustaveroussy.fr). Published Online: November 19, 2020. doi:10.1001/jamaoncol.2020.5591 Conflict of Interest Disclosures: Dr Caramella reported receiving personal fees from Bristol Myers Squibb, AstraZeneca, Pfizer, and Merck Sharp & Dohme outside the submitted work. Dr Ferrara reported receiving personal fees from Merck Sharp & Dohme outside the submitted work. Dr Besse reported receiving grants from AbbVie, Amgen, AstraZeneca, BeiGene, Blueprint Medicines, Bristol Myers Squibb, Boehringer Ingelheim, Celgene, Cristal Therapeutics, Daiichi Sankyo, Eli Lilly, GlaxoSmithKline, Ignyta, Ipsen, Inivata, Janssen, Merck KGaA, Merck Sharp & Dohme, Nektar Therapeutics, Onxeo, OSE Immunotherapeutics, Pfizer, Pharma Mar, Roche-Genentech, Sanofi, Servier, Spectrum Pharmaceuticals, Takeda, Tiziana Pharma, and Tolero Pharmaceuticals related to the submitted work. References 1. Kas B, Talbot H, Ferrara R, et al. Clarification of definitions of hyperprogressive disease during immunotherapy for non-small cell lung cancer.  JAMA Oncol. 2020;6(7):1039-1046. doi:10.1001/jamaoncol.2020.1634PubMedGoogle ScholarCrossref 2. Eisenhauer EA, Therasse P, Bogaerts J, et al. New response evaluation criteria in solid tumours: revised RECIST guideline (version 1.1).  Eur J Cancer. 2009;45(2):228-247. doi:10.1016/j.ejca.2008.10.026PubMedGoogle ScholarCrossref 3. Seymour L, Bogaerts J, Perrone A, et al; RECIST Working Group. iRECIST: guidelines for response criteria for use in trials testing immunotherapeutics.  Lancet Oncol. 2017;18(3):e143-e152. doi:10.1016/S1470-2045(17)30074-8PubMedGoogle ScholarCrossref 4. Matos I, Martin-Liberal J, García-Ruiz A, et al. Capturing hyperprogressive disease with immune-checkpoint inhibitors using RECIST 1.1 criteria.  Clin Cancer Res. 2020;26(8):1846-1855. doi:10.1158/1078-0432.CCR-19-2226PubMedGoogle ScholarCrossref 5. Ferrara R, Mezquita L, Texier M, et al Comparison of fast-progression, hyperprogressive disease, and early deaths in advanced non–small-cell lung cancer treated with PD-1/PD-L1 inhibitors or chemotherapy.  JCO Precis Oncol. 2020;2020(4):829-840. doi:10.1200/PO.20.00021Google ScholarCrossref http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png JAMA Oncology American Medical Association

Clarification of Definitions of Hyperprogressive Disease During Immunotherapy—Reply

Loading next page...
 
/lp/american-medical-association/clarification-of-definitions-of-hyperprogressive-disease-during-ldQ6y3zPD2
Publisher
American Medical Association
Copyright
Copyright 2020 American Medical Association. All Rights Reserved.
ISSN
2374-2437
eISSN
2374-2445
DOI
10.1001/jamaoncol.2020.5591
Publisher site
See Article on Publisher Site

Abstract

In Reply We thank Matos and Garralda for their interest and insightful comments on our article.1 We agree that hyperprogressive disease (HPD), although believed to be associated with immunotherapy, is a pattern of tumoral behavior that in theory could be encountered with other systemic treatments. The objective of our study did not intend to solve this controversy but to provide the more accurate definition of hyperprogression so that future researches on that topic could be reproducible. We selected studies on hyperprogression in the literature that included a prebaseline assessment to estimate the pretreatment tumor growth rate (TGR); most of them had no control group to test our definition with other systemic treatment. Although we agree that TGR is not a perfect tool, we believe that it gives the most chance to describe tumor kinetics. Neither the Response Evaluation Criteria in Solid Tumors (RECIST), version 1.1 criteria nor iRECIST criteria take into account the time interval between baseline and progression, and we are not aware of other criteria that could help in this purpose.2,3 This is one of the limitations of the work published by Matos et al.4 In their study, a 40% increase of the sum of the target lesion between baseline and the first evaluation and/or an increase of 20% plus the appearance of new lesions in 2 different organs was considered as HPD. The moderate concordance between HPD rate according to RECIST or to tumor growth kinetics highlights the need for a more robust definition. In this regard, we have recently reported that using a 50% or greater increase in the sum of the longest diameters of target lesions from baseline (fast progression) may underestimate HPD phenomenon (2.2%) compared with TGR (13.8%).5 In the same study, fast progression occurred at a similar rate in both immune checkpoint inhibitor–treated and chemotherapy-treated patients with non–small cell lung cancer.5 We also agree that the appearance of new lesions should be considered in progression and hyperprogression. This is one of the limitations of the assessment of HPD with TGR. Assessment of HPD with RECIST has also strong limitations. Indeed, the very definition of RECIST is based on the selection of up to 5 target lesions that will be registered, leaving potential other measurable lesions in the nontarget lesions group. Moreover, RECIST measurements cannot be applied to all existing lesions, such as bone metastases, effusions (eg, pleural, peritoneal), lymphangitis, or meningitis. Moreover, we could not find any unquestionable guiding rule on how these new lesions can be taken into account: how can we state that the appearance of 2 (or 3 or 4) new lesions is worse than 1 or which organs are of worse prognosis. All these questions are still pending. Altogether, these findings suggest that HPD definitions should include a comparison to a prebaseline time period, and we absolutely agree on the importance of pursuing efforts in researching how and to what extent HPD can happen. Prebaseline computed tomography scans should be captured in databases of clinical trials to evaluate HPD during the initiation of immune checkpoint inhibitor therapy or other systemic treatments. Back to top Article Information Corresponding Author: Caroline Caramella, MD, Radiology Department, Gustave Roussy, Université Paris-Saclay, 114 rue Edouard Vaillant, Villejuif 94805, France (caroline.caramella@gustaveroussy.fr). Published Online: November 19, 2020. doi:10.1001/jamaoncol.2020.5591 Conflict of Interest Disclosures: Dr Caramella reported receiving personal fees from Bristol Myers Squibb, AstraZeneca, Pfizer, and Merck Sharp & Dohme outside the submitted work. Dr Ferrara reported receiving personal fees from Merck Sharp & Dohme outside the submitted work. Dr Besse reported receiving grants from AbbVie, Amgen, AstraZeneca, BeiGene, Blueprint Medicines, Bristol Myers Squibb, Boehringer Ingelheim, Celgene, Cristal Therapeutics, Daiichi Sankyo, Eli Lilly, GlaxoSmithKline, Ignyta, Ipsen, Inivata, Janssen, Merck KGaA, Merck Sharp & Dohme, Nektar Therapeutics, Onxeo, OSE Immunotherapeutics, Pfizer, Pharma Mar, Roche-Genentech, Sanofi, Servier, Spectrum Pharmaceuticals, Takeda, Tiziana Pharma, and Tolero Pharmaceuticals related to the submitted work. References 1. Kas B, Talbot H, Ferrara R, et al. Clarification of definitions of hyperprogressive disease during immunotherapy for non-small cell lung cancer.  JAMA Oncol. 2020;6(7):1039-1046. doi:10.1001/jamaoncol.2020.1634PubMedGoogle ScholarCrossref 2. Eisenhauer EA, Therasse P, Bogaerts J, et al. New response evaluation criteria in solid tumours: revised RECIST guideline (version 1.1).  Eur J Cancer. 2009;45(2):228-247. doi:10.1016/j.ejca.2008.10.026PubMedGoogle ScholarCrossref 3. Seymour L, Bogaerts J, Perrone A, et al; RECIST Working Group. iRECIST: guidelines for response criteria for use in trials testing immunotherapeutics.  Lancet Oncol. 2017;18(3):e143-e152. doi:10.1016/S1470-2045(17)30074-8PubMedGoogle ScholarCrossref 4. Matos I, Martin-Liberal J, García-Ruiz A, et al. Capturing hyperprogressive disease with immune-checkpoint inhibitors using RECIST 1.1 criteria.  Clin Cancer Res. 2020;26(8):1846-1855. doi:10.1158/1078-0432.CCR-19-2226PubMedGoogle ScholarCrossref 5. Ferrara R, Mezquita L, Texier M, et al Comparison of fast-progression, hyperprogressive disease, and early deaths in advanced non–small-cell lung cancer treated with PD-1/PD-L1 inhibitors or chemotherapy.  JCO Precis Oncol. 2020;2020(4):829-840. doi:10.1200/PO.20.00021Google ScholarCrossref

Journal

JAMA OncologyAmerican Medical Association

Published: Jan 19, 2021

References