TY - JOUR
T1 - Tumour growth rate as a tool for response evaluation during PD-1 treatment for non-small cell lung cancer
T2 - A retrospective analysis
AU - Ten Berge, Deirdre M.H.J.
AU - Hurkmans, Daniel P.
AU - Den Besten, Ilse
AU - Kloover, Jeroen S.
AU - Mathijssen, Ron H.J.
AU - Debets, Reno J.E.M.A.
AU - Smit, Egbert F.
AU - Aerts, Joachim G.J.V.
N1 - Publisher Copyright:
© 2019, European Respiratory Society. All rights reserved.
PY - 2019
Y1 - 2019
N2 - Background: Immune checkpoint inhibitors have emerged as a standard of care treatment for non-small cell lung cancer (NSCLC). To get insight into variations in tumour growth kinetics and their potential predictive values for outcome, we evaluated tumour growth rate (TGR) in patients receiving programmed cell death 1 (PD-1) checkpoint inhibitors. Patients and methods: Differences in TGR before and after the start of treatment were calculated by entering the sum of the longest diameters from computer tomography scans before and after the initiation of therapy into a formula that assumes volumetric exponential tumour growth. TGR variations, possible predictors for TGR changes and its relationship to overall survival (OS) were studied. For comparison, tumour response was assessed using Response Evaluation Criteria in Solid Tumours (RECIST) version 1.1. Results: Among the 58 evaluable patients, 37 patients (64%) showed deceleration of TGR and 16 patients (27%) showed an acceleration of TGR after initiation of therapy, with a significant difference in median OS of 18.0 months versus 6.0 months (hazard ratio 0.35, 95% CI 0.18–0.71) between these groups. Four patients (7%) were defined as having hyperprogressive disease. In five patients (9%), tumour growth remained stable. These TGR categories were not significantly different according to age, sex, histology, smoking or previous radiotherapy. Of the patients defined as having progressive disease by RECIST version 1.1 at first follow-up, 40% showed response to checkpoint inhibitors by a decrease in TGR. Conclusion: Tumour growth kinetics can be used as a clinically relevant predictor for OS in anti-PD-1- treated patients with NSCLC, and may provide additional information to RECIST measurements.
AB - Background: Immune checkpoint inhibitors have emerged as a standard of care treatment for non-small cell lung cancer (NSCLC). To get insight into variations in tumour growth kinetics and their potential predictive values for outcome, we evaluated tumour growth rate (TGR) in patients receiving programmed cell death 1 (PD-1) checkpoint inhibitors. Patients and methods: Differences in TGR before and after the start of treatment were calculated by entering the sum of the longest diameters from computer tomography scans before and after the initiation of therapy into a formula that assumes volumetric exponential tumour growth. TGR variations, possible predictors for TGR changes and its relationship to overall survival (OS) were studied. For comparison, tumour response was assessed using Response Evaluation Criteria in Solid Tumours (RECIST) version 1.1. Results: Among the 58 evaluable patients, 37 patients (64%) showed deceleration of TGR and 16 patients (27%) showed an acceleration of TGR after initiation of therapy, with a significant difference in median OS of 18.0 months versus 6.0 months (hazard ratio 0.35, 95% CI 0.18–0.71) between these groups. Four patients (7%) were defined as having hyperprogressive disease. In five patients (9%), tumour growth remained stable. These TGR categories were not significantly different according to age, sex, histology, smoking or previous radiotherapy. Of the patients defined as having progressive disease by RECIST version 1.1 at first follow-up, 40% showed response to checkpoint inhibitors by a decrease in TGR. Conclusion: Tumour growth kinetics can be used as a clinically relevant predictor for OS in anti-PD-1- treated patients with NSCLC, and may provide additional information to RECIST measurements.
UR - https://www.scopus.com/pages/publications/85083012184
U2 - 10.1183/23120541.00179-2019
DO - 10.1183/23120541.00179-2019
M3 - Article
C2 - 31857994
SN - 2312-0541
VL - 5
JO - ERJ Open Research
JF - ERJ Open Research
IS - 4
M1 - 00179-2019
ER -