核医学与放射治疗

Radiobiological Modeling Based on 18F-Fluorodeoxyglucose Positron Emission Tomography Data for Esophageal Cancer

Abstract

Mariana Guerrero, Shan Tan and Wei Lu

Abstract

Background: We investigated the relationship of standardized uptake values (SUVs) to radiobiological parameters, such a 25 s tumor control probability (TCP), to allow for quantitative prediction of tumor response based on SUVs from 18F fluorodeoxyglucose (18F-FDG) positron emission tomography (PET) before and after treatment for esophageal cancer.
Methods: We analyzed data from 20 esophageal cancer patients treated with chemoradiotherapy (CRT) followed by surgery. Tumor pathologic response to CRT was assessed in surgical specimens. Patients underwent 18F-FDG PET imaging before and after CRT. Rigid image registration was performed between both images. Because TCP in a heterogeneous tumor is a function of average cell survival, we modeled TCP as a function of , a possible surrogate for average cell survival (=). TCP was represented by a sigmoid function with two parameters: SUVR50, the at which TCP=0.5, and γ50, the slope of the curve at SUVR50. The two parameters and their confidence intervals (CIs) were estimated using the maximum-likelihood method. The correlation between SUV before CRT and SUV change was also studied.
Results: A TCP model as a function of SUV before and after treatment was developed for esophageal cancer patients. The maximum-likelihood estimate of SUVR50 was 0.47 (90% CI, 0.30-0.61) and for γ50was 1.62 (90% CI, 0-4.2). High initial SUV and larger metabolic response (larger ) were correlated, and this correlation was stronger among responders. Conclusions: Our TCP model indicates that is a possible surrogate for cell survival in esophageal cancer patients. Although CIs are large as a result of the small patient sample, parameters for a TCP curve can be derived and an individualized TCP can be calculated for future patients. Initial SUV does not predict response, whereas a correlation is found between surrogates for initial tumor burden and cell kill during therapy.