Using fluorodeoxythymidine to monitor anti‐EGFR inhibitor therapy in squamous cell carcinoma xenografts

Abstract

Background-3′-18F-fluoro-3′-deoxy-fluorothymidine ( 18 F-FLT), a nucleoside analog, could monitor effects of molecularly targeted therapeutics on tumor proliferation.

Correlation Between Epidermal Growth Factor Receptor-Specific Nanobody Uptake and Tumor Burden: A Tool for Noninvasive Monitoring of Tumor Response to Therapy

“…This was in agreement with the study reported by Li et al [42]. Although we did not look at the effect of erlotinib treatment on EGFR expression in vivo, other studies reported no significant difference in EGFR expression between erlotinib-treated and placebo groups [43] at the same concentration of erlotinib and in the same tumor model. However, downregulation of total EGFR expression was reported only at a high concentration of erlotinib (20 μM) in vitro [42]; the mechanism by which this occurs remains unknown.…”

Preclinical and Clinical Evidence that Deoxy-2-[18F]fluoro-D-glucose Positron Emission Tomography with Computed Tomography Is a Reliable Tool for the Detection of Early Molecular Responses to Erlotinib in Head and Neck Cancer

“…This could lead to the use of a more specific marker of cell proliferation, such as 3-deoxy-3-18 F-fluorothymidine (29). Indeed, Atkinson et al (30) reported that 3-deoxy-3-18 F-fluorothymidine allowed anti-EGFR inhibitor therapy in squamous cell carcinoma to be monitored. However, 3-deoxy-3-18 F-fluorothymidine is not commercially available.…”

PET Monitoring of Therapy Response in Head and Neck Squamous Cell Carcinoma

“…When nude mice bearing the human squamous cell cancer graft (HNX-OE; nu/nu mice) were irradiated, both 18 F-FDG and 18 F-FLT uptake declined from baseline levels, but the decline in 18 F-FDG uptake occurred mainly during the first week of treatment, whereas the greatest decline in 18 F-FLT uptake was noted during the second treatment week (100). In another study, however, 18 F-FLT PET showed promise in assessing the early response to cetuximab in a squamous cell cancer xenograft model (101). A significant decline in tumor SUV, tumor-to-muscle ratios, and thymidine kinase-1 activity occurred as early as 6 d after single-agent therapy had been initiated with cetuximab.…”