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Investigate the cellular membrane transport mechanisms of the PET tracer [18F]FHPG in HSVtk-expressing glioma models to determine whether it mimics ganciclovir pharmacokinetics.

December 1, 2004British Journal of CancerOpen Access

Monitoring HSVtk suicide gene therapy: the role of [18F]FHPG membrane transport

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Investigate the cellular membrane transport mechanisms of the PET tracer [18F]FHPG in HSVtk-expressing glioma models to determine whether it mimics ganciclovir pharmacokinetics.
Assessed [18F]FHPG uptake in HSVtk-expressing C6 rat glioma cells using nucleoside transport inhibitors (dipyridamol, NBMPR, 2-chloroadenosine) and nucleobase transport inhibitors.
Measured in vivo tracer uptake and tumor-to-background ratios in C6 and C6tk tumor-bearing rats before and after adenine infusion.
Nucleobase transport inhibitors thymine and adenine reduced in vitro tracer uptake by 58% and 55%, respectively, whereas classical nucleoside transport inhibitors produced no significant effect.
Adenine infusion decreased the in vivo [18F]FHPG uptake ratio between C6tk and C6 tumors from 3.0 ± 0.5 to 1.0 ± 0.2, demonstrating tracer entry occurs exclusively via purine nucleobase carriers rather than nucleoside transport.

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Implication

Preclinical study reveals [18F]FHPG enters cells via purine nucleobase transport in glioma models, indicating it cannot reliably mimic ganciclovir pharmacokinetics.

Cite This Study

Buursma et al. (2004) studied this question.

synapsesocial.com/papers/6a86f1bea6ddb97d43d3c5ae https://doi.org/10.1038/sj.bjc.6602216

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Implication

Preclinical study reveals [18F]FHPG enters cells via purine nucleobase transport in glioma models, indicating it cannot reliably mimic ganciclovir pharmacokinetics.

Monitoring HSVtk suicide gene therapy: the role of [18F]FHPG membrane transport

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Discussion

Implication

Cite This Study

Monitoring HSVtk suicide gene therapy: the role of [18F]FHPG membrane transport

Key Points

Discussion

Implication

Cite This Study

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