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使用 (18)F-FLT PET 评估精氨酸脱亚氨酶治疗黑色素瘤异种移植瘤的效果。

Evaluation of arginine deiminase treatment in melanoma xenografts using (18)F-FLT PET.

机构信息

Department of Radiology, Charité CVK-Universitätsmedizin Berlin, 13353, Berlin, Germany,

出版信息

Mol Imaging Biol. 2013 Dec;15(6):768-75. doi: 10.1007/s11307-013-0655-6.

DOI:10.1007/s11307-013-0655-6
PMID:23722880
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4537614/
Abstract

PURPOSE

This study aims to develop a molecular imaging strategy for response assessment of arginine deiminase (ADI) treatment in melanoma xenografts using 3'-[(18)F]fluoro-3'-deoxythymidine ([(18)F]-FLT) positron emission tomography (PET).

PROCEDURES

F-FLT response to ADI therapy was studied in preclinical models of melanoma in vitro and in vivo. The molecular mechanism of response to ADI therapy was investigated, with a particular emphasis on biological pathways known to regulate (18)F-FLT metabolism.

RESULTS

Proliferation of SK-MEL-28 melanoma tumors was potently inhibited by ADI treatment. However, no metabolic response was observed in FLT PET, presumably based on the known ADI-induced degradation of PTEN, followed by instability of the tumor suppressor p53 and a relative overexpression of thymidine kinase 1, the enzyme mainly responsible for intracellular FLT processing.

CONCLUSION

The specific pharmacological properties of ADI preclude using (18)F-FLT to evaluate clinical response in melanoma and argue for further studies to explore the use of other clinically applicable PET tracers in ADI treatment.

摘要

目的

本研究旨在开发一种使用 3'-[(18)F]氟-3'-去氧胸苷 ([(18)F]-FLT) 正电子发射断层扫描 (PET) 评估精氨酸脱亚氨酶 (ADI) 治疗反应的分子成像策略，用于黑色素瘤异种移植。

方法

在黑色素瘤的体外和体内临床前模型中研究了 F-FLT 对 ADI 治疗的反应。研究了 ADI 治疗反应的分子机制，特别强调了已知调节 (18)F-FLT 代谢的生物学途径。

结果

ADI 治疗强烈抑制 SK-MEL-28 黑色素瘤肿瘤的增殖。然而，在 FLT PET 中未观察到代谢反应，这可能基于已知的 ADI 诱导的 PTEN 降解，随后肿瘤抑制因子 p53 不稳定，以及胸苷激酶 1 的相对过表达，该酶主要负责细胞内 FLT 处理。

结论

ADI 的特定药理学特性排除了使用 (18)F-FLT 来评估黑色素瘤的临床反应，并呼吁进一步研究探索在 ADI 治疗中使用其他临床适用的 PET 示踪剂。

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