使用锝-94m-甲氧基异丁基异腈微PET成像多药耐药P-糖蛋白转运功能。
Imaging multidrug resistance P-glycoprotein transport function using microPET with technetium-94m-sestamibi.
作者信息
Bigott Heather M, Prior Julie L, Piwnica-Worms David R, Welch Michael J
机构信息
Mallinckrodt Institute of Radiology, Washington University School of Medicine, 510 South Kingshighway Boulevard, St. Louis, MO 63110, USA.
出版信息
Mol Imaging. 2005 Jan-Mar;4(1):30-9. doi: 10.1162/15353500200504166.
The best characterized mechanism of multidrug resistance (MDR) in cancer involves the MDR1 efflux transporter P-glycoprotein (Pgp). The positron-emitting radiotracer hexakis(2-methoxyisobutylisonitrile)-(94m)Tc ((94m)Tc-MIBI) was synthesized and validated in cell transport studies as a substrate for MDR1 Pgp. In vivo small-scale PET imaging and biodistribution studies of mdr1a/1b (-/-) gene deleted and wild-type mice demonstrated the use of (94m)Tc-MIBI to detect Pgp function. The reversal effect of a Pgp modulator was shown in tissue distribution studies of KB 3-1 (Pgp-) and KB 8-5 (Pgp+) tumor-bearing nude mice. The current (94m)Tc-MIBI experiments parallel previous studies employing (99m)Tc-MIBI, showing essentially identical performance of the two technetium radiotracers and providing biological validation of (94m)Tc-MIBI for PET imaging of multidrug resistance.
癌症中多药耐药（MDR）最具特征的机制涉及MDR1外排转运体P-糖蛋白（Pgp）。发射正电子的放射性示踪剂六（2-甲氧基异丁基异腈）-（94m）锝（（94m）Tc-MIBI）被合成，并在细胞转运研究中作为MDR1 Pgp的底物进行了验证。对mdr1a/1b（-/-）基因敲除小鼠和野生型小鼠进行的体内小规模PET成像和生物分布研究证明了（94m）Tc-MIBI可用于检测Pgp功能。在携带KB 3-1（Pgp-）和KB 8-5（Pgp+）肿瘤的裸鼠的组织分布研究中显示了Pgp调节剂的逆转作用。当前的（94m）Tc-MIBI实验与之前使用（99m）Tc-MIBI的研究相似，表明这两种锝放射性示踪剂的性能基本相同，并为多药耐药的PET成像提供了（94m）Tc-MIBI的生物学验证。
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