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    題名: Mesenchymal stem cell targeting of microscopic tumors and tumor stroma development monitored by noninvasive in vivo positron emission tomography imaging
    作者: Hung, SC;Deng, WP;Yang, WK;Liu, RS;Lee, CC;Su, TC;Lin, RJ;Yang, DM;Chang, CW;Chen, WH;Wei, HJ;Gelovani, JG
    貢獻者: 附設醫院;Univ Texas, MD Anderson Canc Ctr, Dept Expt Diagnost Imaging, Unit 057, Houston, TX 77030 USA;Acad Sinica, Inst Biomed Sci, Nankang, Peoples R China;Taipei Med Univ, Inst Biomed Mat, Taipei, Taiwan;Vet Gen Hosp, Dept Med Res Orthoped, Taipei, Taiwan;Vet Gen Hosp, Dept Nucl Med, Taipei, Taiwan;Vet Gen Hosp, Natl PET Cyclotron Ctr, Taipei, Taiwan;Natl Yang Ming Univ, Sch Med, Taipei 112, Taiwan;China Med Univ Hosp, Lab Cell Gene Therapy, Taichung, Taiwan
    日期: 2005
    上傳時間: 2010-09-24 14:17:29 (UTC+8)
    出版者: AMER ASSOC CANCER RESEARCH
    摘要: The sodium/iodide symporter (NIS) actively transports iodide into thyrocytes. However, in thyroid carcinoma, down-regulated or mis-targeted NIS expression is commonly found and usually correlates with tumor dedifferentiation and loss of radioiodine uptake capacity. In this study, we screened NIS genes of thyroid tumor tissues from three patients with thyroid carcinoma by using reverse transcription-polymerase chain reaction and nucleotide sequencing. We found a novel exon 6 deletion in NIS gene. We then examined the NIS gene from the blood of this patient. The nucleotide sequences of the flanking region of exon 6 were normal. By transient transfection and I-125 uptake assay, we found that the wild type NIS-expressing HepG2 cells accumulated six times more iodide than mutant and mock HepG2 cells. Our data demonstrated that the exon 6 deletion causes an iodide-trapping defect. (c) 2005 Elsevier Ireland Ltd. All rights reserved.
    關聯: CLINICAL CANCER RESEARCH 11(21):7749-7756
    顯示於類別:[台中附設醫院] 期刊論文

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