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New mechanisms of sodium iodide Symporter Repression

New mechanisms of sodium iodide Symporter Repression
碘化钠同向转运蛋白抑制的新机制
批准号:
G0700064/1
负责人:
Christopher McCabe
金额:
$39.96万
依托单位:
依托单位国家:
英国
项目类别:
Research Grant
财政年份:
2007
资助国家:
英国
项目状态:
已结题
起止时间:
2007 至 --

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中文摘要
翻译
甲状腺癌是一种常见的恶性肿瘤。甲状腺癌的主要治疗选择是放射性碘,它集中在甲状腺中,然后杀死癌细胞。其中一个问题是,帮助甲状腺细胞吸收放射性碘的蛋白质NIS在癌细胞中不如在正常细胞中那么活跃。这意味着治疗并不像它可能的那样有效。我们的目标是改变这一点。我们已经发现两个基因PTTG和PBF降低了NIS的功能。因此,我们想探索如何克服这种影响,特别是因为甲状腺和其他癌症具有高水平的PTTG和PBF。如果我们能阻止PTTG和PBF阻止NIS摄取放射性碘,这将改善治疗,并意味着这种治疗在其他正在测试放射性碘的癌症中也可能更有效。
英文摘要
Thyroid cancer is relatively common, and growing in incidence. A main treatment option for thyroid cancer is radioactive iodide, which is concentrated in the thyroid, and then kills cancer cells. One problem with this is that the protein NIS which helps thyroid cells take up the radioactive iodide is not as active in cancer cells as it is in normal cells. This means that the treatment is not as effective as it could be. We are aiming to change this. We have discovered that two genes called PTTG and PBF reduce the ability of the NIS to function. We therefore want to explore how we can overcome this effect, particularly because thyroid and other cancers have high levels of PTTG and PBF. If we can prevent PTTG and PBF from stopping NIS uptaking radioactive iodide, this should improve therapy and mean that this treatment might also work better in other cancers in which radioactive iodide is being tested.
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