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【drug-news】治焦虑不行就治癌症吧!
Cancer cells have multiple ways to avoid apoptosis, programmed cell death the means by which organisms deal with defective cells. One defense is to produce quantities of phosphatic acid, a phospholipid constituent of cellular membranes.
Unlike other phospholipids, phosphatidic acid also acts as a signaling molecule for cells promoting cellular growth and preventing apoptosis. Finnish and Danish researchers have now shown that phosphatidic acid may well be a target molecule for novel anti-cancer drugs.
Siramesine is a drug molecule developed and synthesized by Lundbeck A/S for the treatment of anxiety. Its development was discontinued due to unsatisfying efficacy in clinical trials in 2002. Later professor Marja Jäättelä and co-workers at the Danish cancer institute discovered that siramesine effectively inhibits the growth of both cultured cancer cells as well as solid tumors in mice. Siramesine is known to bind sigma-receptors, which physiological role remains unknown, on the cellular surface and this interaction was also believed to underlie its anti-tumor actions.
Researchers at the University of Helsinki, Finland, lead by Professor Paavo Kinnunen, studied the interaction of this drug with different phospholipids using biophysical methods and different model cellular membranes. In addition a computer simulation was performed as collaboration with MEMPHYS, Odense, Denmark, to further their understanding of this interaction.
"The key finding of our study was that siramesine avidly and specifically binds to phosphatidic acid", says MD Mikko Parry from Helsinki Biophysics & Biomembrane group at the Institute of Biomedicine, University of Helsinki.
"Importantly, this is the first time it's shown that a lipid second messenger can act as a drug target: it is a totally new mechanism of action and constitutes a novel paradigm for developing new, more effective anti-cancer drugs."
http://www.mphtimes.com/us/index.php?option=com_content&view=article&id=527:unsuccessful-drug-against-anxiety-opens-a-novel-gateway-for-the-treatment-of-cancer&catid=89:regulatory-affairs--drug-approvals&Itemid=162 本人已认领该文编译，48小时后若未提交译文，请其他战友自由认领。 Unsatisfying drug for anxiety reveals scientists a promising novel anti-cancer drug target.
疗效不满意的抗焦虑药物提示了有希望的抗肿瘤药物新靶点
Cancer cells have multiple ways to avoid apoptosis, programmed cell death the means by which organisms deal with defective cells. One defense is to produce quantities of phosphatic acid, a phospholipid constituent of cellular membranes.
肿瘤细胞通过多种途径规避凋亡，而机体主要通过这种程序性细胞死亡清除有缺陷的细胞。其中的一项抵御措施就是产生大量的磷脂酸，这是细胞膜的磷脂成分之一。
Unlike other phospholipids, phosphatidic acid also acts as a signaling molecule for cells promoting cellular growth and preventing apoptosis. Finnish and Danish researchers have now shown that phosphatidic acid may well be a target molecule for novel anti-cancer drugs.
与其它磷脂类不同，磷脂酸同时也是一种细胞信号分子，可以促进细胞生长并抵御凋亡。芬兰和丹麦科学家最近发现磷脂酸可能作为抗癌新药的一个可能的靶分子。
Siramesine is a drug molecule developed and synthesized by Lundbeck A/S for the treatment of anxiety. Its development was discontinued due to unsatisfying efficacy in clinical trials in 2002. Later professor Marja Jäättelä and co-workers at the Danish cancer institute discovered that siramesine effectively inhibits the growth of both cultured cancer cells as well as solid tumors in mice. Siramesine is known to bind sigma-receptors, which physiological role remains unknown, on the cellular surface and this interaction was also believed to underlie its anti-tumor actions.
西拉美新是由Lundbeck A/S公司开发合成的一种抗焦虑药物。2002年由于临床疗效不满意而停止了开发进程。随后丹麦肿瘤研究所的Marja Jäättelä教授及其同事发现，西拉美新可以有效地抑制体外培养肿瘤细胞和小鼠体内实体瘤的生长。已知西拉美新可以结合细胞表面的sigma受体，该受体的生理功能仍不清除，目前认为这种结合是其抗肿瘤作用的基础。
Researchers at the University of Helsinki, Finland, lead by Professor Paavo Kinnunen, studied the interaction of this drug with different phospholipids using biophysical methods and different model cellular membranes. In addition a computer simulation was performed as collaboration with MEMPHYS, Odense, Denmark, to further their understanding of this interaction.
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作者:admin@医学,生命科学 2010-12-18 17:11
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