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Sci Transl Med:纳米粒携带抗癌药可有效抵御癌症发展

2012-04-10 T.Shen 生物谷

图中显示的是纳米粒携带抗癌药物导致癌细胞破坏崩解;蓝色为纳米粒,紫色为癌细胞(Image: Medi-mation/Science Photo Library) Copyright ®版权归生物谷所有,若未得到Bioon授权,请勿转载。 近日,国际著名杂志Science Translational Medicine在线刊登了国外研究人员最新研究成果“Preclinical Develo

图中显示的是纳米粒携带抗癌药物导致癌细胞破坏崩解;蓝色为纳米粒,紫色为癌细胞(Image: Medi-mation/Science Photo Library)

Copyright ®版权归生物谷所有,若未得到Bioon授权,请勿转载。

近日,国际著名杂志Science Translational Medicine在线刊登了国外研究人员最新研究成果“Preclinical Development and Clinical Translation of a PSMA-Targeted Docetaxel Nanoparticle with a Differentiated Pharmacological Profile”,文章中研究者揭示了用纳米粒携带抗癌药物对于治疗癌症效果显著。

纳米粒运输治疗法(Drug-smuggling nanoparticles)将会是最新的抵御癌症的方法,早期的实验结果显示,通过纳米粒运输癌症药物治疗的方法可以明显降低人类肿瘤的大小。来自美国波士顿的研究者将癌症药物多西紫杉醇(docetaxel)填入纳米粒中,然后注射入17个癌症患者的血液中,这些患者对药物有一定的耐药性,经过42天后,这些癌症患者中,有两个患者的肿瘤缩小了,其余的患者肿瘤也不再生长了。

当把这种含有癌症药物的纳米粒注射入人的机体内时,多西紫杉醇并不能够识别出健康的细胞核癌细胞,然而,纳米粒却可以起到识别的作用,它可以通过于肿瘤细胞表面的分子反应来识别肿瘤细胞,从而释放抗癌药物,达到抑制肿瘤生长的目的。而且针对每一个肿瘤细胞仅仅需要不到80%的药物。

研究者Jeffrey Hrkach表示,医生们可以自由控制用药浓度,而不需要担心药物的毒性负面效应,不过我们还需要进行更多的临床试验要确定用药量。(生物谷:T.Shen编译)

Copyright ®版权归生物谷所有,若未得到Bioon授权,请勿转载。

doi:10.1126/scitranslmed.3003651
PMC:
PMID:

Preclinical Development and Clinical Translation of a PSMA-Targeted Docetaxel Nanoparticle with a Differentiated Pharmacological Profile

Jeffrey Hrkach1, Daniel Von Hoff2, Mir Mukkaram Ali1, Elizaveta Andrianova1, Jason Auer1, Tarikh Campbell1, David De Witt1, Michael Figa1, Maria Figueiredo1, Allen Horhota1, Susan Low1, Kevin McDonnell1, Erick Peeke1, Beadle Retnarajan1, Abhimanyu Sabnis1, Edward Schnipper1, Jeffrey J. Song1, Young Ho Song1, Jason Summa1, Douglas Tompsett1, Greg Troiano1, Tina Van Geen Hoven1, Jim Wright1, Patricia LoRusso3, Philip W. Kantoff4, Neil H. Bander5, Christopher Sweeney4, Omid C. Farokhzad6,*, Robert Langer7,* and Stephen Zale1,*

We describe the development and clinical translation of a targeted polymeric nanoparticle (TNP) containing the chemotherapeutic docetaxel (DTXL) for the treatment of patients with solid tumors. DTXL-TNP is targeted to prostate-specific membrane antigen, a clinically validated tumor antigen expressed on prostate cancer cells and on the neovasculature of most nonprostate solid tumors. DTXL-TNP was developed from a combinatorial library of more than 100 TNP formulations varying with respect to particle size, targeting ligand density, surface hydrophilicity, drug loading, and drug release properties. Pharmacokinetic and tissue distribution studies in rats showed that the NPs had a blood circulation half-life of about 20 hours and minimal liver accumulation. In tumor-bearing mice, DTXL-TNP exhibited markedly enhanced tumor accumulation at 12 hours and prolonged tumor growth suppression compared to a solvent-based DTXL formulation (sb-DTXL). In tumor-bearing mice, rats, and nonhuman primates, DTXL-TNP displayed pharmacokinetic characteristics consistent with prolonged circulation of NPs in the vascular compartment and controlled release of DTXL, with total DTXL plasma concentrations remaining at least 100-fold higher than sb-DTXL for more than 24 hours. Finally, initial clinical data in patients with advanced solid tumors indicated that DTXL-TNP displays a pharmacological profile differentiated from sb-DTXL, including pharmacokinetics characteristics consistent with preclinical data and cases of tumor shrinkage at doses below the sb-DTXL dose typically used in the clinic.

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    2012-11-25 bsmagic9140
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    2012-04-12 sunylz
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PNAS:日揭示癌干细胞难以彻底消灭的原因

近日,PNAS发表了日本东京大学医学研究所研究人员的一项新研究发现,对于癌症发病和复发起到重要作用的癌干细胞,能够自己分泌其生存必需的各种蛋白质。如果能够破坏这个机制,就有望防止癌症的复发。 癌干细胞是指具有干细胞性质的癌细胞,有“自我复制”以及“多细胞分化”等能力。这类细胞被认为有形成肿瘤乃至发展成癌症的潜力。现在的癌症治疗主要是通过药物和放疗等杀死癌细胞。但是,如果有癌干细胞残留,癌细胞就会

Nature:脑癌形成研究获进展

近日,国际著名杂志Nature在线刊登了美国加州大学旧金山分校,日本理化研究所RIKEN等处研究人员的最新研究成果“Local generation of glia is a major astrocyte source in postnatal cortex,”,文章中,研究者报道了胶质细胞中最大组成成分:星型胶质细胞的一种新来源,证明了产后皮质局部生成星型胶质细胞是胶质细胞一个主要来源的观点,

AACR:药物CLR1404能够检测和治疗恶性肿瘤和某些癌干细胞

图片来自Christine E. Eyler et al. Glioma Stem Cell Proliferation and Tumor Growth Are Promoted by Nitric Oxide Synthase-2, Cell, Volume 146, Issue 1, 53-66, 8 July 2011, DOI:10.1016/j.cell.2011.06.006. C

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