日前，日本一個(gè)研究小組宣布,，他們?cè)趧?dòng)物實(shí)驗(yàn)中發(fā)現(xiàn)一種防止惡性膠質(zhì)瘤復(fù)發(fā)的新方法,，相關(guān)論文已經(jīng)刊登在英國(guó)《科學(xué)報(bào)告》（Scientific Reports）雜志上。
惡性膠質(zhì)瘤是一種非常難以治療的惡性腦腫瘤,，術(shù)后復(fù)發(fā)率較高,。在日本，它是一種患者人數(shù)最多的惡性腦腫瘤,，發(fā)病率為萬(wàn)分之一,。能夠重新制造癌細(xì)胞的“癌干細(xì)胞”被認(rèn)為是導(dǎo)致惡性膠質(zhì)瘤復(fù)發(fā)的原因。
日本山形大學(xué)和國(guó)立癌癥研究中心的聯(lián)合研究小組注意到,，一種被稱為JNK的蛋白激酶對(duì)于維持“癌干細(xì)胞”的存活必不可少,，于是將美國(guó)制藥公司為治療帕金森氏癥而開(kāi)發(fā)的JNK抑制劑注射到腦內(nèi)移植了惡性膠質(zhì)瘤的實(shí)驗(yàn)鼠體內(nèi)。結(jié)果發(fā)現(xiàn),，腫瘤中的“癌干細(xì)胞”減少到原有水平的十分之一以下,。
如果向?qū)嶒?yàn)鼠腦內(nèi)移植“癌干細(xì)胞”,，再連續(xù)10天注射這種藥物，也能夠?qū)?ldquo;癌干細(xì)胞”減少到原有水平的十分之一以下甚至百分之一,。藥物對(duì)腦功能也沒(méi)有影響,。
研究小組負(fù)責(zé)人、山形大學(xué)教授北中千史說(shuō)：“通過(guò)手術(shù)清除膠質(zhì)瘤,，再輔以這種藥物,，也許就能夠阻止復(fù)發(fā)，讓患者長(zhǎng)期存活,。”研究人員已經(jīng)準(zhǔn)備開(kāi)展臨床研究,，有望5至7年后實(shí)現(xiàn)臨床應(yīng)用。（生物谷Bioon.com）
doi:10.1038/srep00516
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Targeting JNK for therapeutic depletion of stem-like glioblastoma cells
Ken-ichiro Matsuda; Atsushi Sato; Masashi Okada; Keita Shibuya; Shizuka Seino; Kaori Suzuki; Eriko Watanabe; Yoshitaka Narita; Soichiro Shibui; Takamasa Kayama; Chifumi Kitanaka
Control of the stem-like tumour cell population is considered key to realizing the long-term survival of patients with glioblastoma, one of the most devastating human malignancies. To date, possible therapeutic targets and targeting methods have been described, but none has yet proven to target stem-like glioblastoma cells in the brain to the extent necessary to provide a survival benefit. Here we show that targeting JNK in vivo, the activity of which is required for the maintenance of stem-like glioblastoma cells, via transient, systemic administration of a small-molecule JNK inhibitor depletes the self-renewing and tumour-initiating populations within established tumours, inhibits tumour formation by stem-like glioblastoma cells in the brain, and provide substantial survival benefit without evidence of adverse events. Our findings not only implicate JNK in the maintenance of stem-like glioblastoma cells but also demonstrate that JNK is a viable, clinically relevant therapeutic target in the control of stem-like glioblastoma cells
