加拿大戴爾豪斯醫(yī)學(xué)院癌癥研究人員帕特里克﹒李博士證明，一種普通的病毒可以感染并殺死癌癥干細(xì)胞。這一突破性發(fā)現(xiàn)發(fā)表在*近出版的美國基因療法學(xué)會(huì)雜志《分子療法》上。
科學(xué)界近幾年才剛認(rèn)識(shí)到癌癥干細(xì)胞的作用，并迫切需要找到一種**它的辦法?！鞍┌Y干細(xì)胞是一種母細(xì)胞。”李博士解釋說?！八鼈儾粩喈a(chǎn)生新的癌細(xì)胞并形成腫瘤?！庇捎诎┌Y干細(xì)胞對(duì)化療和放療不敏感，因此要?dú)⑺浪鼈兎浅＠щy。就像李博士所說，“我們可以殺死腫瘤里的所有常規(guī)癌細(xì)胞，但只要存在癌癥干細(xì)胞，癌癥就會(huì)復(fù)發(fā)。”
“我們認(rèn)為呼腸孤病毒能有效殺死癌癥干細(xì)胞，因?yàn)槲覀兎磸?fù)發(fā)現(xiàn)它能有效殺死常規(guī)癌細(xì)胞。”李博士說。他是世界上**位發(fā)現(xiàn)一種良性自然病毒能有選擇感染并殺死癌細(xì)胞而不損害健康細(xì)胞的人。加拿大一家生物技術(shù)公司對(duì)呼腸孤病毒進(jìn)行臨床試驗(yàn)發(fā)現(xiàn)，這種****而有效。
與大多數(shù)利用試驗(yàn)室培養(yǎng)癌細(xì)胞的研究不同，這次研究所用的是從患者身上切除的新鮮乳腺癌組織。
呼腸孤病毒除了具有殺死癌細(xì)胞和癌癥干細(xì)胞的能力外，還能激發(fā)**的**系統(tǒng)。由于這種**也能誘導(dǎo)**反應(yīng)，李博士和同事正在研究一種方法，在病毒感染并摧毀癌癥細(xì)胞的同時(shí)能加強(qiáng)**系統(tǒng)抗擊癌細(xì)胞的能力?！拔覀兿乱徊焦ぷ骶褪亲屵@種雙重**的方法能夠成熟?！崩畈┦空f?！拔覀円煤裟c孤病毒固有的特點(diǎn)和**系統(tǒng)自身優(yōu)勢(shì)開發(fā)一種強(qiáng)有力的、基于病毒的**療法。”
呼腸孤病毒有效針對(duì)癌癥干細(xì)胞這一研究發(fā)現(xiàn)已引起英國LeadDiscovery制藥公司的注意，他們準(zhǔn)備進(jìn)行這一方面的**研發(fā)。（創(chuàng)賽新聞中心canspecsci.com）
創(chuàng)賽推薦原始出處：
Molecular Therapy (2009); doi:10.1038/mt.2009.58
Oncolytic Reovirus Effectively Targets Breast Cancer Stem Cells
Paola Marcato1, Cheryl A Dean1, Carman A Giacomantonio2 and Patrick WK Lee1,3
1Department of Microbiology and Immunology, Faculty ofMedicine,Dalhousie University, Halifax, Nova Scotia, Canada
2Department of Surgery, Faculty of Medicine, DalhousieUniversity,Halifax, Nova Scotia, Canada
3Department of Pathology, Faculty of Medicine, DalhousieUniversity,Halifax, Nova Scotia, Canada
Abstract
Recent evidence suggests that cancer stem cells (CSCs) play animportant role incancer, as these cells possess enhancedtumor-forming capabilitiesand are resistant to current anticancertherapies. Hence, novelcancer therapies will need to be tested forboth tumor regressionand CSC targeting. Herein we show thatoncolytic reovirus thatinduces regression of human breast cancerprimary tumor samples xenografted in immunocompromised mice also effectively targets and kills CSCs in these tumors. CSCs were identified based on CD24-CD44+ cell surface expression and overexpression of aldehyde dehydrogenase. Upon reovirus treatment, the CSC population was reduced at the same rate as non-CSCs within the tumor. Immunofluorescence of breast tumor tissue samples from the reovirus- and mock-treated mice confirmed that both CSCs and non-CSCs were infectible by reovirus, and terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling (TUNEL) assay showed that both populations died by apoptosis. Ras, which has been shown to mediate reovirus oncolysis, was found to be present at similar levels in all cell types, and this is consistent with their comparable sensitivity to reovirus. These experiments indicate that oncolytic reovirus has the potential to induce tumor regression in breast cancer patients. More important, the CSC population was equally reduced and was as susceptible to reovirus treatment as the non-CSC population.
