當(dāng)前癌癥治療中面對的一個困難是,，如何在治療過程中只針對惡性細(xì)胞而不殺死健康細(xì)胞。加拿大科學(xué)家的一項最新研究將有可能幫助解決這一問題,，開發(fā)能更好地對付癌細(xì)胞而不損害健康細(xì)胞的療法和藥物,。相關(guān)論文1月4日在線發(fā)表于《自然—生物技術(shù)》（Nature Biotechnology）。
加拿大麥克馬斯特大學(xué)研究人員第一次論證了人類正常干細(xì)胞和癌癥干細(xì)胞的區(qū)別,。這一發(fā)現(xiàn)最終能夠幫助發(fā)展對個體病人的癌癥治療方法,，并將會提供一個藥物開發(fā)模型，通過自動篩選來尋找具有摧毀癌細(xì)胞潛力的分子,。
麥克馬斯特大學(xué)干細(xì)胞和癌癥研究中心科學(xué)主管Mick Bhatia表示：“正常干細(xì)胞和癌癥干細(xì)胞很難區(qū)分,，現(xiàn)在我們有辦法了。這一發(fā)現(xiàn)也讓我們可以在實驗室中比較正常干細(xì)胞和癌癥干細(xì)胞,，并按照其表達(dá)的基因和起反應(yīng)的藥物來定義這兩者之間的差別,。最重要的是，現(xiàn)在我們能夠利用這一發(fā)現(xiàn),，找到一種或一系列可以殺滅癌癥干細(xì)胞的藥物,，同時不會傷害正常的健康細(xì)胞。”
Bhatia說：“麥克馬斯特大學(xué)有最好的篩選平臺和化學(xué)實驗室,，發(fā)現(xiàn)可抗擊傳染病分子的Eric Brown和Gerry Wright教授也在這里,，他們經(jīng)驗豐富，現(xiàn)在我們可以把這一切集中起來,。研究小組的目標(biāo)是消滅癌癥,。”（生物谷Bioon.com）
生物谷推薦原始出處：
Nature Biotechnology 4 January 2009 | doi:10.1038/nbt.1516
Characterization of human embryonic stem cells with features of neoplastic progression
Tamra E Werbowetski-Ogilvie1, Marc Bossé1, Morag Stewart1, Angelique Schnerch1, Veronica Ramos-Mejia1, Anne Rouleau1, Tracy Wynder1, Mary-Jo Smith2, Steve Dingwall3, Tim Carter3, Christopher Williams4, Charles Harris4, Joanna Dolling5, Christopher Wynder1, Doug Boreham3 & Mickie Bhatia1
Cultured human embryonic stem (hES) cells can acquire genetic and epigenetic changes that make them vulnerable to transformation. As hES cells with cancer-cell characteristics share properties with normal hES cells, such as self-renewal, teratoma formation and the expression of pluripotency markers, they may be misconstrued as superior hES cells with enhanced 'stemness'. We characterize two variant hES cell lines (v-hESC-1 and v-hESC-2) that express pluripotency markers at high levels and do not harbor chromosomal abnormalities by standard cytogenetic measures. We show that the two lines possess some features of neoplastic progression, including a high proliferative capacity, growth-factor independence, a 9- to 20-fold increase in frequency of tumor-initiating cells, niche independence and aberrant lineage specification, although they are not malignant. Array comparative genomic hybridization reveals an amplification at 20q11.1-11.2 in v-hESC-1 and a deletion at 5q34a-5q34b;5q3 and a mosaic gain of chromosome 12 in v-hESC-2. These results emphasize the need for functional characterization to distinguish partially transformed and normal hES cells.
1 Stem Cell and Cancer Research Institute, Michael G. DeGroote School of Medicine, MDCL 5029, McMaster University, 1200 Main Street West, Hamilton, Ontario L8N 3Z5, Canada.
2 Department of Pathology and Molecular Medicine, Centre for Gene Therapeutics, McMaster University, Hamilton, Ontario L8N 3Z5, Canada.
3 Department of Medical Physics and Applied Radiation Sciences, McMaster University, Hamilton, Ontario L8S 4M1, Canada.
4 PerkinElmer Life and Analytical Sciences, 940 Winter Street, Waltham, Masschusetts 02451, USA.
5 Department of Pathology and Molecular Medicine, Credit Valley Hospital, 2200 Eglinton Avenue West, Mississauga, Ontario L5M 2N1, Canada.
