美國(guó)一份最近的研究報(bào)告顯示，在細(xì)胞水平擊潰復(fù)雜癌癥的研究取得突破,，研究人員找到了能夠揭示癌細(xì)胞形成和生長(zhǎng)的關(guān)鍵信號(hào),，這將為癌癥的診斷和治療提供幫助。
研究人員以研究單核粒細(xì)胞白血?。╦uvenile myelomonocytic leukemia ,，JMML）為例，稱他們現(xiàn)在能夠利用世界最先進(jìn)的流式細(xì)胞儀技術(shù)對(duì)單個(gè)細(xì)胞進(jìn)行詳細(xì)檢測(cè),，能夠觀察到細(xì)胞類型和細(xì)胞信號(hào)的傳導(dǎo)通路,。這項(xiàng)研究成果發(fā)布在10月號(hào)《癌細(xì)胞》（Cancer Cell）雜志上。
流式細(xì)胞儀幫助研究人員檢測(cè)到單核粒細(xì)胞白血病患兒體內(nèi)細(xì)胞產(chǎn)生的信號(hào),。這種疾病是一種兒童骨髓增生性惡性疾病,，難以診斷。在發(fā)病時(shí),，患者體內(nèi)會(huì)有多種細(xì)胞信號(hào)發(fā)生復(fù)雜的變化,。研究人員發(fā)現(xiàn)了大多數(shù)患者身上都出現(xiàn)STAT5信號(hào)，這說(shuō)明JAK-STAT信號(hào)在癌癥發(fā)生的生物學(xué)機(jī)制中起到了關(guān)鍵作用,。這一成果為將來(lái)的治療提出了重要參考,。
美國(guó)加州大學(xué)兒童醫(yī)院和海倫迪勒家庭綜合癌癥中心的Mignon L. Loh是這次研究的負(fù)責(zé)人之一，他在《癌細(xì)胞》雜志舉辦的新聞發(fā)布會(huì)上說(shuō),，這項(xiàng)工作成功地利用了單核粒細(xì)胞白血病患者體內(nèi)的單細(xì)胞信號(hào),。隨著時(shí)間的推移，研究人員看到了在這種疾病診斷,、緩解,、復(fù)發(fā)和轉(zhuǎn)變的整個(gè)過(guò)程中細(xì)胞信號(hào)的變化,。這是一個(gè)子細(xì)胞異常信號(hào)發(fā)展的完整過(guò)程。
這項(xiàng)研究的另一位參與者,、斯坦福大學(xué)醫(yī)學(xué)院的Garry P. Nolan說(shuō),，通過(guò)測(cè)量信號(hào)蛋白如何對(duì)特定的刺激診斷做出反應(yīng)和發(fā)現(xiàn)哪些信號(hào)是受到癌細(xì)胞的影響，我們基本上能夠確定癌細(xì)胞自身增長(zhǎng)的途徑,。在單細(xì)胞水平為癌癥病人進(jìn)行診斷的這種方法使醫(yī)生能夠盡早發(fā)現(xiàn)癌癥,，并可以深入了解癌細(xì)胞對(duì)特定的治療手段如何反應(yīng)或適應(yīng)。單細(xì)胞診斷技術(shù)的另一個(gè)意義就是,，將來(lái)研究人員最終能預(yù)測(cè)癌細(xì)胞可能會(huì)使用哪些途徑規(guī)避目前的療法,，從而及時(shí)采取對(duì)患者最有效的治療措施。（生物谷Bioon.com）
生物谷推薦原始出處：
Cancer Cell,，Vol 14, 335-343,，Garry P. Nolan，Mignon L. Loh
Single-Cell Profiling Identifies Aberrant STAT5 Activation in Myeloid Malignancies with Specific Clinical and Biologic Correlates
Nikesh Kotecha,1,2 Nikki J. Flores,5 Jonathan M. Irish,1,3 Erin F. Simonds,1 Debbie S. Sakai,5 Sophie Archambeault,5 Ernesto Diaz-Flores,5 Marc Coram,4 Kevin M. Shannon,5,6 Garry P. Nolan,1,7, and Mignon L. Loh5,6,7,
1 Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA
2 Biomedical Informatics Program, Stanford University School of Medicine, Stanford, CA 94305, USA
3 Department of Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA
4 Division of Biostatistics, Stanford University School of Medicine, Stanford, CA 94305, USA
5 Department of Pediatrics, University of California, San Francisco, San Francisco, CA 94143, USA
6 UCSF Comprehensive Cancer Center, University of California, San Francisco, San Francisco, CA 94143, USA
Summary
Progress in understanding the molecular pathogenesis of human myeloproliferative disorders (MPDs) has led to guidelines incorporating genetic assays with histopathology during diagnosis. Advances in flow cytometry have made it possible to simultaneously measure cell type and signaling abnormalities arising as a consequence of genetic pathologies. Using flow cytometry, we observed a specific evoked STAT5 signaling signature in a subset of samples from patients suspected of having juvenile myelomonocytic leukemia (JMML), an aggressive MPD with a challenging clinical presentation during active disease. This signature was a specific feature involving JAK-STAT signaling, suggesting a critical role of this pathway in the biological mechanism of this disorder and indicating potential targets for future therapies.
