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cainiaodui新蟲 (小有名氣)
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| Existing data support the endothelial cell-autonomous role for DLL4/NOTCH1 signaling in restricting the angiogenic response. The NOTCH pathway has been implicated in a variety of human cancers in connection with the genetic alterations and epigenetic events that lead to either constitutive NOTCH activation or sensitized response to ligand-induced activation. Interestingly, a recent study has suggested that DLL4 blockade may reduce tumor-initiating cell frequency in certain xenograft models .At present, however, the mechanism underlying DLL4-mediatedtumor initiation and/or progression remains unclear. |
版主 (文壇精英)
| 現(xiàn)有數(shù)據(jù)支持DLL4/NOTCH1信號(hào)血管內(nèi)皮細(xì)胞自主性可限制血管生成反應(yīng)。 Notch通路與遺傳修飾和表觀遺傳修飾有關(guān),這些修飾導(dǎo)致組成性NOTCH活化或配體誘導(dǎo)激活的敏感性增高,這一機(jī)制與多種人類癌癥有關(guān)。有趣的是,最近研究表明,DLL4阻斷在某些異種移植模型中可以減少腫瘤細(xì)胞發(fā)生的頻率。然而,目前對DLL4介導(dǎo)的腫瘤發(fā)生和/或發(fā)展的機(jī)制仍不清楚。 |

鐵桿木蟲 (正式寫手)
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現(xiàn)有的證據(jù)證明了內(nèi)皮細(xì)胞中 DLL/NOTCH1信號(hào)通路具有阻止血管生成的自發(fā)性功能。 NOTCH的激活(NOTCH activation)和對配體誘導(dǎo)反應(yīng)的過度敏感(sensitized response to ligand-induced activation)導(dǎo)致的基因改變和表觀遺傳學(xué)變化 都表明了NOTCH通路與許多種人類癌癥存在關(guān)聯(lián)。 有趣的是 最近的一項(xiàng)研究發(fā)現(xiàn) 對DLL4通路的阻遏可能會(huì)降低一些特定的異種移植模型中 發(fā)現(xiàn)腫瘤起始細(xì)胞(tumor-initiating cell)的概率。 但就目前為止 DLL4介導(dǎo)腫瘤發(fā)生和/或腫瘤發(fā)展的具體機(jī)制尚不明確。 |
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