4月14日，臺(tái)灣《聯(lián)合晚報(bào)》報(bào)道說，臺(tái)灣“中央研究院”院士洪明奇領(lǐng)導(dǎo)的研究團(tuán)隊(duì)從正常細(xì)胞中找到一種癌癥凋亡細(xì)胞的突變種（BIK－DD）,，適度表現(xiàn)后,，可引起癌癥干細(xì)胞的凋亡，卻不會(huì)誤殺正常細(xì)胞,，可望給幾無存活機(jī)會(huì)的胰臟癌患者帶來生機(jī),。
洪明奇14日出席相關(guān)研討會(huì)并發(fā)表特別演講，他的研究成果引起與會(huì)癌癥醫(yī)學(xué)專家熱烈討論,。相關(guān)研究成果刊登在了國際雜志Cancer Cell上,。
報(bào)道說，胰臟癌患者的5年存活率只有3％至4％,，幾乎是所有癌癥患者中最低的,，胰臟癌因此又有“癌癥中的癌癥”之稱。洪明奇完成的動(dòng)物實(shí)驗(yàn)發(fā)現(xiàn),，經(jīng)過癌癥凋亡細(xì)胞突變種治療后的胰臟癌老鼠,，腫瘤均明顯變小，而且六成以上可存活1年以上,；反觀未接受治療的對照組老鼠,，全部在三四十天后即死亡。
洪明奇說,，不少癌癥經(jīng)化學(xué)治療及放射線治療后,，仍會(huì)在一段時(shí)間后復(fù)發(fā)，主要是癌癥干細(xì)胞的分化能力太強(qiáng),，如果未能徹底殲滅,，即可能復(fù)發(fā)并蔓延，防不勝防,。他采取的基因治療模式,，就是想辦法讓癌癥干細(xì)胞自然凋亡，而達(dá)到徹底治療目的,。
洪明奇研究團(tuán)隊(duì)采用的癌癥凋亡細(xì)胞（BIK）一般人體內(nèi)就有,，即存在于正常細(xì)胞里，也存在于癌細(xì)胞中,；但這種凋亡細(xì)胞平常并不會(huì)特別表現(xiàn),，無法殺死癌癥干細(xì)胞。洪明奇找到癌癥凋亡細(xì)胞的突變種（BIK-DD）,，且可調(diào)控到讓它只在癌癥干細(xì)胞中大量表現(xiàn),，而不會(huì)表現(xiàn)于正常細(xì)胞中。（生物谷Bioon.com）
doi:10.1016/j.ccr.2011.12.006
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KrasG12D-Induced IKK2/β/NF-κB Activation by IL-1α and p62 Feedforward Loops Is Required for Development of Pancreatic Ductal Adenocarcinoma
Jianhua Ling1, Ya'an Kang2, Ruiying Zhao1, Qianghua Xia1, 4, Dung-Fang Lee5, Zhe Chang1, 4, Jin Li6, Bailu Peng7, Jason B. Fleming2, Huamin Wang3, 4, Jinsong Liu3, 4, Ihor R. Lemischka5, Mien-Chie Hung1, 4, 8, Paul J. Chiao1, 4, ,
Constitutive Kras and NF-κB activation is identified as signature alterations in pancreatic ductal adenocarcinoma (PDAC). However, how NF-κB is activated in PDAC is not yet understood. Here, we report that pancreas-targeted IKK2/β inactivation inhibited NF-κB activation and PDAC development in KrasG12D and KrasG12D;Ink4a/ArfF/F mice, demonstrating a mechanistic link between IKK2/β and KrasG12D in PDAC inception. Our findings reveal that KrasG12D-activated AP-1 induces IL-1α, which, in turn, activates NF-κB and its target genes IL-1α and p62, to initiate IL-1α/p62 feedforward loops for inducing and sustaining NF-κB activity. Furthermore, IL-1α overexpression correlates with Kras mutation, NF-κB activity, and poor survival in PDAC patients. Therefore, our findings demonstrate the mechanism by which IKK2/β/NF-κB is activated by KrasG12D through dual feedforward loops of IL-1α/p62.
