英國(guó)研究人員日前報(bào)告說(shuō),，他們發(fā)現(xiàn)一種藥物可消除約半數(shù)患小細(xì)胞肺癌的實(shí)驗(yàn)鼠體內(nèi)的腫瘤,。研究人員希望用這種藥物有效治療小細(xì)胞肺癌這一致死率極高的惡性癌癥。
英國(guó)帝國(guó)理工學(xué)院等機(jī)構(gòu)的研究人員在美國(guó)新一期《癌癥研究》雜志上報(bào)告說(shuō),，小細(xì)胞肺癌患者體內(nèi)癌細(xì)胞擴(kuò)散速度很快,，難以用手術(shù)治療。研究人員發(fā)現(xiàn),，一種名為成纖維細(xì)胞生長(zhǎng)因子2的生長(zhǎng)激素在這種癌細(xì)胞快速擴(kuò)散過(guò)程中起主要作用,，而藥物PD173074可阻斷這種激素的作用。動(dòng)物實(shí)驗(yàn)表明,，這種藥物能消除約50％患有小細(xì)胞肺癌的實(shí)驗(yàn)鼠體內(nèi)的腫瘤,。
研究顯示，這種藥物還可增強(qiáng)化療效果,。目前化療是治療小細(xì)胞肺癌的主要手段,，但其通常只在最初治療時(shí)有效，腫瘤細(xì)胞很快就能適應(yīng)并重新擴(kuò)散,。動(dòng)物實(shí)驗(yàn)顯示,，在化療的同時(shí)使用PD173074，可更高效地抑制腫瘤細(xì)胞的生長(zhǎng)和擴(kuò)散,。
研究人員表示,，明年將開(kāi)展臨床試驗(yàn),，希望能在此基礎(chǔ)上找到有效治療小細(xì)胞肺癌的方法。
肺癌分為小細(xì)胞肺癌和非小細(xì)胞肺癌,，小細(xì)胞肺癌在肺癌中所占比例約為五分之一,。（生物谷Bioon.com）
生物谷推薦原始出處：
Cancer Research 69, 8645, November 15, 2009.doi: 10.1158/0008-5472.CAN-09-1576
The Fibroblast Growth Factor Receptor Inhibitor PD173074 Blocks Small Cell Lung Cancer Growth In vitro and In vivo
Olivier E. Pardo1, John Latigo2, Rosemary E. Jeffery3, Emma Nye4, Richard Poulsom3, Bradley Spencer-Dene4, Nick R. Lemoine5, Gordon W. Stamp4, Eric O. Aboagye2 and Michael J. Seckl1
1 Lung Cancer Biology Group, Cancer Research UK Laboratories and 2 Molecular Therapy Group, Clinical Sciences Centre, Hammersmith Hospital Campus of Imperial College London; 3 In Situ Hybridisation and 4 Experimental Pathology Laboratories, Cancer Research UK London Research Institute; and 5 Institute of Cancer, Barts and The London, School of Medicine and Dentistry, London, United Kingdom
Lung cancer is the commonest cancer killer. Small cell lung cancer (SCLC) is initially chemosensitive, but rapidly relapses in a chemoresistant form with an overall survival of <5%. Consequently, novel therapies are urgently required and will likely arise from an improved understanding of the disease biology. Our previous work showed that fibroblast growth factor-2 induces proliferation and chemoresistance in SCLC cells. Here, we show that the selective fibroblast growth factor receptor (FGFR) inhibitor PD173074 blocks H-510 and H-69 SCLC proliferation and clonogenic growth in a dose-dependent fashion and prevents FGF-2–induced chemoresistance. These effects correlate with the inhibition of both FGFR1 and FGFR2 transphosphorylation. We then determined the efficacy of daily oral administration of PD173074 for 28 days in two human SCLC models. In the H-510 xenograft, tumor growth was impaired similar to that seen with single-agent cisplatin administration, increasing median survival compared with control sham–treated animals. Crucially, the effect of cisplatin was significantly potentiated by coadministration of PD173074. More dramatically, in H-69 xenografts, PD173074 induced complete responses lasting >6 months in 50% of mice. These effects were not a consequence of disrupted tumor vasculature but instead correlated with increased apoptosis (caspase 3 and cytokeratin 18 cleavage) in excised tumors. Moreover, in vivo imaging with 3'-deoxy-3'-[18F]fluorothymidine–positron emission tomography ([18F]FLT-PET) showed decreased intratumoral proliferation in live animals treated with the compound at 7 to 14 days. Our results suggest that clinical trials of FGFR inhibitors should be undertaken in patients with SCLC and that [18F]FLT-PET imaging could provide early in vivo evidence of response.
