最新Nature一篇文章報(bào)道唐氏綜合癥患者體內(nèi)有一個(gè)基因會(huì)減緩腫瘤的生長速度，抑制癌細(xì)胞蔓延,。
也許就像人們常說的,，上帝是公平的，他為你關(guān)閉了一扇門時(shí),，會(huì)為你打開一扇窗,。癌癥也是講道義的，命運(yùn)的厄運(yùn)不會(huì)一再的降臨到苦難人的身上,。
唐氏綜合癥（21-三體綜合癥）又名“先天愚型”,，包含一系列的遺傳病，其中最具代表性的第21對染色體的三體現(xiàn)象,，會(huì)導(dǎo)致包括學(xué)習(xí)障礙,、智能障礙和殘疾等高度畸形。
據(jù)報(bào)道,，唐氏綜合癥患者患各種癌癥的幾率比常人低,，人們猜測這可能與其21號染色體上多出的一條染色體上的某些基因表達(dá)的有關(guān)。據(jù)介紹,，1區(qū)的DSCR1（也稱RCAN1）基因被認(rèn)為是降低癌癥發(fā)生率的可能基因,，它編碼的蛋白能抑制血管內(nèi)皮生長因子（VEGF）介導(dǎo)的血管發(fā)生信號傳導(dǎo)。
在本研究中,，Zygmunt Galdzicki和Sandra Ryeom等人發(fā)現(xiàn),，唐氏綜合癥患者和唐氏綜合癥小鼠模型體內(nèi)的組織中DSCR1的表達(dá)量比正常的高。研究人員嘗試在提高DSCR1在癌癥模型小鼠體內(nèi)的表達(dá)量,，結(jié)果發(fā)現(xiàn)能有效的抑制腫瘤血管生長,，進(jìn)而抑制腫瘤發(fā)生。
這些研究結(jié)果證實(shí),，唐氏綜合癥患者引起特殊的染色體而降低了癌癥的發(fā)生率,。并且，表明DSCR1是通過神經(jīng)鈣蛋白信號調(diào)節(jié)腫瘤血管生長的基因,。DSCR1可能成為癌癥治療的新靶位,。(生物谷Bioon.com)
生物谷推薦原始出處：
Nature advance online publication 20 May 2009 | doi:10.1038/nature08062
Down's syndrome suppression of tumour growth and the role of the calcineurin inhibitor DSCR1
Kwan-Hyuck Baek1,8, Alexander Zaslavsky1,8, Ryan C. Lynch1,8, Carmella Britt1, Yoshiaki Okada2, Richard J. Siarey3, M. William Lensch4, In-Hyun Park4, Sam S. Yoon5, Takashi Minami6, Julie R. Korenberg7, Judah Folkman1, George Q. Daley4, William C. Aird2, Zygmunt Galdzicki3 & Sandra Ryeom1
1 Vascular Biology Program, Department of Surgery, Children's Hospital Boston, Massachusetts 02115, USA
2 Center for Vascular Biology Research, Division of Molecular and Vascular Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts 02115, USA
3 Department of Anatomy, Physiology and Genetic, Neuroscience, Molecular and Cellular Biology Program, School of Medicine, Uniformed Services University of the Health Services, Bethesda, Maryland 20814, USA
4 Department of Medicine, Division of Pediatric Hematology Oncology, Children's Hospital Boston, and Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA
5 Division of Surgical Oncology, Department of Surgery, Massachusetts General Hospital, Boston, Maryland 02114, USA
6 Research Center for Advanced Science and Technology, University of Tokyo, Tokyo, 153-8904, Japan
7 Department of Pediatrics and The Brain Institute, The University of Utah, Salt Lake City, Utah 84108, USA
8 These authors contributed equally to this work.
The incidence of many cancer types is significantly reduced in individuals with Down's syndrome1, 2, 3, 4, and it is thought that this broad cancer protection is conferred by the increased expression of one or more of the 231 supernumerary genes on the extra copy of chromosome 21. One such gene is Down's syndrome candidate region-1 (DSCR1, also known as RCAN1), which encodes a protein that suppresses vascular endothelial growth factor (VEGF)-mediated angiogenic signalling by the calcineurin pathway5, 6, 7, 8, 9, 10. Here we show that DSCR1 is increased in Down's syndrome tissues and in a mouse model of Down's syndrome. Furthermore, we show that the modest increase in expression afforded by a single extra transgenic copy of Dscr1 is sufficient to confer significant suppression of tumour growth in mice, and that such resistance is a consequence of a deficit in tumour angiogenesis arising from suppression of the calcineurin pathway. We also provide evidence that attenuation of calcineurin activity by DSCR1, together with another chromosome 21 gene Dyrk1a, may be sufficient to markedly diminish angiogenesis. These data provide a mechanism for the reduced cancer incidence in Down's syndrome and identify the calcineurin signalling pathway, and its regulators DSCR1 and DYRK1A, as potential therapeutic targets in cancers arising in all individuals.
