英國科學(xué)家在最新一期英國《自然—遺傳學(xué)》（Nature Genetics）雜志上發(fā)表論文說,，他們發(fā)現(xiàn)了一種名為UTX的基因，其變異后能夠引發(fā)多種癌癥,。
英國韋爾科姆基金會桑格研究所科學(xué)家說,，位于X染色體上的UTX基因與控制其他基因的開啟與關(guān)閉有關(guān)。在對患有某種腎癌的患者組織樣本進(jìn)行了大規(guī)?；蚝Y查后,，科學(xué)家發(fā)現(xiàn)，變異的UTX基因可導(dǎo)致癌癥,。當(dāng)研究范圍擴(kuò)大到其他類型的癌癥后,，科學(xué)家又發(fā)現(xiàn)，這種變異的UTX基因?qū)Χ喟l(fā)性骨髓瘤和食道癌都起作用,。
該項(xiàng)目的負(fù)責(zé)人之一安迪·富特雷爾說：“與很多癌癥基因不同的是,，變異的UTX基因似乎并不直接參與細(xì)胞分裂或細(xì)胞死亡，而是影響細(xì)胞的基本調(diào)節(jié),，從而引發(fā)癌癥,。”
富特雷爾表示，除了特定的一種腎癌外，10%的多發(fā)性骨髓瘤病例和約８％的食道癌病例與變異的UTX基因有關(guān),。（生物谷Bioon.com）
生物谷推薦原始出處：
Nature Genetics 29 March 2009 | doi:10.1038/ng.349
Somatic mutations of the histone H3K27 demethylase gene UTX in human cancer
Gijs van Haaften1,10,11, Gillian L Dalgliesh1,11, Helen Davies1,11, Lina Chen1, Graham Bignell1, Chris Greenman1, Sarah Edkins1, Claire Hardy1, Sarah O'Meara1, Jon Teague1, Adam Butler1, Jonathan Hinton1, Calli Latimer1, Jenny Andrews1, Syd Barthorpe1, Dave Beare1, Gemma Buck1, Peter J Campbell1, Jennifer Cole1, Simon Forbes1, Mingming Jia1, David Jones1, Chai Yin Kok1, Catherine Leroy1, Meng-Lay Lin1, David J McBride1, Mark Maddison1, Simon Maquire1, Kirsten McLay1, Andrew Menzies1, Tatiana Mironenko1, Lee Mulderrig1, Laura Mudie1, Erin Pleasance1, Rebecca Shepherd1, Raffaella Smith1, Lucy Stebbings1, Philip Stephens1, Gurpreet Tang1, Patrick S Tarpey1, Rachel Turner1, Kelly Turrell1, Jennifer Varian1, Sofie West1, Sara Widaa1, Paul Wray1, V Peter Collins2, Koichi Ichimura2, Simon Law3, John Wong3, Siu Tsan Yuen4, Suet Yi Leung4, Giovanni Tonon5,10, Ronald A DePinho5, Yu-Tzu Tai6, Kenneth C Anderson6, Richard J Kahnoski7, Aaron Massie7, Sok Kean Khoo8, Bin Tean Teh8, Michael R Stratton1,9 & P Andrew Futreal1
Somatically acquired epigenetic changes are present in many cancers. Epigenetic regulation is maintained via post-translational modifications of core histones. Here, we describe inactivating somatic mutations in the histone lysine demethylase gene UTX, pointing to histone H3 lysine methylation deregulation in multiple tumor types. UTX reintroduction into cancer cells with inactivating UTX mutations resulted in slowing of proliferation and marked transcriptional changes. These data identify UTX as a new human cancer gene.
1 Cancer Genome Project, Wellcome Trust Sanger Institute, Hinxton, UK.
2 Department of Pathology, University of Cambridge, Cambridge, UK.
3 Department of Surgery, The University of Hong Kong, Queen Mary Hospital, Hong Kong
4 Department of Pathology, The University of Hong Kong, Queen Mary Hospital, Hong Kong.
5 Center for Applied Cancer Science of the Belfer Institute for Innovative Cancer Science, Departments of Medical Oncology and Medicine and Genetics, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts, USA.
6 Lebow Insitute for Myeloma Therapeutics and Lipper Myeloma Center, Dana-Farber Cancer Institute, Boston, Massachusetts, USA.
7 Department of Urology, Spectrum Health Hospital, Grand Rapids, Michigan, USA.
8 Laboratory of Cancer Genetics, Van Andel Institute, Grand Rapids, Michigan, USA.
9 Institute of Cancer Research, Sutton, Surrey, UK.
10 Present addresses: The Netherlands Cancer Institute, Amsterdam, The Netherlands (G.v.H.) and Multiple Myeloma Unit, Division of Molecular Oncology, San Raffaele del Monte Tabor Scientific Foundation, Milan, Italy (G.Tonon).
11 These authors contributed equally to this work.
