英国科学家在最新一期英国《自然—遗传学》（Nature Genetics）杂志上发表论文说，他们发现了一种名为UTX的基因，其变异后能够引发多种癌症。
英国韦尔科姆基金会桑格研究所科学家说，位于X染色体上的UTX基因与控制其他基因的开启与关闭有关。在对患有某种肾癌的患者组织样本进行了大规模基因筛查后，科学家发现，变异的UTX基因可导致癌症。当研究范围扩大到其他类型的癌症后，科学家又发现，这种变异的UTX基因对多发性骨髓瘤和食道癌都起作用。
该项目的负责人之一安迪·富特雷尔说：“与很多癌症基因不同的是，变异的UTX基因似乎并不直接参与细胞分裂或细胞死亡，而是影响细胞的基本调节，从而引发癌症。”
富特雷尔表示，除了特定的一种肾癌外，10%的多发性骨髓瘤病例和约８％的食道癌病例与变异的UTX基因有关。（生物谷Bioon.com）
生物谷推荐原始出处：
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.
