新加坡與德國的科研人員經(jīng)過三年努力之后,，設(shè)立資料庫，記錄400個癌癥細(xì)胞系的基因突變,，為全球癌癥研究員提供寶貴的資料,。
新加坡科技研究局（新*科研）屬下的生物醫(yī)藥研究院、生物細(xì)胞研究院和生物資訊研究院,，以及德國馬克斯·普朗克生物化學(xué)研究所(Max Planck Institute of Biochemistry)完成了一項(xiàng)重大的癌癥細(xì)胞基因分析,，并且將400個癌癥細(xì)胞系出現(xiàn)的蛋白質(zhì)酪氨酸激酶（protein tyrosine kinase）突變的數(shù)據(jù)，收錄在名為“TYKIVA”的網(wǎng)上資料庫,。
由癌癥研究專家爾里希教授（Axel Ullrich）率領(lǐng)的研究小組,，在最新一期的《癌癥研究》期刊，公布了資料庫的細(xì)節(jié),。
蛋白質(zhì)酪氨酸激酶是細(xì)胞內(nèi)的蛋白質(zhì),，在細(xì)胞生成和活動扮演重要的角色。研究發(fā)現(xiàn)蛋白質(zhì)酪氨酸激酶的缺陷,，與癌細(xì)胞病變息息相關(guān)。自1990年代,，科研人員研究應(yīng)付蛋白質(zhì)酪氨酸激酶病變的藥物,，研制出副作用較少、比較有針對性的癌癥藥物,。
新*科研發(fā)表文告宣布這項(xiàng)消息時說,，TYKIVA網(wǎng)上資料庫的設(shè)立，將能協(xié)助科研人員更好地了解癌細(xì)胞的分子基因和細(xì)胞結(jié)構(gòu),，研制治療癌癥的藥物,。（聯(lián)合早報(bào)）
原始出處:
Cancer Research 67, 11368-11376, December 1, 2007. doi: 10.1158/0008-5472.CAN-07-2703
Experimental Therapeutics, Molecular Targets, and Chemical Biology
Genetic Alterations in the Tyrosine Kinase Transcriptome of Human Cancer Cell Lines
Jens E. Ruhe1, Sylvia Streit1, Stefan Hart1, Chee-Hong Wong2, Katja Specht4, Pjotr Knyazev5, Tatjana Knyazeva5, Liang Seah Tay1, Hooi Linn Loo1, Priscilla Foo1, Winnie Wong1, Sharon Pok1, Shu Jing Lim1, Huimin Ong1, Ming Luo3, Han Kiat Ho1, Kaitian Peng1, Tze Chuen Lee2, Martin Bezler5, Christian Mann5, Silvia Gaertner5, Heinz Hoefler4, Stefano Iacobelli6, Stephan Peter7, Alice Tay3, Sydney Brenner1,3, Byrappa Venkatesh3 and Axel Ullrich1,5
1 Institute of Medical Biology, 2 Bioinformatics Institute, and 3 Institute of Molecular and Cell Biology, Singapore, Singapore; 4 Department of Pathology, Technical University of Munich, Munich, Germany; 5 Max-Planck-Institute for Biochemistry, Martinsried, Germany; 6 Department of Oncology, University of Chieti Medical School, Chieti, Italy; and 7 Department of Urology, Klinikum Darmstadt, Darmstadt, Germany
Requests for reprints: Jens E. Ruhe, U3 Pharma AG, Bunsenstrasse 1, 82152 Martinsried, Germany. E-mail: [email protected] .
Protein tyrosine kinases (PTKs) play a critical role in the manifestation of cancer cell properties, and respective signaling mechanisms have been studied extensively on immortalized tumor cells. To characterize and analyze commonly used cancer cell lines with regard to variations in the primary structure of all expressed PTKs, we conducted a cDNA-based sequence analysis of the entire tyrosine kinase transcriptome of 254 established tumor cell lines. The profiles of cell line intrinsic PTK transcript alterations and the evaluation of 155 identified polymorphisms and 234 somatic mutations are made available in a database designated "Tykiva" (tyrosine kinome variant). Tissue distribution analysis and/or the localization within defined protein domains indicate functional relevance of several genetic alterations. The cysteine replacement of the highly conserved Y367 residue in fibroblast growth factor receptor 4 or the Q26X nonsense mutation in the tumor-suppressor kinase CSK are examples, and may contribute to cell line–specific signaling characteristics and tumor progression. Moreover, known variants, such as epidermal growth factor receptor G719S, that were shown to mediate anticancer drug sensitivity could be detected in other than the previously reported tumor types. Our data therefore provide extensive system information for the design and interpretation of cell line–based cancer research, and may stimulate further investigations into broader clinical applications of current cancer therapeutics. [Cancer Res 2007;67(23):11368–76]
