Somatic mutations affect key pathways in lung adenocarcinoma
| العنوان: | Somatic mutations affect key pathways in lung adenocarcinoma |
|---|---|
| المؤلفون: | Aldi T. Kraja, Brian H. Dunford-Shore, Tittu Mathew, Otis Hall, Barbara A. Weir, Timothy Fennell, William Pao, Jack A. Roth, Alicia Hawes, Heidi Greulich, Steven E. Scherer, Xiaoqi Shi, Giovanni Tonon, Manuel L. Gonzalez-Garay, Yuzhu Tang, Mark B. Orringer, Qunyuan Zhang, Bruce E. Johnson, Li Ding, David G. Beer, Amit Dutt, Margaret R. Spitz, Carrie A. Haipek, Michael A. Province, Yiming Zhu, Liuda Ziaugra, Lucian R. Chirieac, Ken Chen, Rachel Abbott, William D. Travis, George M. Weinstock, Harold E. Varmus, Lucinda Fulton, Daniel C. Koboldt, Kristian Cibulskis, Carrie Sougnez, Christopher S. Sawyer, Richard A. Gibbs, Bradley A. Ozenberger, Thomas J. Giordano, Heather Schmidt, Ling Lin, Jennifer Baldwin, Elaine R. Mardis, Rick Meyer, Tracie L. Miner, David E. Larson, Ignacio I. Wistuba, Jiqiang Yao, Margaret Morgan, Andrew C. Chang, Akihiko Yoshizawa, Shalini N. Jhangiani, Xiaojun Zhao, David A. Wheeler, Stephen R. Broderick, Jody S. Robinson, Kerstin Clerc, Eric S. Lander, Richard K. Wilson, Ginger A. Fewell, Hua Shen, David J. Dooling, Robert S. Fulton, Aleksandar Milosavljevic, John R. Osborne, Gad Getz, Donna M. Muzny, Yanru Ren, Wendy Winckler, Roman K. Thomas, Mark A. Watson, Peter J. Good, Sacha N. Sander, Megan Hanna, Michael D. McLellan, Ginger A. Metcalf, Brian Ng, Michael C. Wendl, Lora Lewis, Seth D. Crosby, Michael C. Zody, Matthew Meyerson, Robert C. Onofrio, Michael S. Lawrence, Marc Ladanyi, Aniko Sabo, Craig Pohl, Stacey Gabriel, Tammi L. Vickery |
| المساهمون: | Ding, L, Getz, G, Wheeler, Da, Mardis, Ea, Mclellan, Md, Cibulskis, K, Sougnez, C, Greulich, H, Muzny, Dm, Morgan, Mb, Fulton, L, Fulton, R, Zhang, Q, Wendl, Mc, Lawrence, M, Larson, De, Chen, K, Dooling, Dj, Sabo, A, Hawes, Ac, Shen, H, Jhangiani, Sh, Lewis, Lr, Hall, O, Zhu, Y, Mathew, T, Ren, Y, Yao, J, Scherer, Se, Clerc, K, Metcalf, Ga, Ng, B, Milosavljevic, A, Gonzalez-Garay, Ml, Osborne, Jr, Meyer, R, Shi, X, Tang, Y, Koboldt, Dc, Lin, L, Abbott, R, Miner, Tl, Pohl, C, Fewell, G, Haipek, C, Schmidt, H, Dunford-Shore, Bh, Kraja, A, Crosby, Sd, Sawyer, C, Vickery, T, Sander, S, Robinson, J, Winckler, W, Baldwin, J, Chirieac, Lr, Dutt, A, Fennell, T, Hanna, M, Johnson, Be, Onofrio, Rc, Thomas, Rk, Tonon, G, Weir, Ba, Zhao, X, Ziaugra, L, Zody, Mc, Giordano, T, Orringer, Mb, Roth, Ja, Spitz, Mr, Wistuba, Ii, Ozenberger, B, Good, Pj, Chang, Ac, Beer, Dg, Watson, Ma, Ladanyi, M, Broderick, S, Yoshizawa, A, Travis, Wd, Pao, W, Province, Ma, Weinstock, Gm, Varmus, He, Gabriel, Sb, Lander, E, Gibbs, Ra, Meyerson, M, Wilson, Rk. |
| سنة النشر: | 2008 |
| مصطلحات موضوعية: | Male, Genetics, Mutation, Lung Neoplasms, Multidisciplinary, Tumor suppressor gene, DNA repair, Gene Dosage, Adenocarcinoma, Bronchiolo-Alveolar, Biology, medicine.disease, medicine.disease_cause, Article, Gene Expression Regulation, Neoplastic, Germline mutation, Proto-Oncogenes, medicine, Humans, Adenocarcinoma, Female, Genes, Tumor Suppressor, Carcinogenesis, Lung cancer, Gene |
| الوصف: | Determining the genetic basis of cancer requires comprehensive analyses of large collections of histopathologically well-classified primary tumours. Here we report the results of a collaborative study to discover somatic mutations in 188 human lung adenocarcinomas. DNA sequencing of 623 genes with known or potential relationships to cancer revealed more than 1,000 somatic mutations across the samples. Our analysis identified 26 genes that are mutated at significantly high frequencies and thus are probably involved in carcinogenesis. The frequently mutated genes include tyrosine kinases, among them the EGFR homologue ERBB4; multiple ephrin receptor genes, notably EPHA3; vascular endothelial growth factor receptor KDR; and NTRK genes. These data provide evidence of somatic mutations in primary lung adenocarcinoma for several tumour suppressor genes involved in other cancers--including NF1, APC, RB1 and ATM--and for sequence changes in PTPRD as well as the frequently deleted gene LRP1B. The observed mutational profiles correlate with clinical features, smoking status and DNA repair defects. These results are reinforced by data integration including single nucleotide polymorphism array and gene expression array. Our findings shed further light on several important signalling pathways involved in lung adenocarcinoma, and suggest new molecular targets for treatment. |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::3809a79f015121d8b06c7fe2ff78f40fTest |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....3809a79f015121d8b06c7fe2ff78f40f |
| قاعدة البيانات: | OpenAIRE |
| الوصف غير متاح. |