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1,041 results on '"Liu, Edison T."'

202. Tracking the evolution of the SARS coronavirus using high-throughput, high-density resequencing arrays

Author

Wong, Christopher W., Albert, Thomas J., Vega, Vinsensius B., Norton, Jason E., Liu, Edison T., Stanton, Lawrence W., Miller, Lance D., Richmond, Todd A, and Cutler, David J

Subjects
Hybridization -- Research, Nucleotide sequence -- Research, DNA microarrays -- Research, Genetic research, Health
Abstract

The development and validation of an oligonucleotide resequencing array is described for interrogating the entire 30kb SARS-Coronavirus (SARS-CoV) genome in a rapid, cost-effective fashion. Further, it is demonstrated that an array-based resequencing-by-hybridization is a fast, reliable, and economical alternative to capillary sequencing for obtaining SARS-CoV genomic sequence on a population scale.

Published
2004

204. A bioinformatics-based strategy identifies c-Myc and Cdc25A as candidates for the Apmt mammary tumor latency modifiers

Author

Cozma, Diana, Lukes, Luanne, Rouse, Jessica, Ting Hu Qiu, Liu, Edison T., and Hunter. Kent W.

Subjects
Quantitative trait loci -- Research, Breast tumors -- Research, Computational biology -- Research, Genetic research, Health
Abstract

A study was conducted to identify potential candidate genes loci, the epistatically interacting modifier, using a combination of bioinformatics and genomic strategies. This study suggested that c-Myc and Cdc25A are Apmt1, Apmt2 and bioinformatics can be used to bypass congenic construction and subsequent mapping in conventional QTL studies.

Published
2002

206. Stromal effects in breast cancer

Author

Liu, Edison T.

Subjects
Breast cancer -- Genetic aspects, Breast cancer -- Research, Fibroblasts -- Research
Abstract

A study to examine the stromal and epithelial compartments of primary breast cancers is conducted. Findings show that the stromal compartments harbor genetic changes that differ from the genetic changes in the epithelial compartment.

Published
2007

207. Development and characterization of patient-derived xenografts to guide precision medicine in bladder cancer.

Author

Pan, Chong-xian, primary, Zhang, Hongyong, additional, Lin, Tzu-yin, additional, Tepper, Clifford, additional, Keck, James, additional, Ghosh, Paramita, additional, Airhart, Susan D., additional, Carvajal-Carmona, Luis, additional, Bult, Carol J., additional, Gandara, David R., additional, Liu, Edison T., additional, and de Vere White, Ralph, additional

Published
2015
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210. Patient-derived xenograft platform to guide precision medicine in bladder cancer.

Author

Pan, Chong-Xian, primary, Zhang, Hongyong, additional, Lin, Tzu-yin, additional, Tepper, Clifford, additional, Keck, James, additional, Ghosh, Paramita, additional, Airhart, Susan D., additional, Bult, Carol J., additional, Gandara, David R., additional, Evans, Christopher P., additional, Liu, Edison T., additional, and deVere White, Ralph, additional

Published
2015
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211. Patient-specific driver gene prediction and risk assessment through integrated network analysis of cancer omics profiles

Author

Bertrand, Denis, primary, Chng, Kern Rei, additional, Sherbaf, Faranak Ghazi, additional, Kiesel, Anja, additional, Chia, Burton K. H., additional, Sia, Yee Yen, additional, Huang, Sharon K., additional, Hoon, Dave S.B., additional, Liu, Edison T., additional, Hillmer, Axel, additional, and Nagarajan, Niranjan, additional

Published
2015
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212. Systems consequences of amplicon formation in human breast cancer

Author

Massachusetts Institute of Technology. Department of Biological Engineering, Wagner, Joel Patrick, Inaki, Koichiro, Menghi, Francesca, Woo, Xing Yi, Jacques, Pierre-Étienne, Lee, Yi Fang, Shreckengast, Phung Trang, Soon, Wendy WeiJia, Malhotra, Ankit, Teo, Audrey S.M., Hillmer, Axel M., Khng, Alexis Jiaying, Ruan, Xiaoan, Ong, Swee Hoe, Bertrand, Denis, Nagarajan, Niranjan, Karuturi, R. Krishna Murthy, Miranda, Alfredo Hidalgo, Liu, Edison T., Massachusetts Institute of Technology. Department of Biological Engineering, Wagner, Joel Patrick, Inaki, Koichiro, Menghi, Francesca, Woo, Xing Yi, Jacques, Pierre-Étienne, Lee, Yi Fang, Shreckengast, Phung Trang, Soon, Wendy WeiJia, Malhotra, Ankit, Teo, Audrey S.M., Hillmer, Axel M., Khng, Alexis Jiaying, Ruan, Xiaoan, Ong, Swee Hoe, Bertrand, Denis, Nagarajan, Niranjan, Karuturi, R. Krishna Murthy, Miranda, Alfredo Hidalgo, and Liu, Edison T.

Abstract

Chromosomal structural variations play an important role in determining the transcriptional landscape of human breast cancers. To assess the nature of these structural variations, we analyzed eight breast tumor samples with a focus on regions of gene amplification using mate-pair sequencing of long-insert genomic DNA with matched transcriptome profiling. We found that tandem duplications appear to be early events in tumor evolution, especially in the genesis of amplicons. In a detailed reconstruction of events on chromosome 17, we found large unpaired inversions and deletions connect a tandemly duplicated ERBB2 with neighboring 17q21.3 amplicons while simultaneously deleting the intervening BRCA1 tumor suppressor locus. This series of events appeared to be unusually common when examined in larger genomic data sets of breast cancers albeit using approaches with lesser resolution. Using siRNAs in breast cancer cell lines, we showed that the 17q21.3 amplicon harbored a significant number of weak oncogenes that appeared consistently coamplified in primary tumors. Down-regulation of BRCA1 expression augmented the cell proliferation in ERBB2-transfected human normal mammary epithelial cells. Coamplification of other functionally tested oncogenic elements in other breast tumors examined, such as RIPK2 and MYC on chromosome 8, also parallel these findings. Our analyses suggest that structural variations efficiently orchestrate the gain and loss of cancer gene cassettes that engage many oncogenic pathways simultaneously and that such oncogenic cassettes are favored during the evolution of a cancer., Singapore. Agency for Science, Technology and Research, National Science Foundation (U.S.) (East Asia and Pacific Summer Institutes (OISE-1108282))

Published
2014

213. Systems biology, integrative biology, predictive biology

Author

Liu, Edison T.

Subjects
Phenotype -- Research, Systems biology -- Research, Biological sciences
Abstract

Systems biology requires the ability to digitalize biological output so that it could be computed, the computational power to analyze comprehensive and massive datasets, and the capacity to integrate heterogeneous data into a usable knowledge format. A brief description on how it could be described as integrative biology and predictive biology is presented.

Published
2005

214. Oncogenes

Author

Burck, Kathy B., primary, Liu, Edison T., additional, and Larrick, James W., additional

Published
1988
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218. Systems consequences of amplicon formation in human breast cancer

Author

Inaki, Koichiro, primary, Menghi, Francesca, additional, Woo, Xing Yi, additional, Wagner, Joel P., additional, Jacques, Pierre-Étienne, additional, Lee, Yi Fang, additional, Shreckengast, Phung Trang, additional, Soon, Wendy WeiJia, additional, Malhotra, Ankit, additional, Teo, Audrey S.M., additional, Hillmer, Axel M., additional, Khng, Alexis Jiaying, additional, Ruan, Xiaoan, additional, Ong, Swee Hoe, additional, Bertrand, Denis, additional, Nagarajan, Niranjan, additional, Karuturi, R. Krishna Murthy, additional, Hidalgo Miranda, Alfredo, additional, and Liu, Edison T., additional

Published
2014
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219. Utilization of a 358-gene panel to molecularly profile solid tumors for association with target-based therapeutic agents.

Author

Rasmussen, Karen Elizabeth, primary, Nehring, Ramlah, additional, Ananda, Guru, additional, Stafford, Grace A., additional, Phillip, Vivek, additional, Mockus, Susan, additional, Srivastava, Anuj, additional, Simons, Allen, additional, Donnelly, Charles, additional, Karuturi, Krishna, additional, Hinerfeld, Douglas, additional, Spotlow, Vanessa, additional, Lundquist, Micaela, additional, Ruan, Xiaoan, additional, Bult, Carol J., additional, Scott, Sean, additional, Love, Tara, additional, Richards, Dan R., additional, and Liu, Edison T., additional

Published
2014
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221. The JAX patient-derived xenograft program: A unique resource to advance genome-guided cancer medicine and therapeutic agent testing.

Author

Bult, Carol J., primary, Airhart, Susan D., additional, Chuang, Jeffrey, additional, Gandour-Edwards, Regina, additional, George, Joshy, additional, Graber, Joel, additional, Karuturi, R. Krishna Murthy, additional, Keck, James, additional, Kim, Hyunsoo, additional, Lara, Primo, additional, Li, Tianhong, additional, Mack, Philip C., additional, Shultz, Lenny, additional, Tepper, Clifford, additional, Burich, Rebekah, additional, Woo, Xing Yi, additional, Yang, Yan, additional, de Vere White, Ralph, additional, Gandara, David R., additional, and Liu, Edison T., additional

Published
2014
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223. Detection of Chromosomal Breakpoints in Patients with Developmental Delay and Speech Disorders

Author

Utami, Kagistia H., primary, Hillmer, Axel M., additional, Aksoy, Irene, additional, Chew, Elaine G. Y., additional, Teo, Audrey S. M., additional, Zhang, Zhenshui, additional, Lee, Charlie W. H., additional, Chen, Pauline J., additional, Seng, Chan Chee, additional, Ariyaratne, Pramila N., additional, Rouam, Sigrid L., additional, Soo, Lim Seong, additional, Yousoof, Saira, additional, Prokudin, Ivan, additional, Peters, Gregory, additional, Collins, Felicity, additional, Wilson, Meredith, additional, Kakakios, Alyson, additional, Haddad, Georges, additional, Menuet, Arnaud, additional, Perche, Olivier, additional, Tay, Stacey Kiat Hong, additional, Sung, Ken W. K., additional, Ruan, Xiaoan, additional, Ruan, Yijun, additional, Liu, Edison T., additional, Briault, Sylvain, additional, Jamieson, Robyn V., additional, Davila, Sonia, additional, and Cacheux, Valere, additional

Published
2014
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230. GWAS of Follicular Lymphoma Reveals Allelic Heterogeneity at 6p21.32 and Suggests Shared Genetic Susceptibility with Diffuse Large B-cell Lymphoma

Author

Smedby, Karin E., Foo, Jia Nee, Skibola, Christine F., Darabi, Hatef, Conde, Lucia, Hjalgrim, Henrik, Kumar, Vikrant, Chang, Ellen T., Rothman, Nathaniel, Cerhan, James R., Brooks-Wilson, Angela R., Rehnberg, Emil, Irwan, Ishak D., Ryder, Lars P., Brown, Peter N., Bracci, Paige M., Agana, Luz, Riby, Jacques, Cozen, Wendy, Davis, Scott, Hartge, Patricia, Morton, Lindsay M., Severson, Richard K., Wang, Sophia S., Slager, Susan L., Fredericksen, Zachary S., Novak, Anne J., Kay, Neil E., Habermann, Thomas M., Armstrong, Bruce, Kricker, Anne, Milliken, Sam, Purdue, Mark P., Vajdic, Claire M., Boyle, Peter, Lan, Qing, Zahm, Shelia H., Zhang, Yawei, Zheng, Tongzhang, Leach, Stephen, Spinelli, John J., Smith, Martyn T., Chanock, Stephen J., Padyukov, Leonid, Alfredsson, Lars, Klareskog, Lars, Glimelius, Bengt, Melbye, Mads, Liu, Edison T., Adami, Hans-Olov, Humphreys, Keith, Liu, Jianjun, Smedby, Karin E., Foo, Jia Nee, Skibola, Christine F., Darabi, Hatef, Conde, Lucia, Hjalgrim, Henrik, Kumar, Vikrant, Chang, Ellen T., Rothman, Nathaniel, Cerhan, James R., Brooks-Wilson, Angela R., Rehnberg, Emil, Irwan, Ishak D., Ryder, Lars P., Brown, Peter N., Bracci, Paige M., Agana, Luz, Riby, Jacques, Cozen, Wendy, Davis, Scott, Hartge, Patricia, Morton, Lindsay M., Severson, Richard K., Wang, Sophia S., Slager, Susan L., Fredericksen, Zachary S., Novak, Anne J., Kay, Neil E., Habermann, Thomas M., Armstrong, Bruce, Kricker, Anne, Milliken, Sam, Purdue, Mark P., Vajdic, Claire M., Boyle, Peter, Lan, Qing, Zahm, Shelia H., Zhang, Yawei, Zheng, Tongzhang, Leach, Stephen, Spinelli, John J., Smith, Martyn T., Chanock, Stephen J., Padyukov, Leonid, Alfredsson, Lars, Klareskog, Lars, Glimelius, Bengt, Melbye, Mads, Liu, Edison T., Adami, Hans-Olov, Humphreys, Keith, and Liu, Jianjun

Abstract

Non-Hodgkin lymphoma (NHL) represents a diverse group of hematological malignancies, of which follicular lymphoma (FL) is a prevalent subtype. A previous genome-wide association study has established a marker, rs10484561 in the human leukocyte antigen (HLA) class II region on 6p21.32 associated with increased FL risk. Here, in a three-stage genome-wide association study, starting with a genome-wide scan of 379 FL cases and 791 controls followed by validation in 1,049 cases and 5,790 controls, we identified a second independent FL-associated locus on 6p21.32, rs2647012 (ORcombined = 0.64, P-combined= 2x10(-21)) located 962 bp away from rs10484561 (r(2)< 0.1 in controls). After mutual adjustment, the associations at the two SNPs remained genome-wide significant (rs2647012: ORadjusted = 0.70, P-adjusted= 4x10(-12); rs10484561: ORadjusted = 1.64, P-adjusted= 5x10(-15)). Haplotype and coalescence analyses indicated that rs2647012 arose on an evolutionarily distinct haplotype from that of rs10484561 and tags a novel allele with an opposite (protective) effect on FL risk. Moreover, in a follow-up analysis of the top 6 FL-associated SNPs in 4,449 cases of other NHL subtypes, rs10484561 was associated with risk of diffuse large B-cell lymphoma (ORcombined = 1.36, P-combined = 1.4x10(-7)). Our results reveal the presence of allelic heterogeneity within the HLA class II region influencing FL susceptibility and indicate a possible shared genetic etiology with diffuse large B-cell lymphoma. These findings suggest that the HLA class II region plays a complex yet important role in NHL.

Published
2011
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231. GWAS of follicular lymphoma reveals allelic heterogeneity at 6p21.32 and suggests shared genetic susceptibility with diffuse large B-cell lymphoma.

Author

Smedby, Karin E, Gibson, Greg1, Smedby, Karin E, Foo, Jia Nee, Skibola, Christine F, Darabi, Hatef, Conde, Lucia, Hjalgrim, Henrik, Kumar, Vikrant, Chang, Ellen T, Rothman, Nathaniel, Cerhan, James R, Brooks-Wilson, Angela R, Rehnberg, Emil, Irwan, Ishak D, Ryder, Lars P, Brown, Peter N, Bracci, Paige M, Agana, Luz, Riby, Jacques, Cozen, Wendy, Davis, Scott, Hartge, Patricia, Morton, Lindsay M, Severson, Richard K, Wang, Sophia S, Slager, Susan L, Fredericksen, Zachary S, Novak, Anne J, Kay, Neil E, Habermann, Thomas M, Armstrong, Bruce, Kricker, Anne, Milliken, Sam, Purdue, Mark P, Vajdic, Claire M, Boyle, Peter, Lan, Qing, Zahm, Shelia H, Zhang, Yawei, Zheng, Tongzhang, Leach, Stephen, Spinelli, John J, Smith, Martyn T, Chanock, Stephen J, Padyukov, Leonid, Alfredsson, Lars, Klareskog, Lars, Glimelius, Bengt, Melbye, Mads, Liu, Edison T, Adami, Hans-Olov, Humphreys, Keith, Liu, Jianjun, Smedby, Karin E, Gibson, Greg1, Smedby, Karin E, Foo, Jia Nee, Skibola, Christine F, Darabi, Hatef, Conde, Lucia, Hjalgrim, Henrik, Kumar, Vikrant, Chang, Ellen T, Rothman, Nathaniel, Cerhan, James R, Brooks-Wilson, Angela R, Rehnberg, Emil, Irwan, Ishak D, Ryder, Lars P, Brown, Peter N, Bracci, Paige M, Agana, Luz, Riby, Jacques, Cozen, Wendy, Davis, Scott, Hartge, Patricia, Morton, Lindsay M, Severson, Richard K, Wang, Sophia S, Slager, Susan L, Fredericksen, Zachary S, Novak, Anne J, Kay, Neil E, Habermann, Thomas M, Armstrong, Bruce, Kricker, Anne, Milliken, Sam, Purdue, Mark P, Vajdic, Claire M, Boyle, Peter, Lan, Qing, Zahm, Shelia H, Zhang, Yawei, Zheng, Tongzhang, Leach, Stephen, Spinelli, John J, Smith, Martyn T, Chanock, Stephen J, Padyukov, Leonid, Alfredsson, Lars, Klareskog, Lars, Glimelius, Bengt, Melbye, Mads, Liu, Edison T, Adami, Hans-Olov, Humphreys, Keith, and Liu, Jianjun

Abstract

Non-Hodgkin lymphoma (NHL) represents a diverse group of hematological malignancies, of which follicular lymphoma (FL) is a prevalent subtype. A previous genome-wide association study has established a marker, rs10484561 in the human leukocyte antigen (HLA) class II region on 6p21.32 associated with increased FL risk. Here, in a three-stage genome-wide association study, starting with a genome-wide scan of 379 FL cases and 791 controls followed by validation in 1,049 cases and 5,790 controls, we identified a second independent FL-associated locus on 6p21.32, rs2647012 (OR(combined) = 0.64, P(combined) = 2 × 10(-21)) located 962 bp away from rs10484561 (r(2)<0.1 in controls). After mutual adjustment, the associations at the two SNPs remained genome-wide significant (rs2647012:OR(adjusted) = 0.70, P(adjusted) = 4 × 10(-12); rs10484561:OR(adjusted) = 1.64, P(adjusted) = 5 × 10(-15)). Haplotype and coalescence analyses indicated that rs2647012 arose on an evolutionarily distinct haplotype from that of rs10484561 and tags a novel allele with an opposite (protective) effect on FL risk. Moreover, in a follow-up analysis of the top 6 FL-associated SNPs in 4,449 cases of other NHL subtypes, rs10484561 was associated with risk of diffuse large B-cell lymphoma (OR(combined) = 1.36, P(combined) = 1.4 × 10(-7)). Our results reveal the presence of allelic heterogeneity within the HLA class II region influencing FL susceptibility and indicate a possible shared genetic etiology with diffuse large B-cell lymphoma. These findings suggest that the HLA class II region plays a complex yet important role in NHL.

Published
2011

232. International network of cancer genome projects

Author

Hudson, Thomas J., Anderson, Warwick, Aretz, Axel, Barker, Anna D., Bell, Cindy, Bernabe, Rosa R., Bhan, M. K., Calvo, Fabien, Eerola, Iiro, Gerhard, Daniela S., Guttmacher, Alan, Guyer, Mark, Hemsley, Fiona M., Jennings, Jennifer L., Kerr, David, Klatt, Peter, Kolar, Patrik, Kusuda, Jun, Lane, David P., Laplace, Frank, Lu, Youyong, Nettekoven, Gerd, Ozenberger, Brad, Peterson, Jane, Rao, T. S., Remacle, Jacques, Schafer, Alan J., Shibata, Tatsuhiro, Stratton, Michael R., Vockley, Joseph G., Watanabe, Koichi, Yang, Huanming, Yuen, Matthew M. F., Knoppers, M., Bobrow, Martin, Cambon-Thomsen, Anne, Dressler, Lynn G., Dyke, Stephanie O. M., Joly, Yann, Kato, Kazuto, Kennedy, Karen L., Nicolas, Pilar, Parker, Michael J., Rial-Sebbag, Emmanuelle, Romeo-Casabona, Carlos M., Shaw, Kenna M., Wallace, Susan, Wiesner, Georgia L., Zeps, Nikolajs, Lichter, Peter, Biankin, Andrew V., Chabannon, Christian, Chin, Lynda, Clement, Bruno, de Alava, Enrique, Degos, Francoise, Ferguson, Martin L., Geary, Peter, Hayes, D. Neil, Johns, Amber L., Nakagawa, Hidewaki, Penny, Robert, Piris, Miguel A., Sarin, Rajiv, Scarpa, Aldo, van de Vijver, Marc, Futreal, P. Andrew, Aburatani, Hiroyuki, Bayes, Monica, Bowtell, David D. L., Campbell, Peter J., Estivill, Xavier, Grimmond, Sean M., Gut, Ivo, Hirst, Martin, Lopez-Otin, Carlos, Majumder, Partha, Marra, Marco, Ning, Zemin, Puente, Xose S., Ruan, Yijun, Stunnenberg, Hendrik G., Swerdlow, Harold, Velculescu, Victor E., Wilson, Richard K., Xue, Hong H., Yang, Liu, Spellman, Paul T., Bader, Gary D., Boutros, Paul C., Flicek, Paul, Getz, Gad, Guigo, Roderic, Guo, Guangwu, Haussler, David, Heath, Simon, Hubbard, Tim J., Jiang, Tao, Jones, Steven M., Li, Qibin, Lopez-Bigas, Nuria, Luo, Ruibang, Pearson, John V., Quesada, Victor, Raphael, Benjamin J., Sander, Chris, Speed, Terence P., Stuart, Joshua M., Teague, Jon W., Totoki, Yasushi, Tsunoda, Tatsuhiko, Valencia, Alfonso, Wheeler, David A., Wu, Honglong, Zhao, Shancen, Zhou, Guangyu, Stein, Lincoln D., Lathrop, Mark, Ouellette, B. F. Francis, Thomas, Gilles, Yoshida, Teruhiko, Axton, Myles, Gunter, Chris, McPherson, John D., Miller, Linda J., Kasprzyk, Arek, Zhang, Junjun, Haider, Syed A., Wang, Jianxin, Yung, Christina K., Cros, Anthony, Liang, Yong, Gnaneshan, Saravanamuttu, Guberman, Jonathan, Hsu, Jack, Chalmers, Don R. C., Hasel, Karl W., Kaan, Terry S. H., Knoppers, Bartha M., Lowrance, William W., Masui, Tohru, Rodriguez, Laura Lyman, Vergely, Catherine, Cloonan, Nicole, Defazio, Anna, Eshleman, James R., Etemadmoghadam, Dariush, Gardiner, Brooke B., Kench, James G., Sutherland, Robert L., Tempero, Margaret A., Waddell, Nicola J., Wilson, Peter J., Gallinger, Steve, Tsao, Ming-Sound, Shaw, Patricia A., Petersen, Gloria M., Mukhopadhyay, Debabrata, DePinho, Ronald A., Thayer, Sarah, Muthuswamy, Lakshmi, Shazand, Kamran, Beck, Timothy, Sam, Michelle, Timms, Lee, Ballin, Vanessa, Ji, Jiafu, Zhang, Xiuqing, Chen, Feng, Hu, Xueda, Yang, Qi, Tian, Geng, Zhang, Lianhai, Xing, Xiaofang, Li, Xianghong, Zhu, Zhenggang, Yu, Yingyan, Yu, Jun, Tost, Joerg, Brennan, Paul, Holcatova, Ivana, Zaridze, David, Brazma, Alvis, Egevad, Lars, Prokhortchouk, Egor, Banks, Rosamonde Elizabeth, Uhlén, Mathias, Viksna, Juris, Pontén, Fredrik, Skryabin, Konstantin, Birney, Ewan, Borg, Ake, Borresen-Dale, Anne-Lise, Caldas, Carlos, Foekens, John A., Martin, Sancha, Reis-Filho, Jorge S., Richardson, Andrea L., Sotiriou, Christos, van't Veer, Laura, Birnbaum, Daniel, Blanche, Helene, Boucher, Pascal, Boyault, Sandrine, Masson-Jacquemier, Jocelyne D., Pauporte, Iris, Pivot, Xavier, Vincent-Salomon, Anne, Tabone, Eric, Theillet, Charles, Treilleux, Isabelle, Bioulac-Sage, Paulette, Decaens, Thomas, Franco, Dominique, Gut, Marta, Samuel, Didier, Zucman-Rossi, Jessica, Eils, Roland, Brors, Benedikt, Korbel, Jan O., Korshunov, Andrey, Landgraf, Pablo, Lehrach, Hans, Pfister, Stefan, Radlwimmer, Bernhard, Reifenberger, Guido, Taylor, Michael D., von Kalle, Christof, Majumder, Partha P., Pederzoli, Paolo, Lawlor, Rita T., Delledonne, Massimo, Bardelli, Alberto, Gress, Thomas, Klimstra, David, Zamboni, Giuseppe, Nakamura, Yusuke, Miyano, Satoru, Fujimoto, Akihiro, Campo, Elias, de Sanjose, Silvia, Montserrat, Emili, Gonzalez-Diaz, Marcos, Jares, Pedro, Himmelbauer, Heinz, Bea, Silvia, Aparicio, Samuel, Easton, Douglas F., Collins, Francis S., Compton, Carolyn C., Lander, Eric S., Burke, Wylie, Green, Anthony R., Hamilton, Stanley R., Kallioniemi, Olli P., Ley, Timothy J., Liu, Edison T., Wainwright, Brandon J., Hudson, Thomas J., Anderson, Warwick, Aretz, Axel, Barker, Anna D., Bell, Cindy, Bernabe, Rosa R., Bhan, M. K., Calvo, Fabien, Eerola, Iiro, Gerhard, Daniela S., Guttmacher, Alan, Guyer, Mark, Hemsley, Fiona M., Jennings, Jennifer L., Kerr, David, Klatt, Peter, Kolar, Patrik, Kusuda, Jun, Lane, David P., Laplace, Frank, Lu, Youyong, Nettekoven, Gerd, Ozenberger, Brad, Peterson, Jane, Rao, T. S., Remacle, Jacques, Schafer, Alan J., Shibata, Tatsuhiro, Stratton, Michael R., Vockley, Joseph G., Watanabe, Koichi, Yang, Huanming, Yuen, Matthew M. F., Knoppers, M., Bobrow, Martin, Cambon-Thomsen, Anne, Dressler, Lynn G., Dyke, Stephanie O. M., Joly, Yann, Kato, Kazuto, Kennedy, Karen L., Nicolas, Pilar, Parker, Michael J., Rial-Sebbag, Emmanuelle, Romeo-Casabona, Carlos M., Shaw, Kenna M., Wallace, Susan, Wiesner, Georgia L., Zeps, Nikolajs, Lichter, Peter, Biankin, Andrew V., Chabannon, Christian, Chin, Lynda, Clement, Bruno, de Alava, Enrique, Degos, Francoise, Ferguson, Martin L., Geary, Peter, Hayes, D. Neil, Johns, Amber L., Nakagawa, Hidewaki, Penny, Robert, Piris, Miguel A., Sarin, Rajiv, Scarpa, Aldo, van de Vijver, Marc, Futreal, P. Andrew, Aburatani, Hiroyuki, Bayes, Monica, Bowtell, David D. L., Campbell, Peter J., Estivill, Xavier, Grimmond, Sean M., Gut, Ivo, Hirst, Martin, Lopez-Otin, Carlos, Majumder, Partha, Marra, Marco, Ning, Zemin, Puente, Xose S., Ruan, Yijun, Stunnenberg, Hendrik G., Swerdlow, Harold, Velculescu, Victor E., Wilson, Richard K., Xue, Hong H., Yang, Liu, Spellman, Paul T., Bader, Gary D., Boutros, Paul C., Flicek, Paul, Getz, Gad, Guigo, Roderic, Guo, Guangwu, Haussler, David, Heath, Simon, Hubbard, Tim J., Jiang, Tao, Jones, Steven M., Li, Qibin, Lopez-Bigas, Nuria, Luo, Ruibang, Pearson, John V., Quesada, Victor, Raphael, Benjamin J., Sander, Chris, Speed, Terence P., Stuart, Joshua M., Teague, Jon W., Totoki, Yasushi, Tsunoda, Tatsuhiko, Valencia, Alfonso, Wheeler, David A., Wu, Honglong, Zhao, Shancen, Zhou, Guangyu, Stein, Lincoln D., Lathrop, Mark, Ouellette, B. F. Francis, Thomas, Gilles, Yoshida, Teruhiko, Axton, Myles, Gunter, Chris, McPherson, John D., Miller, Linda J., Kasprzyk, Arek, Zhang, Junjun, Haider, Syed A., Wang, Jianxin, Yung, Christina K., Cros, Anthony, Liang, Yong, Gnaneshan, Saravanamuttu, Guberman, Jonathan, Hsu, Jack, Chalmers, Don R. C., Hasel, Karl W., Kaan, Terry S. H., Knoppers, Bartha M., Lowrance, William W., Masui, Tohru, Rodriguez, Laura Lyman, Vergely, Catherine, Cloonan, Nicole, Defazio, Anna, Eshleman, James R., Etemadmoghadam, Dariush, Gardiner, Brooke B., Kench, James G., Sutherland, Robert L., Tempero, Margaret A., Waddell, Nicola J., Wilson, Peter J., Gallinger, Steve, Tsao, Ming-Sound, Shaw, Patricia A., Petersen, Gloria M., Mukhopadhyay, Debabrata, DePinho, Ronald A., Thayer, Sarah, Muthuswamy, Lakshmi, Shazand, Kamran, Beck, Timothy, Sam, Michelle, Timms, Lee, Ballin, Vanessa, Ji, Jiafu, Zhang, Xiuqing, Chen, Feng, Hu, Xueda, Yang, Qi, Tian, Geng, Zhang, Lianhai, Xing, Xiaofang, Li, Xianghong, Zhu, Zhenggang, Yu, Yingyan, Yu, Jun, Tost, Joerg, Brennan, Paul, Holcatova, Ivana, Zaridze, David, Brazma, Alvis, Egevad, Lars, Prokhortchouk, Egor, Banks, Rosamonde Elizabeth, Uhlén, Mathias, Viksna, Juris, Pontén, Fredrik, Skryabin, Konstantin, Birney, Ewan, Borg, Ake, Borresen-Dale, Anne-Lise, Caldas, Carlos, Foekens, John A., Martin, Sancha, Reis-Filho, Jorge S., Richardson, Andrea L., Sotiriou, Christos, van't Veer, Laura, Birnbaum, Daniel, Blanche, Helene, Boucher, Pascal, Boyault, Sandrine, Masson-Jacquemier, Jocelyne D., Pauporte, Iris, Pivot, Xavier, Vincent-Salomon, Anne, Tabone, Eric, Theillet, Charles, Treilleux, Isabelle, Bioulac-Sage, Paulette, Decaens, Thomas, Franco, Dominique, Gut, Marta, Samuel, Didier, Zucman-Rossi, Jessica, Eils, Roland, Brors, Benedikt, Korbel, Jan O., Korshunov, Andrey, Landgraf, Pablo, Lehrach, Hans, Pfister, Stefan, Radlwimmer, Bernhard, Reifenberger, Guido, Taylor, Michael D., von Kalle, Christof, Majumder, Partha P., Pederzoli, Paolo, Lawlor, Rita T., Delledonne, Massimo, Bardelli, Alberto, Gress, Thomas, Klimstra, David, Zamboni, Giuseppe, Nakamura, Yusuke, Miyano, Satoru, Fujimoto, Akihiro, Campo, Elias, de Sanjose, Silvia, Montserrat, Emili, Gonzalez-Diaz, Marcos, Jares, Pedro, Himmelbauer, Heinz, Bea, Silvia, Aparicio, Samuel, Easton, Douglas F., Collins, Francis S., Compton, Carolyn C., Lander, Eric S., Burke, Wylie, Green, Anthony R., Hamilton, Stanley R., Kallioniemi, Olli P., Ley, Timothy J., Liu, Edison T., and Wainwright, Brandon J.

Abstract

The International Cancer Genome Consortium (ICGC) was launched to coordinate large-scale cancer genome studies in tumours from 50 different cancer types and/or subtypes that are of clinical and societal importance across the globe. Systematic studies of more than 25,000 cancer genomes at the genomic, epigenomic and transcriptomic levels will reveal the repertoire of oncogenic mutations, uncover traces of the mutagenic influences, define clinically relevant subtypes for prognosis and therapeutic management, and enable the development of new cancer therapies., QC 20110114

Published
2010
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233. Multi-Variant Pathway Association Analysis Reveals the Importance of Genetic Determinants of Estrogen Metabolism in Breast and Endometrial Cancer Susceptibility

Author

Low, Yen Ling, Li, Yuqing, Humphreys, Keith, Thalamuthu, Anbupalam, Li, Yi, Darabi, Hatef, Wedrén, Sara, Bonnard, Carine, Czene, Kamila, Iles, Mark M., Heikkinen, Tuomas, Aittomäki, Kristiina, Blomqvist, Carl, Nevanlinna, Heli, Hall, Per, Liu, Edison T., Liu, Jianjun, Low, Yen Ling, Li, Yuqing, Humphreys, Keith, Thalamuthu, Anbupalam, Li, Yi, Darabi, Hatef, Wedrén, Sara, Bonnard, Carine, Czene, Kamila, Iles, Mark M., Heikkinen, Tuomas, Aittomäki, Kristiina, Blomqvist, Carl, Nevanlinna, Heli, Hall, Per, Liu, Edison T., and Liu, Jianjun

Abstract

Despite the central role of estrogen exposure in breast and endometrial cancer development and numerous studies of genes in the estrogen metabolic pathway, polymorphisms within the pathway have not been consistently associated with these cancers. We posit that this is due to the complexity of multiple weak genetic effects within the metabolic pathway that can only be effectively detected through multi-variant analysis. We conducted a comprehensive association analysis of the estrogen metabolic pathway by interrogating 239 tagSNPs within 35 genes of the pathway in three tumor samples. The discovery sample consisted of 1,596 breast cancer cases, 719 endometrial cancer cases, and 1,730 controls from Sweden; and the validation sample included 2,245 breast cancer cases and 1,287 controls from Finland. We performed admixture maximum likelihood (AML)-based global tests to evaluate the cumulative effect from multiple SNPs within the whole metabolic pathway and three sub-pathways for androgen synthesis, androgen-to-estrogen conversion, and estrogen removal. In the discovery sample, although no single polymorphism was significant after correction for multiple testing, the pathway-based AML global test suggested association with both breast (rho(global) = 0.034) and endometrial (rho(global) = 0.052) cancers. Further testing revealed the association to be focused on polymorphisms within the androgen-to-estrogen conversion sub-pathway, for both breast (rho(global) = 0.008) and endometrial cancer (rho(global) = 0.014). The sub-pathway association was validated in the Finnish sample of breast cancer (rho(global) = 0.015). Further tumor subtype analysis demonstrated that the association of the androgen-to-estrogen conversion sub-pathway was confined to postmenopausal women with sporadic estrogen receptor positive tumors (rho(global) = 0.0003). Gene-based AML analysis suggested CYP19A1 and UGT2B4 to be the major players within the sub-pathway. Our study indicates that the composite

Published
2010
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234. Multi-Variant Pathway Association Analysis Reveals the Importance of Genetic Determinants of Estrogen Metabolism in Breast and Endometrial Cancer Susceptibility

Author

University of Helsinki, Women's Health Research Program, University of Helsinki, Research Program in Genome-Scale Biology, University of Helsinki, Department of Oncology, University of Helsinki, Department of Obstetrics and Gynecology, Low, Yen Ling, Li, Yuqing, Humphreys, Keith, Thalamuthu, Anbupalam, Li, Yi, Darabi, Hatef, Wedren, Sara, Bonnard, Carine, Czene, Kamila, Iles, Mark M., Heikkinen, Tuomas, Aittomäki, Kristiina, Blomqvist, Carl, Nevanlinna, Heli, Hall, Per, Liu, Edison T., Liu, Jianjun, University of Helsinki, Women's Health Research Program, University of Helsinki, Research Program in Genome-Scale Biology, University of Helsinki, Department of Oncology, University of Helsinki, Department of Obstetrics and Gynecology, Low, Yen Ling, Li, Yuqing, Humphreys, Keith, Thalamuthu, Anbupalam, Li, Yi, Darabi, Hatef, Wedren, Sara, Bonnard, Carine, Czene, Kamila, Iles, Mark M., Heikkinen, Tuomas, Aittomäki, Kristiina, Blomqvist, Carl, Nevanlinna, Heli, Hall, Per, Liu, Edison T., and Liu, Jianjun

Published
2010

235. Monochromosome transfer and microarray analysis identify a critical tumor-suppressive region mapping to chromosome 13q14 and THSD1 in esophageal carcinoma

Author

Ko, Josephine M.Y., Chan, Pui Ling, Yau, Wing Lung, Chan, Ho Kin, Chan, King Chi, Yu, Zhuo You, Kwong, Fung Mei, Miller, Lance D., Liu, Edison T., Yang, Li Chun, Lo, Paulisally H.Y., Stanbridge, Eric J., Tang, Johnny C.O., Srivastava, Gopesh, Tsao, Sai Wah, Law, Simon, Lung, Maria L., Ko, Josephine M.Y., Chan, Pui Ling, Yau, Wing Lung, Chan, Ho Kin, Chan, King Chi, Yu, Zhuo You, Kwong, Fung Mei, Miller, Lance D., Liu, Edison T., Yang, Li Chun, Lo, Paulisally H.Y., Stanbridge, Eric J., Tang, Johnny C.O., Srivastava, Gopesh, Tsao, Sai Wah, Law, Simon, and Lung, Maria L.

Abstract

Loss of chromosome 13q regions in esophageal squamous cell carcinoma (ESCC) is a frequent event. Monochromosome transfer approaches provide direct functional evidence for tumor suppression by chromosome 13 in SLMT-1, an ESCC cell line, and identify critical regions at 13q12.3, 13q14.11, and 13q14.3. Differential gene expression profiles of three tumor-suppressing microcell hybrids (MCH) and their tumorigenic parental SLMT-1 cell line were revealed by competitive hybridization using 19k cDNA oligonucleolide microarrays. Nine candidate 13q14 tumor-suppressor genes (TSG), including RB1, showed down-regulation in SLMT-1, compared with NE1, an immortalized normal esophageal epithelial cell line; their average gene expression was restored in MCHs compared with SLMT-1. Reverse transcription-PCR validated gene expression levels in MCHs and a panel of ESCC cell lines. Results suggest that the tumor-suppressing effect is not attributed to RB1, but instead likely involves thrombospondin type I domain-containing 1 (THSD1), a novel candidate TSG mapping to 13q14. Quantitative reverse transcription-PCR detected down-regulation of THSD1 expression in 100\% of ESCC and other cancer cell lines. Mechanisms for THSD1 silencing in ESCC involved loss of heterozygosity and promoter hypermethylation, as analyzed by methylation-specific PCR and clonal bisulfite sequencing. Transfection of wild-type THSD1 into SLMT-1 resulted in significant reduction of colony-forming ability, hence providing functional evidence for its growth-suppressive activity. These findings suggest that THSD1 is a good candidate TSG.

Published
2008

240. Regulation of Transcription through Acetylation of H3K122 on the Lateral Surface of the Histone Octamer

Author

Tropberger, Philipp, primary, Pott, Sebastian, additional, Keller, Claudia, additional, Kamieniarz-Gdula, Kinga, additional, Caron, Matthieu, additional, Richter, Florian, additional, Li, Guohong, additional, Mittler, Gerhard, additional, Liu, Edison T., additional, Bühler, Marc, additional, Margueron, Raphael, additional, and Schneider, Robert, additional

Published
2013
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242. The tandem duplicator phenotype as a distinct genomic configuration in cancer.

Author

Menghi, Francesca, Koichiro Inaki, XingYi Woo, Kumar, Pooja A., Grzeda, Krzysztof R., Malhotra, Ankit, Yadav, Vinod, Hyunsoo Kim, Marquez, Eladio J., Ucar, Duygu, Shreckengast, Phung T., Wagner, Joel P., MacIntyre, George, Murthy Karuturi, Krishna R., Scully, Ralph, Keck, James, Chuang, Jeffrey H., and Liu, Edison T.

Subjects
CANCER, CHROMOTHRIPSIS, TUMOR proteins, GENOMICS, PHENOTYPES, CANCER chemotherapy
Abstract

Next-generation sequencing studies have revealed genome-wide structural variation patterns in cancer, such as chromothripsis and chromoplexy, that do not engage a single discernable driver mutation, and whose clinical relevance is unclear. We devised a robust genomic metric able to identify cancers with a chromotype called tandem duplicator phenotype (TDP) characterized by frequent and distributed tandem duplications (TDs). Enriched only in triple-negative breast cancer (TNBC) and in ovarian, endometrial, and liver cancers, TDP tumors conjointly exhibit tumor protein p53 (TP53) mutations, disruption of breast cancer 1 (BRCA1), and increased expression of DNA replication genes pointing at rereplication in a defective checkpoint environment as a plausible causal mechanism. The resultant TDs in TDP augment global oncogene expression and disrupt tumor suppressor genes. Importantly, the TDP strongly correlates with cisplatin sensitivity in both TNBC cell lines and primary patient-derived xenografts. We conclude that the TDP is a common cancer chromotype that coordinately alters oncogene/tumor suppressor expression with potential as a marker for chemotherapeutic response. [ABSTRACT FROM AUTHOR]

Published
2016
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243. Hormone-replacement therapy influences gene expression profiles and is associated with breast-cancer prognosis : a cohort study

Author

Hall, Per, Ploner, Alexander, Bjohle, Judith, Huang, Fei, Lin, Chin-Yo, Liu, Edison T, Miller, Lance D, Nordgren, Hans, Pawitan, Yudi, Shaw, Peter, Skoog, Lambert, Smeds, Johanna, Wedren, Sara, Ohd, John, Bergh, Jonas, Hall, Per, Ploner, Alexander, Bjohle, Judith, Huang, Fei, Lin, Chin-Yo, Liu, Edison T, Miller, Lance D, Nordgren, Hans, Pawitan, Yudi, Shaw, Peter, Skoog, Lambert, Smeds, Johanna, Wedren, Sara, Ohd, John, and Bergh, Jonas

Abstract

Background: Postmenopausal hormone-replacement therapy (HRT) increases breast-cancer risk. The influence of HRT on the biology of the primary tumor, however, is not well understood. Methods: We obtained breast-cancer gene expression profiles using Affymetrix human genome U133A arrays. We examined the relationship between HRT-regulated gene profiles, tumor characteristics, and recurrence-free survival in 72 postmenopausal women. Results: HRT use in patients with estrogen receptor ( ER) protein positive tumors (n = 72) was associated with an altered regulation of 276 genes. Expression profiles based on these genes clustered ER-positive tumors into two molecular subclasses, one of which was associated with HRT use and had significantly better recurrence free survival despite lower ER levels. A comparison with external data suggested that gene regulation in tumors associated with HRT was negatively correlated with gene regulation induced by short-term estrogen exposure, but positively correlated with the effect of tamoxifen. Conclusion: Our findings suggest that post-menopausal HRT use is associated with a distinct gene expression profile related to better recurrence-free survival and lower ER protein levels. Tentatively, HRT-associated gene expression in tumors resembles the effect of tamoxifen exposure on MCF-7 cells.

Published
2006
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244. Genetic reclassification of histologic grade delineates new clinical subtypes of breast cancer

Author

Ivshina, Anna V., George, Joshy, Senko, Oleg, Mow, Benjamin, Putti, Thomas C., Smeds, Johanna, Lindahl, Thomas, Pawitan, Yudi, Hall, Per, Nordgren, Hans, Wong, John E. L., Liu, Edison T., Bergh, Jonas, Kuznetsov, Vladimir A., Miller, Lance D., Ivshina, Anna V., George, Joshy, Senko, Oleg, Mow, Benjamin, Putti, Thomas C., Smeds, Johanna, Lindahl, Thomas, Pawitan, Yudi, Hall, Per, Nordgren, Hans, Wong, John E. L., Liu, Edison T., Bergh, Jonas, Kuznetsov, Vladimir A., and Miller, Lance D.

Abstract

Histologic grading of breast cancer defines morphologic subtypes informative of metastatic potential, although not without considerable interobserver disagreement and clinical heterogeneity particularly among the moderately differentiated grade 2 (G2) tumors. We posited that a gene expression signature capable of discerning tumors of grade 1 (G1) and grade 3 (W) histology might provide a more objective measure of grade with prognostic benefit for patients with G2 disease. To this end, we studied the expression profiles of 347 primary invasive breast tumors analyzed on Affymetrix microarrays. Using class prediction algorithms, we identified 264 robust grade-associated markers, six of which could accurately classify G1 and G3 tumors, and separate G2 tumors into two highly discriminant classes (termed G2a and G2b genetic grades) with patient survival outcomes highly similar to those with G1 and G3 histology, respectively. Statistical analysis of conventional clinical variables further distinguished G2a and G2b subtypes from each other, but also from histologic G1 and G3 tumors. In multivariate analyses, genetic grade was consistently found to be an independent prognostic indicator of disease recurrence comparable with that of lymph node status and tumor size. When incorporated into the Nottingham prognostic index, genetic grade enhanced detection of patients with less harmful tumors, likely to benefit little from adjuvant therapy. Our findings show that a genetic grade signature can improve prognosis and therapeutic planning for breast cancer patients, and support the view that low- and high-grade disease, as defined genetically, reflect independent pathobiological entities rather than a continuum of cancer progression.

Published
2006
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245. Gene expression profiling spares early breast cancer patients from adjuvant therapy : derived and validated in two population-based cohorts

Author

Pawitan, Yudi, Bjöhle, Judith, Amler, Lukas, Borg, Anna-Lena, Egyhazi, Suzanne, Hall, Per, Han, Xia, Holmberg, Lars, Huang, Fei, Klaar, Sigrid, Liu, Edison T., Miller, Lance, Nordgren, Hans, Ploner, Alexander, Sandelin, Kerstin, Shaw, Peter M., Smeds, Johanna, Skoog, Lambert, Wedrén, Sara, Bergh, Jonas, Pawitan, Yudi, Bjöhle, Judith, Amler, Lukas, Borg, Anna-Lena, Egyhazi, Suzanne, Hall, Per, Han, Xia, Holmberg, Lars, Huang, Fei, Klaar, Sigrid, Liu, Edison T., Miller, Lance, Nordgren, Hans, Ploner, Alexander, Sandelin, Kerstin, Shaw, Peter M., Smeds, Johanna, Skoog, Lambert, Wedrén, Sara, and Bergh, Jonas

Abstract

INTRODUCTION: Adjuvant breast cancer therapy significantly improves survival, but overtreatment and undertreatment are major problems. Breast cancer expression profiling has so far mainly been used to identify women with a poor prognosis as candidates for adjuvant therapy but without demonstrated value for therapy prediction. METHODS: We obtained the gene expression profiles of 159 population-derived breast cancer patients, and used hierarchical clustering to identify the signature associated with prognosis and impact of adjuvant therapies, defined as distant metastasis or death within 5 years. Independent datasets of 76 treated population-derived Swedish patients, 135 untreated population-derived Swedish patients and 78 Dutch patients were used for validation. The inclusion and exclusion criteria for the studies of population-derived Swedish patients were defined. RESULTS: Among the 159 patients, a subset of 64 genes was found to give an optimal separation of patients with good and poor outcomes. Hierarchical clustering revealed three subgroups: patients who did well with therapy, patients who did well without therapy, and patients that failed to benefit from given therapy. The expression profile gave significantly better prognostication (odds ratio, 4.19; P = 0.007) (breast cancer end-points odds ratio, 10.64) compared with the Elston-Ellis histological grading (odds ratio of grade 2 vs 1 and grade 3 vs 1, 2.81 and 3.32 respectively; P = 0.24 and 0.16), tumor stage (odds ratio of stage 2 vs 1 and stage 3 vs 1, 1.11 and 1.28; P = 0.83 and 0.68) and age (odds ratio, 0.11; P = 0.55). The risk groups were consistent and validated in the independent Swedish and Dutch data sets used with 211 and 78 patients, respectively. CONCLUSION: We have identified discriminatory gene expression signatures working both on untreated and systematically treated primary breast cancer patients with the potential to spare them from adjuvant therapy.

Published
2005
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246. Personalizing medicine

Author

Liu, Edison T.

Subjects
The Language of Life: DNA and the Revolution in Personalized Medicine (Nonfiction work) -- Collins, Francis S. -- Book reviews, Books -- Book reviews, Biological sciences, Health
Abstract

The Language of Life: DNA and the Revolution in Personalized Medicine Francis S. Collins Harper, 2010 368 pp., hardcover, $26.99 ISBN: 0061733172 Books about science for the general public have [...]

Published
2010

250. Long Span DNA Paired-End-Tag (DNA-PET) Sequencing Strategy for the Interrogation of Genomic Structural Mutations and Fusion-Point-Guided Reconstruction of Amplicons

Author

Yao, Fei, primary, Ariyaratne, Pramila N., additional, Hillmer, Axel M., additional, Lee, Wah Heng, additional, Li, Guoliang, additional, Teo, Audrey S. M., additional, Woo, Xing Yi, additional, Zhang, Zhenshui, additional, Chen, Jieqi P., additional, Poh, Wan Ting, additional, Zawack, Kelson F. B., additional, Chan, Chee Seng, additional, Leong, See Ting, additional, Neo, Say Chuan, additional, Choi, Poh Sum D., additional, Gao, Song, additional, Nagarajan, Niranjan, additional, Thoreau, Hervé, additional, Shahab, Atif, additional, Ruan, Xiaoan, additional, Cacheux-Rataboul, Valère, additional, Wei, Chia-Lin, additional, Bourque, Guillaume, additional, Sung, Wing-Kin, additional, Liu, Edison T., additional, and Ruan, Yijun, additional

Published
2012
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