Search

Your search keyword '"Lawrence, Michael"' showing total 19 results
Start Over Author "Lawrence, Michael" Journal nature genetics
19 results on '"Lawrence, Michael"'

2. Paired exome analysis of Barrett's esophagus and adenocarcinoma

Author

Stachler, Matthew D, Taylor-Weiner, Amaro, Peng, Shouyong, McKenna, Aaron, Agoston, Agoston T, Odze, Robert D, Davison, Jon M, Nason, Katie S, Loda, Massimo, Leshchiner, Ignaty, Stewart, Chip, Stojanov, Petar, Seepo, Sara, Lawrence, Michael S, Ferrer-Torres, Daysha, Lin, Jules, Chang, Andrew C, Gabriel, Stacey B, Lander, Eric S, Beer, David G, Getz, Gad, Carter, Scott L, and Bass, Adam J

Subjects
Biological Sciences, Genetics, Rare Diseases, Digestive Diseases, Cancer, Clinical Research, Adenocarcinoma, Barrett Esophagus, Class I Phosphatidylinositol 3-Kinases, Cyclin-Dependent Kinase Inhibitor p16, DNA Mutational Analysis, Esophageal Neoplasms, Exome, Gene Amplification, Gene Frequency, Genetic Predisposition to Disease, Genome-Wide Association Study, Humans, Phosphatidylinositol 3-Kinases, Point Mutation, Tumor Suppressor Protein p53, Medical and Health Sciences, Developmental Biology, Agricultural biotechnology, Bioinformatics and computational biology
Abstract

Barrett's esophagus is thought to progress to esophageal adenocarcinoma (EAC) through a stepwise progression with loss of CDKN2A followed by TP53 inactivation and aneuploidy. Here we present whole-exome sequencing from 25 pairs of EAC and Barrett's esophagus and from 5 patients whose Barrett's esophagus and tumor were extensively sampled. Our analysis showed that oncogene amplification typically occurred as a late event and that TP53 mutations often occurred early in Barrett's esophagus progression, including in non-dysplastic epithelium. Reanalysis of additional EAC exome data showed that the majority (62.5%) of EACs emerged following genome doubling and that tumors with genomic doubling had different patterns of genomic alterations, with more frequent oncogenic amplification and less frequent inactivation of tumor suppressors, including CDKN2A. These data suggest that many EACs emerge not through the gradual accumulation of tumor-suppressor alterations but rather through a more direct path whereby a TP53-mutant cell undergoes genome doubling, followed by the acquisition of oncogenic amplifications.

Published
2015

3. A mutational signature reveals alterations underlying deficient homologous recombination repair in breast cancer

Author

Polak, Paz, primary, Kim, Jaegil, additional, Braunstein, Lior Z, additional, Karlic, Rosa, additional, Haradhavala, Nicholas J, additional, Tiao, Grace, additional, Rosebrock, Daniel, additional, Livitz, Dimitri, additional, Kübler, Kirsten, additional, Mouw, Kent W, additional, Kamburov, Atanas, additional, Maruvka, Yosef E, additional, Leshchiner, Ignaty, additional, Lander, Eric S, additional, Golub, Todd R, additional, Zick, Aviad, additional, Orthwein, Alexandre, additional, Lawrence, Michael S, additional, Batra, Rajbir N, additional, Caldas, Carlos, additional, Haber, Daniel A, additional, Laird, Peter W, additional, Shen, Hui, additional, Ellisen, Leif W, additional, D'Andrea, Alan D, additional, Chanock, Stephen J, additional, Foulkes, William D, additional, and Getz, Gad, additional

Published
2017
Full Text
View/download PDF

4. Tumor-suppressor genes that escape from X-inactivation contribute to cancer sex bias

Author

Dunford, Andrew, primary, Weinstock, David M, additional, Savova, Virginia, additional, Schumacher, Steven E, additional, Cleary, John P, additional, Yoda, Akinori, additional, Sullivan, Timothy J, additional, Hess, Julian M, additional, Gimelbrant, Alexander A, additional, Beroukhim, Rameen, additional, Lawrence, Michael S, additional, Getz, Gad, additional, and Lane, Andrew A, additional

Published
2016
Full Text
View/download PDF

5. The genomic landscape and evolution of endometrial carcinoma progression and abdominopelvic metastasis

Author

Gibson, William J, primary, Hoivik, Erling A, additional, Halle, Mari K, additional, Taylor-Weiner, Amaro, additional, Cherniack, Andrew D, additional, Berg, Anna, additional, Holst, Frederik, additional, Zack, Travis I, additional, Werner, Henrica M J, additional, Staby, Kjersti M, additional, Rosenberg, Mara, additional, Stefansson, Ingunn M, additional, Kusonmano, Kanthida, additional, Chevalier, Aaron, additional, Mauland, Karen K, additional, Trovik, Jone, additional, Krakstad, Camilla, additional, Giannakis, Marios, additional, Hodis, Eran, additional, Woie, Kathrine, additional, Bjorge, Line, additional, Vintermyr, Olav K, additional, Wala, Jeremiah A, additional, Lawrence, Michael S, additional, Getz, Gad, additional, Carter, Scott L, additional, Beroukhim, Rameen, additional, and Salvesen, Helga B, additional

Published
2016
Full Text
View/download PDF

6. Pan-cancer network analysis identifies combinations of rare somatic mutations across pathways and protein complexes

Author

Leiserson, Mark D M, primary, Vandin, Fabio, additional, Wu, Hsin-Ta, additional, Dobson, Jason R, additional, Eldridge, Jonathan V, additional, Thomas, Jacob L, additional, Papoutsaki, Alexandra, additional, Kim, Younhun, additional, Niu, Beifang, additional, McLellan, Michael, additional, Lawrence, Michael S, additional, Gonzalez-Perez, Abel, additional, Tamborero, David, additional, Cheng, Yuwei, additional, Ryslik, Gregory A, additional, Lopez-Bigas, Nuria, additional, Getz, Gad, additional, Ding, Li, additional, and Raphael, Benjamin J, additional

Published
2014
Full Text
View/download PDF

7. RNF43 is frequently mutated in colorectal and endometrial cancers

Author

Giannakis, Marios, primary, Hodis, Eran, additional, Jasmine Mu, Xinmeng, additional, Yamauchi, Mai, additional, Rosenbluh, Joseph, additional, Cibulskis, Kristian, additional, Saksena, Gordon, additional, Lawrence, Michael S, additional, Qian, Zhi Rong, additional, Nishihara, Reiko, additional, Van Allen, Eliezer M, additional, Hahn, William C, additional, Gabriel, Stacey B, additional, Lander, Eric S, additional, Getz, Gad, additional, Ogino, Shuji, additional, Fuchs, Charles S, additional, and Garraway, Levi A, additional

Published
2014
Full Text
View/download PDF

8. Exome sequencing identifies BRAF mutations in papillary craniopharyngiomas

Author

Brastianos, Priscilla K, primary, Taylor-Weiner, Amaro, additional, Manley, Peter E, additional, Jones, Robert T, additional, Dias-Santagata, Dora, additional, Thorner, Aaron R, additional, Lawrence, Michael S, additional, Rodriguez, Fausto J, additional, Bernardo, Lindsay A, additional, Schubert, Laura, additional, Sunkavalli, Ashwini, additional, Shillingford, Nick, additional, Calicchio, Monica L, additional, Lidov, Hart G W, additional, Taha, Hala, additional, Martinez-Lage, Maria, additional, Santi, Mariarita, additional, Storm, Phillip B, additional, Lee, John Y K, additional, Palmer, James N, additional, Adappa, Nithin D, additional, Scott, R Michael, additional, Dunn, Ian F, additional, Laws, Edward R, additional, Stewart, Chip, additional, Ligon, Keith L, additional, Hoang, Mai P, additional, Van Hummelen, Paul, additional, Hahn, William C, additional, Louis, David N, additional, Resnick, Adam C, additional, Kieran, Mark W, additional, Getz, Gad, additional, and Santagata, Sandro, additional

Published
2014
Full Text
View/download PDF

9. Somatic mutation of CDKN1B in small intestine neuroendocrine tumors

Author

Francis, Joshua M, primary, Kiezun, Adam, additional, Ramos, Alex H, additional, Serra, Stefano, additional, Pedamallu, Chandra Sekhar, additional, Qian, Zhi Rong, additional, Banck, Michaela S, additional, Kanwar, Rahul, additional, Kulkarni, Amit A, additional, Karpathakis, Anna, additional, Manzo, Veronica, additional, Contractor, Tanupriya, additional, Philips, Juliet, additional, Nickerson, Elizabeth, additional, Pho, Nam, additional, Hooshmand, Susanne M, additional, Brais, Lauren K, additional, Lawrence, Michael S, additional, Pugh, Trevor, additional, McKenna, Aaron, additional, Sivachenko, Andrey, additional, Cibulskis, Kristian, additional, Carter, Scott L, additional, Ojesina, Akinyemi I, additional, Freeman, Samuel, additional, Jones, Robert T, additional, Voet, Douglas, additional, Saksena, Gordon, additional, Auclair, Daniel, additional, Onofrio, Robert, additional, Shefler, Erica, additional, Sougnez, Carrie, additional, Grimsby, Jonna, additional, Green, Lisa, additional, Lennon, Niall, additional, Meyer, Tim, additional, Caplin, Martyn, additional, Chung, Daniel C, additional, Beutler, Andreas S, additional, Ogino, Shuji, additional, Thirlwell, Christina, additional, Shivdasani, Ramesh, additional, Asa, Sylvia L, additional, Harris, Chris R, additional, Getz, Gad, additional, Kulke, Matthew, additional, and Meyerson, Matthew, additional

Published
2013
Full Text
View/download PDF

10. Pan-cancer patterns of somatic copy number alteration

Author

Zack, Travis I, primary, Schumacher, Steven E, additional, Carter, Scott L, additional, Cherniack, Andrew D, additional, Saksena, Gordon, additional, Tabak, Barbara, additional, Lawrence, Michael S, additional, Zhang, Cheng-Zhong, additional, Wala, Jeremiah, additional, Mermel, Craig H, additional, Sougnez, Carrie, additional, Gabriel, Stacey B, additional, Hernandez, Bryan, additional, Shen, Hui, additional, Laird, Peter W, additional, Getz, Gad, additional, Meyerson, Matthew, additional, and Beroukhim, Rameen, additional

Published
2013
Full Text
View/download PDF

11. An APOBEC cytidine deaminase mutagenesis pattern is widespread in human cancers

Author

Roberts, Steven A, primary, Lawrence, Michael S, additional, Klimczak, Leszek J, additional, Grimm, Sara A, additional, Fargo, David, additional, Stojanov, Petar, additional, Kiezun, Adam, additional, Kryukov, Gregory V, additional, Carter, Scott L, additional, Saksena, Gordon, additional, Harris, Shawn, additional, Shah, Ruchir R, additional, Resnick, Michael A, additional, Getz, Gad, additional, and Gordenin, Dmitry A, additional

Published
2013
Full Text
View/download PDF

12. Exome and whole-genome sequencing of esophageal adenocarcinoma identifies recurrent driver events and mutational complexity

Author

Dulak, Austin M, primary, Stojanov, Petar, additional, Peng, Shouyong, additional, Lawrence, Michael S, additional, Fox, Cameron, additional, Stewart, Chip, additional, Bandla, Santhoshi, additional, Imamura, Yu, additional, Schumacher, Steven E, additional, Shefler, Erica, additional, McKenna, Aaron, additional, Carter, Scott L, additional, Cibulskis, Kristian, additional, Sivachenko, Andrey, additional, Saksena, Gordon, additional, Voet, Douglas, additional, Ramos, Alex H, additional, Auclair, Daniel, additional, Thompson, Kristin, additional, Sougnez, Carrie, additional, Onofrio, Robert C, additional, Guiducci, Candace, additional, Beroukhim, Rameen, additional, Zhou, Zhongren, additional, Lin, Lin, additional, Lin, Jules, additional, Reddy, Rishindra, additional, Chang, Andrew, additional, Landrenau, Rodney, additional, Pennathur, Arjun, additional, Ogino, Shuji, additional, Luketich, James D, additional, Golub, Todd R, additional, Gabriel, Stacey B, additional, Lander, Eric S, additional, Beer, David G, additional, Godfrey, Tony E, additional, Getz, Gad, additional, and Bass, Adam J, additional

Published
2013
Full Text
View/download PDF

13. The genetic landscape of high-risk neuroblastoma

Author

Pugh, Trevor J, primary, Morozova, Olena, additional, Attiyeh, Edward F, additional, Asgharzadeh, Shahab, additional, Wei, Jun S, additional, Auclair, Daniel, additional, Carter, Scott L, additional, Cibulskis, Kristian, additional, Hanna, Megan, additional, Kiezun, Adam, additional, Kim, Jaegil, additional, Lawrence, Michael S, additional, Lichenstein, Lee, additional, McKenna, Aaron, additional, Pedamallu, Chandra Sekhar, additional, Ramos, Alex H, additional, Shefler, Erica, additional, Sivachenko, Andrey, additional, Sougnez, Carrie, additional, Stewart, Chip, additional, Ally, Adrian, additional, Birol, Inanc, additional, Chiu, Readman, additional, Corbett, Richard D, additional, Hirst, Martin, additional, Jackman, Shaun D, additional, Kamoh, Baljit, additional, Khodabakshi, Alireza Hadj, additional, Krzywinski, Martin, additional, Lo, Allan, additional, Moore, Richard A, additional, Mungall, Karen L, additional, Qian, Jenny, additional, Tam, Angela, additional, Thiessen, Nina, additional, Zhao, Yongjun, additional, Cole, Kristina A, additional, Diamond, Maura, additional, Diskin, Sharon J, additional, Mosse, Yael P, additional, Wood, Andrew C, additional, Ji, Lingyun, additional, Sposto, Richard, additional, Badgett, Thomas, additional, London, Wendy B, additional, Moyer, Yvonne, additional, Gastier-Foster, Julie M, additional, Smith, Malcolm A, additional, Auvil, Jaime M Guidry, additional, Gerhard, Daniela S, additional, Hogarty, Michael D, additional, Jones, Steven J M, additional, Lander, Eric S, additional, Gabriel, Stacey B, additional, Getz, Gad, additional, Seeger, Robert C, additional, Khan, Javed, additional, Marra, Marco A, additional, Meyerson, Matthew, additional, and Maris, John M, additional

Published
2013
Full Text
View/download PDF

14. Exome sequencing identifies recurrent SPOP, FOXA1 and MED12 mutations in prostate cancer

Author

Barbieri, Christopher E, primary, Baca, Sylvan C, additional, Lawrence, Michael S, additional, Demichelis, Francesca, additional, Blattner, Mirjam, additional, Theurillat, Jean-Philippe, additional, White, Thomas A, additional, Stojanov, Petar, additional, Van Allen, Eliezer, additional, Stransky, Nicolas, additional, Nickerson, Elizabeth, additional, Chae, Sung-Suk, additional, Boysen, Gunther, additional, Auclair, Daniel, additional, Onofrio, Robert C, additional, Park, Kyung, additional, Kitabayashi, Naoki, additional, MacDonald, Theresa Y, additional, Sheikh, Karen, additional, Vuong, Terry, additional, Guiducci, Candace, additional, Cibulskis, Kristian, additional, Sivachenko, Andrey, additional, Carter, Scott L, additional, Saksena, Gordon, additional, Voet, Douglas, additional, Hussain, Wasay M, additional, Ramos, Alex H, additional, Winckler, Wendy, additional, Redman, Michelle C, additional, Ardlie, Kristin, additional, Tewari, Ashutosh K, additional, Mosquera, Juan Miguel, additional, Rupp, Niels, additional, Wild, Peter J, additional, Moch, Holger, additional, Morrissey, Colm, additional, Nelson, Peter S, additional, Kantoff, Philip W, additional, Gabriel, Stacey B, additional, Golub, Todd R, additional, Meyerson, Matthew, additional, Lander, Eric S, additional, Getz, Gad, additional, Rubin, Mark A, additional, and Garraway, Levi A, additional

Published
2012
Full Text
View/download PDF

15. Tumor-suppressor genes that escape from X-inactivation contribute to cancer sex bias

Author

Dunford, Andrew, Weinstock, David M, Savova, Virginia, Schumacher, Steven E, Cleary, John P, Yoda, Akinori, Sullivan, Timothy J, Hess, Julian M, Gimelbrant, Alexander A, Beroukhim, Rameen, Lawrence, Michael S, Getz, Gad, and Lane, Andrew A

Abstract

There is a striking and unexplained male predominance across many cancer types. A subset of X-chromosome genes can escape X-inactivation, which would protect females from complete functional loss by a single mutation. To identify putative 'escape from X-inactivation tumor-suppressor' (EXITS) genes, we examined somatic alterations from >4,100 cancers across 21 tumor types for sex bias. Six of 783 non-pseudoautosomal region (PAR) X-chromosome genes (ATRX, CNKSR2, DDX3X, KDM5C, KDM6A, and MAGEC3) harbored loss-of-function mutations more frequently in males (based on a false discovery rate < 0.1), in comparison to zero of 18,055 autosomal and PAR genes (Fisher's exact P < 0.0001). Male-biased mutations in genes that escape X-inactivation were observed in combined analysis across many cancers and in several individual tumor types, suggesting a generalized phenomenon. We conclude that biallelic expression of EXITS genes in females explains a portion of the reduced cancer incidence in females as compared to males across a variety of tumor types.

Published
2017
Full Text
View/download PDF

16. Genomic sequencing of colorectal adenocarcinomas identifies a recurrent VTI1A-TCF7L2 fusion

Author

Bass, Adam J, primary, Lawrence, Michael S, additional, Brace, Lear E, additional, Ramos, Alex H, additional, Drier, Yotam, additional, Cibulskis, Kristian, additional, Sougnez, Carrie, additional, Voet, Douglas, additional, Saksena, Gordon, additional, Sivachenko, Andrey, additional, Jing, Rui, additional, Parkin, Melissa, additional, Pugh, Trevor, additional, Verhaak, Roel G, additional, Stransky, Nicolas, additional, Boutin, Adam T, additional, Barretina, Jordi, additional, Solit, David B, additional, Vakiani, Evi, additional, Shao, Wenlin, additional, Mishina, Yuji, additional, Warmuth, Markus, additional, Jimenez, Jose, additional, Chiang, Derek Y, additional, Signoretti, Sabina, additional, Kaelin, William G, additional, Spardy, Nicole, additional, Hahn, William C, additional, Hoshida, Yujin, additional, Ogino, Shuji, additional, DePinho, Ronald A, additional, Chin, Lynda, additional, Garraway, Levi A, additional, Fuchs, Charles S, additional, Baselga, Jose, additional, Tabernero, Josep, additional, Gabriel, Stacey, additional, Lander, Eric S, additional, Getz, Gad, additional, and Meyerson, Matthew, additional

Published
2011
Full Text
View/download PDF

17. Paired exome analysis of Barrett's esophagus and adenocarcinoma.

Author

Taylor-Weiner, Amaro, Peng, Shouyong, Stojanov, Petar, Lin, Jules, Bass, Adam J, Stewart, Chip, Seepo, Sara, Odze, Robert D, Nason, Katie S, Stachler, Matthew D, Carter, Scott L, Lander, Eric S, Leshchiner, Ignaty, Lawrence, Michael S, McKenna, Aaron, Chang, Andrew C, Agoston, Agoston T, Beer, David G, Loda, Massimo, and Davison, Jon M

Subjects
BARRETT'S esophagus, ADENOCARCINOMA, DYSPLASIA, ONCOGENES, TRANSFORMING growth factors-beta
Abstract

Barrett's esophagus is thought to progress to esophageal adenocarcinoma (EAC) through a stepwise progression with loss of CDKN2A followed by TP53 inactivation and aneuploidy. Here we present whole-exome sequencing from 25 pairs of EAC and Barrett's esophagus and from 5 patients whose Barrett's esophagus and tumor were extensively sampled. Our analysis showed that oncogene amplification typically occurred as a late event and that TP53 mutations often occurred early in Barrett's esophagus progression, including in non-dysplastic epithelium. Reanalysis of additional EAC exome data showed that the majority (62.5%) of EACs emerged following genome doubling and that tumors with genomic doubling had different patterns of genomic alterations, with more frequent oncogenic amplification and less frequent inactivation of tumor suppressors, including CDKN2A. These data suggest that many EACs emerge not through the gradual accumulation of tumor-suppressor alterations but rather through a more direct path whereby a TP53-mutant cell undergoes genome doubling, followed by the acquisition of oncogenic amplifications. [ABSTRACT FROM AUTHOR]

Published
2015
Full Text
View/download PDF

18. Pan-cancer network analysis identifies combinations of rare somatic mutations across pathways and protein complexes.

Author

Leiserson, Mark D M, Raphael, Benjamin J, Thomas, Jacob L, Vandin, Fabio, Ding, Li, Eldridge, Jonathan V, Kim, Younhun, McLellan, Michael, Gonzalez-Perez, Abel, Cheng, Yuwei, Dobson, Jason R, Niu, Beifang, Ryslik, Gregory A, Lopez-Bigas, Nuria, Wu, Hsin-Ta, Getz, Gad, Papoutsaki, Alexandra, Lawrence, Michael S, and Tamborero, David

Subjects
CANCER, DNA mutational analysis, HETEROGENEITY, SOMATIC hybrids, PROTEINS
Abstract

Cancers exhibit extensive mutational heterogeneity, and the resulting long-tail phenomenon complicates the discovery of genes and pathways that are significantly mutated in cancer. We perform a pan-cancer analysis of mutated networks in 3,281 samples from 12 cancer types from The Cancer Genome Atlas (TCGA) using HotNet2, a new algorithm to find mutated subnetworks that overcomes the limitations of existing single-gene, pathway and network approaches. We identify 16 significantly mutated subnetworks that comprise well-known cancer signaling pathways as well as subnetworks with less characterized roles in cancer, including cohesin, condensin and others. Many of these subnetworks exhibit co-occurring mutations across samples. These subnetworks contain dozens of genes with rare somatic mutations across multiple cancers; many of these genes have additional evidence supporting a role in cancer. By illuminating these rare combinations of mutations, pan-cancer network analyses provide a roadmap to investigate new diagnostic and therapeutic opportunities across cancer types. [ABSTRACT FROM AUTHOR]

Published
2015
Full Text
View/download PDF

19. Distinct patterns of somatic genome alterations in lung adenocarcinomas and squamous cell carcinomas

Author

Campbell, Joshua D, Alexandrov, Anton, Kim, Jaegil, Wala, Jeremiah, Berger, Alice H, Pedamallu, Chandra Sekhar, Shukla, Sachet A, Guo, Guangwu, Brooks, Angela N, Murray, Bradley A, Imielinski, Marcin, Hu, Xin, Ling, Shiyun, Akbani, Rehan, Rosenberg, Mara, Cibulskis, Carrie, Ramachandran, Aruna, Collisson, Eric A, Kwiatkowski, David J, Lawrence, Michael S, Weinstein, John N, Verhaak, Roel G W, Wu, Catherine J, Hammerman, Peter S, Cherniack, Andrew D, Getz, Gad, Artyomov, Maxim N, Schreiber, Robert, Govindan, Ramaswamy, and Meyerson, Matthew

Abstract

To compare lung adenocarcinoma (ADC) and lung squamous cell carcinoma (SqCC) and to identify new drivers of lung carcinogenesis, we examined the exome sequences and copy number profiles of 660 lung ADC and 484 lung SqCC tumor–normal pairs. Recurrent alterations in lung SqCCs were more similar to those of other squamous carcinomas than to alterations in lung ADCs. New significantly mutated genes included PPP3CA, DOT1L, and FTSJD1 in lung ADC, RASA1 in lung SqCC, and KLF5, EP300, and CREBBP in both tumor types. New amplification peaks encompassed MIR21 in lung ADC, MIR205 in lung SqCC, and MAPK1 in both. Lung ADCs lacking receptor tyrosine kinase–Ras–Raf pathway alterations had mutations in SOS1, VAV1, RASA1, and ARHGAP35. Regarding neoantigens, 47% of the lung ADC and 53% of the lung SqCC tumors had at least five predicted neoepitopes. Although targeted therapies for lung ADC and SqCC are largely distinct, immunotherapies may aid in treatment for both subtypes.

Published
2016
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results