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367 results on '"McKenna, Aaron"'

1. Campylobacter spp. within the UK poultry industry : prevalence, risk factors and the chicken microbiome

Author

McKenna, Aaron and Green, Brian

Subjects
636.5, Chicken, Campylobacter, Poultry, Microbiome, Farm
Abstract

Campylobacteriosis as a disease, is of huge significance to the human population worldwide. It remains the number one cause of human zoonosis within the EU with over 245,000 cases of campylobacteriosis reported in 2018 with many more cases thought to have gone unreported. Campylobacter is of particular significance for the poultry industry due to the fact chickens are a significant reservoir for Campylobacter spp. and ultimately cause a food safety risk should chicken meat be mishandled or improperly cooked. As such there has been a huge focus on Campylobacter reduction across the EU which has seen measures introduced to educate consumers on poultry meat handling and cooking as well as to force poultry producers to reduce levels within the supply chain. Within the UK, the Foods Standards Agency (FSA) have pressurised retailers to reduce Campylobacter loading on chicken products within their stores. This in turn has resulted in significant efforts to reduce levels of Campylobacter along the supply chain, particularly on farm. To date a fail-safe method of excluding Campylobacter from commercial UK and Irish poultry farms remains elusive. This body of research is unique in that it was done in conjunction with the commercial poultry industry, subsequently allowing access to a greater depth of metadata associated with Campylobacter prevalence on farm. Questions that were off interest to this work were i) the understanding of prevalence at a UK level and associated risk factors ii) the effect of Campylobacter on chicken health and performance at commercial farm level iii) investigate the chicken gut microbiome over time and how this may influence Campylobacter appearance and performance; and iv) assess the impact of farming production system parameters on the chicken microbiome, its influence on Campylobacter and performance. Our results are the first to analyse Campylobacter prevalence on farm during the period 2014 - 2016, during which Campylobacter reduction was a clear focus for the industry. We identified a year on year reduction in Campylobacter positive flocks from 60% in 2014 to 46% in 2016. Furthermore, we identified key risk factors associated with Campylobacter for UK poultry farmers. Unsurprisingly seasonality was a clear risk but other factors such as those in relation to farm infrastructure were identified and will ultimately inform the industry on best practice for the future. This research also sets out clearly the impact Campylobacter can have on flock performance, providing a clear incentive for farmers to invest and adhere to best practice biosecurity. Nonetheless, it is recognised that biosecurity alone will not prevent Campylobacter colonisation and further understanding of the chicken gut microbiome, how it interacts with Campylobacter and how commercial farm practices influence this, is required. Our chicken gut microbiome analysis clearly shows rapidly increasing microbial diversity up to day 12 with variation observed both in terms of genera and abundance, before a stabilization of the microbial diversity after day 20. In particular, we identified a shift from competitive to environmental drivers of microbial community from days 12 to 20 creating a window of opportunity whereby Campylobacter can appear. Additionally, we demonstrated for the first time how different production systems influence chicken microbial communities and as such could ultimately lead to improved performance and better intervention strategies against Campylobacter within the food chain.

Published
2021

2. Estimation of cell lineage trees by maximum-likelihood phylogenetics

Author

Feng, Jean, DeWitt III, William S, McKenna, Aaron, Simon, Noah, Willis, Amy, and Matsen IV, Frederick A

Subjects
Quantitative Biology - Quantitative Methods, Statistics - Applications
Abstract

CRISPR technology has enabled large-scale cell lineage tracing for complex multicellular organisms by mutating synthetic genomic barcodes during organismal development. However, these sophisticated biological tools currently use ad-hoc and outmoded computational methods to reconstruct the cell lineage tree from the mutated barcodes. Because these methods are agnostic to the biological mechanism, they are unable to take full advantage of the data's structure. We propose a statistical model for the mutation process and develop a procedure to estimate the tree topology, branch lengths, and mutation parameters by iteratively applying penalized maximum likelihood estimation. In contrast to existing techniques, our method estimates time along each branch, rather than number of mutation events, thus providing a detailed account of tissue-type differentiation. Via simulations, we demonstrate that our method is substantially more accurate than existing approaches. Our reconstructed trees also better recapitulate known aspects of zebrafish development and reproduce similar results across fish replicates.

Published
2019

3. Massively parallel profiling and predictive modeling of the outcomes of CRISPR/Cas9-mediated double-strand break repair

Author

Chen, Wei, McKenna, Aaron, Schreiber, Jacob, Haeussler, Maximilian, Yin, Yi, Agarwal, Vikram, Noble, William Stafford, and Shendure, Jay

Subjects
Biological Sciences, Genetics, Human Genome, Biotechnology, 1.1 Normal biological development and functioning, 2.1 Biological and endogenous factors, Generic health relevance, Base Sequence, CRISPR-Cas Systems, DNA Breaks, Double-Stranded, DNA Cleavage, DNA End-Joining Repair, Gene Editing, Genome, Human, Humans, Models, Genetic, Mutation, Sequence Deletion, Environmental Sciences, Information and Computing Sciences, Developmental Biology, Biological sciences, Chemical sciences, Environmental sciences
Abstract

Non-homologous end-joining (NHEJ) plays an important role in double-strand break (DSB) repair of DNA. Recent studies have shown that the error patterns of NHEJ are strongly biased by sequence context, but these studies were based on relatively few templates. To investigate this more thoroughly, we systematically profiled ∼1.16 million independent mutational events resulting from CRISPR/Cas9-mediated cleavage and NHEJ-mediated DSB repair of 6872 synthetic target sequences, introduced into a human cell line via lentiviral infection. We find that: (i) insertions are dominated by 1 bp events templated by sequence immediately upstream of the cleavage site, (ii) deletions are predominantly associated with microhomology and (iii) targets exhibit variable but reproducible diversity with respect to the number and relative frequency of the mutational outcomes to which they give rise. From these data, we trained a model that uses local sequence context to predict the distribution of mutational outcomes. Exploiting the bias of NHEJ outcomes towards microhomology mediated events, we demonstrate the programming of deletion patterns by introducing microhomology to specific locations in the vicinity of the DSB site. We anticipate that our results will inform investigations of DSB repair mechanisms as well as the design of CRISPR/Cas9 experiments for diverse applications including genome-wide screens, gene therapy, lineage tracing and molecular recording.

Published
2019

6. Simultaneous single-cell profiling of lineages and cell types in the vertebrate brain.

Author

Raj, Bushra, Wagner, Daniel E, McKenna, Aaron, Pandey, Shristi, Klein, Allon M, Shendure, Jay, Gagnon, James A, and Schier, Alexander F

Subjects
Brain, Animals, Zebrafish, Humans, Mice, Sequence Analysis, RNA, Cell Lineage, Single-Cell Analysis, Transcriptome, CRISPR-Cas Systems, Gene Editing
Abstract

The lineage relationships among the hundreds of cell types generated during development are difficult to reconstruct. A recent method, GESTALT, used CRISPR-Cas9 barcode editing for large-scale lineage tracing, but was restricted to early development and did not identify cell types. Here we present scGESTALT, which combines the lineage recording capabilities of GESTALT with cell-type identification by single-cell RNA sequencing. The method relies on an inducible system that enables barcodes to be edited at multiple time points, capturing lineage information from later stages of development. Sequencing of ∼60,000 transcriptomes from the juvenile zebrafish brain identified >100 cell types and marker genes. Using these data, we generate lineage trees with hundreds of branches that help uncover restrictions at the level of cell types, brain regions, and gene expression cascades during differentiation. scGESTALT can be applied to other multicellular organisms to simultaneously characterize molecular identities and lineage histories of thousands of cells during development and disease.

Published
2018

12. 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

13. Genomic Correlate of Exceptional Erlotinib Response in Head and Neck Squamous Cell Carcinoma

Author

Van Allen, Eliezer M, Lui, Vivian WY, Egloff, Ann Marie, Goetz, Eva M, Li, Hua, Johnson, Jonas T, Duvvuri, Umamaheswar, Bauman, Julie E, Stransky, Nicolas, Zeng, Yan, Gilbert, Breean R, Pendleton, Kelsey P, Wang, Lin, Chiosea, Simion, Sougnez, Carrie, Wagle, Nikhil, Zhang, Fan, Du, Yu, Close, David, Johnston, Paul A, McKenna, Aaron, Carter, Scott L, Golub, Todd R, Getz, Gad, Mills, Gordon B, Garraway, Levi A, and Grandis, Jennifer R

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Oncology and Carcinogenesis, Genetics, Dental/Oral and Craniofacial Disease, Cancer, Clinical Research, Cancer Genomics, Human Genome, Lung, Orphan Drug, Clinical Trials and Supportive Activities, Rare Diseases, Lung Cancer, Adult, Antineoplastic Agents, Biomarkers, Tumor, Biopsy, Carcinoma, Squamous Cell, Chemotherapy, Adjuvant, DNA Mutational Analysis, Drug Administration Schedule, ErbB Receptors, Erlotinib Hydrochloride, Genetic Predisposition to Disease, Head and Neck Neoplasms, Humans, Male, Mitogen-Activated Protein Kinase 1, Molecular Targeted Therapy, Mutation, Neoadjuvant Therapy, Neoplasm Staging, Phenotype, Phosphorylation, Predictive Value of Tests, Protein Kinase Inhibitors, Randomized Controlled Trials as Topic, Remission Induction, Squamous Cell Carcinoma of Head and Neck, Time Factors, Tongue Neoplasms, Treatment Outcome, Public Health and Health Services, Oncology and carcinogenesis
Abstract

ImportanceRandomized clinical trials demonstrate no benefit for epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors in unselected patients with head and neck squamous cell carcinoma (HNSCC). However, a patient with stage IVA HNSCC received 13 days of neoadjuvant erlotinib and experienced a near-complete histologic response.ObjectiveTo determine a mechanism of exceptional response to erlotinib therapy in HNSCC.Design, setting, and participantsSingle patient with locally advanced HNSCC who received erlotinib monotherapy in a window-of-opportunity clinical trial (patients scheduled to undergo primary cancer surgery are treated briefly with an investigational agent). Whole-exome sequencing of pretreatment tumor and germline patient samples was performed at a quaternary care academic medical center, and a candidate somatic variant was experimentally investigated for mediating erlotinib response.InterventionA brief course of erlotinib monotherapy followed by surgical resection.Main outcomes and measuresIdentification of pretreatment tumor somatic alterations that may contribute to the exceptional response to erlotinib. Hypotheses were formulated regarding enhanced erlotinib response in preclinical models harboring the patient tumor somatic variant MAPK1 E322K following the identification of tumor somatic variants.ResultsNo EGFR alterations were observed in the pretreatment tumor DNA. Paradoxically, the tumor harbored an activating MAPK1 E322K mutation (allelic fraction 0.13), which predicts ERK activation and erlotinib resistance in EGFR-mutant lung cancer. The HNSCC cells with MAPK1 E322K exhibited enhanced EGFR phosphorylation and erlotinib sensitivity compared with wild-type MAPK1 cells.Conclusions and relevanceSelective erlotinib use in HNSCC may be informed by precision oncology approaches.

Published
2015

16. Widespread genetic heterogeneity in multiple myeloma: implications for targeted therapy.

Author

Lohr, Jens, Stojanov, Petar, Carter, Scott, Cruz-Gordillo, Peter, Lawrence, Michael, Auclair, Daniel, Sougnez, Carrie, Knoechel, Birgit, Gould, Joshua, Saksena, Gordon, Cibulskis, Kristian, McKenna, Aaron, Chapman, Michael, Straussman, Ravid, Levy, Joan, Perkins, Louise, Keats, Jonathan, Schumacher, Steven, Rosenberg, Mara, Getz, Gad, and Golub, Todd

Subjects
Blotting, Western, Gene Dosage, Genetic Heterogeneity, Humans, Multiple Myeloma, Mutation, Sequence Analysis, DNA
Abstract

We performed massively parallel sequencing of paired tumor/normal samples from 203 multiple myeloma (MM) patients and identified significantly mutated genes and copy number alterations and discovered putative tumor suppressor genes by determining homozygous deletions and loss of heterozygosity. We observed frequent mutations in KRAS (particularly in previously treated patients), NRAS, BRAF, FAM46C, TP53, and DIS3 (particularly in nonhyperdiploid MM). Mutations were often present in subclonal populations, and multiple mutations within the same pathway (e.g., KRAS, NRAS, and BRAF) were observed in the same patient. In vitro modeling predicts only partial treatment efficacy of targeting subclonal mutations, and even growth promotion of nonmutated subclones in some cases. These results emphasize the importance of heterogeneity analysis for treatment decisions.

Published
2014

17. The Somatic Genomic Landscape of Glioblastoma

Author

Brennan, Cameron W, Verhaak, Roel GW, McKenna, Aaron, Campos, Benito, Noushmehr, Houtan, Salama, Sofie R, Zheng, Siyuan, Chakravarty, Debyani, Sanborn, J Zachary, Berman, Samuel H, Beroukhim, Rameen, Bernard, Brady, Wu, Chang-Jiun, Genovese, Giannicola, Shmulevich, Ilya, Barnholtz-Sloan, Jill, Zou, Lihua, Vegesna, Rahulsimham, Shukla, Sachet A, Ciriello, Giovanni, Yung, WK, Zhang, Wei, Sougnez, Carrie, Mikkelsen, Tom, Aldape, Kenneth, Bigner, Darell D, Van Meir, Erwin G, Prados, Michael, Sloan, Andrew, Black, Keith L, Eschbacher, Jennifer, Finocchiaro, Gaetano, Friedman, William, Andrews, David W, Guha, Abhijit, Iacocca, Mary, O’Neill, Brian P, Foltz, Greg, Myers, Jerome, Weisenberger, Daniel J, Penny, Robert, Kucherlapati, Raju, Perou, Charles M, Hayes, D Neil, Gibbs, Richard, Marra, Marco, Mills, Gordon B, Lander, Eric, Spellman, Paul, Wilson, Richard, Sander, Chris, Weinstein, John, Meyerson, Matthew, Gabriel, Stacey, Laird, Peter W, Haussler, David, Getz, Gad, Chin, Lynda, Network, TCGA Research, Benz, Christopher, Barrett, Wendi, Ostrom, Quinn, Wolinsky, Yingli, Bose, Bikash, Boulos, Paul T, Boulos, Madgy, Brown, Jenn, Czerinski, Christine, Eppley, Matthew, Kempista, Thelma, Kitko, Teresa, Koyfman, Yakov, Rabeno, Brenda, Rastogi, Pawan, Sugarman, Michael, Swanson, Patricia, Yalamanchii, Kennedy, Otey, Ilana P, Liu, Yingchun Spring, Xiao, Yonghong, Auman, J Todd, Chen, Peng-Chieh, Hadjipanayis, Angela, Lee, Eunjung, Lee, Semin, Park, Peter J, Seidman, Jonathan, Yang, Lixing, Kalkanis, Steven, Poisson, Laila M, Raghunathan, Aditya, Scarpace, Lisa, Bressler, Ryan, and Eakin, Andrea

Subjects
Biological Sciences, Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Genetics, Brain Disorders, Brain Cancer, Biotechnology, Orphan Drug, Cancer, Cancer Genomics, Neurosciences, Human Genome, Rare Diseases, Precision Medicine, 2.1 Biological and endogenous factors, 4.1 Discovery and preclinical testing of markers and technologies, 5.1 Pharmaceuticals, 4.2 Evaluation of markers and technologies, Brain Neoplasms, Female, Gene Expression Profiling, Gene Regulatory Networks, Glioblastoma, Humans, Male, Mutation, Proteome, Signal Transduction, TCGA Research Network, Medical and Health Sciences, Developmental Biology, Biological sciences, Biomedical and clinical sciences
Abstract

We describe the landscape of somatic genomic alterations based on multidimensional and comprehensive characterization of more than 500 glioblastoma tumors (GBMs). We identify several novel mutated genes as well as complex rearrangements of signature receptors, including EGFR and PDGFRA. TERT promoter mutations are shown to correlate with elevated mRNA expression, supporting a role in telomerase reactivation. Correlative analyses confirm that the survival advantage of the proneural subtype is conferred by the G-CIMP phenotype, and MGMT DNA methylation may be a predictive biomarker for treatment response only in classical subtype GBM. Integrative analysis of genomic and proteomic profiles challenges the notion of therapeutic inhibition of a pathway as an alternative to inhibition of the target itself. These data will facilitate the discovery of therapeutic and diagnostic target candidates, the validation of research and clinical observations and the generation of unanticipated hypotheses that can advance our molecular understanding of this lethal cancer.

Published
2013

18. Comprehensive genomic characterization of squamous cell lung cancers

Author

Hammerman, Peter S, Lawrence, Michael S, Voet, Douglas, Jing, Rui, Cibulskis, Kristian, Sivachenko, Andrey, Stojanov, Petar, McKenna, Aaron, Lander, Eric S, Gabriel, Stacey, Getz, Gad, Sougnez, Carrie, Imielinski, Marcin, Helman, Elena, Hernandez, Bryan, Pho, Nam H, Meyerson, Matthew, Chu, Andy, Chun, Hye-Jung E, Mungall, Andrew J, Pleasance, Erin, Gordon Robertson, A, Sipahimalani, Payal, Stoll, Dominik, Balasundaram, Miruna, Birol, Inanc, Butterfield, Yaron SN, Chuah, Eric, Coope, Robin JN, Corbett, Richard, Dhalla, Noreen, Guin, Ranabir, He, An, Hirst, Carrie, Hirst, Martin, Holt, Robert A, Lee, Darlene, Li, Haiyan I, Mayo, Michael, Moore, Richard A, Mungall, Karen, Ming Nip, Ka, Olshen, Adam, Schein, Jacqueline E, Slobodan, Jared R, Tam, Angela, Thiessen, Nina, Varhol, Richard, Zeng, Thomas, Zhao, Yongjun, Jones, Steven JM, Marra, Marco A, Saksena, Gordon, Cherniack, Andrew D, Schumacher, Stephen E, Tabak, Barbara, Carter, Scott L, Nguyen, Huy, Onofrio, Robert C, Crenshaw, Andrew, Ardlie, Kristin, Beroukhim, Rameen, Winckler, Wendy, Protopopov, Alexei, Zhang, Jianhua, Hadjipanayis, Angela, Lee, Semin, Xi, Ruibin, Yang, Lixing, Ren, Xiaojia, Zhang, Hailei, Shukla, Sachet, Chen, Peng-Chieh, Haseley, Psalm, Lee, Eunjung, Chin, Lynda, Park, Peter J, Kucherlapati, Raju, Socci, Nicholas D, Liang, Yupu, Schultz, Nikolaus, Borsu, Laetitia, Lash, Alex E, Viale, Agnes, Sander, Chris, Ladanyi, Marc, Todd Auman, J, Hoadley, Katherine A, Wilkerson, Matthew D, Shi, Yan, Liquori, Christina, Meng, Shaowu, Li, Ling, Turman, Yidi J, Topal, Michael D, and Tan, Donghui

Subjects
Biological Sciences, Biomedical and Clinical Sciences, Genetics, Oncology and Carcinogenesis, Rare Diseases, Biotechnology, Cancer Genomics, Human Genome, Lung, Cancer, Lung Cancer, Orphan Drug, 2.1 Biological and endogenous factors, Adenocarcinoma, Adenocarcinoma of Lung, Carcinoma, Squamous Cell, DNA Mutational Analysis, Gene Deletion, Gene Expression Profiling, Gene Expression Regulation, Neoplastic, Genes, p16, Genes, p53, Genome, Human, Genomics, Humans, Lung Neoplasms, Molecular Targeted Therapy, Mutation, Mutation Rate, Phosphatidylinositol 3-Kinases, Signal Transduction, Cancer Genome Atlas Research Network, General Science & Technology
Abstract

Lung squamous cell carcinoma is a common type of lung cancer, causing approximately 400,000 deaths per year worldwide. Genomic alterations in squamous cell lung cancers have not been comprehensively characterized, and no molecularly targeted agents have been specifically developed for its treatment. As part of The Cancer Genome Atlas, here we profile 178 lung squamous cell carcinomas to provide a comprehensive landscape of genomic and epigenomic alterations. We show that the tumour type is characterized by complex genomic alterations, with a mean of 360 exonic mutations, 165 genomic rearrangements, and 323 segments of copy number alteration per tumour. We find statistically recurrent mutations in 11 genes, including mutation of TP53 in nearly all specimens. Previously unreported loss-of-function mutations are seen in the HLA-A class I major histocompatibility gene. Significantly altered pathways included NFE2L2 and KEAP1 in 34%, squamous differentiation genes in 44%, phosphatidylinositol-3-OH kinase pathway genes in 47%, and CDKN2A and RB1 in 72% of tumours. We identified a potential therapeutic target in most tumours, offering new avenues of investigation for the treatment of squamous cell lung cancers.

Published
2012

19. Medulloblastoma exome sequencing uncovers subtype-specific somatic mutations.

Author

Pugh, Trevor J, Weeraratne, Shyamal Dilhan, Archer, Tenley C, Pomeranz Krummel, Daniel A, Auclair, Daniel, Bochicchio, James, Carneiro, Mauricio O, Carter, Scott L, Cibulskis, Kristian, Erlich, Rachel L, Greulich, Heidi, Lawrence, Michael S, Lennon, Niall J, McKenna, Aaron, Meldrim, James, Ramos, Alex H, Ross, Michael G, Russ, Carsten, Shefler, Erica, Sivachenko, Andrey, Sogoloff, Brian, Stojanov, Petar, Tamayo, Pablo, Mesirov, Jill P, Amani, Vladimir, Teider, Natalia, Sengupta, Soma, Francois, Jessica Pierre, Northcott, Paul A, Taylor, Michael D, Yu, Furong, Crabtree, Gerald R, Kautzman, Amanda G, Gabriel, Stacey B, Getz, Gad, Jäger, Natalie, Jones, David TW, Lichter, Peter, Pfister, Stefan M, Roberts, Thomas M, Meyerson, Matthew, Pomeroy, Scott L, and Cho, Yoon-Jae

Subjects
Humans, Medulloblastoma, Cerebellar Neoplasms, DNA Helicases, Histone-Lysine N-Methyltransferase, Intracellular Signaling Peptides and Proteins, DNA-Binding Proteins, Receptors, Cell Surface, Neoplasm Proteins, Proto-Oncogene Proteins, Nuclear Proteins, Transcription Factors, Repressor Proteins, Signal Transduction, Protein Structure, Tertiary, Mutation, Genome, Human, Models, Molecular, Child, Tumor Suppressor Protein p53, Wnt Proteins, beta Catenin, TCF Transcription Factors, Hedgehog Proteins, DEAD-box RNA Helicases, Promoter Regions, Genetic, LIM Domain Proteins, Exome, Patched Receptors, Patched-1 Receptor, Histone Methyltransferases, Brain Disorders, Pediatric Cancer, Cancer, Human Genome, Biotechnology, Pediatric, Brain Cancer, Rare Diseases, Genetics, Neurosciences, Genetic Testing, Aetiology, 2.1 Biological and endogenous factors, General Science & Technology
Abstract

Medulloblastomas are the most common malignant brain tumours in children. Identifying and understanding the genetic events that drive these tumours is critical for the development of more effective diagnostic, prognostic and therapeutic strategies. Recently, our group and others described distinct molecular subtypes of medulloblastoma on the basis of transcriptional and copy number profiles. Here we use whole-exome hybrid capture and deep sequencing to identify somatic mutations across the coding regions of 92 primary medulloblastoma/normal pairs. Overall, medulloblastomas have low mutation rates consistent with other paediatric tumours, with a median of 0.35 non-silent mutations per megabase. We identified twelve genes mutated at statistically significant frequencies, including previously known mutated genes in medulloblastoma such as CTNNB1, PTCH1, MLL2, SMARCA4 and TP53. Recurrent somatic mutations were newly identified in an RNA helicase gene, DDX3X, often concurrent with CTNNB1 mutations, and in the nuclear co-repressor (N-CoR) complex genes GPS2, BCOR and LDB1. We show that mutant DDX3X potentiates transactivation of a TCF promoter and enhances cell viability in combination with mutant, but not wild-type, β-catenin. Together, our study reveals the alteration of WNT, hedgehog, histone methyltransferase and now N-CoR pathways across medulloblastomas and within specific subtypes of this disease, and nominates the RNA helicase DDX3X as a component of pathogenic β-catenin signalling in medulloblastoma.

Published
2012

20. Genome Report: chromosome-scale genome assembly of the African spiny mouse (Acomys cahirinus)

Author

Nguyen, Elizabeth Dong, primary, Fard, Vahid Nikoonejad, additional, Kim, Bernard Y, additional, Collins, Sarah, additional, Galey, Miranda, additional, Nelson, Branden R, additional, Wakenight, Paul, additional, Gable, Simone M, additional, McKenna, Aaron, additional, Bammler, Theo K, additional, MacDonald, Jim, additional, Okamura, Daryl M, additional, Shendure, Jay, additional, Beier, David R, additional, Ramirez, Jan Marino, additional, Majesky, Mark W, additional, Millen, Kathleen J, additional, Tollis, Marc, additional, and Miller, Danny E, additional

Published
2023
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26. Chromosome-scale genome assembly of the African spiny mouse (Acomys cahirinus)

Author

Nguyen, Elizabeth D, primary, Nikoonejad Fard, Vahid, additional, Kim, Bernard, additional, Collins, Sarah, additional, Galey, Miranda, additional, Nelson, Branden R, additional, Wakenight, Paul, additional, Gable, Simone M, additional, McKenna, Aaron, additional, Bammler, Theo K, additional, MacDonald, Jim, additional, Okamura, Daryl M, additional, Shendure, Jay, additional, Beier, David R., additional, Marino Ramirez, Jan, additional, Majesky, Mark W, additional, Millen, Kathleen J, additional, Tollis, Marc, additional, and Miller, Danny E., additional

Published
2023
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27. Data from MAP Kinase Pathway Alterations in BRAF-Mutant Melanoma Patients with Acquired Resistance to Combined RAF/MEK Inhibition

Author

Wagle, Nikhil, primary, Van Allen, Eliezer M., primary, Treacy, Daniel J., primary, Frederick, Dennie T., primary, Cooper, Zachary A., primary, Taylor-Weiner, Amaro, primary, Rosenberg, Mara, primary, Goetz, Eva M., primary, Sullivan, Ryan J., primary, Farlow, Deborah N., primary, Friedrich, Dennis C., primary, Anderka, Kristin, primary, Perrin, Danielle, primary, Johannessen, Cory M., primary, McKenna, Aaron, primary, Cibulskis, Kristian, primary, Kryukov, Gregory, primary, Hodis, Eran, primary, Lawrence, Donald P., primary, Fisher, Sheila, primary, Getz, Gad, primary, Gabriel, Stacey B., primary, Carter, Scott L., primary, Flaherty, Keith T., primary, Wargo, Jennifer A., primary, and Garraway, Levi A., primary

Published
2023
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28. Supplementary Table S1 from Genomic Characterization of Brain Metastases Reveals Branched Evolution and Potential Therapeutic Targets

Author

Brastianos, Priscilla K., primary, Carter, Scott L., primary, Santagata, Sandro, primary, Cahill, Daniel P., primary, Taylor-Weiner, Amaro, primary, Jones, Robert T., primary, Van Allen, Eliezer M., primary, Lawrence, Michael S., primary, Horowitz, Peleg M., primary, Cibulskis, Kristian, primary, Ligon, Keith L., primary, Tabernero, Josep, primary, Seoane, Joan, primary, Martinez-Saez, Elena, primary, Curry, William T., primary, Dunn, Ian F., primary, Paek, Sun Ha, primary, Park, Sung-Hye, primary, McKenna, Aaron, primary, Chevalier, Aaron, primary, Rosenberg, Mara, primary, Barker, Frederick G., primary, Gill, Corey M., primary, Van Hummelen, Paul, primary, Thorner, Aaron R., primary, Johnson, Bruce E., primary, Hoang, Mai P., primary, Choueiri, Toni K., primary, Signoretti, Sabina, primary, Sougnez, Carrie, primary, Rabin, Michael S., primary, Lin, Nancy U., primary, Winer, Eric P., primary, Stemmer-Rachamimov, Anat, primary, Meyerson, Matthew, primary, Garraway, Levi, primary, Gabriel, Stacey, primary, Lander, Eric S., primary, Beroukhim, Rameen, primary, Batchelor, Tracy T., primary, Baselga, José, primary, Louis, David N., primary, Getz, Gad, primary, and Hahn, William C., primary

Published
2023
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29. Data from Genomic Characterization of Brain Metastases Reveals Branched Evolution and Potential Therapeutic Targets

Author

Brastianos, Priscilla K., primary, Carter, Scott L., primary, Santagata, Sandro, primary, Cahill, Daniel P., primary, Taylor-Weiner, Amaro, primary, Jones, Robert T., primary, Van Allen, Eliezer M., primary, Lawrence, Michael S., primary, Horowitz, Peleg M., primary, Cibulskis, Kristian, primary, Ligon, Keith L., primary, Tabernero, Josep, primary, Seoane, Joan, primary, Martinez-Saez, Elena, primary, Curry, William T., primary, Dunn, Ian F., primary, Paek, Sun Ha, primary, Park, Sung-Hye, primary, McKenna, Aaron, primary, Chevalier, Aaron, primary, Rosenberg, Mara, primary, Barker, Frederick G., primary, Gill, Corey M., primary, Van Hummelen, Paul, primary, Thorner, Aaron R., primary, Johnson, Bruce E., primary, Hoang, Mai P., primary, Choueiri, Toni K., primary, Signoretti, Sabina, primary, Sougnez, Carrie, primary, Rabin, Michael S., primary, Lin, Nancy U., primary, Winer, Eric P., primary, Stemmer-Rachamimov, Anat, primary, Meyerson, Matthew, primary, Garraway, Levi, primary, Gabriel, Stacey, primary, Lander, Eric S., primary, Beroukhim, Rameen, primary, Batchelor, Tracy T., primary, Baselga, José, primary, Louis, David N., primary, Getz, Gad, primary, and Hahn, William C., primary

Published
2023
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30. Supplementary Methods, Figures S1 - S20 from Genomic Characterization of Brain Metastases Reveals Branched Evolution and Potential Therapeutic Targets

Author

Brastianos, Priscilla K., primary, Carter, Scott L., primary, Santagata, Sandro, primary, Cahill, Daniel P., primary, Taylor-Weiner, Amaro, primary, Jones, Robert T., primary, Van Allen, Eliezer M., primary, Lawrence, Michael S., primary, Horowitz, Peleg M., primary, Cibulskis, Kristian, primary, Ligon, Keith L., primary, Tabernero, Josep, primary, Seoane, Joan, primary, Martinez-Saez, Elena, primary, Curry, William T., primary, Dunn, Ian F., primary, Paek, Sun Ha, primary, Park, Sung-Hye, primary, McKenna, Aaron, primary, Chevalier, Aaron, primary, Rosenberg, Mara, primary, Barker, Frederick G., primary, Gill, Corey M., primary, Van Hummelen, Paul, primary, Thorner, Aaron R., primary, Johnson, Bruce E., primary, Hoang, Mai P., primary, Choueiri, Toni K., primary, Signoretti, Sabina, primary, Sougnez, Carrie, primary, Rabin, Michael S., primary, Lin, Nancy U., primary, Winer, Eric P., primary, Stemmer-Rachamimov, Anat, primary, Meyerson, Matthew, primary, Garraway, Levi, primary, Gabriel, Stacey, primary, Lander, Eric S., primary, Beroukhim, Rameen, primary, Batchelor, Tracy T., primary, Baselga, José, primary, Louis, David N., primary, Getz, Gad, primary, and Hahn, William C., primary

Published
2023
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31. Supplementary File 3 from Genomic Characterization of Brain Metastases Reveals Branched Evolution and Potential Therapeutic Targets

Author

Brastianos, Priscilla K., primary, Carter, Scott L., primary, Santagata, Sandro, primary, Cahill, Daniel P., primary, Taylor-Weiner, Amaro, primary, Jones, Robert T., primary, Van Allen, Eliezer M., primary, Lawrence, Michael S., primary, Horowitz, Peleg M., primary, Cibulskis, Kristian, primary, Ligon, Keith L., primary, Tabernero, Josep, primary, Seoane, Joan, primary, Martinez-Saez, Elena, primary, Curry, William T., primary, Dunn, Ian F., primary, Paek, Sun Ha, primary, Park, Sung-Hye, primary, McKenna, Aaron, primary, Chevalier, Aaron, primary, Rosenberg, Mara, primary, Barker, Frederick G., primary, Gill, Corey M., primary, Van Hummelen, Paul, primary, Thorner, Aaron R., primary, Johnson, Bruce E., primary, Hoang, Mai P., primary, Choueiri, Toni K., primary, Signoretti, Sabina, primary, Sougnez, Carrie, primary, Rabin, Michael S., primary, Lin, Nancy U., primary, Winer, Eric P., primary, Stemmer-Rachamimov, Anat, primary, Meyerson, Matthew, primary, Garraway, Levi, primary, Gabriel, Stacey, primary, Lander, Eric S., primary, Beroukhim, Rameen, primary, Batchelor, Tracy T., primary, Baselga, José, primary, Louis, David N., primary, Getz, Gad, primary, and Hahn, William C., primary

Published
2023
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32. Supplementary File Legends from Genomic Characterization of Brain Metastases Reveals Branched Evolution and Potential Therapeutic Targets

Author

Brastianos, Priscilla K., primary, Carter, Scott L., primary, Santagata, Sandro, primary, Cahill, Daniel P., primary, Taylor-Weiner, Amaro, primary, Jones, Robert T., primary, Van Allen, Eliezer M., primary, Lawrence, Michael S., primary, Horowitz, Peleg M., primary, Cibulskis, Kristian, primary, Ligon, Keith L., primary, Tabernero, Josep, primary, Seoane, Joan, primary, Martinez-Saez, Elena, primary, Curry, William T., primary, Dunn, Ian F., primary, Paek, Sun Ha, primary, Park, Sung-Hye, primary, McKenna, Aaron, primary, Chevalier, Aaron, primary, Rosenberg, Mara, primary, Barker, Frederick G., primary, Gill, Corey M., primary, Van Hummelen, Paul, primary, Thorner, Aaron R., primary, Johnson, Bruce E., primary, Hoang, Mai P., primary, Choueiri, Toni K., primary, Signoretti, Sabina, primary, Sougnez, Carrie, primary, Rabin, Michael S., primary, Lin, Nancy U., primary, Winer, Eric P., primary, Stemmer-Rachamimov, Anat, primary, Meyerson, Matthew, primary, Garraway, Levi, primary, Gabriel, Stacey, primary, Lander, Eric S., primary, Beroukhim, Rameen, primary, Batchelor, Tracy T., primary, Baselga, José, primary, Louis, David N., primary, Getz, Gad, primary, and Hahn, William C., primary

Published
2023
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33. Supplementary Table S7 from The Genomic Landscape of Pediatric Ewing Sarcoma

Author

Crompton, Brian D., primary, Stewart, Chip, primary, Taylor-Weiner, Amaro, primary, Alexe, Gabriela, primary, Kurek, Kyle C., primary, Calicchio, Monica L., primary, Kiezun, Adam, primary, Carter, Scott L., primary, Shukla, Sachet A., primary, Mehta, Swapnil S., primary, Thorner, Aaron R., primary, de Torres, Carmen, primary, Lavarino, Cinzia, primary, Suñol, Mariona, primary, McKenna, Aaron, primary, Sivachenko, Andrey, primary, Cibulskis, Kristian, primary, Lawrence, Michael S., primary, Stojanov, Petar, primary, Rosenberg, Mara, primary, Ambrogio, Lauren, primary, Auclair, Daniel, primary, Seepo, Sara, primary, Blumenstiel, Brendan, primary, DeFelice, Matthew, primary, Imaz-Rosshandler, Ivan, primary, Schwarz-Cruz y Celis, Angela, primary, Rivera, Miguel N., primary, Rodriguez-Galindo, Carlos, primary, Fleming, Mark D., primary, Golub, Todd R., primary, Getz, Gad, primary, Mora, Jaume, primary, and Stegmaier, Kimberly, primary

Published
2023
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34. Supplementary Table 3 from MAP Kinase Pathway Alterations in BRAF-Mutant Melanoma Patients with Acquired Resistance to Combined RAF/MEK Inhibition

Author

Wagle, Nikhil, primary, Van Allen, Eliezer M., primary, Treacy, Daniel J., primary, Frederick, Dennie T., primary, Cooper, Zachary A., primary, Taylor-Weiner, Amaro, primary, Rosenberg, Mara, primary, Goetz, Eva M., primary, Sullivan, Ryan J., primary, Farlow, Deborah N., primary, Friedrich, Dennis C., primary, Anderka, Kristin, primary, Perrin, Danielle, primary, Johannessen, Cory M., primary, McKenna, Aaron, primary, Cibulskis, Kristian, primary, Kryukov, Gregory, primary, Hodis, Eran, primary, Lawrence, Donald P., primary, Fisher, Sheila, primary, Getz, Gad, primary, Gabriel, Stacey B., primary, Carter, Scott L., primary, Flaherty, Keith T., primary, Wargo, Jennifer A., primary, and Garraway, Levi A., primary

Published
2023
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35. Supplementary Table 2 from MAP Kinase Pathway Alterations in BRAF-Mutant Melanoma Patients with Acquired Resistance to Combined RAF/MEK Inhibition

Author

Wagle, Nikhil, primary, Van Allen, Eliezer M., primary, Treacy, Daniel J., primary, Frederick, Dennie T., primary, Cooper, Zachary A., primary, Taylor-Weiner, Amaro, primary, Rosenberg, Mara, primary, Goetz, Eva M., primary, Sullivan, Ryan J., primary, Farlow, Deborah N., primary, Friedrich, Dennis C., primary, Anderka, Kristin, primary, Perrin, Danielle, primary, Johannessen, Cory M., primary, McKenna, Aaron, primary, Cibulskis, Kristian, primary, Kryukov, Gregory, primary, Hodis, Eran, primary, Lawrence, Donald P., primary, Fisher, Sheila, primary, Getz, Gad, primary, Gabriel, Stacey B., primary, Carter, Scott L., primary, Flaherty, Keith T., primary, Wargo, Jennifer A., primary, and Garraway, Levi A., primary

Published
2023
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36. Data from The Genetic Landscape of Clinical Resistance to RAF Inhibition in Metastatic Melanoma

Author

Van Allen, Eliezer M., primary, Wagle, Nikhil, primary, Sucker, Antje, primary, Treacy, Daniel J., primary, Johannessen, Cory M., primary, Goetz, Eva M., primary, Place, Chelsea S., primary, Taylor-Weiner, Amaro, primary, Whittaker, Steven, primary, Kryukov, Gregory V., primary, Hodis, Eran, primary, Rosenberg, Mara, primary, McKenna, Aaron, primary, Cibulskis, Kristian, primary, Farlow, Deborah, primary, Zimmer, Lisa, primary, Hillen, Uwe, primary, Gutzmer, Ralf, primary, Goldinger, Simone M., primary, Ugurel, Selma, primary, Gogas, Helen J., primary, Egberts, Friederike, primary, Berking, Carola, primary, Trefzer, Uwe, primary, Loquai, Carmen, primary, Weide, Benjamin, primary, Hassel, Jessica C., primary, Gabriel, Stacey B., primary, Carter, Scott L., primary, Getz, Gad, primary, Garraway, Levi A., primary, and Schadendorf, Dirk, primary

Published
2023
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37. Supplementary Table S2 from The Genetic Landscape of Clinical Resistance to RAF Inhibition in Metastatic Melanoma

Author

Van Allen, Eliezer M., primary, Wagle, Nikhil, primary, Sucker, Antje, primary, Treacy, Daniel J., primary, Johannessen, Cory M., primary, Goetz, Eva M., primary, Place, Chelsea S., primary, Taylor-Weiner, Amaro, primary, Whittaker, Steven, primary, Kryukov, Gregory V., primary, Hodis, Eran, primary, Rosenberg, Mara, primary, McKenna, Aaron, primary, Cibulskis, Kristian, primary, Farlow, Deborah, primary, Zimmer, Lisa, primary, Hillen, Uwe, primary, Gutzmer, Ralf, primary, Goldinger, Simone M., primary, Ugurel, Selma, primary, Gogas, Helen J., primary, Egberts, Friederike, primary, Berking, Carola, primary, Trefzer, Uwe, primary, Loquai, Carmen, primary, Weide, Benjamin, primary, Hassel, Jessica C., primary, Gabriel, Stacey B., primary, Carter, Scott L., primary, Getz, Gad, primary, Garraway, Levi A., primary, and Schadendorf, Dirk, primary

Published
2023
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38. Supplementary File 2 from Genomic Characterization of Brain Metastases Reveals Branched Evolution and Potential Therapeutic Targets

Author

Brastianos, Priscilla K., primary, Carter, Scott L., primary, Santagata, Sandro, primary, Cahill, Daniel P., primary, Taylor-Weiner, Amaro, primary, Jones, Robert T., primary, Van Allen, Eliezer M., primary, Lawrence, Michael S., primary, Horowitz, Peleg M., primary, Cibulskis, Kristian, primary, Ligon, Keith L., primary, Tabernero, Josep, primary, Seoane, Joan, primary, Martinez-Saez, Elena, primary, Curry, William T., primary, Dunn, Ian F., primary, Paek, Sun Ha, primary, Park, Sung-Hye, primary, McKenna, Aaron, primary, Chevalier, Aaron, primary, Rosenberg, Mara, primary, Barker, Frederick G., primary, Gill, Corey M., primary, Van Hummelen, Paul, primary, Thorner, Aaron R., primary, Johnson, Bruce E., primary, Hoang, Mai P., primary, Choueiri, Toni K., primary, Signoretti, Sabina, primary, Sougnez, Carrie, primary, Rabin, Michael S., primary, Lin, Nancy U., primary, Winer, Eric P., primary, Stemmer-Rachamimov, Anat, primary, Meyerson, Matthew, primary, Garraway, Levi, primary, Gabriel, Stacey, primary, Lander, Eric S., primary, Beroukhim, Rameen, primary, Batchelor, Tracy T., primary, Baselga, José, primary, Louis, David N., primary, Getz, Gad, primary, and Hahn, William C., primary

Published
2023
Full Text
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39. Supplementary Methods, Figure Legends, Figures S1 - S6, Tables S1, S3 - S6, S8 - S15, S17 from The Genomic Landscape of Pediatric Ewing Sarcoma

Author

Crompton, Brian D., primary, Stewart, Chip, primary, Taylor-Weiner, Amaro, primary, Alexe, Gabriela, primary, Kurek, Kyle C., primary, Calicchio, Monica L., primary, Kiezun, Adam, primary, Carter, Scott L., primary, Shukla, Sachet A., primary, Mehta, Swapnil S., primary, Thorner, Aaron R., primary, de Torres, Carmen, primary, Lavarino, Cinzia, primary, Suñol, Mariona, primary, McKenna, Aaron, primary, Sivachenko, Andrey, primary, Cibulskis, Kristian, primary, Lawrence, Michael S., primary, Stojanov, Petar, primary, Rosenberg, Mara, primary, Ambrogio, Lauren, primary, Auclair, Daniel, primary, Seepo, Sara, primary, Blumenstiel, Brendan, primary, DeFelice, Matthew, primary, Imaz-Rosshandler, Ivan, primary, Schwarz-Cruz y Celis, Angela, primary, Rivera, Miguel N., primary, Rodriguez-Galindo, Carlos, primary, Fleming, Mark D., primary, Golub, Todd R., primary, Getz, Gad, primary, Mora, Jaume, primary, and Stegmaier, Kimberly, primary

Published
2023
Full Text
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40. Supplementary File 1 from Genomic Characterization of Brain Metastases Reveals Branched Evolution and Potential Therapeutic Targets

Author

Brastianos, Priscilla K., primary, Carter, Scott L., primary, Santagata, Sandro, primary, Cahill, Daniel P., primary, Taylor-Weiner, Amaro, primary, Jones, Robert T., primary, Van Allen, Eliezer M., primary, Lawrence, Michael S., primary, Horowitz, Peleg M., primary, Cibulskis, Kristian, primary, Ligon, Keith L., primary, Tabernero, Josep, primary, Seoane, Joan, primary, Martinez-Saez, Elena, primary, Curry, William T., primary, Dunn, Ian F., primary, Paek, Sun Ha, primary, Park, Sung-Hye, primary, McKenna, Aaron, primary, Chevalier, Aaron, primary, Rosenberg, Mara, primary, Barker, Frederick G., primary, Gill, Corey M., primary, Van Hummelen, Paul, primary, Thorner, Aaron R., primary, Johnson, Bruce E., primary, Hoang, Mai P., primary, Choueiri, Toni K., primary, Signoretti, Sabina, primary, Sougnez, Carrie, primary, Rabin, Michael S., primary, Lin, Nancy U., primary, Winer, Eric P., primary, Stemmer-Rachamimov, Anat, primary, Meyerson, Matthew, primary, Garraway, Levi, primary, Gabriel, Stacey, primary, Lander, Eric S., primary, Beroukhim, Rameen, primary, Batchelor, Tracy T., primary, Baselga, José, primary, Louis, David N., primary, Getz, Gad, primary, and Hahn, William C., primary

Published
2023
Full Text
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41. Supplementary Table 4 from MAP Kinase Pathway Alterations in BRAF-Mutant Melanoma Patients with Acquired Resistance to Combined RAF/MEK Inhibition

Author

Wagle, Nikhil, primary, Van Allen, Eliezer M., primary, Treacy, Daniel J., primary, Frederick, Dennie T., primary, Cooper, Zachary A., primary, Taylor-Weiner, Amaro, primary, Rosenberg, Mara, primary, Goetz, Eva M., primary, Sullivan, Ryan J., primary, Farlow, Deborah N., primary, Friedrich, Dennis C., primary, Anderka, Kristin, primary, Perrin, Danielle, primary, Johannessen, Cory M., primary, McKenna, Aaron, primary, Cibulskis, Kristian, primary, Kryukov, Gregory, primary, Hodis, Eran, primary, Lawrence, Donald P., primary, Fisher, Sheila, primary, Getz, Gad, primary, Gabriel, Stacey B., primary, Carter, Scott L., primary, Flaherty, Keith T., primary, Wargo, Jennifer A., primary, and Garraway, Levi A., primary

Published
2023
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42. Supplementary Table 1 from MAP Kinase Pathway Alterations in BRAF-Mutant Melanoma Patients with Acquired Resistance to Combined RAF/MEK Inhibition

Author

Wagle, Nikhil, primary, Van Allen, Eliezer M., primary, Treacy, Daniel J., primary, Frederick, Dennie T., primary, Cooper, Zachary A., primary, Taylor-Weiner, Amaro, primary, Rosenberg, Mara, primary, Goetz, Eva M., primary, Sullivan, Ryan J., primary, Farlow, Deborah N., primary, Friedrich, Dennis C., primary, Anderka, Kristin, primary, Perrin, Danielle, primary, Johannessen, Cory M., primary, McKenna, Aaron, primary, Cibulskis, Kristian, primary, Kryukov, Gregory, primary, Hodis, Eran, primary, Lawrence, Donald P., primary, Fisher, Sheila, primary, Getz, Gad, primary, Gabriel, Stacey B., primary, Carter, Scott L., primary, Flaherty, Keith T., primary, Wargo, Jennifer A., primary, and Garraway, Levi A., primary

Published
2023
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43. Supplementary Table 6 from MAP Kinase Pathway Alterations in BRAF-Mutant Melanoma Patients with Acquired Resistance to Combined RAF/MEK Inhibition

Author

Wagle, Nikhil, primary, Van Allen, Eliezer M., primary, Treacy, Daniel J., primary, Frederick, Dennie T., primary, Cooper, Zachary A., primary, Taylor-Weiner, Amaro, primary, Rosenberg, Mara, primary, Goetz, Eva M., primary, Sullivan, Ryan J., primary, Farlow, Deborah N., primary, Friedrich, Dennis C., primary, Anderka, Kristin, primary, Perrin, Danielle, primary, Johannessen, Cory M., primary, McKenna, Aaron, primary, Cibulskis, Kristian, primary, Kryukov, Gregory, primary, Hodis, Eran, primary, Lawrence, Donald P., primary, Fisher, Sheila, primary, Getz, Gad, primary, Gabriel, Stacey B., primary, Carter, Scott L., primary, Flaherty, Keith T., primary, Wargo, Jennifer A., primary, and Garraway, Levi A., primary

Published
2023
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44. Supplementary Figures from MAP Kinase Pathway Alterations in BRAF-Mutant Melanoma Patients with Acquired Resistance to Combined RAF/MEK Inhibition

Author

Wagle, Nikhil, primary, Van Allen, Eliezer M., primary, Treacy, Daniel J., primary, Frederick, Dennie T., primary, Cooper, Zachary A., primary, Taylor-Weiner, Amaro, primary, Rosenberg, Mara, primary, Goetz, Eva M., primary, Sullivan, Ryan J., primary, Farlow, Deborah N., primary, Friedrich, Dennis C., primary, Anderka, Kristin, primary, Perrin, Danielle, primary, Johannessen, Cory M., primary, McKenna, Aaron, primary, Cibulskis, Kristian, primary, Kryukov, Gregory, primary, Hodis, Eran, primary, Lawrence, Donald P., primary, Fisher, Sheila, primary, Getz, Gad, primary, Gabriel, Stacey B., primary, Carter, Scott L., primary, Flaherty, Keith T., primary, Wargo, Jennifer A., primary, and Garraway, Levi A., primary

Published
2023
Full Text
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45. Supplementary Table Legends from The Genetic Landscape of Clinical Resistance to RAF Inhibition in Metastatic Melanoma

Author

Van Allen, Eliezer M., primary, Wagle, Nikhil, primary, Sucker, Antje, primary, Treacy, Daniel J., primary, Johannessen, Cory M., primary, Goetz, Eva M., primary, Place, Chelsea S., primary, Taylor-Weiner, Amaro, primary, Whittaker, Steven, primary, Kryukov, Gregory V., primary, Hodis, Eran, primary, Rosenberg, Mara, primary, McKenna, Aaron, primary, Cibulskis, Kristian, primary, Farlow, Deborah, primary, Zimmer, Lisa, primary, Hillen, Uwe, primary, Gutzmer, Ralf, primary, Goldinger, Simone M., primary, Ugurel, Selma, primary, Gogas, Helen J., primary, Egberts, Friederike, primary, Berking, Carola, primary, Trefzer, Uwe, primary, Loquai, Carmen, primary, Weide, Benjamin, primary, Hassel, Jessica C., primary, Gabriel, Stacey B., primary, Carter, Scott L., primary, Getz, Gad, primary, Garraway, Levi A., primary, and Schadendorf, Dirk, primary

Published
2023
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46. Data Supplement from MAP Kinase Pathway Alterations in BRAF-Mutant Melanoma Patients with Acquired Resistance to Combined RAF/MEK Inhibition

Author

Wagle, Nikhil, primary, Van Allen, Eliezer M., primary, Treacy, Daniel J., primary, Frederick, Dennie T., primary, Cooper, Zachary A., primary, Taylor-Weiner, Amaro, primary, Rosenberg, Mara, primary, Goetz, Eva M., primary, Sullivan, Ryan J., primary, Farlow, Deborah N., primary, Friedrich, Dennis C., primary, Anderka, Kristin, primary, Perrin, Danielle, primary, Johannessen, Cory M., primary, McKenna, Aaron, primary, Cibulskis, Kristian, primary, Kryukov, Gregory, primary, Hodis, Eran, primary, Lawrence, Donald P., primary, Fisher, Sheila, primary, Getz, Gad, primary, Gabriel, Stacey B., primary, Carter, Scott L., primary, Flaherty, Keith T., primary, Wargo, Jennifer A., primary, and Garraway, Levi A., primary

Published
2023
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47. Supplementary Table 5 from MAP Kinase Pathway Alterations in BRAF-Mutant Melanoma Patients with Acquired Resistance to Combined RAF/MEK Inhibition

Author

Wagle, Nikhil, primary, Van Allen, Eliezer M., primary, Treacy, Daniel J., primary, Frederick, Dennie T., primary, Cooper, Zachary A., primary, Taylor-Weiner, Amaro, primary, Rosenberg, Mara, primary, Goetz, Eva M., primary, Sullivan, Ryan J., primary, Farlow, Deborah N., primary, Friedrich, Dennis C., primary, Anderka, Kristin, primary, Perrin, Danielle, primary, Johannessen, Cory M., primary, McKenna, Aaron, primary, Cibulskis, Kristian, primary, Kryukov, Gregory, primary, Hodis, Eran, primary, Lawrence, Donald P., primary, Fisher, Sheila, primary, Getz, Gad, primary, Gabriel, Stacey B., primary, Carter, Scott L., primary, Flaherty, Keith T., primary, Wargo, Jennifer A., primary, and Garraway, Levi A., primary

Published
2023
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48. Prospective Derivation of a Living Organoid Biobank of Colorectal Cancer Patients

Author

van de Wetering, Marc, Francies, Hayley E., Francis, Joshua M., Bounova, Gergana, Iorio, Francesco, Pronk, Apollo, van Houdt, Winan, van Gorp, Joost, Taylor-Weiner, Amaro, Kester, Lennart, McLaren-Douglas, Anne, Blokker, Joyce, Jaksani, Sridevi, Bartfeld, Sina, Volckman, Richard, van Sluis, Peter, Li, Vivian S.W., Seepo, Sara, Sekhar Pedamallu, Chandra, Cibulskis, Kristian, Carter, Scott L., McKenna, Aaron, Lawrence, Michael S., Lichtenstein, Lee, Stewart, Chip, Koster, Jan, Versteeg, Rogier, van Oudenaarden, Alexander, Saez-Rodriguez, Julio, Vries, Robert G.J., Getz, Gad, Wessels, Lodewyk, Stratton, Michael R., McDermott, Ultan, Meyerson, Matthew, Garnett, Mathew J., and Clevers, Hans

Published
2015
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