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Your search keyword '"Shah, Sohrab P"' showing total 723 results
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723 results on '"Shah, Sohrab P"'

1. Cancer phylogenetic tree inference at scale from 1000s of single cell genomes

Author

Salehi, Sohrab, Dorri, Fatemeh, Chern, Kevin, Kabeer, Farhia, Rusk, Nicole, Funnell, Tyler, Williams, Marc J., Lai, Daniel, Andronescu, Mirela, Campbell, Kieran R., McPherson, Andrew, Aparicio, Samuel, Roth, Andrew, Shah, Sohrab P., and Bouchard-Côté, Alexandre

Subjects
Phylogenetics, Cancer evolution, Bayesian statistics, MCMC, Copy number evolution, PDX, Triple negative breast cancer, Archaeology, CC1-960, Science
Abstract

A new generation of scalable single cell whole genome sequencing (scWGS) methods allows unprecedented high resolution measurement of the evolutionary dynamics of cancer cell populations. Phylogenetic reconstruction is central to identifying sub-populations and distinguishing the mutational processes that gave rise to them. Existing phylogenetic tree building models do not scale to the tens of thousands of high resolution genomes achievable with current scWGS methods. We constructed a phylogenetic model and associated Bayesian inference procedure, sitka, specifically for scWGS data. The method is based on a novel phylogenetic encoding of copy number (CN) data, the sitka transformation, that simplifies the site dependencies induced by rearrangements while still forming a sound foundation to phylogenetic inference. The sitka transformation allows us to design novel scalable Markov chain Monte Carlo (MCMC) algorithms. Moreover, we introduce a novel point mutation calling method that incorporates the CN data and the underlying phylogenetic tree to overcome the low per-cell coverage of scWGS. We demonstrate our method on three single cell datasets, including a novel PDX series, and analyse the topological properties of the inferred trees. Sitka is freely available at https://github.com/UBC-Stat-ML/sitkatree.git

Published
2023
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2. Transformer-based segmentation of adnexal lesions and ovarian implants in CT images

Author

Rangnekar, Aneesh, Boehm, Kevin M., Aherne, Emily A., Nikolovski, Ines, Gangai, Natalie, Liu, Ying, Zamarin, Dimitry, Roche, Kara L., Shah, Sohrab P., Lakhman, Yulia, and Veeraraghavan, Harini

Subjects
Electrical Engineering and Systems Science - Image and Video Processing
Abstract

Two self-supervised pretrained transformer-based segmentation models (SMIT and Swin UNETR) fine-tuned on a dataset of ovarian cancer CT images provided reasonably accurate delineations of the tumors in an independent test dataset. Tumors in the adnexa were segmented more accurately by both transformers (SMIT and Swin UNETR) than the omental implants. AI-assisted labeling performed on 72 out of 245 omental implants resulted in smaller manual editing effort of 39.55 mm compared to full manual correction of partial labels of 106.49 mm and resulted in overall improved accuracy performance. Both SMIT and Swin UNETR did not generate any false detection of omental metastases in the urinary bladder and relatively few false detections in the small bowel, with 2.16 cc on average for SMIT and 7.37 cc for Swin UNETR respectively.

Published
2024

4. DNA liquid biopsy-based prediction of cancer-associated venous thromboembolism

Author

Jee, Justin, Brannon, A. Rose, Singh, Rohan, Derkach, Andriy, Fong, Christopher, Lee, Adrian, Gray, Lauren, Pichotta, Karl, Luthra, Anisha, Diosdado, Monica, Haque, Mohammad, Guo, Jiannan, Hernandez, Jennifer, Garg, Kavita, Wilhelm, Clare, Arcila, Maria E., Pavlakis, Nick, Clarke, Stephen, Shah, Sohrab P., Razavi, Pedram, Reis-Filho, Jorge S., Ladanyi, Marc, Schultz, Nikolaus, Zwicker, Jeffrey, Berger, Michael F., Li, Bob T., and Mantha, Simon

Published
2024
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6. Single-cell mtDNA dynamics in tumors is driven by coregulation of nuclear and mitochondrial genomes

Author

Kim, Minsoo, Gorelick, Alexander N., Vàzquez-García, Ignacio, Williams, Marc J., Salehi, Sohrab, Shi, Hongyu, Weiner, Adam C., Ceglia, Nick, Funnell, Tyler, Park, Tricia, Boscenco, Sonia, O’Flanagan, Ciara H., Jiang, Hui, Grewal, Diljot, Tang, Cerise, Rusk, Nicole, Gammage, Payam A., McPherson, Andrew, Aparicio, Sam, Shah, Sohrab P., and Reznik, Ed

Published
2024
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7. Epigenetic dysregulation from chromosomal transit in micronuclei.

Author

Agustinus, Albert S, Al-Rawi, Duaa, Dameracharla, Bhargavi, Raviram, Ramya, Jones, Bailey SCL, Stransky, Stephanie, Scipioni, Lorenzo, Luebeck, Jens, Di Bona, Melody, Norkunaite, Danguole, Myers, Robert M, Duran, Mercedes, Choi, Seongmin, Weigelt, Britta, Yomtoubian, Shira, McPherson, Andrew, Toufektchan, Eléonore, Keuper, Kristina, Mischel, Paul S, Mittal, Vivek, Shah, Sohrab P, Maciejowski, John, Storchova, Zuzana, Gratton, Enrico, Ly, Peter, Landau, Dan, Bakhoum, Mathieu F, Koche, Richard P, Sidoli, Simone, Bafna, Vineet, David, Yael, and Bakhoum, Samuel F

Subjects
Chromosomes, Chromatin, Animals, Humans, Mice, Neoplasms, Chromosomal Instability, Histones, Epigenesis, Genetic, Human Genome, Genetics, Cancer, General Science & Technology
Abstract

Chromosomal instability (CIN) and epigenetic alterations are characteristics of advanced and metastatic cancers1-4, but whether they are mechanistically linked is unknown. Here we show that missegregation of mitotic chromosomes, their sequestration in micronuclei5,6 and subsequent rupture of the micronuclear envelope7 profoundly disrupt normal histone post-translational modifications (PTMs), a phenomenon conserved across humans and mice, as well as in cancer and non-transformed cells. Some of the changes in histone PTMs occur because of the rupture of the micronuclear envelope, whereas others are inherited from mitotic abnormalities before the micronucleus is formed. Using orthogonal approaches, we demonstrate that micronuclei exhibit extensive differences in chromatin accessibility, with a strong positional bias between promoters and distal or intergenic regions, in line with observed redistributions of histone PTMs. Inducing CIN causes widespread epigenetic dysregulation, and chromosomes that transit in micronuclei experience heritable abnormalities in their accessibility long after they have been reincorporated into the primary nucleus. Thus, as well as altering genomic copy number, CIN promotes epigenetic reprogramming and heterogeneity in cancer.

Published
2023

11. Ovarian cancer mutational processes drive site-specific immune evasion

Author

Vázquez-García, Ignacio, Uhlitz, Florian, Ceglia, Nicholas, Lim, Jamie L. P., Wu, Michelle, Mohibullah, Neeman, Niyazov, Juliana, Ruiz, Arvin Eric B., Boehm, Kevin M., Bojilova, Viktoria, Fong, Christopher J., Funnell, Tyler, Grewal, Diljot, Havasov, Eliyahu, Leung, Samantha, Pasha, Arfath, Patel, Druv M., Pourmaleki, Maryam, Rusk, Nicole, Shi, Hongyu, Vanguri, Rami, Williams, Marc J., Zhang, Allen W., Broach, Vance, Chi, Dennis S., Da Cruz Paula, Arnaud, Gardner, Ginger J., Kim, Sarah H., Lennon, Matthew, Long Roche, Kara, Sonoda, Yukio, Zivanovic, Oliver, Kundra, Ritika, Viale, Agnes, Derakhshan, Fatemeh N., Geneslaw, Luke, Issa Bhaloo, Shirin, Maroldi, Ana, Nunez, Rahelly, Pareja, Fresia, Stylianou, Anthe, Vahdatinia, Mahsa, Bykov, Yonina, Grisham, Rachel N., Liu, Ying L., Lakhman, Yulia, Nikolovski, Ines, Kelly, Daniel, Gao, Jianjiong, Schietinger, Andrea, Hollmann, Travis J., Bakhoum, Samuel F., Soslow, Robert A., Ellenson, Lora H., Abu-Rustum, Nadeem R., Aghajanian, Carol, Friedman, Claire F., McPherson, Andrew, Weigelt, Britta, Zamarin, Dmitriy, and Shah, Sohrab P.

Published
2022
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12. Single-cell genomic variation induced by mutational processes in cancer

Author

Funnell, Tyler, O’Flanagan, Ciara H., Williams, Marc J., McPherson, Andrew, McKinney, Steven, Kabeer, Farhia, Lee, Hakwoo, Salehi, Sohrab, Vázquez-García, Ignacio, Shi, Hongyu, Leventhal, Emily, Masud, Tehmina, Eirew, Peter, Yap, Damian, Zhang, Allen W., Lim, Jamie L. P., Wang, Beixi, Brimhall, Jazmine, Biele, Justina, Ting, Jerome, Au, Vinci, Van Vliet, Michael, Liu, Yi Fei, Beatty, Sean, Lai, Daniel, Pham, Jenifer, Grewal, Diljot, Abrams, Douglas, Havasov, Eliyahu, Leung, Samantha, Bojilova, Viktoria, Moore, Richard A., Rusk, Nicole, Uhlitz, Florian, Ceglia, Nicholas, Weiner, Adam C., Zaikova, Elena, Douglas, J. Maxwell, Zamarin, Dmitriy, Weigelt, Britta, Kim, Sarah H., Da Cruz Paula, Arnaud, Reis-Filho, Jorge S., Martin, Spencer D., Li, Yangguang, Xu, Hong, de Algara, Teresa Ruiz, Lee, So Ra, Llanos, Viviana Cerda, Huntsman, David G., McAlpine, Jessica N., Shah, Sohrab P., and Aparicio, Samuel

Published
2022
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13. Non-coding somatic mutations converge on the PAX8 pathway in ovarian cancer.

Author

Corona, Rosario I, Seo, Ji-Heui, Lin, Xianzhi, Hazelett, Dennis J, Reddy, Jessica, Fonseca, Marcos AS, Abassi, Forough, Lin, Yvonne G, Mhawech-Fauceglia, Paulette Y, Shah, Sohrab P, Huntsman, David G, Gusev, Alexander, Karlan, Beth Y, Berman, Benjamin P, Freedman, Matthew L, Gayther, Simon A, and Lawrenson, Kate

Subjects
Ovary, Humans, Ovarian Neoplasms, Muscle Proteins, DNA-Binding Proteins, Transcription Factors, Repressor Proteins, Epigenesis, Genetic, Gene Expression Regulation, Neoplastic, Binding Sites, Mutation, Polymorphism, Single Nucleotide, Adult, Aged, Middle Aged, Female, Kruppel-Like Transcription Factors, Gene Regulatory Networks, Enhancer Elements, Genetic, Gene Knockout Techniques, Epigenomics, PAX8 Transcription Factor, Whole Genome Sequencing, Carcinoma, Ovarian Epithelial, Chromatin Immunoprecipitation Sequencing, RNA-Seq
Abstract

The functional consequences of somatic non-coding mutations in ovarian cancer (OC) are unknown. To identify regulatory elements (RE) and genes perturbed by acquired non-coding variants, here we establish epigenomic and transcriptomic landscapes of primary OCs using H3K27ac ChIP-seq and RNA-seq, and then integrate these with whole genome sequencing data from 232 OCs. We identify 25 frequently mutated regulatory elements, including an enhancer at 6p22.1 which associates with differential expression of ZSCAN16 (P = 6.6 × 10-4) and ZSCAN12 (P = 0.02). CRISPR/Cas9 knockout of this enhancer induces downregulation of both genes. Globally, there is an enrichment of single nucleotide variants in active binding sites for TEAD4 (P = 6 × 10-11) and its binding partner PAX8 (P = 2×10-10), a known lineage-specific transcription factor in OC. In addition, the collection of cis REs associated with PAX8 comprise the most frequently mutated set of enhancers in OC (P = 0.003). These data indicate that non-coding somatic mutations disrupt the PAX8 transcriptional network during OC development.

Published
2020

14. Overall survival with circulating tumor DNA-guided therapy in advanced non-small-cell lung cancer

Author

Jee, Justin, Lebow, Emily S., Yeh, Randy, Das, Jeeban P., Namakydoust, Azadeh, Paik, Paul K., Chaft, Jamie E., Jayakumaran, Gowtham, Rose Brannon, A., Benayed, Ryma, Zehir, Ahmet, Donoghue, Mark, Schultz, Nikolaus, Chakravarty, Debyani, Kundra, Ritika, Madupuri, Ramyasree, Murciano-Goroff, Yonina R., Tu, Hai-Yan, Xu, Chong-Rui, Martinez, Andrés, Wilhelm, Clare, Galle, Jesse, Daly, Bobby, Yu, Helena A., Offin, Michael, Hellmann, Matthew D., Lito, Piro, Arbour, Kathryn C., Zauderer, Marjorie G., Kris, Mark G., Ng, Kenneth K., Eng, Juliana, Preeshagul, Isabel, Victoria Lai, W., Fiore, John J., Iqbal, Afsheen, Molena, Daniela, Rocco, Gaetano, Park, Bernard J., Lim, Lee P., Li, Mark, Tong-Li, Candace, De Silva, Madhawa, Chan, David L., Diakos, Connie I., Itchins, Malinda, Clarke, Stephen, Pavlakis, Nick, Lee, Adrian, Rekhtman, Natasha, Chang, Jason, Travis, William D., Riely, Gregory J., Solit, David B., Gonen, Mithat, Rusch, Valerie W., Rimner, Andreas, Gomez, Daniel, Drilon, Alexander, Scher, Howard I., Shah, Sohrab P., Berger, Michael F., Arcila, Maria E., Ladanyi, Marc, Levine, Ross L., Shen, Ronglai, Razavi, Pedram, Reis-Filho, Jorge S., Jones, David R., Rudin, Charles M., Isbell, James M., and Li, Bob T.

Published
2022
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15. Multimodal integration of radiology, pathology and genomics for prediction of response to PD-(L)1 blockade in patients with non-small cell lung cancer

Author

Vanguri, Rami S., Luo, Jia, Aukerman, Andrew T., Egger, Jacklynn V., Fong, Christopher J., Horvat, Natally, Pagano, Andrew, Araujo-Filho, Jose de Arimateia Batista, Geneslaw, Luke, Rizvi, Hira, Sosa, Ramon, Boehm, Kevin M., Yang, Soo-Ryum, Bodd, Francis M., Ventura, Katia, Hollmann, Travis J., Ginsberg, Michelle S., Gao, Jianjiong, Hellmann, Matthew D., Sauter, Jennifer L., and Shah, Sohrab P.

Published
2022
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17. Fundamental immune–oncogenicity trade-offs define driver mutation fitness

Author

Hoyos, David, Zappasodi, Roberta, Schulze, Isabell, Sethna, Zachary, de Andrade, Kelvin César, Bajorin, Dean F., Bandlamudi, Chaitanya, Callahan, Margaret K., Funt, Samuel A., Hadrup, Sine R., Holm, Jeppe S., Rosenberg, Jonathan E., Shah, Sohrab P., Vázquez-García, Ignacio, Weigelt, Britta, Wu, Michelle, Zamarin, Dmitriy, Campitelli, Laura F., Osborne, Edward J., Klinger, Mark, Robins, Harlan S., Khincha, Payal P., Savage, Sharon A., Balachandran, Vinod P., Wolchok, Jedd D., Hellmann, Matthew D., Merghoub, Taha, Levine, Arnold J., Łuksza, Marta, and Greenbaum, Benjamin D.

Published
2022
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18. Multimodal data integration using machine learning improves risk stratification of high-grade serous ovarian cancer

Author

Boehm, Kevin M., Aherne, Emily A., Ellenson, Lora, Nikolovski, Ines, Alghamdi, Mohammed, Vázquez-García, Ignacio, Zamarin, Dmitriy, Long Roche, Kara, Liu, Ying, Patel, Druv, Aukerman, Andrew, Pasha, Arfath, Rose, Doori, Selenica, Pier, Causa Andrieu, Pamela I., Fong, Chris, Capanu, Marinela, Reis-Filho, Jorge S., Vanguri, Rami, Veeraraghavan, Harini, Gangai, Natalie, Sosa, Ramon, Leung, Samantha, McPherson, Andrew, Gao, JianJiong, Lakhman, Yulia, and Shah, Sohrab P.

Published
2022
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19. Clonal somatic copy number altered driver events inform drug sensitivity in high-grade serous ovarian cancer

Author

Martins, Filipe Correia, Couturier, Dominique-Laurent, de Santiago, Ines, Sauer, Carolin Margarethe, Vias, Maria, Angelova, Mihaela, Sanders, Deborah, Piskorz, Anna, Hall, James, Hosking, Karen, Amirthanayagam, Anumithra, Cosulich, Sabina, Carnevalli, Larissa, Davies, Barry, Watkins, Thomas B. K., Funingana, Ionut G., Bolton, Helen, Haldar, Krishnayan, Latimer, John, Baldwin, Peter, Crawford, Robin, Eldridge, Matthew, Basu, Bristi, Jimenez-Linan, Mercedes, Mcpherson, Andrew W., McGranahan, Nicholas, Litchfield, Kevin, Shah, Sohrab P., McNeish, Iain, Caldas, Carlos, Evan, Gerard, Swanton, Charles, and Brenton, James D.

Published
2022
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20. Accurate determination of CRISPR-mediated gene fitness in transplantable tumours

Author

Eirew, Peter, O’Flanagan, Ciara, Ting, Jerome, Salehi, Sohrab, Brimhall, Jazmine, Wang, Beixi, Biele, Justina, Algara, Teresa, Lee, So Ra, Hoang, Corey, Yap, Damian, McKinney, Steven, Bates, Cherie, Kong, Esther, Lai, Daniel, Beatty, Sean, Andronescu, Mirela, Zaikova, Elena, Funnell, Tyler, Ceglia, Nicholas, Chia, Stephen, Gelmon, Karen, Mar, Colin, Shah, Sohrab, Roth, Andrew, Bouchard-Côté, Alexandre, and Aparicio, Samuel

Published
2022
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21. Single-cell profiling reveals a memory B cell-like subtype of follicular lymphoma with increased transformation risk

Author

Wang, Xuehai, Nissen, Michael, Gracias, Deanne, Kusakabe, Manabu, Simkin, Guillermo, Jiang, Aixiang, Duns, Gerben, Sarkozy, Clementine, Hilton, Laura, Chavez, Elizabeth A., Segat, Gabriela C., Wong, Rachel, Kim, Jubin, Aoki, Tomohiro, Islam, Rashedul, May, Christina, Hung, Stacy, Tyshchenko, Kate, Brinkman, Ryan R., Hirst, Martin, Karsan, Aly, Freeman, Ciara, Sehn, Laurie H., Morin, Ryan D., Roth, Andrew J., Savage, Kerry J., Craig, Jeffrey W., Shah, Sohrab P., Steidl, Christian, Scott, David W., and Weng, Andrew P.

Published
2022
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25. The driver landscape of sporadic chordoma.

Author

Tarpey, Patrick S, Behjati, Sam, Young, Matthew D, Martincorena, Inigo, Alexandrov, Ludmil B, Farndon, Sarah J, Guzzo, Charlotte, Hardy, Claire, Latimer, Calli, Butler, Adam P, Teague, Jon W, Shlien, Adam, Futreal, P Andrew, Shah, Sohrab, Bashashati, Ali, Jamshidi, Farzad, Nielsen, Torsten O, Huntsman, David, Baumhoer, Daniel, Brandner, Sebastian, Wunder, Jay, Dickson, Brendan, Cogswell, Patricia, Sommer, Josh, Phillips, Joanna J, Amary, M Fernanda, Tirabosco, Roberto, Pillay, Nischalan, Yip, Stephen, Stratton, Michael R, Flanagan, Adrienne M, and Campbell, Peter J

Subjects
Cell Line, Tumor, Humans, Chordoma, Bone Neoplasms, T-Box Domain Proteins, Fetal Proteins, Vesicular Transport Proteins, Case-Control Studies, Gene Duplication, Mutation, Polymorphism, Single Nucleotide, Phosphatidylinositol 3-Kinases, Class I Phosphatidylinositol 3-Kinases, Cell Line, Tumor, Polymorphism, Single Nucleotide
Abstract

Chordoma is a malignant, often incurable bone tumour showing notochordal differentiation. Here, we defined the somatic driver landscape of 104 cases of sporadic chordoma. We reveal somatic duplications of the notochordal transcription factor brachyury (T) in up to 27% of cases. These variants recapitulate the rearrangement architecture of the pathogenic germline duplications of T that underlie familial chordoma. In addition, we find potentially clinically actionable PI3K signalling mutations in 16% of cases. Intriguingly, one of the most frequently altered genes, mutated exclusively by inactivating mutation, was LYST (10%), which may represent a novel cancer gene in chordoma.Chordoma is a rare often incurable malignant bone tumour. Here, the authors investigate driver mutations of sporadic chordoma in 104 cases, revealing duplications in notochordal transcription factor brachyury (T), PI3K signalling mutations, and mutations in LYST, a potential novel cancer gene in chordoma.

Published
2017

26. Kronos: a workflow assembler for genome analytics and informatics

Author

Taghiyar, M Jafar, Rosner, Jamie, Grewal, Diljot, Grande, Bruno M, Aniba, Radhouane, Grewal, Jasleen, Boutros, Paul C, Morin, Ryan D, Bashashati, Ali, and Shah, Sohrab P

Subjects
High-Throughput Nucleotide Sequencing, Software, Whole Genome Sequencing, genomics, workflow, pipeline, reproducibility
Abstract

BackgroundThe field of next-generation sequencing informatics has matured to a point where algorithmic advances in sequence alignment and individual feature detection methods have stabilized. Practical and robust implementation of complex analytical workflows (where such tools are structured into "best practices" for automated analysis of next-generation sequencing datasets) still requires significant programming investment and expertise.ResultsWe present Kronos, a software platform for facilitating the development and execution of modular, auditable, and distributable bioinformatics workflows. Kronos obviates the need for explicit coding of workflows by compiling a text configuration file into executable Python applications. Making analysis modules would still require programming. The framework of each workflow includes a run manager to execute the encoded workflows locally (or on a cluster or cloud), parallelize tasks, and log all runtime events. The resulting workflows are highly modular and configurable by construction, facilitating flexible and extensible meta-applications that can be modified easily through configuration file editing. The workflows are fully encoded for ease of distribution and can be instantiated on external systems, a step toward reproducible research and comparative analyses. We introduce a framework for building Kronos components that function as shareable, modular nodes in Kronos workflows.ConclusionsThe Kronos platform provides a standard framework for developers to implement custom tools, reuse existing tools, and contribute to the community at large. Kronos is shipped with both Docker and Amazon Web Services Machine Images. It is free, open source, and available through the Python Package Index and at https://github.com/jtaghiyar/kronos.

Published
2017

27. Enhancing Knowledge Discovery from Cancer Genomics Data with Galaxy

Author

Albuquerque, Marco A, Grande, Bruno M, Ritch, Elie J, Pararajalingam, Prasath, Jessa, Selin, Krzywinski, Martin, Grewal, Jasleen K, Shah, Sohrab P, Boutros, Paul C, and Morin, Ryan D

Subjects
Human Genome, Hematology, Biotechnology, Lymphoma, Genetics, Cancer, Rare Diseases, Algorithms, Genomics, Humans, Internet, Lymphoma, Large B-Cell, Diffuse, Mutation, Software, Workflow, Driver, Genome, Pipeline, Tool, Cloud
Abstract

The field of cancer genomics has demonstrated the power of massively parallel sequencing techniques to inform on the genes and specific alterations that drive tumor onset and progression. Although large comprehensive sequence data sets continue to be made increasingly available, data analysis remains an ongoing challenge, particularly for laboratories lacking dedicated resources and bioinformatics expertise. To address this, we have produced a collection of Galaxy tools that represent many popular algorithms for detecting somatic genetic alterations from cancer genome and exome data. We developed new methods for parallelization of these tools within Galaxy to accelerate runtime and have demonstrated their usability and summarized their runtimes on multiple cloud service providers. Some tools represent extensions or refinement of existing toolkits to yield visualizations suited to cohort-wide cancer genomic analysis. For example, we present Oncocircos and Oncoprintplus, which generate data-rich summaries of exome-derived somatic mutation. Workflows that integrate these to achieve data integration and visualizations are demonstrated on a cohort of 96 diffuse large B-cell lymphomas and enabled the discovery of multiple candidate lymphoma-related genes. Our toolkit is available from our GitHub repository as Galaxy tool and dependency definitions and has been deployed using virtualization on multiple platforms including Docker.

Published
2017

28. Joint Inference of Genome Structure and Content in Heterogeneous Tumour Samples

Author

McPherson, Andrew, Roth, Andrew, Ha, Gavin, Shah, Sohrab P., Chauve, Cedric, and Sahinalp, S. Cenk

Subjects
Quantitative Biology - Genomics, Computer Science - Computational Engineering, Finance, and Science
Abstract

For a genomically unstable cancer, a single tumour biopsy will often contain a mixture of competing tumour clones. These tumour clones frequently differ with respect to their genomic content (copy number of each gene) and structure (order of genes on each chromosome). Modern bulk genome sequencing mixes the signals of tumour clones and contaminating normal cells, complicating inference of genomic content and structure. We propose a method to unmix tumour and contaminating normal signals and jointly predict genomic structure and content of each tumour clone. We use genome graphs to represent tumour clones, and model the likelihood of the observed reads given clones and mixing proportions. Our use of haplotype blocks allows us to accurately measure allele specific read counts, and infer allele specific copy number for each clone. The proposed method is a heuristic local search based on applying incremental, locally optimal modifications of the genome graphs. Using simulated data, we show that our method predicts copy counts and gene adjacencies with reasonable accuracy., Comment: Presented at RECOMB 2015

Published
2015

29. Multimodal histopathologic models stratify hormone receptor-positive early breast cancer

Author

Boehm, Kevin Michael, primary, El Nahhas, Omar S. M., additional, Marra, Antonio, additional, Selenica, Pier, additional, Wen, Hannah Y, additional, Weigelt, Britta, additional, Paul, Evan D, additional, Cekan, Pavol, additional, Erber, Ramona, additional, Loeffler, Chiara M. L., additional, Guerini-Rocco, Elena, additional, Fusco, Nicola, additional, Frascarelli, Chiara, additional, Mane, Eltjona, additional, Munzone, Elisabetta, additional, Dellapasqua, Silvia, additional, Zagami, Paola, additional, Curigliano, Giuseppe, additional, Razavi, Pedram, additional, Reis-Filho, Jorge S., additional, Pareja, Fresia, additional, Chandarlapaty, Sarat, additional, Shah, Sohrab P, additional, and Kather, Jakob Nikolas, additional

Published
2024
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30. FIGURE 4 from Weakly Supervised Deep Learning Predicts Immunotherapy Response in Solid Tumors Based on PD-L1 Expression

Author

Ligero, Marta, primary, Serna, Garazi, primary, El Nahhas, Omar S.M., primary, Sansano, Irene, primary, Mauchanski, Siarhei, primary, Viaplana, Cristina, primary, Calderaro, Julien, primary, Toledo, Rodrigo A., primary, Dienstmann, Rodrigo, primary, Vanguri, Rami S., primary, Sauter, Jennifer L., primary, Sanchez-Vega, Francisco, primary, Shah, Sohrab P., primary, Ramón y Cajal, Santiago, primary, Garralda, Elena, primary, Nuciforo, Paolo, primary, Perez-Lopez, Raquel, primary, and Kather, Jakob Nikolas, primary

Published
2024
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31. Divergent clonal selection dominates medulloblastoma at recurrence

Author

Morrissy, A Sorana, Garzia, Livia, Shih, David JH, Zuyderduyn, Scott, Huang, Xi, Skowron, Patryk, Remke, Marc, Cavalli, Florence MG, Ramaswamy, Vijay, Lindsay, Patricia E, Jelveh, Salomeh, Donovan, Laura K, Wang, Xin, Luu, Betty, Zayne, Kory, Li, Yisu, Mayoh, Chelsea, Thiessen, Nina, Mercier, Eloi, Mungall, Karen L, Ma, Yusanne, Tse, Kane, Zeng, Thomas, Shumansky, Karey, Roth, Andrew JL, Shah, Sohrab, Farooq, Hamza, Kijima, Noriyuki, Holgado, Borja L, Lee, John JY, Matan-Lithwick, Stuart, Liu, Jessica, Mack, Stephen C, Manno, Alex, Michealraj, KA, Nor, Carolina, Peacock, John, Qin, Lei, Reimand, Juri, Rolider, Adi, Thompson, Yuan Y, Wu, Xiaochong, Pugh, Trevor, Ally, Adrian, Bilenky, Mikhail, Butterfield, Yaron SN, Carlsen, Rebecca, Cheng, Young, Chuah, Eric, Corbett, Richard D, Dhalla, Noreen, He, An, Lee, Darlene, Li, Haiyan I, Long, William, Mayo, Michael, Plettner, Patrick, Qian, Jenny Q, Schein, Jacqueline E, Tam, Angela, Wong, Tina, Birol, Inanc, Zhao, Yongjun, Faria, Claudia C, Pimentel, José, Nunes, Sofia, Shalaby, Tarek, Grotzer, Michael, Pollack, Ian F, Hamilton, Ronald L, Li, Xiao-Nan, Bendel, Anne E, Fults, Daniel W, Walter, Andrew W, Kumabe, Toshihiro, Tominaga, Teiji, Collins, V Peter, Cho, Yoon-Jae, Hoffman, Caitlin, Lyden, David, Wisoff, Jeffrey H, Garvin, James H, Stearns, Duncan S, Massimi, Luca, Schüller, Ulrich, Sterba, Jaroslav, Zitterbart, Karel, Puget, Stephanie, Ayrault, Olivier, Dunn, Sandra E, Tirapelli, Daniela PC, Carlotti, Carlos G, Wheeler, Helen, Hallahan, Andrew R, Ingram, Wendy, MacDonald, Tobey J, Olson, Jeffrey J, Van Meir, Erwin G, Lee, Ji-Yeoun, and Wang, Kyu-Chang

Subjects
Pediatric, Biotechnology, Genetics, Brain Disorders, Human Genome, Brain Cancer, Rare Diseases, Cancer, Animals, Cerebellar Neoplasms, Clone Cells, Craniospinal Irradiation, DNA Mutational Analysis, Disease Models, Animal, Drosophila melanogaster, Female, Genome, Human, Humans, Male, Medulloblastoma, Mice, Molecular Targeted Therapy, Neoplasm Recurrence, Local, Radiotherapy, Image-Guided, Selection, Genetic, Signal Transduction, Xenograft Model Antitumor Assays, General Science & Technology
Abstract

The development of targeted anti-cancer therapies through the study of cancer genomes is intended to increase survival rates and decrease treatment-related toxicity. We treated a transposon-driven, functional genomic mouse model of medulloblastoma with 'humanized' in vivo therapy (microneurosurgical tumour resection followed by multi-fractionated, image-guided radiotherapy). Genetic events in recurrent murine medulloblastoma exhibit a very poor overlap with those in matched murine diagnostic samples (

Published
2016

32. Weakly supervised deep learning predicts immunotherapy response in solid tumors based on PD-L1 expression

Author

Ligero, Marta, primary, Serna, Garazi, additional, El Nahhas, Omar S.M., additional, Sansano, Irene, additional, Mauchanski, Siarhei, additional, Viaplana, Cristina, additional, Calderaro, Julien, additional, Toledo, Rodrigo A, additional, Dienstmann, Rodrigo, additional, Vanguri, Rami S., additional, Sauter, Jennifer L., additional, Sanchez-Vega, Francisco, additional, Shah, Sohrab P, additional, Ramón y Cajal, Santiago, additional, Garralda, Elena, additional, Nuciforo, Paolo, additional, Perez-Lopez, Raquel, additional, and Kather, Jakob Nikolas, additional

Published
2023
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33. TMEM30A loss-of-function mutations drive lymphomagenesis and confer therapeutically exploitable vulnerability in B-cell lymphoma

Author

Ennishi, Daisuke, Healy, Shannon, Bashashati, Ali, Saberi, Saeed, Hother, Christoffer, Mottok, Anja, Chan, Fong Chun, Chong, Lauren, Abraham, Libin, Kridel, Robert, Boyle, Merrill, Meissner, Barbara, Aoki, Tomohiro, Takata, Katsuyoshi, Woolcock, Bruce W., Viganò, Elena, Gold, Michael, Molday, Laurie L., Molday, Robert S., Telenius, Adele, Li, Michael Y., Wretham, Nicole, Dos Santos, Nancy, Wong, Mark, Viller, Natasja N., Uger, Robert A., Duns, Gerben, Baticados, Abigail, Madero, Angel, Bristow, Brianna N., Farinha, Pedro, Slack, Graham W., Ben-Neriah, Susana, Lai, Daniel, Zhang, Allen W., Salehi, Sohrab, Shulha, Hennady P., Chiu, Derek S., Mostafavi, Sara, Gerrie, Alina S., Huang, Da Wei, Rushton, Christopher, Villa, Diego, Sehn, Laurie H., Savage, Kerry J., Mungall, Andrew J., Weng, Andrew P., Bally, Marcel B., Morin, Ryan D., Cohen Freue, Gabriela V., Staudt, Louis M., Connors, Joseph M., Marra, Marco A., Shah, Sohrab P., Gascoyne, Randy D., Scott, David W., and Steidl, Christian

Published
2020
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34. Multifocal endometriotic lesions associated with cancer are clonal and carry a high mutation burden

Author

Anglesio, Michael S, Bashashati, Ali, Wang, Yi Kan, Senz, Janine, Ha, Gavin, Yang, Winnie, Aniba, Mohamed R, Prentice, Leah M, Farahani, Hossein, Li Chang, Hector, Karnezis, Anthony N, Marra, Marco A, Yong, Paul J, Hirst, Martin, Gilks, Blake, Shah, Sohrab P, and Huntsman, David G

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Rare Diseases, Ovarian Cancer, Human Genome, Cancer, Genetics, Endometriosis, 2.1 Biological and endogenous factors, Aetiology, Adenocarcinoma, Clear Cell, Class I Phosphatidylinositol 3-Kinases, DNA, Neoplasm, DNA-Binding Proteins, Female, Genome-Wide Association Study, Humans, Mutation, Nuclear Proteins, Ovarian Neoplasms, Phosphatidylinositol 3-Kinases, Precancerous Conditions, Sequence Analysis, DNA, Transcription Factors, endometriosis, ovarian cancer, clear cell carcinoma, cancer precursor, sequencing, Clinical Sciences, Pathology, Clinical sciences, Oncology and carcinogenesis
Abstract

Endometriosis is a significant risk factor for clear cell and endometrioid ovarian cancers and is often found contiguous with these cancers. Using whole-genome shotgun sequencing of seven clear cell ovarian carcinomas (CCC) and targeted sequencing in synchronous endometriosis, we have investigated how this carcinoma may evolve from endometriosis. In every case we observed multiple tumour-associated somatic mutations in at least one concurrent endometriotic lesion. ARID1A and PIK3CA mutations appeared consistently in concurrent endometriosis when present in the primary CCC. In several cases, one or more endometriotic lesions carried the near-complete complement of somatic mutations present in the index CCC tumour. Ancestral mutations were detected in both tumour-adjacent and -distant endometriotic lesions, regardless of any cytological atypia. These findings provide objective evidence that multifocal benign endometriotic lesions are clonally related and that CCCs arising in these patients progress from endometriotic lesions that may already carry sufficient cancer-associated mutations to be considered neoplasms themselves, albeit with low malignant potential. We speculate that genomically distinct classes of endometriosis exist and that ovarian endometriosis with high mutational burden represents one class at high risk for malignant transformation.

Published
2015

35. Regulation of pH by Carbonic Anhydrase 9 Mediates Survival of Pancreatic Cancer Cells With Activated KRAS in Response to Hypoxia

Author

McDonald, Paul C., Chafe, Shawn C., Brown, Wells S., Saberi, Saeed, Swayampakula, Mridula, Venkateswaran, Geetha, Nemirovsky, Oksana, Gillespie, Jordan A., Karasinska, Joanna M., Kalloger, Steve E., Supuran, Claudiu T., Schaeffer, David F., Bashashati, Ali, Shah, Sohrab P., Topham, James T., Yapp, Donald T., Li, Jinyang, Renouf, Daniel J., Stanger, Ben Z., and Dedhar, Shoukat

Published
2019
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37. Author Correction: Fundamental immune–oncogenicity trade-offs define driver mutation fitness

Author

Hoyos, David, Zappasodi, Roberta, Schulze, Isabell, Sethna, Zachary, de Andrade, Kelvin César, Bajorin, Dean F., Bandlamudi, Chaitanya, Callahan, Margaret K., Funt, Samuel A., Hadrup, Sine R., Holm, Jeppe S., Rosenberg, Jonathan E., Shah, Sohrab P., Vázquez-García, Ignacio, Weigelt, Britta, Wu, Michelle, Zamarin, Dmitriy, Campitelli, Laura F., Osborne, Edward J., Klinger, Mark, Robins, Harlan S., Khincha, Payal P., Savage, Sharon A., Balachandran, Vinod P., Wolchok, Jedd D., Hellmann, Matthew D., Merghoub, Taha, Levine, Arnold J., Łuksza, Marta, and Greenbaum, Benjamin D.

Published
2022
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38. Small cell carcinoma of the ovary, hypercalcemic type, displays frequent inactivating germline and somatic mutations in SMARCA4

Author

Ramos, Pilar, Karnezis, Anthony N, Craig, David W, Sekulic, Aleksandar, Russell, Megan L, Hendricks, William PD, Corneveaux, Jason J, Barrett, Michael T, Shumansky, Karey, Yang, Yidong, Shah, Sohrab P, Prentice, Leah M, Marra, Marco A, Kiefer, Jeffrey, Zismann, Victoria L, McEachron, Troy A, Salhia, Bodour, Prat, Jaime, D'Angelo, Emanuela, Clarke, Blaise A, Pressey, Joseph G, Farley, John H, Anthony, Stephen P, Roden, Richard BS, Cunliffe, Heather E, Huntsman, David G, and Trent, Jeffrey M

Subjects
Cancer, Rare Diseases, Ovarian Cancer, Genetics, Base Sequence, Carcinoma, Small Cell, Chromatin Assembly and Disassembly, Chromosome Mapping, Computational Biology, DNA Helicases, DNA, Complementary, Electrophoresis, Polyacrylamide Gel, Exome, Female, Gene Library, Humans, Immunohistochemistry, Molecular Sequence Data, Mutation, Nuclear Proteins, Ovarian Neoplasms, Sequence Analysis, DNA, Transcription Factors, Biological Sciences, Medical and Health Sciences, Developmental Biology
Abstract

Small cell carcinoma of the ovary of hypercalcemic type (SCCOHT) is an extremely rare, aggressive cancer affecting children and young women. We identified germline and somatic inactivating mutations in the SWI/SNF chromatin-remodeling gene SMARCA4 in 75% (9/12) of SCCOHT cases in addition to SMARCA4 protein loss in 82% (14/17) of SCCOHT tumors but in only 0.4% (2/485) of other primary ovarian tumors. These data implicate SMARCA4 in SCCOHT oncogenesis.

Published
2014

39. Tumor-associated antigen PRAME exhibits dualistic functions that are targetable in diffuse large B cell lymphoma

Author

Takata, Katsuyoshi, Chong, Lauren C., Ennishi, Daisuke, Aoki, Tomohiro, Li, Michael Yu, Thakur, Avinash, Healy, Shannon, Vigano, Elena, Dao, Tao, Kwon, Daniel, Duns, Gerben, Nielsen, Julie S., Ben-Neriah, Susana, Tse, Ethan, Hung, Stacy S., Boyle, Merrill, Mun, Sung Soo, Bourne, Christopher M., Woolcock, Bruce, Telenius, Adele, Kishida, Makoto, Rai, Shinya, Zhang, Allen W., Bashashati, Ali, Saberi, Saeed, DAntonio, Gianluca, Nelson, Brad H., Shah, Sohrab P., Hoodless, Pamela A., Melnick, Ari M., Gascoyne, Randy D., Connors, Joseph M., Scheinberg, David A., Beguelin, Wendy, Scott, David W., and Steidl, Christian

Subjects
Oncology, Experimental, Gene mutations -- Research, Immune response -- Genetic aspects, Non-Hodgkin's lymphomas -- Genetic aspects -- Care and treatment, Tumor antigens -- Genetic aspects, Cancer -- Research, Health care industry
Abstract

PRAME is a prominent member of the cancer testis antigen family of proteins, which triggers autologous T cell-mediated immune responses. Integrative genomic analysis in diffuse large B cell lymphoma (DLBCL) uncovered recurrent and highly focal deletions of 22q11.22, including the PRAME gene, which were associated with poor outcome. PRAME-deleted tumors showed cytotoxic T cell immune escape and were associated with cold tumor microenvironments. In addition, PRAME downmodulation was strongly associated with somatic EZH2 Y641 mutations in DLBCL. In turn, PRC2-regulated genes were repressed in isogenic PRAME-KO lymphoma cell lines, and PRAME was found to directly interact with EZH2 as a negative regulator. EZH2 inhibition with EPZ-6438 abrogated these extrinsic and intrinsic effects, leading to PRAME expression and microenvironment restoration in vivo. Our data highlight multiple functions of PRAME during lymphomagenesis and provide a preclinical rationale for synergistic therapies combining epigenetic reprogramming with PRAME-targeted therapies., Introduction The current treatment standard of combined immunochemotherapy with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) has achieved significant improvement in patient outcomes in diffuse large B cell lymphoma (DLBCL) [...]

Published
2022
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40. TERT promoter mutation in adult granulosa cell tumor of the ovary

Author

Pilsworth, Jessica A., Cochrane, Dawn R., Xia, Zhouchunyang, Aubert, Geraldine, Färkkilä, Anniina E.M., Horlings, Hugo M., Yanagida, Satoshi, Yang, Winnie, Lim, Jamie L.P., Wang, Yi Kan, Bashashati, Ali, Keul, Jacqueline, Wong, Adele, Norris, Kevin, Brucker, Sara Y., Taran, Florin-Andrei, Krämer, Bernhard, Staebler, Annette, van Meurs, Hannah, Oliva, Esther, Shah, Sohrab P., Kommoss, Stefan, Kommoss, Friedrich, Gilks, C. Blake, Baird, Duncan M., and Huntsman, David G.

Published
2018
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41. Probabilistic cell-type assignment of single-cell RNA-seq for tumor microenvironment profiling

Author

Zhang, Allen W., O’Flanagan, Ciara, Chavez, Elizabeth A., Lim, Jamie L. P., Ceglia, Nicholas, McPherson, Andrew, Wiens, Matt, Walters, Pascale, Chan, Tim, Hewitson, Brittany, Lai, Daniel, Mottok, Anja, Sarkozy, Clementine, Chong, Lauren, Aoki, Tomohiro, Wang, Xuehai, Weng, Andrew P, McAlpine, Jessica N., Aparicio, Samuel, Steidl, Christian, Campbell, Kieran R., and Shah, Sohrab P.

Published
2019
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42. The clonal and mutational evolution spectrum of primary triple-negative breast cancers

Author

Shah, Sohrab P, Roth, Andrew, Goya, Rodrigo, Oloumi, Arusha, Ha, Gavin, Zhao, Yongjun, Turashvili, Gulisa, Ding, Jiarui, Tse, Kane, Haffari, Gholamreza, Bashashati, Ali, Prentice, Leah M, Khattra, Jaswinder, Burleigh, Angela, Yap, Damian, Bernard, Virginie, McPherson, Andrew, Shumansky, Karey, Crisan, Anamaria, Giuliany, Ryan, Heravi-Moussavi, Alireza, Rosner, Jamie, Lai, Daniel, Birol, Inanc, Varhol, Richard, Tam, Angela, Dhalla, Noreen, Zeng, Thomas, Ma, Kevin, Chan, Simon K, Griffith, Malachi, Moradian, Annie, Cheng, S-W Grace, Morin, Gregg B, Watson, Peter, Gelmon, Karen, Chia, Stephen, Chin, Suet-Feung, Curtis, Christina, Rueda, Oscar M, Pharoah, Paul D, Damaraju, Sambasivarao, Mackey, John, Hoon, Kelly, Harkins, Timothy, Tadigotla, Vasisht, Sigaroudinia, Mahvash, Gascard, Philippe, Tlsty, Thea, Costello, Joseph F, Meyer, Irmtraud M, Eaves, Connie J, Wasserman, Wyeth W, Jones, Steven, Huntsman, David, Hirst, Martin, Caldas, Carlos, Marra, Marco A, and Aparicio, Samuel

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Breast Cancer, Cancer, 4.1 Discovery and preclinical testing of markers and technologies, Detection, screening and diagnosis, Alleles, Breast Neoplasms, Clone Cells, DNA Copy Number Variations, DNA Mutational Analysis, Disease Progression, Evolution, Molecular, Female, Gene Expression Profiling, Gene Expression Regulation, Neoplastic, Genotype, High-Throughput Nucleotide Sequencing, Humans, INDEL Mutation, Mutation, Point Mutation, Precision Medicine, Reproducibility of Results, Sequence Analysis, RNA, General Science & Technology
Abstract

Primary triple-negative breast cancers (TNBCs), a tumour type defined by lack of oestrogen receptor, progesterone receptor and ERBB2 gene amplification, represent approximately 16% of all breast cancers. Here we show in 104 TNBC cases that at the time of diagnosis these cancers exhibit a wide and continuous spectrum of genomic evolution, with some having only a handful of coding somatic aberrations in a few pathways, whereas others contain hundreds of coding somatic mutations. High-throughput RNA sequencing (RNA-seq) revealed that only approximately 36% of mutations are expressed. Using deep re-sequencing measurements of allelic abundance for 2,414 somatic mutations, we determine for the first time-to our knowledge-in an epithelial tumour subtype, the relative abundance of clonal frequencies among cases representative of the population. We show that TNBCs vary widely in their clonal frequencies at the time of diagnosis, with the basal subtype of TNBC showing more variation than non-basal TNBC. Although p53 (also known as TP53), PIK3CA and PTEN somatic mutations seem to be clonally dominant compared to other genes, in some tumours their clonal frequencies are incompatible with founder status. Mutations in cytoskeletal, cell shape and motility proteins occurred at lower clonal frequencies, suggesting that they occurred later during tumour progression. Taken together, our results show that understanding the biology and therapeutic responses of patients with TNBC will require the determination of individual tumour clonal genotypes.

Published
2012

43. Eleven grand challenges in single-cell data science

Author

Lähnemann, David, Köster, Johannes, Szczurek, Ewa, McCarthy, Davis J., Hicks, Stephanie C., Robinson, Mark D., Vallejos, Catalina A., Campbell, Kieran R., Beerenwinkel, Niko, Mahfouz, Ahmed, Pinello, Luca, Skums, Pavel, Stamatakis, Alexandros, Attolini, Camille Stephan-Otto, Aparicio, Samuel, Baaijens, Jasmijn, Balvert, Marleen, Barbanson, Buys de, Cappuccio, Antonio, Corleone, Giacomo, Dutilh, Bas E., Florescu, Maria, Guryev, Victor, Holmer, Rens, Jahn, Katharina, Lobo, Thamar Jessurun, Keizer, Emma M., Khatri, Indu, Kielbasa, Szymon M., Korbel, Jan O., Kozlov, Alexey M., Kuo, Tzu-Hao, Lelieveldt, Boudewijn P.F., Mandoiu, Ion I., Marioni, John C., Marschall, Tobias, Mölder, Felix, Niknejad, Amir, Rączkowska, Alicja, Reinders, Marcel, Ridder, Jeroen de, Saliba, Antoine-Emmanuel, Somarakis, Antonios, Stegle, Oliver, Theis, Fabian J., Yang, Huan, Zelikovsky, Alex, McHardy, Alice C., Raphael, Benjamin J., Shah, Sohrab P., and Schönhuth, Alexander

Published
2020
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44. Chemogenomic profiling of breast cancer patient-derived xenografts reveals targetable vulnerabilities for difficult-to-treat tumors

Author

Savage, Paul, Pacis, Alain, Kuasne, Hellen, Liu, Leah, Lai, Daniel, Wan, Adrian, Dankner, Matthew, Martinez, Constanza, Muñoz-Ramos, Valentina, Pilon, Virginie, Monast, Anie, Zhao, Hong, Souleimanova, Margarita, Annis, Matthew G., Aguilar-Mahecha, Adriana, Lafleur, Josiane, Bertos, Nicholas R., Asselah, Jamil, Bouganim, Nathaniel, Petrecca, Kevin, Siegel, Peter M., Omeroglu, Atilla, Shah, Sohrab P., Aparicio, Samuel, Basik, Mark, Meterissian, Sarkis, and Park, Morag

Published
2020
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46. Genetic profiling of MYC and BCL2 in diffuse large B-cell lymphoma determines cell-of-origin–specific clinical impact

Author

Ennishi, Daisuke, Mottok, Anja, Ben-Neriah, Susana, Shulha, Hennady P., Farinha, Pedro, Chan, Fong Chun, Meissner, Barbara, Boyle, Merrill, Hother, Christoffer, Kridel, Robert, Lai, Daniel, Saberi, Saeed, Bashashati, Ali, Shah, Sohrab P., Morin, Ryan D., Marra, Marco A., Savage, Kerry J., Sehn, Laurie H., Steidl, Christian, Connors, Joseph M., Gascoyne, Randy D., and Scott, David W.

Published
2017
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48. Abstract 102: Transient chromosomal instability as a driver of ovarian cancer genome evolution

Author

Vazquez-Garcia, Ignacio, primary, Uhlitz, Florian, additional, Williams, Marc J., additional, Li, Jun, additional, Shi, Hongyu, additional, Freeman, Samuel, additional, Myers, Matthew, additional, Consortium, MSK SPECTRUM, additional, Weigelt, Britta, additional, Zamarin, Dmitriy, additional, McPherson, Andrew, additional, Bakhoum, Samuel F., additional, and Shah, Sohrab P., additional

Published
2023
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50. Chafe et al Supplementary Materials and Methods from Targeting Hypoxia-Induced Carbonic Anhydrase IX Enhances Immune-Checkpoint Blockade Locally and Systemically

Author

Chafe, Shawn C., primary, McDonald, Paul C., primary, Saberi, Saeed, primary, Nemirovsky, Oksana, primary, Venkateswaran, Geetha, primary, Burugu, Samantha, primary, Gao, Dongxia, primary, Delaidelli, Alberto, primary, Kyle, Alastair H., primary, Baker, Jennifer H.E., primary, Gillespie, Jordan A., primary, Bashashati, Ali, primary, Minchinton, Andrew I., primary, Zhou, Youwen, primary, Shah, Sohrab P., primary, and Dedhar, Shoukat, primary

Published
2023
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