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321 results on '"Bourgon, Richard"'

1. Automated Clinical Data Extraction with Knowledge Conditioned LLMs

Author

Li, Diya, Kadav, Asim, Gao, Aijing, Li, Rui, and Bourgon, Richard

Subjects
Computer Science - Computation and Language, Computer Science - Artificial Intelligence
Abstract

The extraction of lung lesion information from clinical and medical imaging reports is crucial for research on and clinical care of lung-related diseases. Large language models (LLMs) can be effective at interpreting unstructured text in reports, but they often hallucinate due to a lack of domain-specific knowledge, leading to reduced accuracy and posing challenges for use in clinical settings. To address this, we propose a novel framework that aligns generated internal knowledge with external knowledge through in-context learning (ICL). Our framework employs a retriever to identify relevant units of internal or external knowledge and a grader to evaluate the truthfulness and helpfulness of the retrieved internal-knowledge rules, to align and update the knowledge bases. Our knowledge-conditioned approach also improves the accuracy and reliability of LLM outputs by addressing the extraction task in two stages: (i) lung lesion finding detection and primary structured field parsing, followed by (ii) further parsing of lesion description text into additional structured fields. Experiments with expert-curated test datasets demonstrate that this ICL approach can increase the F1 score for key fields (lesion size, margin and solidity) by an average of 12.9% over existing ICL methods.

Published
2024

2. Improving Precancerous Case Characterization via Transformer-based Ensemble Learning

Author

Zhong, Yizhen, Xiao, Jiajie, Vetterli, Thomas, Matin, Mahan, Loo, Ellen, Lin, Jimmy, Bourgon, Richard, and Shapira, Ofer

Subjects
Computer Science - Machine Learning
Abstract

The application of natural language processing (NLP) to cancer pathology reports has been focused on detecting cancer cases, largely ignoring precancerous cases. Improving the characterization of precancerous adenomas assists in developing diagnostic tests for early cancer detection and prevention, especially for colorectal cancer (CRC). Here we developed transformer-based deep neural network NLP models to perform the CRC phenotyping, with the goal of extracting precancerous lesion attributes and distinguishing cancer and precancerous cases. We achieved 0.914 macro-F1 scores for classifying patients into negative, non-advanced adenoma, advanced adenoma and CRC. We further improved the performance to 0.923 using an ensemble of classifiers for cancer status classification and lesion size named entity recognition (NER). Our results demonstrated the potential of using NLP to leverage real-world health record data to facilitate the development of diagnostic tests for early cancer prevention.

Published
2022

4. Activation of NF-κB and p300/CBP potentiates cancer chemoimmunotherapy through induction of MHC-I antigen presentation

Author

Zhou, Yixuan, Bastian, Ingmar Niels, Long, Mark D, Dow, Michelle, Li, Weihua, Liu, Tao, Ngu, Rachael Katie, Antonucci, Laura, Huang, Jian Yu, Phung, Qui T, Zhao, Xi-He, Banerjee, Sourav, Lin, Xue-Jia, Wang, Hongxia, Dang, Brian, Choi, Sylvia, Karin, Daniel, Su, Hua, Ellisman, Mark H, Jamieson, Christina, Bosenberg, Marcus, Cheng, Zhang, Haybaeck, Johannes, Kenner, Lukas, Fisch, Kathleen M, Bourgon, Richard, Hernandez, Genevive, Lill, Jennie R, Liu, Song, Carter, Hannah, Mellman, Ira, Karin, Michael, and Shalapour, Shabnam

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Immunology, Cancer, Animals, Antigen Presentation, Antineoplastic Agents, Apoptosis, B7-H1 Antigen, Biomarkers, Tumor, CD8-Positive T-Lymphocytes, Cell Proliferation, Drug Therapy, Combination, Gene Expression Regulation, Neoplastic, Histocompatibility Antigens Class I, Humans, Immune Checkpoint Inhibitors, Immunotherapy, Mice, NF-kappa B, Neoplasms, Oxaliplatin, Prognosis, Survival Rate, Tumor Cells, Cultured, Xenograft Model Antitumor Assays, p300-CBP Transcription Factors, histone acetylation, MHC-I, antigen presentation, immune checkpoint inhibitors, NF-κB
Abstract

Many cancers evade immune rejection by suppressing major histocompatibility class I (MHC-I) antigen processing and presentation (AgPP). Such cancers do not respond to immune checkpoint inhibitor therapies (ICIT) such as PD-1/PD-L1 [PD-(L)1] blockade. Certain chemotherapeutic drugs augment tumor control by PD-(L)1 inhibitors through potentiation of T-cell priming but whether and how chemotherapy enhances MHC-I-dependent cancer cell recognition by cytotoxic T cells (CTLs) is not entirely clear. We now show that the lysine acetyl transferases p300/CREB binding protein (CBP) control MHC-I AgPPM expression and neoantigen amounts in human cancers. Moreover, we found that two distinct DNA damaging drugs, the platinoid oxaliplatin and the topoisomerase inhibitor mitoxantrone, strongly up-regulate MHC-I AgPP in a manner dependent on activation of nuclear factor kappa B (NF-κB), p300/CBP, and other transcription factors, but independently of autocrine IFNγ signaling. Accordingly, NF-κB and p300 ablations prevent chemotherapy-induced MHC-I AgPP and abrogate rejection of low MHC-I-expressing tumors by reinvigorated CD8+ CTLs. Drugs like oxaliplatin and mitoxantrone may be used to overcome resistance to PD-(L)1 inhibitors in tumors that had "epigenetically down-regulated," but had not permanently lost MHC-I AgPP activity.

Published
2021

6. TGFβ attenuates tumour response to PD-L1 blockade by contributing to exclusion of T cells.

Author

Mariathasan, Sanjeev, Turley, Shannon J, Nickles, Dorothee, Castiglioni, Alessandra, Yuen, Kobe, Wang, Yulei, Kadel, Edward E, Koeppen, Hartmut, Astarita, Jillian L, Cubas, Rafael, Jhunjhunwala, Suchit, Banchereau, Romain, Yang, Yagai, Guan, Yinghui, Chalouni, Cecile, Ziai, James, Şenbabaoğlu, Yasin, Santoro, Stephen, Sheinson, Daniel, Hung, Jeffrey, Giltnane, Jennifer M, Pierce, Andrew A, Mesh, Kathryn, Lianoglou, Steve, Riegler, Johannes, Carano, Richard AD, Eriksson, Pontus, Höglund, Mattias, Somarriba, Loan, Halligan, Daniel L, van der Heijden, Michiel S, Loriot, Yohann, Rosenberg, Jonathan E, Fong, Lawrence, Mellman, Ira, Chen, Daniel S, Green, Marjorie, Derleth, Christina, Fine, Gregg D, Hegde, Priti S, Bourgon, Richard, and Powles, Thomas

Subjects
Urothelium, CD8-Positive T-Lymphocytes, Fibroblasts, Animals, Humans, Mice, Urologic Neoplasms, Neoplasm Metastasis, Disease Models, Animal, Collagen, Transforming Growth Factor beta, Antibodies, Antibodies, Monoclonal, Antigens, Neoplasm, Treatment Outcome, Immunotherapy, Cohort Studies, Signal Transduction, Drug Resistance, Neoplasm, Phenotype, Mutation, Tumor Microenvironment, Antibodies, Monoclonal, Humanized, Cell Cycle Checkpoints, B7-H1 Antigen, Monoclonal, Humanized, Antigens, Neoplasm, Disease Models, Animal, Drug Resistance, General Science & Technology
Abstract

Therapeutic antibodies that block the programmed death-1 (PD-1)-programmed death-ligand 1 (PD-L1) pathway can induce robust and durable responses in patients with various cancers, including metastatic urothelial cancer. However, these responses only occur in a subset of patients. Elucidating the determinants of response and resistance is key to improving outcomes and developing new treatment strategies. Here we examined tumours from a large cohort of patients with metastatic urothelial cancer who were treated with an anti-PD-L1 agent (atezolizumab) and identified major determinants of clinical outcome. Response to treatment was associated with CD8+ T-effector cell phenotype and, to an even greater extent, high neoantigen or tumour mutation burden. Lack of response was associated with a signature of transforming growth factor β (TGFβ) signalling in fibroblasts. This occurred particularly in patients with tumours, which showed exclusion of CD8+ T cells from the tumour parenchyma that were instead found in the fibroblast- and collagen-rich peritumoural stroma; a common phenotype among patients with metastatic urothelial cancer. Using a mouse model that recapitulates this immune-excluded phenotype, we found that therapeutic co-administration of TGFβ-blocking and anti-PD-L1 antibodies reduced TGFβ signalling in stromal cells, facilitated T-cell penetration into the centre of tumours, and provoked vigorous anti-tumour immunity and tumour regression. Integration of these three independent biological features provides the best basis for understanding patient outcome in this setting and suggests that TGFβ shapes the tumour microenvironment to restrain anti-tumour immunity by restricting T-cell infiltration.

Published
2018

7. Atezolizumab as first-line treatment in cisplatin-ineligible patients with locally advanced and metastatic urothelial carcinoma: a single-arm, multicentre, phase 2 trial.

Author

Balar, Arjun, Galsky, Matthew, Rosenberg, Jonathan, Powles, Thomas, Petrylak, Daniel, Bellmunt, Joaquim, Loriot, Yohann, Necchi, Andrea, Hoffman-Censits, Jean, Perez-Gracia, Jose, Dawson, Nancy, van der Heijden, Michiel, Dreicer, Robert, Srinivas, Sandy, Retz, Margitta, Joseph, Richard, Drakaki, Alexandra, Vaishampayan, Ulka, Sridhar, Srikala, Quinn, David, Durán, Ignacio, Shaffer, David, Eigl, Bernhard, Grivas, Petros, Yu, Evan, Li, Shi, Kadel, Edward, Boyd, Zachary, Bourgon, Richard, Hegde, Priti, Mariathasan, Sanjeev, Thåström, AnnChristine, Abidoye, Oyewale, Fine, Gregg, and Bajorin, Dean

Subjects
Aged, Aged, 80 and over, Antibodies, Monoclonal, Antibodies, Monoclonal, Humanized, Antineoplastic Agents, B7-H1 Antigen, Biomarkers, Tumor, Carcinoma, Transitional Cell, Cisplatin, Contraindications, Female, Humans, Infusions, Intravenous, Kaplan-Meier Estimate, Lymphatic Metastasis, Male, Middle Aged, Response Evaluation Criteria in Solid Tumors, Urologic Neoplasms
Abstract

BACKGROUND: First-line chemotherapy for patients with cisplatin-ineligible locally advanced or metastatic urothelial carcinoma is associated with short response duration, poor survival, and high toxicity. This study assessed atezolizumab (anti-programmed death-ligand 1 [PD-L1]) as treatment for metastatic urothelial cancer in cisplatin-ineligible patients. METHODS: For this single-arm, multicentre, phase 2 study, in 47 academic medical centres and community oncology practices in seven countries in North America and Europe, we recruited previously untreated patients with locally advanced or metastatic urothelial cancer who were cisplatin ineligible. Patients were given 1200 mg intravenous atezolizumab every 21 days until progression. The primary endpoint was independently confirmed objective response rate per Response Evaluation Criteria in Solid Tumors version 1.1 (central review), assessed in prespecified subgroups based on PD-L1 expression and in all patients. All participants who received one or more doses of atezolizumab were included in the primary and safety analyses. This study was registered with ClinicalTrials.gov, number NCT02108652. FINDINGS: Between June 9, 2014, and March 30, 2015, we enrolled 123 patients, of whom 119 received one or more doses of atezolizumab. At 17·2 months median follow-up, the objective response rate was 23% (95% CI 16 to 31), the complete response rate was 9% (n=11), and 19 of 27 responses were ongoing. Median response duration was not reached. Responses occurred across all PD-L1 and poor prognostic factor subgroups. Median progression-free survival was 2·7 months (2·1 to 4·2). Median overall survival was 15·9 months (10·4 to not estimable). Tumour mutation load was associated with response. Treatment-related adverse events that occurred in 10% or more of patients were fatigue (36 [30%] patients), diarrhoea (14 [12%] patients), and pruritus (13 [11%] patients). One treatment-related death (sepsis) occurred. Nine (8%) patients had an adverse event leading to treatment discontinuation. Immune-mediated events occurred in 14 (12%) patients. INTERPRETATION: Atezolizumab showed encouraging durable response rates, survival, and tolerability, supporting its therapeutic use in untreated metastatic urothelial cancer. FUNDING: F Hoffmann-La Roche, Genentech.

Published
2017

8. Cross-tissue organization of the fibroblast lineage

Author

Buechler, Matthew B., Pradhan, Rachana N., Krishnamurty, Akshay T., Cox, Christian, Calviello, Aslihan Karabacak, Wang, Amber W., Yang, Yeqing Angela, Tam, Lucinda, Caothien, Roger, Roose-Girma, Merone, Modrusan, Zora, Arron, Joseph R., Bourgon, Richard, Müller, Sören, and Turley, Shannon. J.

Published
2021
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9. Gremlin 1+ fibroblastic niche maintains dendritic cell homeostasis in lymphoid tissues

Author

Kapoor, Varun N., Müller, Sören, Keerthivasan, Shilpa, Brown, Markus, Chalouni, Cecile, Storm, Elaine E., Castiglioni, Alessandra, Lane, Ryan, Nitschke, Maximilian, Dominguez, Claudia X., Astarita, Jillian L., Krishnamurty, Akshay T., Carbone, Catherine B., Senbabaoglu, Yasin, Wang, Amber W., Wu, Xiumin, Cremasco, Viviana, Roose-Girma, Merone, Tam, Lucinda, Doerr, Jonas, Chen, Mark Z., Lee, Wyne P., Modrusan, Zora, Yang, Yeqing Angela, Bourgon, Richard, Sandoval, Wendy, Shaw, Andrey S., de Sauvage, Frederic J., Mellman, Ira, Moussion, Christine, and Turley, Shannon J.

Published
2021
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10. Peripheral T cell expansion predicts tumour infiltration and clinical response

Author

Wu, Thomas D., Madireddi, Shravan, de Almeida, Patricia E., Banchereau, Romain, Chen, Ying-Jiun J., Chitre, Avantika S., Chiang, Eugene Y., Iftikhar, Hina, O’Gorman, William E., Au-Yeung, Amelia, Takahashi, Chikara, Goldstein, Leonard D., Poon, Chungkee, Keerthivasan, Shilpa, de Almeida Nagata, Denise E., Du, Xiangnan, Lee, Hyang-Mi, Banta, Karl L., Mariathasan, Sanjeev, Das Thakur, Meghna, Huseni, Mahrukh A., Ballinger, Marcus, Estay, Ivette, Caplazi, Patrick, Modrusan, Zora, Delamarre, Lélia, Mellman, Ira, Bourgon, Richard, and Grogan, Jane L.

Published
2020
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11. Integrated digital pathology and transcriptome analysis identifies molecular mediators of T-cell exclusion in ovarian cancer

Author

Desbois, Mélanie, Udyavar, Akshata R., Ryner, Lisa, Kozlowski, Cleopatra, Guan, Yinghui, Dürrbaum, Milena, Lu, Shan, Fortin, Jean-Philippe, Koeppen, Hartmut, Ziai, James, Chang, Ching-Wei, Keerthivasan, Shilpa, Plante, Marie, Bourgon, Richard, Bais, Carlos, Hegde, Priti, Daemen, Anneleen, Turley, Shannon, and Wang, Yulei

Published
2020
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12. Transcription Factors Bind Thousands of Active and Inactive Regions in the Drosophila Blastoderm

Author

Li, Xiao-Yong, MacArthur, Stewart, Bourgon, Richard, Nix, David, Pollard, Daniel A., Iyer, Venky N., Hechmer, Aaron, Simirenko, Lisa, Stapleton, Mark, Luengo Hendriks, Cris L., Chu, Hou Cheng, Ogawa, Nobuo, Inwood, William, Sementchenko, Victor, Beaton, Amy, Weiszmann, Richard, Celniker, Susan E., Knowles, David W., Gingeras, Tom, Speed, Terence P., Eisen, Michael B., and Biggin, Mark D.

Subjects
Applied life sciences
Published
2008

14. Genome-wide analysis of Polycomb targets in Drosophila

Author

Schwartz, Yuri B., Kahn, Tatyana G., Nix, David A., Li, Xiao-Yong, Bourgon, Richard, Biggin, Mark, and Pirrotta, Vincenzo

Subjects
Applied life sciences
Abstract

Polycomb Group (PcG) complexes are multiprotein assemblages that bind to chromatin and establish chromatin states leading to epigenetic silencing. PcG proteins regulate homeotic genes in flies and vertebrates but little is known about other PcG targets and the role of the PcG in development, differentiation and disease. We have determined the distribution of the PcG proteins PC, E(Z) and PSC and of histone H3 K27 trimethylation in the Drosophila genome. At more than 200 PcG target genes, binding sites for the three PcG proteins colocalize to presumptive Polycomb Response Elements (PREs). In contrast, H3 me3K27 forms broad domains including the entire transcription unit and regulatory regions. PcG targets are highly enriched in genes encoding transcription factors but receptors, signaling proteins, morphogens and regulators representing all major developmental pathways are also included.

Published
2006

17. Supplementary Data from Single-Cell RNA Sequencing Reveals Stromal Evolution into LRRC15+ Myofibroblasts as a Determinant of Patient Response to Cancer Immunotherapy

Author

Dominguez, Claudia X., primary, Müller, Sören, primary, Keerthivasan, Shilpa, primary, Koeppen, Hartmut, primary, Hung, Jeffrey, primary, Gierke, Sarah, primary, Breart, Beatrice, primary, Foreman, Oded, primary, Bainbridge, Travis W., primary, Castiglioni, Alessandra, primary, Senbabaoglu, Yasin, primary, Modrusan, Zora, primary, Liang, Yuxin, primary, Junttila, Melissa R., primary, Klijn, Christiaan, primary, Bourgon, Richard, primary, and Turley, Shannon J., primary

Published
2023
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18. Data from Single-Cell RNA Sequencing Reveals Stromal Evolution into LRRC15+ Myofibroblasts as a Determinant of Patient Response to Cancer Immunotherapy

Author

Dominguez, Claudia X., primary, Müller, Sören, primary, Keerthivasan, Shilpa, primary, Koeppen, Hartmut, primary, Hung, Jeffrey, primary, Gierke, Sarah, primary, Breart, Beatrice, primary, Foreman, Oded, primary, Bainbridge, Travis W., primary, Castiglioni, Alessandra, primary, Senbabaoglu, Yasin, primary, Modrusan, Zora, primary, Liang, Yuxin, primary, Junttila, Melissa R., primary, Klijn, Christiaan, primary, Bourgon, Richard, primary, and Turley, Shannon J., primary

Published
2023
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22. Supplementary Tables 5 - 10 from High-Throughput Detection of Clinically Relevant Mutations in Archived Tumor Samples by Multiplexed PCR and Next-Generation Sequencing

Author

Bourgon, Richard, primary, Lu, Shan, primary, Yan, Yibing, primary, Lackner, Mark R., primary, Wang, Weiru, primary, Weigman, Victor, primary, Wang, David, primary, Guan, Yinghui, primary, Ryner, Lisa, primary, Koeppen, Hartmut, primary, Patel, Rajesh, primary, Hampton, Garret M., primary, Amler, Lukas C., primary, and Wang, Yulei, primary

Published
2023
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23. CCR Translation for This Article from DNA Methylation Profiling Defines Clinically Relevant Biological Subsets of Non–Small Cell Lung Cancer

Author

Walter, Kim, primary, Holcomb, Thomas, primary, Januario, Tom, primary, Du, Pan, primary, Evangelista, Marie, primary, Kartha, Nithya, primary, Iniguez, Leonardo, primary, Soriano, Robert, primary, Huw, Ling, primary, Stern, Howard, primary, Modrusan, Zora, primary, Seshagiri, Somasekar, primary, Hampton, Garret M., primary, Amler, Lukas C., primary, Bourgon, Richard, primary, Yauch, Robert L., primary, and Shames, David S., primary

Published
2023
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24. Supplementary Methods and Tables from Loss of NAPRT1 Expression by Tumor-Specific Promoter Methylation Provides a Novel Predictive Biomarker for NAMPT Inhibitors

Author

Shames, David S., primary, Elkins, Kristi, primary, Walter, Kimberly, primary, Holcomb, Thomas, primary, Du, Pan, primary, Mohl, Dane, primary, Xiao, Yang, primary, Pham, Thinh, primary, Haverty, Peter M., primary, Liederer, Bianca, primary, Liang, Xiaorong, primary, Yauch, Robert L., primary, O'Brien, Thomas, primary, Bourgon, Richard, primary, Koeppen, Hartmut, primary, and Belmont, Lisa D., primary

Published
2023
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25. Supplementary Methods, Figures 1-9, Tables 1-4 from DNA Methylation Profiling Defines Clinically Relevant Biological Subsets of Non–Small Cell Lung Cancer

Author

Walter, Kim, primary, Holcomb, Thomas, primary, Januario, Tom, primary, Du, Pan, primary, Evangelista, Marie, primary, Kartha, Nithya, primary, Iniguez, Leonardo, primary, Soriano, Robert, primary, Huw, Ling, primary, Stern, Howard, primary, Modrusan, Zora, primary, Seshagiri, Somasekar, primary, Hampton, Garret M., primary, Amler, Lukas C., primary, Bourgon, Richard, primary, Yauch, Robert L., primary, and Shames, David S., primary

Published
2023
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26. Supplementary Figure 1 from Loss of NAPRT1 Expression by Tumor-Specific Promoter Methylation Provides a Novel Predictive Biomarker for NAMPT Inhibitors

Author

Shames, David S., primary, Elkins, Kristi, primary, Walter, Kimberly, primary, Holcomb, Thomas, primary, Du, Pan, primary, Mohl, Dane, primary, Xiao, Yang, primary, Pham, Thinh, primary, Haverty, Peter M., primary, Liederer, Bianca, primary, Liang, Xiaorong, primary, Yauch, Robert L., primary, O'Brien, Thomas, primary, Bourgon, Richard, primary, Koeppen, Hartmut, primary, and Belmont, Lisa D., primary

Published
2023
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27. Supplementary Materials and Methods, Figures 1 - 6, Tables 1 - 4 from High-Throughput Detection of Clinically Relevant Mutations in Archived Tumor Samples by Multiplexed PCR and Next-Generation Sequencing

Author

Bourgon, Richard, primary, Lu, Shan, primary, Yan, Yibing, primary, Lackner, Mark R., primary, Wang, Weiru, primary, Weigman, Victor, primary, Wang, David, primary, Guan, Yinghui, primary, Ryner, Lisa, primary, Koeppen, Hartmut, primary, Patel, Rajesh, primary, Hampton, Garret M., primary, Amler, Lukas C., primary, and Wang, Yulei, primary

Published
2023
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28. Supplementary Table 3 from Comparative Oncogenomics Identifies PSMB4 and SHMT2 as Potential Cancer Driver Genes

Author

Lee, Genee Y., primary, Haverty, Peter M., primary, Li, Li, primary, Kljavin, Noelyn M., primary, Bourgon, Richard, primary, Lee, James, primary, Stern, Howard, primary, Modrusan, Zora, primary, Seshagiri, Somasekar, primary, Zhang, Zemin, primary, Davis, David, primary, Stokoe, David, primary, Settleman, Jeffrey, primary, de Sauvage, Frederic J., primary, and Neve, Richard M., primary

Published
2023
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29. Data from Comparative Oncogenomics Identifies PSMB4 and SHMT2 as Potential Cancer Driver Genes

Author

Lee, Genee Y., primary, Haverty, Peter M., primary, Li, Li, primary, Kljavin, Noelyn M., primary, Bourgon, Richard, primary, Lee, James, primary, Stern, Howard, primary, Modrusan, Zora, primary, Seshagiri, Somasekar, primary, Zhang, Zemin, primary, Davis, David, primary, Stokoe, David, primary, Settleman, Jeffrey, primary, de Sauvage, Frederic J., primary, and Neve, Richard M., primary

Published
2023
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30. Supplementary Table 7 from Comparative Oncogenomics Identifies PSMB4 and SHMT2 as Potential Cancer Driver Genes

Author

Lee, Genee Y., primary, Haverty, Peter M., primary, Li, Li, primary, Kljavin, Noelyn M., primary, Bourgon, Richard, primary, Lee, James, primary, Stern, Howard, primary, Modrusan, Zora, primary, Seshagiri, Somasekar, primary, Zhang, Zemin, primary, Davis, David, primary, Stokoe, David, primary, Settleman, Jeffrey, primary, de Sauvage, Frederic J., primary, and Neve, Richard M., primary

Published
2023
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31. Supplementary Table 2 from Comparative Oncogenomics Identifies PSMB4 and SHMT2 as Potential Cancer Driver Genes

Author

Lee, Genee Y., primary, Haverty, Peter M., primary, Li, Li, primary, Kljavin, Noelyn M., primary, Bourgon, Richard, primary, Lee, James, primary, Stern, Howard, primary, Modrusan, Zora, primary, Seshagiri, Somasekar, primary, Zhang, Zemin, primary, Davis, David, primary, Stokoe, David, primary, Settleman, Jeffrey, primary, de Sauvage, Frederic J., primary, and Neve, Richard M., primary

Published
2023
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32. Supplementary Table 4 from Comparative Oncogenomics Identifies PSMB4 and SHMT2 as Potential Cancer Driver Genes

Author

Lee, Genee Y., primary, Haverty, Peter M., primary, Li, Li, primary, Kljavin, Noelyn M., primary, Bourgon, Richard, primary, Lee, James, primary, Stern, Howard, primary, Modrusan, Zora, primary, Seshagiri, Somasekar, primary, Zhang, Zemin, primary, Davis, David, primary, Stokoe, David, primary, Settleman, Jeffrey, primary, de Sauvage, Frederic J., primary, and Neve, Richard M., primary

Published
2023
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33. Supplementary Table 5 from Comparative Oncogenomics Identifies PSMB4 and SHMT2 as Potential Cancer Driver Genes

Author

Lee, Genee Y., primary, Haverty, Peter M., primary, Li, Li, primary, Kljavin, Noelyn M., primary, Bourgon, Richard, primary, Lee, James, primary, Stern, Howard, primary, Modrusan, Zora, primary, Seshagiri, Somasekar, primary, Zhang, Zemin, primary, Davis, David, primary, Stokoe, David, primary, Settleman, Jeffrey, primary, de Sauvage, Frederic J., primary, and Neve, Richard M., primary

Published
2023
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34. Supplementary Table 6 from Comparative Oncogenomics Identifies PSMB4 and SHMT2 as Potential Cancer Driver Genes

Author

Lee, Genee Y., primary, Haverty, Peter M., primary, Li, Li, primary, Kljavin, Noelyn M., primary, Bourgon, Richard, primary, Lee, James, primary, Stern, Howard, primary, Modrusan, Zora, primary, Seshagiri, Somasekar, primary, Zhang, Zemin, primary, Davis, David, primary, Stokoe, David, primary, Settleman, Jeffrey, primary, de Sauvage, Frederic J., primary, and Neve, Richard M., primary

Published
2023
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35. Supplementary Table 1 from Comparative Oncogenomics Identifies PSMB4 and SHMT2 as Potential Cancer Driver Genes

Author

Lee, Genee Y., primary, Haverty, Peter M., primary, Li, Li, primary, Kljavin, Noelyn M., primary, Bourgon, Richard, primary, Lee, James, primary, Stern, Howard, primary, Modrusan, Zora, primary, Seshagiri, Somasekar, primary, Zhang, Zemin, primary, Davis, David, primary, Stokoe, David, primary, Settleman, Jeffrey, primary, de Sauvage, Frederic J., primary, and Neve, Richard M., primary

Published
2023
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36. Atezolizumab in patients with locally advanced and metastatic urothelial carcinoma who have progressed following treatment with platinum-based chemotherapy: a single-arm, multicentre, phase 2 trial

Author

Rosenberg, Jonathan E, Hoffman-Censits, Jean, Powles, Tom, van der Heijden, Michiel S, Balar, Arjun V, Necchi, Andrea, Dawson, Nancy, O'Donnell, Peter H, Balmanoukian, Ani, Loriot, Yohann, Srinivas, Sandy, Retz, Margitta M, Grivas, Petros, Joseph, Richard W, Galsky, Matthew D, Fleming, Mark T, Petrylak, Daniel P, Perez-Gracia, Jose Luis, Burris, Howard A, Castellano, Daniel, Canil, Christina, Bellmunt, Joaquim, Bajorin, Dean, Nickles, Dorothee, Bourgon, Richard, Frampton, Garrett M, Cui, Na, Mariathasan, Sanjeev, Abidoye, Oyewale, Fine, Gregg D, and Dreicer, Robert

Published
2016
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37. HLApollo: A superior transformer model for pan-allelic peptide-MHC-I presentation prediction, with diverse negative coverage, deconvolution and protein language features

Author

Thrift, William John, primary, Lounsbury, Nicolas W., additional, Broadwell, Quade, additional, Heidersbach, Amy, additional, Freund, Emily, additional, Abdolazimi, Yassan, additional, Phung, Qui T, additional, Chen, Jieming, additional, Capietto, Aude-Hélène, additional, Tong, Ann-Jay, additional, Rose, Christopher M., additional, Blanchette, Craig, additional, Lill, Jennie R, additional, Haley, Benjamin, additional, Delamarre, Lélia, additional, Bourgon, Richard, additional, Liu, Kai, additional, and Jhunjhunwala, Suchit, additional

Published
2022
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39. Reproducible pharmacogenomics profiling of cancer cell line panels

Author

Haverty, Peter M., Lin, Eva, Tan, Jenille, Yu, Yihong, Lam, Billy, Lianoglou, Steve, Neve, Richard M., Martin, Scott, Settleman, Jeff, Yauch, Robert L., and Bourgon, Richard

Subjects
Oncology, Experimental, Cancer cells -- Research, Cancer -- Research, Pharmacogenetics -- Methods, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

The use of large-scale genomic and drug response screening of cancer cell lines depends crucially on the reproducibility of results. Here we consider two previously published screens, plus a later critique of these studies. Using independent data, we show that consistency is achievable, and provide a systematic description of the best laboratory and analysis practices for future studies., Human cancer cell lines are vital models for studying anti-cancer therapeutics and determinants of drug sensitivity. With the rapidly growing recognition of intra-tumour and inter-patient heterogeneity, the optimal use of [...]

Published
2016
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40. A resource for cell line authentication, annotation and quality control

Author

Yu, Mamie, Selvaraj, Suresh K., Liang-Chu, May M.Y., Aghajani, Sahar, Busse, Matthew, Yuan, Jean, Lee, Genee, Peale, Franklin, Klijn, Christiaan, Bourgon, Richard, Kaminker, Joshua S., and Neve, Richard M.

Subjects
Cell lines -- Health aspects -- Identification and classification, Medical research -- Standards, Medicine, Experimental -- Standards, Methodology -- Standards, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Cell line misidentification, contamination and poor annotation affect scientific reproducibility. Here we outline simple measures to detect or avoid cross-contamination, present a framework for cell line annotation linked to short [...]

Published
2015
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43. Transcriptomic profiling of adjuvant colorectal cancer identifies three key prognostic biological processes and a disease specific role for granzyme B

Author

Daemen, Anneleen, primary, Udyavar, Akshata R., additional, Sandmann, Thomas, additional, Li, Congfen, additional, Bosch, Linda J. W., additional, O’Gorman, William, additional, Li, Yijin, additional, Au-Yeung, Amelia, additional, Takahashi, Chikara, additional, Kabbarah, Omar, additional, Bourgon, Richard, additional, Hegde, Priti, additional, Bais, Carlos, additional, and Das Thakur, Meghna, additional

Published
2021
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44. Abstract PO-007: Plasma-based detection of pancreatic cancer: A multiomics approach

Author

Hsu, Teng-Kuei, primary, Liu, Tzu-Yu, additional, Gould, Billie, additional, Decapite, Christine, additional, Zureikat, Amer, additional, Paniccia, Alessandro, additional, Ariazi, Eric, additional, Bertin, Marvin, additional, Bourgon, Richard, additional, Coil, Kaitlyn, additional, Donnella, Hayley, additional, Drake, Adam, additional, Granka, Julie M., additional, Kaur, Preet, additional, Louie, Maggie C., additional, Mahajan, Shivani, additional, Pasupathy, Amit, additional, Shapira, Ofer, additional, Ulz, Peter, additional, Yang, Chun, additional, Lin, C. Jimmy, additional, and Brand, Randall, additional

Published
2021
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45. Indication-specific tumor evolution and its impact on neoantigen targeting and biomarkers for individualized cancer immunotherapies

Author

Lo, Amy A, primary, Wallace, Andrew, additional, Oreper, Daniel, additional, Lounsbury, Nicolas, additional, Havnar, Charles, additional, Pechuan-Jorge, Ximo, additional, Wu, Thomas D, additional, Bourgon, Richard, additional, Jones, Ryan, additional, Krogh, Katrina, additional, Yang, Guang-Yu, additional, and Zill, Oliver A, additional

Published
2021
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46. Single-cell dissection of cellular components and interactions shaping the tumor immune phenotypes in ovarian cancer

Author

Hornburg, Milena, primary, Desbois, Mélanie, additional, Lu, Shan, additional, Guan, Yinghui, additional, Lo, Amy A., additional, Kaufman, Susan, additional, Elrod, Ashley, additional, Lotstein, Alina, additional, DesRochers, Teresa M., additional, Munoz-Rodriguez, Jose L., additional, Wang, Xingwei, additional, Giltnane, Jennifer, additional, Mayba, Oleg, additional, Turley, Shannon J., additional, Bourgon, Richard, additional, Daemen, Anneleen, additional, and Wang, Yulei, additional

Published
2021
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48. Recurrent R-spondin fusions in colon cancer

Author

Seshagiri, Somasekar, Stawiski, Eric W., Durinck, Steffen, Modrusan, Zora, Storm, Elaine E., Conboy, Caitlin B., Chaudhuri, Subhra, Guan, Yinghui, Janakiraman, Vasantharajan, Jaiswal, Bijay S., Guillory, Joseph, Ha, Connie, Dijkgraaf, Gerrit J.P., Stinson, Jeremy, Gnad, Florian, Huntley, Melanie A., Degenhardt, Jeremiah D., Haverty, Peter M., Bourgon, Richard, Wang, Weiru, Koeppen, Hartmut, Gentleman, Robert, Starr, Timothy K., Zhang, Zemin, Largaespada, David A., Wu, Thomas D., and de Sauvage, Frederic J.

Subjects
Gene mutations -- Analysis -- Research, Genomics -- Analysis -- Research, Colon cancer -- Analysis -- Genetic aspects -- Care and treatment -- Patient outcomes -- Research, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Identifying and understanding changes in cancer genomes is essential for the development of targeted therapeutics (1). Here we analyse systematically more than 70 pairs of primary human colon tumours by applying next-generation sequencing to characterize their exomes, transcriptomes and copy-number alterations. We have identified 36,303 protein-altering somatic changes that include several new recurrent mutations in the Wnt pathway gene TCF7L2, chromatin-remodelling genes such as TET2 and TET3 and receptor tyrosine kinases including ERBB3. Our analysis for significantly mutated cancer genes identified 23 candidates, including the cell cycle checkpoint kinase ATM. Copy-number and RNA-seq data analysis identified amplifications and corresponding overexpression of IGF2in a subset of colon tumours. Furthermore, using RNA-seq data we identified multiple fusion transcripts including recurrent gene fusions involving R-spondin family members RSPO2 and RRSPO3 that together occur in 10% of colon tumours. The RSPO fusions were mutually exclusive with APC mutations, indicating that they probably have a role in the activation of Wnt signalling and tumorigenesis. Consistent with this we show that the RSPO fusion proteins were capable of potentiating Wnt signalling. The R-spondin gene fusions and several other gene mutations identified in this study provide new potential opportunities for therapeutic intervention in colon cancer., Colorectal cancer (CRC) is the fourth most prevalent cancer, accounting for over 50,000 deaths per year in the United States (2). Approximately 15% of CRCs have microsatellite instability (MSI) arising [...]

Published
2012

49. Development of a gene expression-based prognostic signature for IDH wild-type glioblastoma

Author

Johnson, Radia M, Phillips, Heidi S, Bais, Carlos, Brennan, Cameron W, Cloughesy, Timothy F, Daemen, Anneleen, Herrlinger, Ulrich, Jenkins, Robert B, Lai, Albert, Mancao, Christoph, Weller, Michael, Wick, Wolfgang, Bourgon, Richard, Garcia, Josep, and University of Zurich

Subjects
610 Medicine & health, 10040 Clinic for Neurology
Published
2020

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