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2. A Genomically and Clinically Annotated Patient-Derived Xenograft (PDX) Resource for Preclinical Research in Non-Small Cell Lung Cancer

Author

Woo, Xing Yi, Srivastava, Anuj, Mack, Philip C, Graber, Joel H, Sanderson, Brian J, Lloyd, Michael W, Chen, Mandy, Domanskyi, Sergii, Gandour-Edwards, Regina, Tsai, Rebekah A, Keck, James, Cheng, Mingshan, Bundy, Margaret, Jocoy, Emily L, Riess, Jonathan W, Holland, William, Grubb, Stephen C, Peterson, James G, Stafford, Grace A, Paisie, Carolyn, Neuhauser, Steven B, Karuturi, R Krishna Murthy, George, Joshy, Simons, Allen K, Chavaree, Margaret, Tepper, Clifford G, Goodwin, Neal, Airhart, Susan D, Lara, Primo N, Openshaw, Thomas H, Liu, Edison T, Gandara, David R, and Bult, Carol J

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Orphan Drug, Lung Cancer, Biotechnology, Genetics, Human Genome, Rare Diseases, Cancer, Lung, Development of treatments and therapeutic interventions, 5.1 Pharmaceuticals, Good Health and Well Being, Humans, Animals, Carcinoma, Non-Small-Cell Lung, Lung Neoplasms, Heterografts, Xenograft Model Antitumor Assays, Adenocarcinoma of Lung, Disease Models, Animal, Oncology & Carcinogenesis, Biochemistry and cell biology, Oncology and carcinogenesis
Abstract

Patient-derived xenograft (PDX) models are an effective preclinical in vivo platform for testing the efficacy of novel drugs and drug combinations for cancer therapeutics. Here we describe a repository of 79 genomically and clinically annotated lung cancer PDXs available from The Jackson Laboratory that have been extensively characterized for histopathologic features, mutational profiles, gene expression, and copy-number aberrations. Most of the PDXs are models of non-small cell lung cancer (NSCLC), including 37 lung adenocarcinoma (LUAD) and 33 lung squamous cell carcinoma (LUSC) models. Other lung cancer models in the repository include four small cell carcinomas, two large cell neuroendocrine carcinomas, two adenosquamous carcinomas, and one pleomorphic carcinoma. Models with both de novo and acquired resistance to targeted therapies with tyrosine kinase inhibitors are available in the collection. The genomic profiles of the LUAD and LUSC PDX models are consistent with those observed in patient tumors from The Cancer Genome Atlas and previously characterized gene expression-based molecular subtypes. Clinically relevant mutations identified in the original patient tumors were confirmed in engrafted PDX tumors. Treatment studies performed in a subset of the models recapitulated the responses expected on the basis of the observed genomic profiles. These models therefore serve as a valuable preclinical platform for translational cancer research.SignificancePatient-derived xenografts of lung cancer retain key features observed in the originating patient tumors and show expected responses to treatment with standard-of-care agents, providing experimentally tractable and reproducible models for preclinical investigations.

Published
2022

7. The Maine Cancer Genomics Initiative: Implementing a Community Cancer Genomics Program Across an Entire Rural State

Author

Rueter, Jens, Anderson, Eric C., Graham, Leah C., Antov, Andrey, Helbig, Petra, Gaitor, Lory, Bourne, Jennifer, Edelman, Emily, Reed, E. Kate, Reddi, Honey V., Mockus, Susan, DiPalazzo, John, Lu-Emerson, Christine, Inhorn, Roger, Sinclair, Sarah J., Thomas, Christian A., Brooks, Philip L., Rasmussen, Karen, Han, Paul, and Liu, Edison T.

Published
2023
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10. Bridging Tumor Genomics to Patient Outcomes Through an Integrated Patient-Derived Xenograft Platform

Author

Gandara, David R, Mack, Philip C, Bult, Carol, Li, Tianhong, Lara, Primo N, Riess, Jonathan W, Astrow, Stephanie H, Gandour-Edwards, Regina, Cooke, David T, Yoneda, Ken Y, Moore, Elizabeth H, Pan, Chong-xian, Burich, Rebekah A, David, Elizabeth A, Keck, James G, Airhart, Susan, Goodwin, Neal, de Vere White, Ralph W, and Liu, Edison T

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Genetics, Cancer, Biotechnology, Human Genome, Lung, Lung Cancer, Development of treatments and therapeutic interventions, 5.1 Pharmaceuticals, Good Health and Well Being, Animals, Antineoplastic Agents, Carcinoma, Non-Small-Cell Lung, Genomics, Humans, Lung Neoplasms, Mice, Mice, Inbred NOD, Mice, SCID, Xenograft Model Antitumor Assays, Clinical trials, Lung cancer, Mouse model, Patient derived xenograft, Clinical Sciences, Oncology & Carcinogenesis, Clinical sciences, Oncology and carcinogenesis
Abstract

New approaches to optimization of cancer drug development in the laboratory and the clinic will be required to fully achieve the goal of individualized, precision cancer therapy. Improved preclinical models that more closely reflect the now recognized genomic complexity of human cancers are needed. Here we describe a collaborative research project that integrates core resources of The Jackson Laboratory Basic Science Cancer Center with genomics and clinical research facilities at the UC Davis Comprehensive Cancer Center to establish a clinically and genomically annotated patient-derived xenograft (PDX) platform designed to enhance new drug development and strategies for targeted therapies. Advanced stage non-small-cell lung cancer (NSCLC) was selected for initial studies because of emergence of a number of "druggable" molecular targets, and recent recognition of substantial inter- and intrapatient tumor heterogeneity. Additionally, clonal evolution after targeted therapy interventions make this tumor type ideal for investigation of this platform. Using the immunodeficient NOD scid gamma mouse, > 200 NSCLC tumor biopsies have been xenotransplanted. During the annotation process, patient tumors and subsequent PDXs are compared at multiple levels, including histomorphology, clinically applicable molecular biomarkers, global gene expression patterns, gene copy number variations, and DNA/chromosomal alterations. NSCLC PDXs are grouped into panels of interest according to oncogene subtype and/or histologic subtype. Multiregimen drug testing, paired with next-generation sequencing before and after therapy and timed tumor pharmacodynamics enables determination of efficacy, signaling pathway alterations, and mechanisms of sensitivity-resistance in individual models. This approach should facilitate derivation of new therapeutic strategies and the transition to individualized therapy.

Published
2015

13. Alterations in the Rho pathway contribute to Epstein-Barr virus–induced lymphomagenesis in immunosuppressed environments

Author

Cho, Sung-Yup, Sung, Chang Ohk, Chae, Jeesoo, Lee, Jieun, Na, Deukchae, Kang, Wonyoung, Kang, Jinjoo, Min, Seoyeon, Lee, Ahra, Kwak, Eunhye, Kim, Jooyoung, Choi, Boram, Kim, Hyunsoo, Chuang, Jeffrey H., Pak, Hyo-Kyung, Park, Chan-Sik, Park, Sanghui, Ko, Young Hyeh, Lee, Dakeun, Roh, Jin, Cho, Min-Sun, Park, Seongyeol, Ju, Young Seok, Suh, Yun-Suhk, Kong, Seong-Ho, Lee, Hyuk-Joon, Keck, James, Banchereau, Jacques, Liu, Edison T., Kim, Woo-Ho, Park, Hansoo, Yang, Han-Kwang, Kim, Jong-Il, and Lee, Charles

Published
2018
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14. GWAS of Follicular Lymphoma Reveals Allelic Heterogeneity at 6p21.32 and Suggests Shared Genetic Susceptibility with Diffuse Large B-cell Lymphoma

Author

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

Subjects
Human Genome, Hematology, Rare Diseases, Cancer, Lymphoma, Genetics, Aetiology, 2.1 Biological and endogenous factors, Chromosomes, Human, Pair 6, Denmark, Gene Frequency, Genetic Predisposition to Disease, Genetic Variation, Genome, Human, Genome-Wide Association Study, Haplotypes, Histocompatibility Antigens Class II, Humans, Lymphoma, Follicular, Lymphoma, Large B-Cell, Diffuse, Polymorphism, Single Nucleotide, Risk Factors, Sweden, Developmental Biology
Abstract

Non-Hodgkin lymphoma (NHL) represents a diverse group of hematological malignancies, of which follicular lymphoma (FL) is a prevalent subtype. A previous genome-wide association study has established a marker, rs10484561 in the human leukocyte antigen (HLA) class II region on 6p21.32 associated with increased FL risk. Here, in a three-stage genome-wide association study, starting with a genome-wide scan of 379 FL cases and 791 controls followed by validation in 1,049 cases and 5,790 controls, we identified a second independent FL-associated locus on 6p21.32, rs2647012 (OR(combined)  = 0.64, P(combined)  = 2 × 10(-21)) located 962 bp away from rs10484561 (r(2)

Published
2011

24. Data from Monochromosome Transfer and Microarray Analysis Identify a Critical Tumor-Suppressive Region Mapping to Chromosome 13q14 and THSD1 in Esophageal Carcinoma

Author

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

Published
2023
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25. Supplementary Figures S1-S3 from Monochromosome Transfer and Microarray Analysis Identify a Critical Tumor-Suppressive Region Mapping to Chromosome 13q14 and THSD1 in Esophageal Carcinoma

Author

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

Published
2023
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27. The tandem duplicator phenotype as a distinct genomic configuration in cancer

Author

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

Published
2016

28. Supplementary Table from A Genomically and Clinically Annotated Patient-Derived Xenograft Resource for Preclinical Research in Non–Small Cell Lung Cancer

Author

Woo, Xing Yi, primary, Srivastava, Anuj, primary, Mack, Philip C., primary, Graber, Joel H., primary, Sanderson, Brian J., primary, Lloyd, Michael W., primary, Chen, Mandy, primary, Domanskyi, Sergii, primary, Gandour-Edwards, Regina, primary, Tsai, Rebekah A., primary, Keck, James, primary, Cheng, Mingshan, primary, Bundy, Margaret, primary, Jocoy, Emily L., primary, Riess, Jonathan W., primary, Holland, William, primary, Grubb, Stephen C., primary, Peterson, James G., primary, Stafford, Grace A., primary, Paisie, Carolyn, primary, Neuhauser, Steven B., primary, Karuturi, R. Krishna Murthy, primary, George, Joshy, primary, Simons, Allen K., primary, Chavaree, Margaret, primary, Tepper, Clifford G., primary, Goodwin, Neal, primary, Airhart, Susan D., primary, Lara, Primo N., primary, Openshaw, Thomas H., primary, Liu, Edison T., primary, Gandara, David R., primary, and Bult, Carol J., primary

Published
2023
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29. Data from A Genomically and Clinically Annotated Patient-Derived Xenograft Resource for Preclinical Research in Non–Small Cell Lung Cancer

Author

Woo, Xing Yi, primary, Srivastava, Anuj, primary, Mack, Philip C., primary, Graber, Joel H., primary, Sanderson, Brian J., primary, Lloyd, Michael W., primary, Chen, Mandy, primary, Domanskyi, Sergii, primary, Gandour-Edwards, Regina, primary, Tsai, Rebekah A., primary, Keck, James, primary, Cheng, Mingshan, primary, Bundy, Margaret, primary, Jocoy, Emily L., primary, Riess, Jonathan W., primary, Holland, William, primary, Grubb, Stephen C., primary, Peterson, James G., primary, Stafford, Grace A., primary, Paisie, Carolyn, primary, Neuhauser, Steven B., primary, Karuturi, R. Krishna Murthy, primary, George, Joshy, primary, Simons, Allen K., primary, Chavaree, Margaret, primary, Tepper, Clifford G., primary, Goodwin, Neal, primary, Airhart, Susan D., primary, Lara, Primo N., primary, Openshaw, Thomas H., primary, Liu, Edison T., primary, Gandara, David R., primary, and Bult, Carol J., primary

Published
2023
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30. Supplementary Figure from A Genomically and Clinically Annotated Patient-Derived Xenograft Resource for Preclinical Research in Non–Small Cell Lung Cancer

Author

Woo, Xing Yi, primary, Srivastava, Anuj, primary, Mack, Philip C., primary, Graber, Joel H., primary, Sanderson, Brian J., primary, Lloyd, Michael W., primary, Chen, Mandy, primary, Domanskyi, Sergii, primary, Gandour-Edwards, Regina, primary, Tsai, Rebekah A., primary, Keck, James, primary, Cheng, Mingshan, primary, Bundy, Margaret, primary, Jocoy, Emily L., primary, Riess, Jonathan W., primary, Holland, William, primary, Grubb, Stephen C., primary, Peterson, James G., primary, Stafford, Grace A., primary, Paisie, Carolyn, primary, Neuhauser, Steven B., primary, Karuturi, R. Krishna Murthy, primary, George, Joshy, primary, Simons, Allen K., primary, Chavaree, Margaret, primary, Tepper, Clifford G., primary, Goodwin, Neal, primary, Airhart, Susan D., primary, Lara, Primo N., primary, Openshaw, Thomas H., primary, Liu, Edison T., primary, Gandara, David R., primary, and Bult, Carol J., primary

Published
2023
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32. Data from Genetic Reclassification of Histologic Grade Delineates New Clinical Subtypes of Breast Cancer

Author

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

Published
2023
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33. Supplementary File 3 from Genetic Reclassification of Histologic Grade Delineates New Clinical Subtypes of Breast Cancer

Author

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

Published
2023
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34. Supplementary File 1 from Genetic Reclassification of Histologic Grade Delineates New Clinical Subtypes of Breast Cancer

Author

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

Published
2023
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36. Supplementary File 2 from Genetic Reclassification of Histologic Grade Delineates New Clinical Subtypes of Breast Cancer

Author

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

Published
2023
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38. CTCF-Mediated Human 3D Genome Architecture Reveals Chromatin Topology for Transcription

Author

Tang, Zhonghui, Luo, Oscar Junhong, Li, Xingwang, Zheng, Meizhen, Zhu, Jacqueline Jufen, Szalaj, Przemyslaw, Trzaskoma, Pawel, Magalska, Adriana, Wlodarczyk, Jakub, Ruszczycki, Blazej, Michalski, Paul, Piecuch, Emaly, Wang, Ping, Wang, Danjuan, Tian, Simon Zhongyuan, Penrad-Mobayed, May, Sachs, Laurent M., Ruan, Xiaoan, Wei, Chia-Lin, Liu, Edison T., Wilczynski, Grzegorz M., Plewczynski, Dariusz, Li, Guoliang, and Ruan, Yijun

Published
2015
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39. Mechanism of tandem duplication formation in BRCA1-mutant cells

Author

Willis, Nicholas A., Frock, Richard L., Menghi, Francesca, Duffey, Erin E., Panday, Arvind, Camacho, Virginia, Hasty, E. Paul, Liu, Edison T., Alt, Frederick W., and Scully, Ralph

Subjects
DNA replication -- Health aspects, Cancer cells -- Genetic aspects -- Health aspects, Gene mutation -- Health aspects, Breast cancer -- Genetic aspects, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Small, approximately 10-kilobase microhomology-mediated tandem duplications are abundant in the genomes of BRCA1-linked but not BRCA2-linked breast cancer. Here we define the mechanism underlying this rearrangement signature. We show that, in primary mammalian cells, BRCA1, but not BRCA2, suppresses the formation of tandem duplications at a site-specific chromosomal replication fork barrier imposed by the binding of Tus proteins to an array of Ter sites. BRCA1 has no equivalent role at chromosomal double-stranded DNA breaks, indicating that tandem duplications form specifically at stalled forks. Tandem duplications in BRCA1 mutant cells arise by a replication restart-bypass mechanism terminated by end joining or by microhomology-mediated template switching, the latter forming complex tandem duplication breakpoints. Solitary DNA ends form directly at TusTer, implicating misrepair of these lesions in tandem duplication formation. Furthermore, BRCA1 inactivation is strongly associated with 10 kilobase tandem duplications in ovarian cancer. This tandem duplicator phenotype may be a general signature of BRCA1-deficient cancer., Author(s): Nicholas A. Willis [1]; Richard L. Frock [2]; Francesca Menghi [3]; Erin E. Duffey [1]; Arvind Panday [1]; Virginia Camacho [4]; E. Paul Hasty [5]; Edison T. Liu [3, [...]

Published
2017
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46. Genomic and Molecular Classification of Breast Cancer

Author

Loi, Sherene M., Demonty, Gaston, Desmedt, Christine, Durgecq, Virginie, Liu, Edison T., Sotiriou, Christos, Piccart, Martine J., editor, Hung, Mien-Chie, editor, Solin, Lawrence J., editor, Cardoso, Fatima, editor, and Wood, William C., editor

Published
2006
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47. A Genomically and Clinically Annotated Patient-Derived Xenograft Resource for Preclinical Research in Non–Small Cell Lung Cancer

Author

Woo, Xing Yi, primary, Srivastava, Anuj, additional, Mack, Philip C., additional, Graber, Joel H., additional, Sanderson, Brian J., additional, Lloyd, Michael W., additional, Chen, Mandy, additional, Domanskyi, Sergii, additional, Gandour-Edwards, Regina, additional, Tsai, Rebekah A., additional, Keck, James, additional, Cheng, Mingshan, additional, Bundy, Margaret, additional, Jocoy, Emily L., additional, Riess, Jonathan W., additional, Holland, William, additional, Grubb, Stephen C., additional, Peterson, James G., additional, Stafford, Grace A., additional, Paisie, Carolyn, additional, Neuhauser, Steven B., additional, Karuturi, R. Krishna Murthy, additional, George, Joshy, additional, Simons, Allen K., additional, Chavaree, Margaret, additional, Tepper, Clifford G., additional, Goodwin, Neal, additional, Airhart, Susan D., additional, Lara, Primo N., additional, Openshaw, Thomas H., additional, Liu, Edison T., additional, Gandara, David R., additional, and Bult, Carol J., additional

Published
2022
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48. Genomic and epigenomic BRCA alterations predict adaptive resistance and response to platinum-based therapy in patients with triple-negative breast and ovarian carcinomas

Author

Menghi, Francesca, primary, Banda, Kalyan, additional, Kumar, Pooja, additional, Straub, Robert, additional, Dobrolecki, Lacey, additional, Rodriguez, Isabel V., additional, Yost, Susan E., additional, Chandok, Harshpreet, additional, Radke, Marc R., additional, Somlo, George, additional, Yuan, Yuan, additional, Lewis, Michael T., additional, Swisher, Elizabeth M., additional, and Liu, Edison T., additional

Published
2022
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