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1. Endocrine-Therapy-Resistant ESR1 Variants Revealed by Genomic Characterization of Breast-Cancer-Derived Xenografts

Author

Shunqiang Li, Dong Shen, Jieya Shao, Robert Crowder, Wenbin Liu, Aleix Prat, Xiaping He, Shuying Liu, Jeremy Hoog, Charles Lu, Li Ding, Obi L. Griffith, Christopher Miller, Dave Larson, Robert S. Fulton, Michelle Harrison, Tom Mooney, Joshua F. McMichael, Jingqin Luo, Yu Tao, Rodrigo Goncalves, Christopher Schlosberg, Jeffrey F. Hiken, Laila Saied, Cesar Sanchez, Therese Giuntoli, Caroline Bumb, Crystal Cooper, Robert T. Kitchens, Austin Lin, Chanpheng Phommaly, Sherri R. Davies, Jin Zhang, Megha Shyam Kavuri, Donna McEachern, Yi Yu Dong, Cynthia Ma, Timothy Pluard, Michael Naughton, Ron Bose, Rama Suresh, Reida McDowell, Loren Michel, Rebecca Aft, William Gillanders, Katherine DeSchryver, Richard K. Wilson, Shaomeng Wang, Gordon B. Mills, Ana Gonzalez-Angulo, John R. Edwards, Christopher Maher, Charles M. Perou, Elaine R. Mardis, and Matthew J. Ellis

Subjects
Biology (General), QH301-705.5
Abstract

To characterize patient-derived xenografts (PDXs) for functional studies, we made whole-genome comparisons with originating breast cancers representative of the major intrinsic subtypes. Structural and copy number aberrations were found to be retained with high fidelity. However, at the single-nucleotide level, variable numbers of PDX-specific somatic events were documented, although they were only rarely functionally significant. Variant allele frequencies were often preserved in the PDXs, demonstrating that clonal representation can be transplantable. Estrogen-receptor-positive PDXs were associated with ESR1 ligand-binding-domain mutations, gene amplification, or an ESR1/YAP1 translocation. These events produced different endocrine-therapy-response phenotypes in human, cell line, and PDX endocrine-response studies. Hence, deeply sequenced PDX models are an important resource for the search for genome-forward treatment options and capture endocrine-drug-resistance etiologies that are not observed in standard cell lines. The originating tumor genome provides a benchmark for assessing genetic drift and clonal representation after transplantation.

Published
2013
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2. Endocrine-Therapy-Resistant ESR1 Variants Revealed by Genomic Characterization of Breast-Cancer-Derived Xenografts

Author

Shunqiang Li, Obi L. Griffith, Yiyu Dong, Jin Zhang, Laila Saied, Shuying Liu, Therese Giuntoli, Robert S. Fulton, Christopher G. Maher, Crystal Cooper, Jeremy Hoog, Wenbin Liu, Ron Bose, Austin Lin, Dave Larson, Robert J. Crowder, Chanpheng Phommaly, Xiaping He, Megha Shyam Kavuri, Rodrigo Franco Gonçalves, Yu Tao, Cynthia X. Ma, Caroline Bumb, Christopher A. Miller, Charles Lu, Ana M. Gonzalez-Angulo, John R. Edwards, Jeffrey F. Hiken, César Sánchez, Timothy J. Pluard, Dong Shen, Elaine R. Mardis, Michael Naughton, Li Ding, Gordon B. Mills, Rama Suresh, Reida G. McDowell, Joshua F. McMichael, R.T. Kitchens, Richard K. Wilson, Christopher E. Schlosberg, Sherri R. Davies, Jieya Shao, Aleix Prat, Loren S. Michel, Matthew J. Ellis, Rebecca Aft, Shaomeng Wang, Katherine DeSchryver, Jingqin Luo, Thomas B. Mooney, Michelle Harrison, Donna McEachern, Charles M. Perou, William E. Gillanders, and Universitat de Barcelona

Subjects
Genome instability, Somatic cell, Molecular biology, Breast Neoplasms, Genomics, Biology, Genome, Genomic Instability, Translocation, Genetic, General Biochemistry, Genetics and Molecular Biology, Càncer de mama, Mice, 03 medical and health sciences, 0302 clinical medicine, Breast cancer, Gene duplication, Animals, Humans, Point Mutation, RNA, Neoplasm, Allele, lcsh:QH301-705.5, Alleles, Adaptor Proteins, Signal Transducing, Neoplasm Staging, 030304 developmental biology, Biologia molecular, Genetics, 0303 health sciences, Estradiol, Estrogen Receptor alpha, Gene Amplification, YAP-Signaling Proteins, Phosphoproteins, Phenotype, Neoplasm Proteins, 3. Good health, Transplantation, Genòmica, lcsh:Biology (General), Estudi de casos, Drug Resistance, Neoplasm, 030220 oncology & carcinogenesis, Heterografts, Female, Case studies, Transcription Factors
Abstract

SummaryTo characterize patient-derived xenografts (PDXs) for functional studies, we made whole-genome comparisons with originating breast cancers representative of the major intrinsic subtypes. Structural and copy number aberrations were found to be retained with high fidelity. However, at the single-nucleotide level, variable numbers of PDX-specific somatic events were documented, although they were only rarely functionally significant. Variant allele frequencies were often preserved in the PDXs, demonstrating that clonal representation can be transplantable. Estrogen-receptor-positive PDXs were associated with ESR1 ligand-binding-domain mutations, gene amplification, or an ESR1/YAP1 translocation. These events produced different endocrine-therapy-response phenotypes in human, cell line, and PDX endocrine-response studies. Hence, deeply sequenced PDX models are an important resource for the search for genome-forward treatment options and capture endocrine-drug-resistance etiologies that are not observed in standard cell lines. The originating tumor genome provides a benchmark for assessing genetic drift and clonal representation after transplantation.

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