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Your search keyword '"Freeman, Samuel S."' showing total 7 results
Start Over Author "Freeman, Samuel S." Publication Type Electronic Resources
7 results on '"Freeman, Samuel S."'

1. Structural Alterations Driving Castration-Resistant Prostate Cancer Revealed by Linked-Read Genome Sequencing

Author

Koch Institute for Integrative Cancer Research at MIT, Viswanathan, Srinivas R., Ha, Gavin, Hoff, Andreas M., Wala, Jeremiah A., Carrot-Zhang, Jian, Whelan, Christopher W., Haradhvala, Nicholas J., Freeman, Samuel S., Reed, Sarah C., Rhoades, Justin, Polak, Paz, Cipicchio, Michelle, Wankowicz, Stephanie A., Wong, Alicia, Kamath, Tushar, Zhang, Zhenwei, Gydush, Gregory J., Rotem, Denisse, Love, J. Christopher, Getz, Gad, Gabriel, Stacey, Zhang, Cheng-Zhong, Dehm, Scott M., Nelson, Peter S., Van Allen, Eliezer M., Choudhury, Atish D., Adalsteinsson, Viktor A., Beroukhim, Rameen, Taplin, Mary-Ellen, Meyerson, Matthew, Koch Institute for Integrative Cancer Research at MIT, Viswanathan, Srinivas R., Ha, Gavin, Hoff, Andreas M., Wala, Jeremiah A., Carrot-Zhang, Jian, Whelan, Christopher W., Haradhvala, Nicholas J., Freeman, Samuel S., Reed, Sarah C., Rhoades, Justin, Polak, Paz, Cipicchio, Michelle, Wankowicz, Stephanie A., Wong, Alicia, Kamath, Tushar, Zhang, Zhenwei, Gydush, Gregory J., Rotem, Denisse, Love, J. Christopher, Getz, Gad, Gabriel, Stacey, Zhang, Cheng-Zhong, Dehm, Scott M., Nelson, Peter S., Van Allen, Eliezer M., Choudhury, Atish D., Adalsteinsson, Viktor A., Beroukhim, Rameen, Taplin, Mary-Ellen, and Meyerson, Matthew

Abstract

© 2018 Elsevier Inc. Nearly all prostate cancer deaths are from metastatic castration-resistant prostate cancer (mCRPC), but there have been few whole-genome sequencing (WGS) studies of this disease state. We performed linked-read WGS on 23 mCRPC biopsy specimens and analyzed cell-free DNA sequencing data from 86 patients with mCRPC. In addition to frequent rearrangements affecting known prostate cancer genes, we observed complex rearrangements of the AR locus in most cases. Unexpectedly, these rearrangements include highly recurrent tandem duplications involving an upstream enhancer of AR in 70%–87% of cases compared with <2% of primary prostate cancers. A subset of cases displayed AR or MYC enhancer duplication in the context of a genome-wide tandem duplicator phenotype associated with CDK12 inactivation. Our findings highlight the complex genomic structure of mCRPC, nominate alterations that may inform prostate cancer treatment, and suggest that additional recurrent events in the non-coding mCRPC genome remain to be discovered. Linked-read genome sequencing data from patients highlight that amplification of an enhancer upstream of the androgen receptor locus is a key feature of metastatic castration-resistant prostate cancer.

Published
2022

2. Sensitive Detection of Minimal Residual Disease in Patients Treated for Early-Stage Breast Cancer

Author

Parsons, Heather A., Rhoades, Justin, Reed, Sarah C., Gydush, Gregory, Ram, Priyanka, Exman, Pedro, Xiong, Kan, Lo, Christopher C., Li, Tianyu, Fleharty, Mark, Kirkner, Gregory J., Rotem, Denisse, Cohen, Ofir, Yu, Fangyan, Fitarelli-Kiehl, Mariana, Leong, Ka Wai, Hughes, Melissa E., Rosenberg, Shoshana M., Collins, Laura C., Miller, Kathy D., Blumenstiel, Brendan, Trippa, Lorenzo, Cibulskis, Carrie, Neuberg, Donna S., DeFelice, Matthew, Freeman, Samuel S., Lennon, Niall J., Wagle, Nikhil, Ha, Gavin, Stover, Daniel G., Choudhury, Atish D., Getz, Gad, Winer, Eric P., Meyerson, Matthew, Lin, Nancy U., Krop, Ian, Love, J. Christopher, Makrigiorgos, G. Mike, Partridge, Ann H., Mayer, Erica L., Golub, Todd R., Adalsteinsson, Viktor A., Parsons, Heather A., Rhoades, Justin, Reed, Sarah C., Gydush, Gregory, Ram, Priyanka, Exman, Pedro, Xiong, Kan, Lo, Christopher C., Li, Tianyu, Fleharty, Mark, Kirkner, Gregory J., Rotem, Denisse, Cohen, Ofir, Yu, Fangyan, Fitarelli-Kiehl, Mariana, Leong, Ka Wai, Hughes, Melissa E., Rosenberg, Shoshana M., Collins, Laura C., Miller, Kathy D., Blumenstiel, Brendan, Trippa, Lorenzo, Cibulskis, Carrie, Neuberg, Donna S., DeFelice, Matthew, Freeman, Samuel S., Lennon, Niall J., Wagle, Nikhil, Ha, Gavin, Stover, Daniel G., Choudhury, Atish D., Getz, Gad, Winer, Eric P., Meyerson, Matthew, Lin, Nancy U., Krop, Ian, Love, J. Christopher, Makrigiorgos, G. Mike, Partridge, Ann H., Mayer, Erica L., Golub, Todd R., and Adalsteinsson, Viktor A.

Abstract

© 2020 American Association for Cancer Research. Purpose: Existing cell-free DNA (cfDNA) methods lack the sensitivity needed for detecting minimal residual disease (MRD) following therapy. We developed a test for tracking hundreds of patient-specific mutations to detect MRD with a 1,000-fold lower error rate than conventional sequencing. Experimental Design: We compared the sensitivity of our approach to digital droplet PCR (ddPCR) in a dilution series, then retrospectively identified two cohorts of patients who had undergone prospective plasma sampling and clinical data collection: 16 patients with ER+/HER2- metastatic breast cancer (MBC) sampled within 6 months following metastatic diagnosis and 142 patients with stage 0 to III breast cancer who received curative-intent treatment with most sampled at surgery and 1 year postoperative. We performed whole-exome sequencing of tumors and designed individualized MRD tests, which we applied to serial cfDNA samples. Results: Our approach was 100-fold more sensitive than ddPCR when tracking 488 mutations, but most patients had fewer identifiable tumor mutations to track in cfDNA (median = 57; range = 2–346). Clinical sensitivity was 81% (n = 13/16) in newly diagnosed MBC, 23% (n = 7/30) at postoperative and 19% (n = 6/32) at 1 year in early-stage disease, and highest in patients with the most tumor mutations available to track. MRD detection at 1 year was strongly associated with distant recurrence [HR = 20.8; 95% confidence interval, 7.3–58.9]. Median lead time from first positive sample to recurrence was 18.9 months (range = 3.4–39.2 months). Conclusions: Tracking large numbers of individualized tumor mutations in cfDNA can improve MRD detection, but its sensitivity is driven by the number of tumor mutations available to track.

Published
2022

3. Genome-scale screens identify factors regulating tumor cell responses to natural killer cells

Author

Massachusetts Institute of Technology. Department of Biological Engineering, Sheffer, Michal, Lowry, Emily, Beelen, Nicky, Borah, Minasri, Amara, Suha Naffar-Abu, Mader, Chris C., Roth, Jennifer A., Tsherniak, Aviad, Freeman, Samuel S., Dashevsky, Olga, Gandolfi, Sara, Bender, Samantha, Bryan, Jordan G., Zhu, Cong, Wang, Li, Tariq, Ifrah, Kamath, Govinda M., Simoes, Ricardo De Matos, Dhimolea, Eugen, Yu, Channing, Hu, Yiguo, Dufva, Olli, Giannakis, Marios, Syrgkanis, Vasilis, Fraenkel, Ernest, Golub, Todd, Romee, Rizwan, Mustjoki, Satu, Culhane, Aedin C., Wieten, Lotte, Mitsiades, Constantine S., Massachusetts Institute of Technology. Department of Biological Engineering, Sheffer, Michal, Lowry, Emily, Beelen, Nicky, Borah, Minasri, Amara, Suha Naffar-Abu, Mader, Chris C., Roth, Jennifer A., Tsherniak, Aviad, Freeman, Samuel S., Dashevsky, Olga, Gandolfi, Sara, Bender, Samantha, Bryan, Jordan G., Zhu, Cong, Wang, Li, Tariq, Ifrah, Kamath, Govinda M., Simoes, Ricardo De Matos, Dhimolea, Eugen, Yu, Channing, Hu, Yiguo, Dufva, Olli, Giannakis, Marios, Syrgkanis, Vasilis, Fraenkel, Ernest, Golub, Todd, Romee, Rizwan, Mustjoki, Satu, Culhane, Aedin C., Wieten, Lotte, and Mitsiades, Constantine S.

Abstract

To systematically define molecular features in human tumor cells that determine their degree of sensitivity to human allogeneic natural killer (NK) cells, we quantified the NK cell responsiveness of hundreds of molecularly annotated 'DNA-barcoded' solid tumor cell lines in multiplexed format and applied genome-scale CRISPR-based gene-editing screens in several solid tumor cell lines, to functionally interrogate which genes in tumor cells regulate the response to NK cells. In these orthogonal studies, NK cell-sensitive tumor cells tend to exhibit 'mesenchymal-like' transcriptional programs; high transcriptional signature for chromatin remodeling complexes; high levels of B7-H6 (NCR3LG1); and low levels of HLA-E/antigen presentation genes. Importantly, transcriptional signatures of NK cell-sensitive tumor cells correlate with immune checkpoint inhibitor (ICI) resistance in clinical samples. This study provides a comprehensive map of mechanisms regulating tumor cell responses to NK cells, with implications for future biomarker-driven applications of NK cell immunotherapies.

Published
2021

4. Genomic Heterogeneity as a Barrier to Precision Medicine in Gastroesophageal Adenocarcinoma.

Author

Pectasides, Eirini, Pectasides, Eirini, Stachler, Matthew D, Derks, Sarah, Liu, Yang, Maron, Steven, Islam, Mirazul, Alpert, Lindsay, Kwak, Heewon, Kindler, Hedy, Polite, Blase, Sharma, Manish R, Allen, Kenisha, O'Day, Emily, Lomnicki, Samantha, Maranto, Melissa, Kanteti, Rajani, Fitzpatrick, Carrie, Weber, Christopher, Setia, Namrata, Xiao, Shu-Yuan, Hart, John, Nagy, Rebecca J, Kim, Kyoung-Mee, Choi, Min-Gew, Min, Byung-Hoon, Nason, Katie S, O'Keefe, Lea, Watanabe, Masayuki, Baba, Hideo, Lanman, Rick, Agoston, Agoston T, Oh, David J, Dunford, Andrew, Thorner, Aaron R, Ducar, Matthew D, Wollison, Bruce M, Coleman, Haley A, Ji, Yuan, Posner, Mitchell C, Roggin, Kevin, Turaga, Kiran, Chang, Paul, Hogarth, Kyle, Siddiqui, Uzma, Gelrud, Andres, Ha, Gavin, Freeman, Samuel S, Rhoades, Justin, Reed, Sarah, Gydush, Greg, Rotem, Denisse, Davison, Jon, Imamura, Yu, Adalsteinsson, Viktor, Lee, Jeeyun, Bass, Adam J, Catenacci, Daniel V, Pectasides, Eirini, Pectasides, Eirini, Stachler, Matthew D, Derks, Sarah, Liu, Yang, Maron, Steven, Islam, Mirazul, Alpert, Lindsay, Kwak, Heewon, Kindler, Hedy, Polite, Blase, Sharma, Manish R, Allen, Kenisha, O'Day, Emily, Lomnicki, Samantha, Maranto, Melissa, Kanteti, Rajani, Fitzpatrick, Carrie, Weber, Christopher, Setia, Namrata, Xiao, Shu-Yuan, Hart, John, Nagy, Rebecca J, Kim, Kyoung-Mee, Choi, Min-Gew, Min, Byung-Hoon, Nason, Katie S, O'Keefe, Lea, Watanabe, Masayuki, Baba, Hideo, Lanman, Rick, Agoston, Agoston T, Oh, David J, Dunford, Andrew, Thorner, Aaron R, Ducar, Matthew D, Wollison, Bruce M, Coleman, Haley A, Ji, Yuan, Posner, Mitchell C, Roggin, Kevin, Turaga, Kiran, Chang, Paul, Hogarth, Kyle, Siddiqui, Uzma, Gelrud, Andres, Ha, Gavin, Freeman, Samuel S, Rhoades, Justin, Reed, Sarah, Gydush, Greg, Rotem, Denisse, Davison, Jon, Imamura, Yu, Adalsteinsson, Viktor, Lee, Jeeyun, Bass, Adam J, and Catenacci, Daniel V

Abstract

Gastroesophageal adenocarcinoma (GEA) is a lethal disease where targeted therapies, even when guided by genomic biomarkers, have had limited efficacy. A potential reason for the failure of such therapies is that genomic profiling results could commonly differ between the primary and metastatic tumors. To evaluate genomic heterogeneity, we sequenced paired primary GEA and synchronous metastatic lesions across multiple cohorts, finding extensive differences in genomic alterations, including discrepancies in potentially clinically relevant alterations. Multiregion sequencing showed significant discrepancy within the primary tumor (PT) and between the PT and disseminated disease, with oncogene amplification profiles commonly discordant. In addition, a pilot analysis of cell-free DNA (cfDNA) sequencing demonstrated the feasibility of detecting genomic amplifications not detected in PT sampling. Lastly, we profiled paired primary tumors, metastatic tumors, and cfDNA from patients enrolled in the personalized antibodies for GEA (PANGEA) trial of targeted therapies in GEA and found that genomic biomarkers were recurrently discrepant between the PT and untreated metastases. Divergent primary and metastatic tissue profiling led to treatment reassignment in 32% (9/28) of patients. In discordant primary and metastatic lesions, we found 87.5% concordance for targetable alterations in metastatic tissue and cfDNA, suggesting the potential for cfDNA profiling to enhance selection of therapy.Significance: We demonstrate frequent baseline heterogeneity in targetable genomic alterations in GEA, indicating that current tissue sampling practices for biomarker testing do not effectively guide precision medicine in this disease and that routine profiling of metastatic lesions and/or cfDNA should be systematically evaluated. Cancer Discov; 8(1); 37-48. ©2017 AACR.See related commentary by Sundar and Tan, p. 14See related article by Janjigian et al., p. 49This article is highlighted in the

Published
2018

5. Scalable whole-exome sequencing of cell-free DNA reveals high concordance with metastatic tumors

Author

Massachusetts Institute of Technology. Department of Chemical Engineering, Koch Institute for Integrative Cancer Research at MIT, Adalsteinsson, Viktor A., Loginov, Denis, Ding, Huiming, Leeson, Rachel, Barry, Rachel M, Love, John C, Ha, Gavin, Freeman, Samuel S., Choudhury, Atish D., Stover, Daniel G., Parsons, Heather A., Gydush, Gregory, Reed, Sarah C., Rotem, Denisse, Rhoades, Justin, Livitz, Dimitri, Rosebrock, Daniel, Leshchiner, Ignaty, Kim, Jaegil, Stewart, Chip, Rosenberg, Mara, Francis, Joshua M., Zhang, Cheng-Zhong, Cohen, Ofir, Oh, Coyin, Polak, Paz, Lloyd, Max, Mahmud, Sairah, Helvie, Karla, Merrill, Margaret S., Santiago, Rebecca A., O’Connor, Edward P., Jeong, Seong H., Kramkowski, Joseph F., Zhang, Zhenwei, Polacek, Laura, Lohr, Jens G., Schleicher, Molly, Lipscomb, Emily, Saltzman, Andrea, Oliver, Nelly M., Marini, Lori, Waks, Adrienne G., Harshman, Lauren C., Tolaney, Sara M., Van Allen, Eliezer M., Winer, Eric P., Lin, Nancy U., Nakabayashi, Mari, Taplin, Mary-Ellen, Johannessen, Cory M., Garraway, Levi A., Golub, Todd R., Boehm, Jesse S., Wagle, Nikhil, Getz, Gad, Meyerson, Matthew, Massachusetts Institute of Technology. Department of Chemical Engineering, Koch Institute for Integrative Cancer Research at MIT, Adalsteinsson, Viktor A., Loginov, Denis, Ding, Huiming, Leeson, Rachel, Barry, Rachel M, Love, John C, Ha, Gavin, Freeman, Samuel S., Choudhury, Atish D., Stover, Daniel G., Parsons, Heather A., Gydush, Gregory, Reed, Sarah C., Rotem, Denisse, Rhoades, Justin, Livitz, Dimitri, Rosebrock, Daniel, Leshchiner, Ignaty, Kim, Jaegil, Stewart, Chip, Rosenberg, Mara, Francis, Joshua M., Zhang, Cheng-Zhong, Cohen, Ofir, Oh, Coyin, Polak, Paz, Lloyd, Max, Mahmud, Sairah, Helvie, Karla, Merrill, Margaret S., Santiago, Rebecca A., O’Connor, Edward P., Jeong, Seong H., Kramkowski, Joseph F., Zhang, Zhenwei, Polacek, Laura, Lohr, Jens G., Schleicher, Molly, Lipscomb, Emily, Saltzman, Andrea, Oliver, Nelly M., Marini, Lori, Waks, Adrienne G., Harshman, Lauren C., Tolaney, Sara M., Van Allen, Eliezer M., Winer, Eric P., Lin, Nancy U., Nakabayashi, Mari, Taplin, Mary-Ellen, Johannessen, Cory M., Garraway, Levi A., Golub, Todd R., Boehm, Jesse S., Wagle, Nikhil, Getz, Gad, and Meyerson, Matthew

Abstract

Whole-exome sequencing of cell-free DNA (cfDNA) could enable comprehensive profiling of tumors from blood but the genome-wide concordance between cfDNA and tumor biopsies is uncertain. Here we report ichorCNA, software that quantifies tumor content in cfDNA from 0.1× coverage whole-genome sequencing data without prior knowledge of tumor mutations. We apply ichorCNA to 1439 blood samples from 520 patients with metastatic prostate or breast cancers. In the earliest tested sample for each patient, 34% of patients have ≥10% tumor-derived cfDNA, sufficient for standard coverage whole-exome sequencing. Using whole-exome sequencing, we validate the concordance of clonal somatic mutations (88%), copy number alterations (80%), mutational signatures, and neoantigens between cfDNA and matched tumor biopsies from 41 patients with ≥10% cfDNA tumor content. In summary, we provide methods to identify patients eligible for comprehensive cfDNA profiling, revealing its applicability to many patients, and demonstrate high concordance of cfDNA and metastatic tumor whole-exome sequencing., American Association for Cancer Research (Award U2C-AACR-DT0712)

Published
2017

6. Transcriptomic Characterization of SF3B1 Mutation Reveals Its Pleiotropic Effects in Chronic Lymphocytic Leukemia.

Author

Wang, Lili, Wang, Lili, Brooks, Angela N, Fan, Jean, Wan, Youzhong, Gambe, Rutendo, Li, Shuqiang, Hergert, Sarah, Yin, Shanye, Freeman, Samuel S, Levin, Joshua Z, Fan, Lin, Seiler, Michael, Buonamici, Silvia, Smith, Peter G, Chau, Kevin F, Cibulskis, Carrie L, Zhang, Wandi, Rassenti, Laura Z, Ghia, Emanuela M, Kipps, Thomas J, Fernandes, Stacey, Bloch, Donald B, Kotliar, Dylan, Landau, Dan A, Shukla, Sachet A, Aster, Jon C, Reed, Robin, DeLuca, David S, Brown, Jennifer R, Neuberg, Donna, Getz, Gad, Livak, Kenneth J, Meyerson, Matthew M, Kharchenko, Peter V, Wu, Catherine J, Wang, Lili, Wang, Lili, Brooks, Angela N, Fan, Jean, Wan, Youzhong, Gambe, Rutendo, Li, Shuqiang, Hergert, Sarah, Yin, Shanye, Freeman, Samuel S, Levin, Joshua Z, Fan, Lin, Seiler, Michael, Buonamici, Silvia, Smith, Peter G, Chau, Kevin F, Cibulskis, Carrie L, Zhang, Wandi, Rassenti, Laura Z, Ghia, Emanuela M, Kipps, Thomas J, Fernandes, Stacey, Bloch, Donald B, Kotliar, Dylan, Landau, Dan A, Shukla, Sachet A, Aster, Jon C, Reed, Robin, DeLuca, David S, Brown, Jennifer R, Neuberg, Donna, Getz, Gad, Livak, Kenneth J, Meyerson, Matthew M, Kharchenko, Peter V, and Wu, Catherine J

Abstract

Mutations in SF3B1, which encodes a spliceosome component, are associated with poor outcome in chronic lymphocytic leukemia (CLL), but how these contribute to CLL progression remains poorly understood. We undertook a transcriptomic characterization of primary human CLL cells to identify transcripts and pathways affected by SF3B1 mutation. Splicing alterations, identified in the analysis of bulk cells, were confirmed in single SF3B1-mutated CLL cells and also found in cell lines ectopically expressing mutant SF3B1. SF3B1 mutation was found to dysregulate multiple cellular functions including DNA damage response, telomere maintenance, and Notch signaling (mediated through KLF8 upregulation, increased TERC and TERT expression, or altered splicing of DVL2 transcript, respectively). SF3B1 mutation leads to diverse changes in CLL-related pathways.

Published
2016

7. Characterization of HPV and host genome interactions in primary head and neck cancers.

Author

Parfenov, Michael, Parfenov, Michael, Pedamallu, Chandra Sekhar, Gehlenborg, Nils, Freeman, Samuel S, Danilova, Ludmila, Bristow, Christopher A, Lee, Semin, Hadjipanayis, Angela G, Ivanova, Elena V, Wilkerson, Matthew D, Protopopov, Alexei, Yang, Lixing, Seth, Sahil, Song, Xingzhi, Tang, Jiabin, Ren, Xiaojia, Zhang, Jianhua, Pantazi, Angeliki, Santoso, Netty, Xu, Andrew W, Mahadeshwar, Harshad, Wheeler, David A, Haddad, Robert I, Jung, Joonil, Ojesina, Akinyemi I, Issaeva, Natalia, Yarbrough, Wendell G, Hayes, D Neil, Grandis, Jennifer R, El-Naggar, Adel K, Meyerson, Matthew, Park, Peter J, Chin, Lynda, Seidman, JG, Hammerman, Peter S, Kucherlapati, Raju, Cancer Genome Atlas Network, Parfenov, Michael, Parfenov, Michael, Pedamallu, Chandra Sekhar, Gehlenborg, Nils, Freeman, Samuel S, Danilova, Ludmila, Bristow, Christopher A, Lee, Semin, Hadjipanayis, Angela G, Ivanova, Elena V, Wilkerson, Matthew D, Protopopov, Alexei, Yang, Lixing, Seth, Sahil, Song, Xingzhi, Tang, Jiabin, Ren, Xiaojia, Zhang, Jianhua, Pantazi, Angeliki, Santoso, Netty, Xu, Andrew W, Mahadeshwar, Harshad, Wheeler, David A, Haddad, Robert I, Jung, Joonil, Ojesina, Akinyemi I, Issaeva, Natalia, Yarbrough, Wendell G, Hayes, D Neil, Grandis, Jennifer R, El-Naggar, Adel K, Meyerson, Matthew, Park, Peter J, Chin, Lynda, Seidman, JG, Hammerman, Peter S, Kucherlapati, Raju, and Cancer Genome Atlas Network

Abstract

Previous studies have established that a subset of head and neck tumors contains human papillomavirus (HPV) sequences and that HPV-driven head and neck cancers display distinct biological and clinical features. HPV is known to drive cancer by the actions of the E6 and E7 oncoproteins, but the molecular architecture of HPV infection and its interaction with the host genome in head and neck cancers have not been comprehensively described. We profiled a cohort of 279 head and neck cancers with next generation RNA and DNA sequencing and show that 35 (12.5%) tumors displayed evidence of high-risk HPV types 16, 33, or 35. Twenty-five cases had integration of the viral genome into one or more locations in the human genome with statistical enrichment for genic regions. Integrations had a marked impact on the human genome and were associated with alterations in DNA copy number, mRNA transcript abundance and splicing, and both inter- and intrachromosomal rearrangements. Many of these events involved genes with documented roles in cancer. Cancers with integrated vs. nonintegrated HPV displayed different patterns of DNA methylation and both human and viral gene expressions. Together, these data provide insight into the mechanisms by which HPV interacts with the human genome beyond expression of viral oncoproteins and suggest that specific integration events are an integral component of viral oncogenesis.

Published
2014

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