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Peter S. Choi, Ph.D.
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Assistant Professor of Pathology and Laboratory Medicine
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Department: Pathology and Laboratory Medicine
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Graduate Group Affiliations
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Contact information
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3501 Civic Center Blvd
54 Colket Translational Research Building, Room 4064
Philadelphia, PA 19104
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54 Colket Translational Research Building, Room 4064
Philadelphia, PA 19104
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Office: 267-425-5490
32 Fax: 267-425-0025
32 Lab: 267-426-2853
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32 Fax: 267-425-0025
32 Lab: 267-426-2853
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Email:
choip@chop.edu
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choip@chop.edu
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Publications
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Education:
21 9 B.S. 14 (Biology) c
2b Cornell University, 2002.
21 a Ph.D. 17 (Immunology) c
2c Stanford University, 2012.
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Permanent link21 9 B.S. 14 (Biology) c
2b Cornell University, 2002.
21 a Ph.D. 17 (Immunology) c
2c Stanford University, 2012.
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d1 Our laboratory is interested in the genetics of cancer and in particular, how genetic alterations affecting processes such as RNA splicing drive cancer and expose potential therapeutic vulnerabilities.
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10 Keywords
72 Cancer biology; Lung cancer; Genome editing; RNA splicing; Next-generation sequencing; Synthetic lethality
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18 Research Details
299 Alternative splicing is an essential mode of gene regulation that greatly diversifies the coding potential of the transcriptome. However, this process is often dysregulated in human cancer. Recent large-scale genomic surveys of multiple cancer types have identified somatic alterations in splicing factors and other RNA-binding proteins, demonstrating that global changes in RNA processing can play a significant role in tumorigenesis. Despite our ability to comprehensively detect the landscape of alternatively spliced transcripts through next-generation sequencing, it has remained difficult to predict much of the functional impact of aberrant splicing.
34d Our group aims to decipher how patterns of alternative splicing control cellular processes, and when perturbed, can lead to pathogenic states such as cancer. We are particularly interested in characterizing RNA-binding proteins known to be mutated in cancer and their functional role in alternative splicing and other steps in RNA processing. We are also interested in understanding how the expression of specific isoforms may regulate fundamental pathways involved in cell division and cell death. To tackle these questions, we make extensive use of genome editing to engineer faithful models of cancer-associated mutations and more rapidly characterize the function of alternatively spliced isoforms. We are also applying genome-wide CRISPR/Cas9 screens to identify genotype-specific dependencies in a systematic and unbiased fashion.
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19 Rotation Projects
45 Potential rotation projects include (but are not limited to):
41 -Characterization of cancer-specific alternative splicing
3a -Role of RNA-binding proteins in tumor suppression
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47 Please contact Peter Choi (choip@chop.edu) for further details.
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15 Lab Personnel
3c Josue Medor - PhD Graduate Student (CAMB CB Program)
3e Amanda Weiss - PhD Graduate Student (CAMB G&E Program)
47 Benjamin Wales-McGrath - PhD Graduate Student (CAMB G&E Program)
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Description of Research Expertise
23 Research Interestsd1 Our laboratory is interested in the genetics of cancer and in particular, how genetic alterations affecting processes such as RNA splicing drive cancer and expose potential therapeutic vulnerabilities.
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10 Keywords
72 Cancer biology; Lung cancer; Genome editing; RNA splicing; Next-generation sequencing; Synthetic lethality
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18 Research Details
299 Alternative splicing is an essential mode of gene regulation that greatly diversifies the coding potential of the transcriptome. However, this process is often dysregulated in human cancer. Recent large-scale genomic surveys of multiple cancer types have identified somatic alterations in splicing factors and other RNA-binding proteins, demonstrating that global changes in RNA processing can play a significant role in tumorigenesis. Despite our ability to comprehensively detect the landscape of alternatively spliced transcripts through next-generation sequencing, it has remained difficult to predict much of the functional impact of aberrant splicing.
34d Our group aims to decipher how patterns of alternative splicing control cellular processes, and when perturbed, can lead to pathogenic states such as cancer. We are particularly interested in characterizing RNA-binding proteins known to be mutated in cancer and their functional role in alternative splicing and other steps in RNA processing. We are also interested in understanding how the expression of specific isoforms may regulate fundamental pathways involved in cell division and cell death. To tackle these questions, we make extensive use of genome editing to engineer faithful models of cancer-associated mutations and more rapidly characterize the function of alternatively spliced isoforms. We are also applying genome-wide CRISPR/Cas9 screens to identify genotype-specific dependencies in a systematic and unbiased fashion.
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19 Rotation Projects
45 Potential rotation projects include (but are not limited to):
41 -Characterization of cancer-specific alternative splicing
3a -Role of RNA-binding proteins in tumor suppression
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47 Please contact Peter Choi (choip@chop.edu) for further details.
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15 Lab Personnel
3c Josue Medor - PhD Graduate Student (CAMB CB Program)
3e Amanda Weiss - PhD Graduate Student (CAMB G&E Program)
47 Benjamin Wales-McGrath - PhD Graduate Student (CAMB G&E Program)
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11a Yang K, Islas N, Jewell S, Wu D, Jha A, Radens CM, Pleiss JA, Lynch KW, Barash Y*, Choi PS*: Machine learning-optimized targeted detection of alternative splicing. Nucleic Acids Research 53(3), Dec 2024 Notes: *Co-corresponding 14
1f8 Tang S, Sethunath V, Metaferia NY, Nogueira MF, Gallant DS, Garner ER, Lairson LA, Penney CM, Li J, Gelbard MK, Alaiwi SA, Seo JH, Hwang JH, Strathdee CA, Baca SC, AbuHammad S, Zhang X, Doench JG, Hahn WC, Takeda DY, Freedman ML, Choi PS*, Viswanathan SR*.: A genome-scale CRISPR screen reveals PRMT1 as a critical regulator of androgen receptor signaling in prostate cancer. Cell Rep 38: 110417, Feb 2022 Notes: *Co-corresponding.
1f9 Li Ji*, Choi Peter S*, Chaffer Christine L, Labella Katherine, Hwang Justin H, Giacomelli Andrew O, Kim Jong Wook, Ilic Nina, Doench John G, Ly Seav Huong, Dai Chao, Hagel Kimberly, Hong Andrew L, Gjoerup Ole, Goel Shom, Ge Jennifer Y, Root David E, Zhao Jean J, Brooks Angela N, Weinberg Robert A, Hahn William C: An alternative splicing switch in FLNB promotes the mesenchymal cell state in human breast cancer. eLife 7, Jul 2018.
14e Zhang Xiaoyang*, Choi Peter S*, Francis Joshua M, Imielinski Marcin, Watanabe Hideo, Cherniack Andrew D, Meyerson Matthew: Identification of focally amplified lineage-specific super-enhancers in human epithelial cancers. Nature Genetics 48(2): 176-82, Feb 2016.
ce Choi Peter S, Meyerson Matthew: Targeted genomic rearrangements using CRISPR/Cas technology. Nature Communications 5: 3728, Apr 2014.
142 Choi Peter S, Li Yulin, Felsher Dean W: Addiction to multiple oncogenes can be exploited to prevent the emergence of therapeutic resistance. Proceedings of the National Academy of Sciences of the United States of America 111(32): E3316-24, Aug 2014.
135 Li Yulin, Choi Peter S, Casey Stephanie C, Dill David L, Felsher Dean W: MYC through miR-17-92 suppresses specific target genes to maintain survival, autonomous proliferation, and a neoplastic state. Cancer Cell 26(2): 262-72, Aug 2014.
18e Choi Peter S*, van Riggelen Jan*, Gentles Andrew J, Bachireddy Pavan, Rakhra Kavya, Adam Stacey J, Plevritis Sylvia K, Felsher Dean W: Lymphomas that recur after MYC suppression continue to exhibit oncogene addiction. Proceedings of the National Academy of Sciences of the United States of America 108(42): 17432-7, Oct 2011.
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Selected Publications
ea Lee AR, Tangiyan A, Singh I, Choi PS: Incomplete paralog compensation generates selective dependency on TRA2A in cancer. PLOS Genetics 21(5): e1011685, May 2025.11a Yang K, Islas N, Jewell S, Wu D, Jha A, Radens CM, Pleiss JA, Lynch KW, Barash Y*, Choi PS*: Machine learning-optimized targeted detection of alternative splicing. Nucleic Acids Research 53(3), Dec 2024 Notes: *Co-corresponding 14
1f8 Tang S, Sethunath V, Metaferia NY, Nogueira MF, Gallant DS, Garner ER, Lairson LA, Penney CM, Li J, Gelbard MK, Alaiwi SA, Seo JH, Hwang JH, Strathdee CA, Baca SC, AbuHammad S, Zhang X, Doench JG, Hahn WC, Takeda DY, Freedman ML, Choi PS*, Viswanathan SR*.: A genome-scale CRISPR screen reveals PRMT1 as a critical regulator of androgen receptor signaling in prostate cancer. Cell Rep 38: 110417, Feb 2022 Notes: *Co-corresponding.
1f9 Li Ji*, Choi Peter S*, Chaffer Christine L, Labella Katherine, Hwang Justin H, Giacomelli Andrew O, Kim Jong Wook, Ilic Nina, Doench John G, Ly Seav Huong, Dai Chao, Hagel Kimberly, Hong Andrew L, Gjoerup Ole, Goel Shom, Ge Jennifer Y, Root David E, Zhao Jean J, Brooks Angela N, Weinberg Robert A, Hahn William C: An alternative splicing switch in FLNB promotes the mesenchymal cell state in human breast cancer. eLife 7, Jul 2018.
14e Zhang Xiaoyang*, Choi Peter S*, Francis Joshua M, Imielinski Marcin, Watanabe Hideo, Cherniack Andrew D, Meyerson Matthew: Identification of focally amplified lineage-specific super-enhancers in human epithelial cancers. Nature Genetics 48(2): 176-82, Feb 2016.
ce Choi Peter S, Meyerson Matthew: Targeted genomic rearrangements using CRISPR/Cas technology. Nature Communications 5: 3728, Apr 2014.
142 Choi Peter S, Li Yulin, Felsher Dean W: Addiction to multiple oncogenes can be exploited to prevent the emergence of therapeutic resistance. Proceedings of the National Academy of Sciences of the United States of America 111(32): E3316-24, Aug 2014.
135 Li Yulin, Choi Peter S, Casey Stephanie C, Dill David L, Felsher Dean W: MYC through miR-17-92 suppresses specific target genes to maintain survival, autonomous proliferation, and a neoplastic state. Cancer Cell 26(2): 262-72, Aug 2014.
18e Choi Peter S*, van Riggelen Jan*, Gentles Andrew J, Bachireddy Pavan, Rakhra Kavya, Adam Stacey J, Plevritis Sylvia K, Felsher Dean W: Lymphomas that recur after MYC suppression continue to exhibit oncogene addiction. Proceedings of the National Academy of Sciences of the United States of America 108(42): 17432-7, Oct 2011.
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