Figure 2 from <i>In Vivo</i> Modeling of Patient Genetic Heterogeneity Identifies New Ways to Target Cholangiocarcinoma

<p><i>In vivo</i> CRISPR-Cas9 screening identifies transforming mutations that interact with mutant Ras. <b>A,</b> Schematic of this study in which high-content sequencing data are collated from patients with ICC and the mutational profile of these tumors rationalized t...

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Автор: Nicholas T. Younger (14956251) (author)
Інші автори: Mollie L. Wilson (14956254) (author), Anabel Martinez Lyons (14956257) (author), Edward J. Jarman (9773166) (author), Alison M. Meynert (14956260) (author), Graeme R. Grimes (14160170) (author), Konstantinos Gournopanos (14956263) (author), Scott H. Waddell (14956266) (author), Peter A. Tennant (14956269) (author), David H. Wilson (14956272) (author), Rachel V. Guest (14956275) (author), Stephen J. Wigmore (14915943) (author), Juan Carlos Acosta (14956278) (author), Timothy J. Kendall (14956281) (author), Martin S. Taylor (14956284) (author), Duncan Sproul (13971883) (author), Pleasantine Mill (256953) (author), Luke Boulter (14956287) (author)
Опубліковано: 2025
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author Nicholas T. Younger (14956251)
author2 Mollie L. Wilson (14956254)
Anabel Martinez Lyons (14956257)
Edward J. Jarman (9773166)
Alison M. Meynert (14956260)
Graeme R. Grimes (14160170)
Konstantinos Gournopanos (14956263)
Scott H. Waddell (14956266)
Peter A. Tennant (14956269)
David H. Wilson (14956272)
Rachel V. Guest (14956275)
Stephen J. Wigmore (14915943)
Juan Carlos Acosta (14956278)
Timothy J. Kendall (14956281)
Martin S. Taylor (14956284)
Duncan Sproul (13971883)
Pleasantine Mill (256953)
Luke Boulter (14956287)
author2_role author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author_facet Nicholas T. Younger (14956251)
Mollie L. Wilson (14956254)
Anabel Martinez Lyons (14956257)
Edward J. Jarman (9773166)
Alison M. Meynert (14956260)
Graeme R. Grimes (14160170)
Konstantinos Gournopanos (14956263)
Scott H. Waddell (14956266)
Peter A. Tennant (14956269)
David H. Wilson (14956272)
Rachel V. Guest (14956275)
Stephen J. Wigmore (14915943)
Juan Carlos Acosta (14956278)
Timothy J. Kendall (14956281)
Martin S. Taylor (14956284)
Duncan Sproul (13971883)
Pleasantine Mill (256953)
Luke Boulter (14956287)
author_role author
dc.creator.none.fl_str_mv Nicholas T. Younger (14956251)
Mollie L. Wilson (14956254)
Anabel Martinez Lyons (14956257)
Edward J. Jarman (9773166)
Alison M. Meynert (14956260)
Graeme R. Grimes (14160170)
Konstantinos Gournopanos (14956263)
Scott H. Waddell (14956266)
Peter A. Tennant (14956269)
David H. Wilson (14956272)
Rachel V. Guest (14956275)
Stephen J. Wigmore (14915943)
Juan Carlos Acosta (14956278)
Timothy J. Kendall (14956281)
Martin S. Taylor (14956284)
Duncan Sproul (13971883)
Pleasantine Mill (256953)
Luke Boulter (14956287)
dc.date.none.fl_str_mv 2025-11-24T22:22:14Z
dc.identifier.none.fl_str_mv 10.1158/0008-5472.30698871
dc.relation.none.fl_str_mv https://figshare.com/articles/figure/Figure_2_from_i_In_Vivo_i_Modeling_of_Patient_Genetic_Heterogeneity_Identifies_New_Ways_to_Target_Cholangiocarcinoma/30698871
dc.rights.none.fl_str_mv CC BY
info:eu-repo/semantics/openAccess
dc.subject.none.fl_str_mv Cancer
Cancer Biology
Molecular and Cellular Biology
Therapeutic Research and Development
Methods and Technology
Cell Signaling
Computational Methods
Sequence analysis
Drug Targets
Gastrointestinal Cancers
Liver cancer
Gene Technologies
Comparative genomics
Oncogenes & Tumor Suppressors
Kras
Preclinical Models
Animal models of cancer
dc.title.none.fl_str_mv Figure 2 from <i>In Vivo</i> Modeling of Patient Genetic Heterogeneity Identifies New Ways to Target Cholangiocarcinoma
dc.type.none.fl_str_mv Image
Figure
info:eu-repo/semantics/publishedVersion
image
description <p><i>In vivo</i> CRISPR-Cas9 screening identifies transforming mutations that interact with mutant Ras. <b>A,</b> Schematic of this study in which high-content sequencing data are collated from patients with ICC and the mutational profile of these tumors rationalized to identify novel, high confidence drivers of ICC. These putative drivers are used as input for an <i>in vivo</i> SpCas9/CRISPR screen to identify novel functional processes that drive ICC growth. <b>B,</b> Macroscopic images of the livers following injection with either NRAS<sup>G12V</sup> or KRAS<sup>G12D</sup> alone (left) or in combination with ICC<sup>Lib</sup> (right; dotted line, tumor). Scale bar, 1 cm. <b>C,</b> Quantification of macroscopic tumors per mouse at 10 weeks in mice bearing Nras<sup>G12V</sup> -expressing tumors and 8 weeks in those with Kras<sup>G12D</sup>-driven cancer. Each circle represents a different animal. <b>D,</b> The number of samples containing Indels in a particular gene following whole exome sequencing. Top graph lists those mutations found in both NRAS<sup>G12V</sup> and KRAS<sup>G12D</sup> tumors, and bottom graphs denote those mutations that are found only in KRAS<sup>G12D</sup> - or NRAS<sup>G12V</sup> -expressing tumors. Sample frequency (%) denotes the proportion of tumors containing any given mutation, whereas (count) is absolute number. (<i>N</i> represents anatomically discreet tumors recovered from at least four individual animals, KRAS<sup>G12D</sup><i>N</i> = 14 and NRAS<sup>G12V</sup><i>N</i> = 10.) <b>E,</b> PCA showing how samples group based on their transcriptomic signature and gRNA-induced mutations associated with each tumor type.</p>
eu_rights_str_mv openAccess
id Manara_8b023457956b4da37779c92ef9ce8cb9
identifier_str_mv 10.1158/0008-5472.30698871
network_acronym_str Manara
network_name_str ManaraRepo
oai_identifier_str oai:figshare.com:article/30698871
publishDate 2025
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rights_invalid_str_mv CC BY
spelling Figure 2 from <i>In Vivo</i> Modeling of Patient Genetic Heterogeneity Identifies New Ways to Target CholangiocarcinomaNicholas T. Younger (14956251)Mollie L. Wilson (14956254)Anabel Martinez Lyons (14956257)Edward J. Jarman (9773166)Alison M. Meynert (14956260)Graeme R. Grimes (14160170)Konstantinos Gournopanos (14956263)Scott H. Waddell (14956266)Peter A. Tennant (14956269)David H. Wilson (14956272)Rachel V. Guest (14956275)Stephen J. Wigmore (14915943)Juan Carlos Acosta (14956278)Timothy J. Kendall (14956281)Martin S. Taylor (14956284)Duncan Sproul (13971883)Pleasantine Mill (256953)Luke Boulter (14956287)CancerCancer BiologyMolecular and Cellular BiologyTherapeutic Research and DevelopmentMethods and TechnologyCell SignalingComputational MethodsSequence analysisDrug TargetsGastrointestinal CancersLiver cancerGene TechnologiesComparative genomicsOncogenes & Tumor SuppressorsKrasPreclinical ModelsAnimal models of cancer<p><i>In vivo</i> CRISPR-Cas9 screening identifies transforming mutations that interact with mutant Ras. <b>A,</b> Schematic of this study in which high-content sequencing data are collated from patients with ICC and the mutational profile of these tumors rationalized to identify novel, high confidence drivers of ICC. These putative drivers are used as input for an <i>in vivo</i> SpCas9/CRISPR screen to identify novel functional processes that drive ICC growth. <b>B,</b> Macroscopic images of the livers following injection with either NRAS<sup>G12V</sup> or KRAS<sup>G12D</sup> alone (left) or in combination with ICC<sup>Lib</sup> (right; dotted line, tumor). Scale bar, 1 cm. <b>C,</b> Quantification of macroscopic tumors per mouse at 10 weeks in mice bearing Nras<sup>G12V</sup> -expressing tumors and 8 weeks in those with Kras<sup>G12D</sup>-driven cancer. Each circle represents a different animal. <b>D,</b> The number of samples containing Indels in a particular gene following whole exome sequencing. Top graph lists those mutations found in both NRAS<sup>G12V</sup> and KRAS<sup>G12D</sup> tumors, and bottom graphs denote those mutations that are found only in KRAS<sup>G12D</sup> - or NRAS<sup>G12V</sup> -expressing tumors. Sample frequency (%) denotes the proportion of tumors containing any given mutation, whereas (count) is absolute number. (<i>N</i> represents anatomically discreet tumors recovered from at least four individual animals, KRAS<sup>G12D</sup><i>N</i> = 14 and NRAS<sup>G12V</sup><i>N</i> = 10.) <b>E,</b> PCA showing how samples group based on their transcriptomic signature and gRNA-induced mutations associated with each tumor type.</p>2025-11-24T22:22:14ZImageFigureinfo:eu-repo/semantics/publishedVersionimage10.1158/0008-5472.30698871https://figshare.com/articles/figure/Figure_2_from_i_In_Vivo_i_Modeling_of_Patient_Genetic_Heterogeneity_Identifies_New_Ways_to_Target_Cholangiocarcinoma/30698871CC BYinfo:eu-repo/semantics/openAccessoai:figshare.com:article/306988712025-11-24T22:22:14Z
spellingShingle Figure 2 from <i>In Vivo</i> Modeling of Patient Genetic Heterogeneity Identifies New Ways to Target Cholangiocarcinoma
Nicholas T. Younger (14956251)
Cancer
Cancer Biology
Molecular and Cellular Biology
Therapeutic Research and Development
Methods and Technology
Cell Signaling
Computational Methods
Sequence analysis
Drug Targets
Gastrointestinal Cancers
Liver cancer
Gene Technologies
Comparative genomics
Oncogenes & Tumor Suppressors
Kras
Preclinical Models
Animal models of cancer
status_str publishedVersion
title Figure 2 from <i>In Vivo</i> Modeling of Patient Genetic Heterogeneity Identifies New Ways to Target Cholangiocarcinoma
title_full Figure 2 from <i>In Vivo</i> Modeling of Patient Genetic Heterogeneity Identifies New Ways to Target Cholangiocarcinoma
title_fullStr Figure 2 from <i>In Vivo</i> Modeling of Patient Genetic Heterogeneity Identifies New Ways to Target Cholangiocarcinoma
title_full_unstemmed Figure 2 from <i>In Vivo</i> Modeling of Patient Genetic Heterogeneity Identifies New Ways to Target Cholangiocarcinoma
title_short Figure 2 from <i>In Vivo</i> Modeling of Patient Genetic Heterogeneity Identifies New Ways to Target Cholangiocarcinoma
title_sort Figure 2 from <i>In Vivo</i> Modeling of Patient Genetic Heterogeneity Identifies New Ways to Target Cholangiocarcinoma
topic Cancer
Cancer Biology
Molecular and Cellular Biology
Therapeutic Research and Development
Methods and Technology
Cell Signaling
Computational Methods
Sequence analysis
Drug Targets
Gastrointestinal Cancers
Liver cancer
Gene Technologies
Comparative genomics
Oncogenes & Tumor Suppressors
Kras
Preclinical Models
Animal models of cancer