Loading…

Abstract 797: Glioblastoma animal model using CRISPR-Cas9 technology

Current in vivo model system poses limitation on fully recapitulating genomic characteristics of a tumor due to high complexity and poor understanding of the heterogeneous microenvironment conditions in cancer pathogenesis. In an effort to address such issues, strategic models are required. In prese...

Full description

Saved in:
Bibliographic Details
Published in:Cancer research (Chicago, Ill.) Ill.), 2017-07, Vol.77 (13_Supplement), p.797-797
Main Authors: Jeong, Da Eun, Lee, Kee Hang, Kim, Sung Soo, Bae, Yoon Kyung, Nam, Hyun, Hwang, Ji Yoon, Pyeon, Hee Jang, Song, Hye Jin, Joo, Kyeung Min
Format: Article
Language:English
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
cited_by
cites
container_end_page 797
container_issue 13_Supplement
container_start_page 797
container_title Cancer research (Chicago, Ill.)
container_volume 77
creator Jeong, Da Eun
Lee, Kee Hang
Kim, Sung Soo
Bae, Yoon Kyung
Nam, Hyun
Hwang, Ji Yoon
Pyeon, Hee Jang
Song, Hye Jin
Joo, Kyeung Min
description Current in vivo model system poses limitation on fully recapitulating genomic characteristics of a tumor due to high complexity and poor understanding of the heterogeneous microenvironment conditions in cancer pathogenesis. In an effort to address such issues, strategic models are required. In present study, we propose that the most representative cancer models have consistent tumor microenvironments and genomic mutations. The Clustered regularly interspaced short palindromic repeats (CRISPR)-Cas9 system is a powerful genome editing tool for efficient and precise genome engineering. Here, we employed CRISPR-Cas9 system in vivo to generate Cre-dependent Cas9 knock-in mouse (B6;129-Gt(ROSA)26Sortm1(CAG-cas9*,-EGFP)Fezh/J, Jackson lab.). The Cre-dependent Cas9 mouse models harbor combinations of genomic alterations including well-established oncogenes such as EGFRviii, c-MET, PDGFRa, IDH1 R132H and KRAS, EGFR, ALK, BRAF in Brain and Lung cancer models, respectively. While, they also consist of tumor suppressor genes including PTEN, NF1, Ink4a/ARF, Rb, TP53 and TP53, PTEN, NKx-1, APC in both Brain and Lung models, respectively. Cre-dependent model allows us to study in-depth into the tumor initiation and progression, while able to follow up in the role of tumor microenvironment in cancer maintenance. A better understanding of cancer models for preclinical research including their uses, as well as their limitations, may aid future potential studies regarding the development and implementation of new immune targeted therapies and potential validation of novel therapeutic biomarkers. Citation Format: Da Eun Jeong, Kee Hang Lee, Sung Soo Kim, Yoon Kyung Bae, Hyun Nam, Ji Yoon Hwang, Hee Jang Pyeon, Hye Jin Song, Kyeung Min Joo. Glioblastoma animal model using CRISPR-Cas9 technology [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 797. doi:10.1158/1538-7445.AM2017-797
doi_str_mv 10.1158/1538-7445.AM2017-797
format article
fullrecord <record><control><sourceid>crossref</sourceid><recordid>TN_cdi_crossref_primary_10_1158_1538_7445_AM2017_797</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>10_1158_1538_7445_AM2017_797</sourcerecordid><originalsourceid>FETCH-LOGICAL-c917-6c049842662e8827fd2ad665964be69c931e7fb57b64bf1ddb057be99b4ce72d3</originalsourceid><addsrcrecordid>eNo9kM1OwzAQhC0EEqHwBhz8Aim2419uUYBSqQhUerdsxylBTozicOjb46oVp90daVbzDQD3GC0xZvIBs0qWglK2rN8IwqIUSlyA4l--BAVCSJaMCnINblL6zifDiBXgqbZpnoybYfY8wlXoow0mzXEw0Iz9YAIcYusD_E39uIfNdv35sS0bkxScvfsaY4j7wy246kxI_u48F2D38rxrXsvN-2rd1JvSqRyKO0SVpIRz4qUkomuJaTlnilPruXKqwl50lgmbhQ63rUV590pZ6rwgbbUA9PTWTTGlyXf6Z8oJp4PGSB-L0EdifSTWpyJ0hqr-AOzhT98</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>Abstract 797: Glioblastoma animal model using CRISPR-Cas9 technology</title><source>EZB Electronic Journals Library</source><creator>Jeong, Da Eun ; Lee, Kee Hang ; Kim, Sung Soo ; Bae, Yoon Kyung ; Nam, Hyun ; Hwang, Ji Yoon ; Pyeon, Hee Jang ; Song, Hye Jin ; Joo, Kyeung Min</creator><creatorcontrib>Jeong, Da Eun ; Lee, Kee Hang ; Kim, Sung Soo ; Bae, Yoon Kyung ; Nam, Hyun ; Hwang, Ji Yoon ; Pyeon, Hee Jang ; Song, Hye Jin ; Joo, Kyeung Min</creatorcontrib><description>Current in vivo model system poses limitation on fully recapitulating genomic characteristics of a tumor due to high complexity and poor understanding of the heterogeneous microenvironment conditions in cancer pathogenesis. In an effort to address such issues, strategic models are required. In present study, we propose that the most representative cancer models have consistent tumor microenvironments and genomic mutations. The Clustered regularly interspaced short palindromic repeats (CRISPR)-Cas9 system is a powerful genome editing tool for efficient and precise genome engineering. Here, we employed CRISPR-Cas9 system in vivo to generate Cre-dependent Cas9 knock-in mouse (B6;129-Gt(ROSA)26Sortm1(CAG-cas9*,-EGFP)Fezh/J, Jackson lab.). The Cre-dependent Cas9 mouse models harbor combinations of genomic alterations including well-established oncogenes such as EGFRviii, c-MET, PDGFRa, IDH1 R132H and KRAS, EGFR, ALK, BRAF in Brain and Lung cancer models, respectively. While, they also consist of tumor suppressor genes including PTEN, NF1, Ink4a/ARF, Rb, TP53 and TP53, PTEN, NKx-1, APC in both Brain and Lung models, respectively. Cre-dependent model allows us to study in-depth into the tumor initiation and progression, while able to follow up in the role of tumor microenvironment in cancer maintenance. A better understanding of cancer models for preclinical research including their uses, as well as their limitations, may aid future potential studies regarding the development and implementation of new immune targeted therapies and potential validation of novel therapeutic biomarkers. Citation Format: Da Eun Jeong, Kee Hang Lee, Sung Soo Kim, Yoon Kyung Bae, Hyun Nam, Ji Yoon Hwang, Hee Jang Pyeon, Hye Jin Song, Kyeung Min Joo. Glioblastoma animal model using CRISPR-Cas9 technology [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 797. doi:10.1158/1538-7445.AM2017-797</description><identifier>ISSN: 0008-5472</identifier><identifier>EISSN: 1538-7445</identifier><identifier>DOI: 10.1158/1538-7445.AM2017-797</identifier><language>eng</language><ispartof>Cancer research (Chicago, Ill.), 2017-07, Vol.77 (13_Supplement), p.797-797</ispartof><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids></links><search><creatorcontrib>Jeong, Da Eun</creatorcontrib><creatorcontrib>Lee, Kee Hang</creatorcontrib><creatorcontrib>Kim, Sung Soo</creatorcontrib><creatorcontrib>Bae, Yoon Kyung</creatorcontrib><creatorcontrib>Nam, Hyun</creatorcontrib><creatorcontrib>Hwang, Ji Yoon</creatorcontrib><creatorcontrib>Pyeon, Hee Jang</creatorcontrib><creatorcontrib>Song, Hye Jin</creatorcontrib><creatorcontrib>Joo, Kyeung Min</creatorcontrib><title>Abstract 797: Glioblastoma animal model using CRISPR-Cas9 technology</title><title>Cancer research (Chicago, Ill.)</title><description>Current in vivo model system poses limitation on fully recapitulating genomic characteristics of a tumor due to high complexity and poor understanding of the heterogeneous microenvironment conditions in cancer pathogenesis. In an effort to address such issues, strategic models are required. In present study, we propose that the most representative cancer models have consistent tumor microenvironments and genomic mutations. The Clustered regularly interspaced short palindromic repeats (CRISPR)-Cas9 system is a powerful genome editing tool for efficient and precise genome engineering. Here, we employed CRISPR-Cas9 system in vivo to generate Cre-dependent Cas9 knock-in mouse (B6;129-Gt(ROSA)26Sortm1(CAG-cas9*,-EGFP)Fezh/J, Jackson lab.). The Cre-dependent Cas9 mouse models harbor combinations of genomic alterations including well-established oncogenes such as EGFRviii, c-MET, PDGFRa, IDH1 R132H and KRAS, EGFR, ALK, BRAF in Brain and Lung cancer models, respectively. While, they also consist of tumor suppressor genes including PTEN, NF1, Ink4a/ARF, Rb, TP53 and TP53, PTEN, NKx-1, APC in both Brain and Lung models, respectively. Cre-dependent model allows us to study in-depth into the tumor initiation and progression, while able to follow up in the role of tumor microenvironment in cancer maintenance. A better understanding of cancer models for preclinical research including their uses, as well as their limitations, may aid future potential studies regarding the development and implementation of new immune targeted therapies and potential validation of novel therapeutic biomarkers. Citation Format: Da Eun Jeong, Kee Hang Lee, Sung Soo Kim, Yoon Kyung Bae, Hyun Nam, Ji Yoon Hwang, Hee Jang Pyeon, Hye Jin Song, Kyeung Min Joo. Glioblastoma animal model using CRISPR-Cas9 technology [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 797. doi:10.1158/1538-7445.AM2017-797</description><issn>0008-5472</issn><issn>1538-7445</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><recordid>eNo9kM1OwzAQhC0EEqHwBhz8Aim2419uUYBSqQhUerdsxylBTozicOjb46oVp90daVbzDQD3GC0xZvIBs0qWglK2rN8IwqIUSlyA4l--BAVCSJaMCnINblL6zifDiBXgqbZpnoybYfY8wlXoow0mzXEw0Iz9YAIcYusD_E39uIfNdv35sS0bkxScvfsaY4j7wy246kxI_u48F2D38rxrXsvN-2rd1JvSqRyKO0SVpIRz4qUkomuJaTlnilPruXKqwl50lgmbhQ63rUV590pZ6rwgbbUA9PTWTTGlyXf6Z8oJp4PGSB-L0EdifSTWpyJ0hqr-AOzhT98</recordid><startdate>20170701</startdate><enddate>20170701</enddate><creator>Jeong, Da Eun</creator><creator>Lee, Kee Hang</creator><creator>Kim, Sung Soo</creator><creator>Bae, Yoon Kyung</creator><creator>Nam, Hyun</creator><creator>Hwang, Ji Yoon</creator><creator>Pyeon, Hee Jang</creator><creator>Song, Hye Jin</creator><creator>Joo, Kyeung Min</creator><scope>AAYXX</scope><scope>CITATION</scope></search><sort><creationdate>20170701</creationdate><title>Abstract 797: Glioblastoma animal model using CRISPR-Cas9 technology</title><author>Jeong, Da Eun ; Lee, Kee Hang ; Kim, Sung Soo ; Bae, Yoon Kyung ; Nam, Hyun ; Hwang, Ji Yoon ; Pyeon, Hee Jang ; Song, Hye Jin ; Joo, Kyeung Min</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c917-6c049842662e8827fd2ad665964be69c931e7fb57b64bf1ddb057be99b4ce72d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jeong, Da Eun</creatorcontrib><creatorcontrib>Lee, Kee Hang</creatorcontrib><creatorcontrib>Kim, Sung Soo</creatorcontrib><creatorcontrib>Bae, Yoon Kyung</creatorcontrib><creatorcontrib>Nam, Hyun</creatorcontrib><creatorcontrib>Hwang, Ji Yoon</creatorcontrib><creatorcontrib>Pyeon, Hee Jang</creatorcontrib><creatorcontrib>Song, Hye Jin</creatorcontrib><creatorcontrib>Joo, Kyeung Min</creatorcontrib><collection>CrossRef</collection><jtitle>Cancer research (Chicago, Ill.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jeong, Da Eun</au><au>Lee, Kee Hang</au><au>Kim, Sung Soo</au><au>Bae, Yoon Kyung</au><au>Nam, Hyun</au><au>Hwang, Ji Yoon</au><au>Pyeon, Hee Jang</au><au>Song, Hye Jin</au><au>Joo, Kyeung Min</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Abstract 797: Glioblastoma animal model using CRISPR-Cas9 technology</atitle><jtitle>Cancer research (Chicago, Ill.)</jtitle><date>2017-07-01</date><risdate>2017</risdate><volume>77</volume><issue>13_Supplement</issue><spage>797</spage><epage>797</epage><pages>797-797</pages><issn>0008-5472</issn><eissn>1538-7445</eissn><abstract>Current in vivo model system poses limitation on fully recapitulating genomic characteristics of a tumor due to high complexity and poor understanding of the heterogeneous microenvironment conditions in cancer pathogenesis. In an effort to address such issues, strategic models are required. In present study, we propose that the most representative cancer models have consistent tumor microenvironments and genomic mutations. The Clustered regularly interspaced short palindromic repeats (CRISPR)-Cas9 system is a powerful genome editing tool for efficient and precise genome engineering. Here, we employed CRISPR-Cas9 system in vivo to generate Cre-dependent Cas9 knock-in mouse (B6;129-Gt(ROSA)26Sortm1(CAG-cas9*,-EGFP)Fezh/J, Jackson lab.). The Cre-dependent Cas9 mouse models harbor combinations of genomic alterations including well-established oncogenes such as EGFRviii, c-MET, PDGFRa, IDH1 R132H and KRAS, EGFR, ALK, BRAF in Brain and Lung cancer models, respectively. While, they also consist of tumor suppressor genes including PTEN, NF1, Ink4a/ARF, Rb, TP53 and TP53, PTEN, NKx-1, APC in both Brain and Lung models, respectively. Cre-dependent model allows us to study in-depth into the tumor initiation and progression, while able to follow up in the role of tumor microenvironment in cancer maintenance. A better understanding of cancer models for preclinical research including their uses, as well as their limitations, may aid future potential studies regarding the development and implementation of new immune targeted therapies and potential validation of novel therapeutic biomarkers. Citation Format: Da Eun Jeong, Kee Hang Lee, Sung Soo Kim, Yoon Kyung Bae, Hyun Nam, Ji Yoon Hwang, Hee Jang Pyeon, Hye Jin Song, Kyeung Min Joo. Glioblastoma animal model using CRISPR-Cas9 technology [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 797. doi:10.1158/1538-7445.AM2017-797</abstract><doi>10.1158/1538-7445.AM2017-797</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record>
fulltext fulltext
identifier ISSN: 0008-5472
ispartof Cancer research (Chicago, Ill.), 2017-07, Vol.77 (13_Supplement), p.797-797
issn 0008-5472
1538-7445
language eng
recordid cdi_crossref_primary_10_1158_1538_7445_AM2017_797
source EZB Electronic Journals Library
title Abstract 797: Glioblastoma animal model using CRISPR-Cas9 technology
url http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-06T18%3A54%3A02IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-crossref&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Abstract%20797:%20Glioblastoma%20animal%20model%20using%20CRISPR-Cas9%20technology&rft.jtitle=Cancer%20research%20(Chicago,%20Ill.)&rft.au=Jeong,%20Da%20Eun&rft.date=2017-07-01&rft.volume=77&rft.issue=13_Supplement&rft.spage=797&rft.epage=797&rft.pages=797-797&rft.issn=0008-5472&rft.eissn=1538-7445&rft_id=info:doi/10.1158/1538-7445.AM2017-797&rft_dat=%3Ccrossref%3E10_1158_1538_7445_AM2017_797%3C/crossref%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c917-6c049842662e8827fd2ad665964be69c931e7fb57b64bf1ddb057be99b4ce72d3%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_id=info:pmid/&rfr_iscdi=true