Acquired/intratumoral mutation of KRAS during metastatic progression of colorectal carcinogenesis
Mutations at codons 12 and 13 of the KRAS gene have been identified as level I predictive biomarkers against the treatment of advanced colorectal cancer with anti-epidermal growth factor receptor (EGFR) monoclonal antibodies. It is thought that the genetic analysis of KRAS mutations associated with...
Gespeichert in:
Veröffentlicht in: | Oncology letters 2012-03, Vol.3 (3), p.649-653 |
---|---|
Hauptverfasser: | , , , , , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
container_end_page | 653 |
---|---|
container_issue | 3 |
container_start_page | 649 |
container_title | Oncology letters |
container_volume | 3 |
creator | OTSUKA, KAZUNORI SATOYOSHI, RIKA NANJO, HIROSHI MIYAZAWA, HIDEAKI ABE, YUKI TANAKA, MASAMITSU YAMAMOTO, YUZO SHIBATA, HIROYUKI |
description | Mutations at codons 12 and 13 of the KRAS gene have been identified as level I predictive biomarkers against the treatment of advanced colorectal cancer with anti-epidermal growth factor receptor (EGFR) monoclonal antibodies. It is thought that the genetic analysis of KRAS mutations associated with metastatic colorectal cancer can be routinely conducted using DNA obtained on one occasion from one organ, from the primary or a metastatic site, whichever is preferentially available. However, the issue of tumor heterogeneity resulting from acquired/intratumoral mutations remains. Recently, the possibility of acquired/intratumoral mutations in the KRAS gene has been reported by two research groups and has ranged from 7.4 to 15.4%. Specimens were collected from advanced colorectal cancer patients with resected primary, and at least one metastatic, site. Direct sequence analysis was performed for KRAS, BRAF and PIK3CA, and immunohistochemistry for glutathione S-transferase II (GSTP) and EGFR. In the current study, we identified an acquired mutation rate of approximately 11.1% in the KRAS gene (1/9). This figure is not negligible. Our observation indicates, particularly in the case of metastatic recurrence after a long interval, that there may be considerable tumor heterogeneity resulting from acquired or intratumoral mutations of the KRAS gene. |
doi_str_mv | 10.3892/ol.2011.543 |
format | Article |
fullrecord | <record><control><sourceid>pubmed_cross</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_3362436</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>22740969</sourcerecordid><originalsourceid>FETCH-LOGICAL-c478t-cdc41b31accb5db7e5a05c7d3f54b99f3fb796b5c7b6c2bf82f87e8c68a53ef33</originalsourceid><addsrcrecordid>eNpVkE1LxDAQhoMo7rLuybv05EW62yRtkl6EZfELFwQ_ziFJkxppm5q0gv_e1l1XHQIzZJ55J3kBOIXJArMcLV21QAmEiyzFB2AKaY5imDB0uK9pOgHzEN6SITICGSPHYIIQTZOc5FMgVuq9t14XS9t0XnR97byoorrvRGddEzkT3T-unqKi97Ypo1p3IowtFbXelV6HsKOUq5zXqhuGlfDKNq7UjQ42nIAjI6qg57s8Ay_XV8_r23jzcHO3Xm1ilVLWxapQKZQYCqVkVkiqM5FkihbYZKnMc4ONpDmRw5UkCknDkGFUM0WYyLA2GM_A5Va37WWtC6XH_1S89bYW_pM7Yfn_TmNfeek-OMYEpZgMAhdbAeVdCF6b_SxM-Gg2dxUfzeaD2QN99nfdnv2xdgDOt0BoRVPYwoXft1Rxgr8PSXP8BfI2i5g</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>Acquired/intratumoral mutation of KRAS during metastatic progression of colorectal carcinogenesis</title><source>Spandidos Publications Journals</source><source>EZB-FREE-00999 freely available EZB journals</source><source>PubMed Central</source><creator>OTSUKA, KAZUNORI ; SATOYOSHI, RIKA ; NANJO, HIROSHI ; MIYAZAWA, HIDEAKI ; ABE, YUKI ; TANAKA, MASAMITSU ; YAMAMOTO, YUZO ; SHIBATA, HIROYUKI</creator><creatorcontrib>OTSUKA, KAZUNORI ; SATOYOSHI, RIKA ; NANJO, HIROSHI ; MIYAZAWA, HIDEAKI ; ABE, YUKI ; TANAKA, MASAMITSU ; YAMAMOTO, YUZO ; SHIBATA, HIROYUKI</creatorcontrib><description>Mutations at codons 12 and 13 of the KRAS gene have been identified as level I predictive biomarkers against the treatment of advanced colorectal cancer with anti-epidermal growth factor receptor (EGFR) monoclonal antibodies. It is thought that the genetic analysis of KRAS mutations associated with metastatic colorectal cancer can be routinely conducted using DNA obtained on one occasion from one organ, from the primary or a metastatic site, whichever is preferentially available. However, the issue of tumor heterogeneity resulting from acquired/intratumoral mutations remains. Recently, the possibility of acquired/intratumoral mutations in the KRAS gene has been reported by two research groups and has ranged from 7.4 to 15.4%. Specimens were collected from advanced colorectal cancer patients with resected primary, and at least one metastatic, site. Direct sequence analysis was performed for KRAS, BRAF and PIK3CA, and immunohistochemistry for glutathione S-transferase II (GSTP) and EGFR. In the current study, we identified an acquired mutation rate of approximately 11.1% in the KRAS gene (1/9). This figure is not negligible. Our observation indicates, particularly in the case of metastatic recurrence after a long interval, that there may be considerable tumor heterogeneity resulting from acquired or intratumoral mutations of the KRAS gene.</description><identifier>ISSN: 1792-1074</identifier><identifier>EISSN: 1792-1082</identifier><identifier>DOI: 10.3892/ol.2011.543</identifier><identifier>PMID: 22740969</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>acquired/intratumor mutation ; BRAF ; colorectal cancer ; KRAS ; PIK3CA</subject><ispartof>Oncology letters, 2012-03, Vol.3 (3), p.649-653</ispartof><rights>Copyright © 2012, Spandidos Publications</rights><rights>Copyright © 2012, Spandidos Publications 2012</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c478t-cdc41b31accb5db7e5a05c7d3f54b99f3fb796b5c7b6c2bf82f87e8c68a53ef33</citedby><cites>FETCH-LOGICAL-c478t-cdc41b31accb5db7e5a05c7d3f54b99f3fb796b5c7b6c2bf82f87e8c68a53ef33</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3362436/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3362436/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,5571,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22740969$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>OTSUKA, KAZUNORI</creatorcontrib><creatorcontrib>SATOYOSHI, RIKA</creatorcontrib><creatorcontrib>NANJO, HIROSHI</creatorcontrib><creatorcontrib>MIYAZAWA, HIDEAKI</creatorcontrib><creatorcontrib>ABE, YUKI</creatorcontrib><creatorcontrib>TANAKA, MASAMITSU</creatorcontrib><creatorcontrib>YAMAMOTO, YUZO</creatorcontrib><creatorcontrib>SHIBATA, HIROYUKI</creatorcontrib><title>Acquired/intratumoral mutation of KRAS during metastatic progression of colorectal carcinogenesis</title><title>Oncology letters</title><addtitle>Oncol Lett</addtitle><description>Mutations at codons 12 and 13 of the KRAS gene have been identified as level I predictive biomarkers against the treatment of advanced colorectal cancer with anti-epidermal growth factor receptor (EGFR) monoclonal antibodies. It is thought that the genetic analysis of KRAS mutations associated with metastatic colorectal cancer can be routinely conducted using DNA obtained on one occasion from one organ, from the primary or a metastatic site, whichever is preferentially available. However, the issue of tumor heterogeneity resulting from acquired/intratumoral mutations remains. Recently, the possibility of acquired/intratumoral mutations in the KRAS gene has been reported by two research groups and has ranged from 7.4 to 15.4%. Specimens were collected from advanced colorectal cancer patients with resected primary, and at least one metastatic, site. Direct sequence analysis was performed for KRAS, BRAF and PIK3CA, and immunohistochemistry for glutathione S-transferase II (GSTP) and EGFR. In the current study, we identified an acquired mutation rate of approximately 11.1% in the KRAS gene (1/9). This figure is not negligible. Our observation indicates, particularly in the case of metastatic recurrence after a long interval, that there may be considerable tumor heterogeneity resulting from acquired or intratumoral mutations of the KRAS gene.</description><subject>acquired/intratumor mutation</subject><subject>BRAF</subject><subject>colorectal cancer</subject><subject>KRAS</subject><subject>PIK3CA</subject><issn>1792-1074</issn><issn>1792-1082</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><recordid>eNpVkE1LxDAQhoMo7rLuybv05EW62yRtkl6EZfELFwQ_ziFJkxppm5q0gv_e1l1XHQIzZJ55J3kBOIXJArMcLV21QAmEiyzFB2AKaY5imDB0uK9pOgHzEN6SITICGSPHYIIQTZOc5FMgVuq9t14XS9t0XnR97byoorrvRGddEzkT3T-unqKi97Ypo1p3IowtFbXelV6HsKOUq5zXqhuGlfDKNq7UjQ42nIAjI6qg57s8Ay_XV8_r23jzcHO3Xm1ilVLWxapQKZQYCqVkVkiqM5FkihbYZKnMc4ONpDmRw5UkCknDkGFUM0WYyLA2GM_A5Va37WWtC6XH_1S89bYW_pM7Yfn_TmNfeek-OMYEpZgMAhdbAeVdCF6b_SxM-Gg2dxUfzeaD2QN99nfdnv2xdgDOt0BoRVPYwoXft1Rxgr8PSXP8BfI2i5g</recordid><startdate>20120301</startdate><enddate>20120301</enddate><creator>OTSUKA, KAZUNORI</creator><creator>SATOYOSHI, RIKA</creator><creator>NANJO, HIROSHI</creator><creator>MIYAZAWA, HIDEAKI</creator><creator>ABE, YUKI</creator><creator>TANAKA, MASAMITSU</creator><creator>YAMAMOTO, YUZO</creator><creator>SHIBATA, HIROYUKI</creator><general>D.A. Spandidos</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>5PM</scope></search><sort><creationdate>20120301</creationdate><title>Acquired/intratumoral mutation of KRAS during metastatic progression of colorectal carcinogenesis</title><author>OTSUKA, KAZUNORI ; SATOYOSHI, RIKA ; NANJO, HIROSHI ; MIYAZAWA, HIDEAKI ; ABE, YUKI ; TANAKA, MASAMITSU ; YAMAMOTO, YUZO ; SHIBATA, HIROYUKI</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c478t-cdc41b31accb5db7e5a05c7d3f54b99f3fb796b5c7b6c2bf82f87e8c68a53ef33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>acquired/intratumor mutation</topic><topic>BRAF</topic><topic>colorectal cancer</topic><topic>KRAS</topic><topic>PIK3CA</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>OTSUKA, KAZUNORI</creatorcontrib><creatorcontrib>SATOYOSHI, RIKA</creatorcontrib><creatorcontrib>NANJO, HIROSHI</creatorcontrib><creatorcontrib>MIYAZAWA, HIDEAKI</creatorcontrib><creatorcontrib>ABE, YUKI</creatorcontrib><creatorcontrib>TANAKA, MASAMITSU</creatorcontrib><creatorcontrib>YAMAMOTO, YUZO</creatorcontrib><creatorcontrib>SHIBATA, HIROYUKI</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Oncology letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>OTSUKA, KAZUNORI</au><au>SATOYOSHI, RIKA</au><au>NANJO, HIROSHI</au><au>MIYAZAWA, HIDEAKI</au><au>ABE, YUKI</au><au>TANAKA, MASAMITSU</au><au>YAMAMOTO, YUZO</au><au>SHIBATA, HIROYUKI</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Acquired/intratumoral mutation of KRAS during metastatic progression of colorectal carcinogenesis</atitle><jtitle>Oncology letters</jtitle><addtitle>Oncol Lett</addtitle><date>2012-03-01</date><risdate>2012</risdate><volume>3</volume><issue>3</issue><spage>649</spage><epage>653</epage><pages>649-653</pages><issn>1792-1074</issn><eissn>1792-1082</eissn><abstract>Mutations at codons 12 and 13 of the KRAS gene have been identified as level I predictive biomarkers against the treatment of advanced colorectal cancer with anti-epidermal growth factor receptor (EGFR) monoclonal antibodies. It is thought that the genetic analysis of KRAS mutations associated with metastatic colorectal cancer can be routinely conducted using DNA obtained on one occasion from one organ, from the primary or a metastatic site, whichever is preferentially available. However, the issue of tumor heterogeneity resulting from acquired/intratumoral mutations remains. Recently, the possibility of acquired/intratumoral mutations in the KRAS gene has been reported by two research groups and has ranged from 7.4 to 15.4%. Specimens were collected from advanced colorectal cancer patients with resected primary, and at least one metastatic, site. Direct sequence analysis was performed for KRAS, BRAF and PIK3CA, and immunohistochemistry for glutathione S-transferase II (GSTP) and EGFR. In the current study, we identified an acquired mutation rate of approximately 11.1% in the KRAS gene (1/9). This figure is not negligible. Our observation indicates, particularly in the case of metastatic recurrence after a long interval, that there may be considerable tumor heterogeneity resulting from acquired or intratumoral mutations of the KRAS gene.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>22740969</pmid><doi>10.3892/ol.2011.543</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
fulltext | fulltext |
identifier | ISSN: 1792-1074 |
ispartof | Oncology letters, 2012-03, Vol.3 (3), p.649-653 |
issn | 1792-1074 1792-1082 |
language | eng |
recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_3362436 |
source | Spandidos Publications Journals; EZB-FREE-00999 freely available EZB journals; PubMed Central |
subjects | acquired/intratumor mutation BRAF colorectal cancer KRAS PIK3CA |
title | Acquired/intratumoral mutation of KRAS during metastatic progression of colorectal carcinogenesis |
url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-23T07%3A47%3A02IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-pubmed_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Acquired/intratumoral%20mutation%20of%20KRAS%20during%20metastatic%20progression%20of%20colorectal%20carcinogenesis&rft.jtitle=Oncology%20letters&rft.au=OTSUKA,%20KAZUNORI&rft.date=2012-03-01&rft.volume=3&rft.issue=3&rft.spage=649&rft.epage=653&rft.pages=649-653&rft.issn=1792-1074&rft.eissn=1792-1082&rft_id=info:doi/10.3892/ol.2011.543&rft_dat=%3Cpubmed_cross%3E22740969%3C/pubmed_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_id=info:pmid/22740969&rfr_iscdi=true |