Clinicopathological features and prognostic roles of KRAS, BRAF, PIK3CA and NRAS mutations in advanced gastric cancer
RAS-RAF-MEK-ERK and PI3K-AKT pathways form a significant cascade for potential molecular target therapy in advanced cancer. The clinical significance of mutations in these genes in advanced gastric cancer (AGC) is uncertain. We collected formalin-fixed, paraffin-embedded and fresh frozen tumor sampl...
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| creator | Takahashi, Naoki Yamada, Yasuhide Taniguchi, Hirokazu Fukahori, Masaru Sasaki, Yusuke Shoji, Hirokazu Honma, Yoshitaka Iwasa, Satoru Takashima, Atsuo Kato, Ken Hamaguchi, Tetsuya Shimada, Yasuhiro |
| description | RAS-RAF-MEK-ERK and PI3K-AKT pathways form a significant cascade for potential molecular target therapy in advanced cancer. The clinical significance of mutations in these genes in advanced gastric cancer (AGC) is uncertain.
We collected formalin-fixed, paraffin-embedded and fresh frozen tumor samples from AGC patients and analyzed the KRAS, NRAS, BRAF and PIK3CA mutations by direct-sequencing. We retrospectively investigated the clinicopathological features of these mutations in AGC patients, and selected patients with metastatic gastric cancer.
Among 167 AGC patients, mutations of KRAS codons 12/13 (N = 8/164, 4.9%), PIK3CA (N = 9/163, 5.5%), and NRAS codon 12/13(N = 3/159, 1.9%) were detected. Comparison of the clinicopathological features of the mutated KRAS, PIK3CA, NRAS genes with an all-wild type of these genes showed that the frequency of the intestinal type was significantly higher in patients whose tumor tissue contained KRAS mutations (P = 0.014). Among 125 patients with metastatic gastric cancer, patients with NRAS codon 12/13 mutations in their tumors had shorter overall survival compared with NRAS wild-type patients (MST: 14.7 vs 8.8 months, P = 0.011). By multivariate analyses, NRAS codon 12/13 mutation was an indicator for poor prognosis in patients with metastatic gastric cancer (adjusted HR 5.607, 95% CI: 1.637-19.203).
Our study indicated that mutations of KRAS, PIK3CA and NRAS were rare in AGC. NRAS mutations were likely to associate with poor prognosis in metastatic state of AGC patients, but further validation of other research is required. |
| doi_str_mv | 10.1186/1756-0500-7-271 |
| format | Article |
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We collected formalin-fixed, paraffin-embedded and fresh frozen tumor samples from AGC patients and analyzed the KRAS, NRAS, BRAF and PIK3CA mutations by direct-sequencing. We retrospectively investigated the clinicopathological features of these mutations in AGC patients, and selected patients with metastatic gastric cancer.
Among 167 AGC patients, mutations of KRAS codons 12/13 (N = 8/164, 4.9%), PIK3CA (N = 9/163, 5.5%), and NRAS codon 12/13(N = 3/159, 1.9%) were detected. Comparison of the clinicopathological features of the mutated KRAS, PIK3CA, NRAS genes with an all-wild type of these genes showed that the frequency of the intestinal type was significantly higher in patients whose tumor tissue contained KRAS mutations (P = 0.014). Among 125 patients with metastatic gastric cancer, patients with NRAS codon 12/13 mutations in their tumors had shorter overall survival compared with NRAS wild-type patients (MST: 14.7 vs 8.8 months, P = 0.011). By multivariate analyses, NRAS codon 12/13 mutation was an indicator for poor prognosis in patients with metastatic gastric cancer (adjusted HR 5.607, 95% CI: 1.637-19.203).
Our study indicated that mutations of KRAS, PIK3CA and NRAS were rare in AGC. NRAS mutations were likely to associate with poor prognosis in metastatic state of AGC patients, but further validation of other research is required.</description><identifier>ISSN: 1756-0500</identifier><identifier>EISSN: 1756-0500</identifier><identifier>DOI: 10.1186/1756-0500-7-271</identifier><identifier>PMID: 24774510</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Analysis ; Chemotherapy ; Class I Phosphatidylinositol 3-Kinases ; Codon ; Cohort Studies ; Comparative analysis ; Female ; Genes ; Genetic aspects ; GTP Phosphohydrolases - genetics ; Health aspects ; Humans ; Kinases ; Male ; Medical research ; Membrane Proteins - genetics ; Metastasis ; Middle Aged ; Mutation ; Mutation - genetics ; Neoplasm Staging ; Phosphatidylinositol 3-Kinases - genetics ; Prognosis ; Proto-Oncogene Proteins - genetics ; Proto-Oncogene Proteins B-raf - genetics ; Proto-Oncogene Proteins p21(ras) ; ras Proteins - genetics ; Stomach Neoplasms - genetics ; Stomach Neoplasms - pathology ; Studies</subject><ispartof>BMC research notes, 2014-04, Vol.7 (1), p.271-271, Article 271</ispartof><rights>COPYRIGHT 2014 BioMed Central Ltd.</rights><rights>2014 Takahashi et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.</rights><rights>Copyright © 2014 Takahashi et al.; licensee BioMed Central Ltd. 2014 Takahashi et al.; licensee BioMed Central Ltd.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b5621-2c6bb4aebcb8df737c2eb6fc1e99df81c77e30a4b4a61c61e22b2a442b9f2af83</citedby><cites>FETCH-LOGICAL-b5621-2c6bb4aebcb8df737c2eb6fc1e99df81c77e30a4b4a61c61e22b2a442b9f2af83</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/PMC4012089/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4012089/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24774510$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Takahashi, Naoki</creatorcontrib><creatorcontrib>Yamada, Yasuhide</creatorcontrib><creatorcontrib>Taniguchi, Hirokazu</creatorcontrib><creatorcontrib>Fukahori, Masaru</creatorcontrib><creatorcontrib>Sasaki, Yusuke</creatorcontrib><creatorcontrib>Shoji, Hirokazu</creatorcontrib><creatorcontrib>Honma, Yoshitaka</creatorcontrib><creatorcontrib>Iwasa, Satoru</creatorcontrib><creatorcontrib>Takashima, Atsuo</creatorcontrib><creatorcontrib>Kato, Ken</creatorcontrib><creatorcontrib>Hamaguchi, Tetsuya</creatorcontrib><creatorcontrib>Shimada, Yasuhiro</creatorcontrib><title>Clinicopathological features and prognostic roles of KRAS, BRAF, PIK3CA and NRAS mutations in advanced gastric cancer</title><title>BMC research notes</title><addtitle>BMC Res Notes</addtitle><description>RAS-RAF-MEK-ERK and PI3K-AKT pathways form a significant cascade for potential molecular target therapy in advanced cancer. The clinical significance of mutations in these genes in advanced gastric cancer (AGC) is uncertain.
We collected formalin-fixed, paraffin-embedded and fresh frozen tumor samples from AGC patients and analyzed the KRAS, NRAS, BRAF and PIK3CA mutations by direct-sequencing. We retrospectively investigated the clinicopathological features of these mutations in AGC patients, and selected patients with metastatic gastric cancer.
Among 167 AGC patients, mutations of KRAS codons 12/13 (N = 8/164, 4.9%), PIK3CA (N = 9/163, 5.5%), and NRAS codon 12/13(N = 3/159, 1.9%) were detected. Comparison of the clinicopathological features of the mutated KRAS, PIK3CA, NRAS genes with an all-wild type of these genes showed that the frequency of the intestinal type was significantly higher in patients whose tumor tissue contained KRAS mutations (P = 0.014). Among 125 patients with metastatic gastric cancer, patients with NRAS codon 12/13 mutations in their tumors had shorter overall survival compared with NRAS wild-type patients (MST: 14.7 vs 8.8 months, P = 0.011). By multivariate analyses, NRAS codon 12/13 mutation was an indicator for poor prognosis in patients with metastatic gastric cancer (adjusted HR 5.607, 95% CI: 1.637-19.203).
Our study indicated that mutations of KRAS, PIK3CA and NRAS were rare in AGC. NRAS mutations were likely to associate with poor prognosis in metastatic state of AGC patients, but further validation of other research is required.</description><subject>Analysis</subject><subject>Chemotherapy</subject><subject>Class I Phosphatidylinositol 3-Kinases</subject><subject>Codon</subject><subject>Cohort Studies</subject><subject>Comparative analysis</subject><subject>Female</subject><subject>Genes</subject><subject>Genetic aspects</subject><subject>GTP Phosphohydrolases - genetics</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Kinases</subject><subject>Male</subject><subject>Medical research</subject><subject>Membrane Proteins - genetics</subject><subject>Metastasis</subject><subject>Middle Aged</subject><subject>Mutation</subject><subject>Mutation - genetics</subject><subject>Neoplasm Staging</subject><subject>Phosphatidylinositol 3-Kinases - genetics</subject><subject>Prognosis</subject><subject>Proto-Oncogene Proteins - genetics</subject><subject>Proto-Oncogene Proteins B-raf - genetics</subject><subject>Proto-Oncogene Proteins p21(ras)</subject><subject>ras Proteins - genetics</subject><subject>Stomach Neoplasms - genetics</subject><subject>Stomach Neoplasms - pathology</subject><subject>Studies</subject><issn>1756-0500</issn><issn>1756-0500</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp1kk1v1DAQhiMEoqVw5oYscQGpaf2RxM6lUrqisGpFUfm4Wo5jp64Se7GdCv49DluWBhX5YHvmmXesd5xlLxE8QohVx4iWVQ5LCHOaY4oeZfu7yON7573sWQg3EFaIMfQ028MFpUWJ4H42rQZjjXQbEa_d4HojxQC0EnHyKgBhO7DxrrcuRCOBd0MKOg3Or5rPh-D0qjk7BJ_W52TV_EY_pjAYpyiicTYAY4HoboWVqgO9CNEnCTlf_fPsiRZDUC_u9oPs69m7L6sP-cXl-_WqucjbssIox7Jq20KoVras05RQiVVbaYlUXXeaIUmpIlAUiamQrJDCuMWiKHBbayw0IwfZyVZ3M7Wj6qSy0YuBb7wZhf_JnTB8mbHmmvfulhcQYcjqJHC6FWiN-4_AMiPdyGfb-Ww7pzwNJYm8uXuFd98nFSIfTZBqGIRVbgoclQQXDBEy93v9D3rjJm-TR4nCuIRlXcK_VC8GxY3VLvWWsyhvygIyQlg9U0cPUGl1akwTt0qbFF8UvF0UJCaqH7EXUwh8ffltyR5vWeldCF7pnScI8vlrPuDCq_uz2PF__iL5Bfl33PM</recordid><startdate>20140429</startdate><enddate>20140429</enddate><creator>Takahashi, Naoki</creator><creator>Yamada, Yasuhide</creator><creator>Taniguchi, Hirokazu</creator><creator>Fukahori, Masaru</creator><creator>Sasaki, Yusuke</creator><creator>Shoji, Hirokazu</creator><creator>Honma, Yoshitaka</creator><creator>Iwasa, Satoru</creator><creator>Takashima, Atsuo</creator><creator>Kato, Ken</creator><creator>Hamaguchi, Tetsuya</creator><creator>Shimada, Yasuhiro</creator><general>BioMed Central Ltd</general><general>BioMed Central</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>IOV</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20140429</creationdate><title>Clinicopathological features and prognostic roles of KRAS, BRAF, PIK3CA and NRAS mutations in advanced gastric cancer</title><author>Takahashi, Naoki ; Yamada, Yasuhide ; Taniguchi, Hirokazu ; Fukahori, Masaru ; Sasaki, Yusuke ; Shoji, Hirokazu ; Honma, Yoshitaka ; Iwasa, Satoru ; Takashima, Atsuo ; Kato, Ken ; Hamaguchi, Tetsuya ; Shimada, Yasuhiro</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b5621-2c6bb4aebcb8df737c2eb6fc1e99df81c77e30a4b4a61c61e22b2a442b9f2af83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Analysis</topic><topic>Chemotherapy</topic><topic>Class I Phosphatidylinositol 3-Kinases</topic><topic>Codon</topic><topic>Cohort Studies</topic><topic>Comparative analysis</topic><topic>Female</topic><topic>Genes</topic><topic>Genetic aspects</topic><topic>GTP Phosphohydrolases - genetics</topic><topic>Health aspects</topic><topic>Humans</topic><topic>Kinases</topic><topic>Male</topic><topic>Medical research</topic><topic>Membrane Proteins - genetics</topic><topic>Metastasis</topic><topic>Middle Aged</topic><topic>Mutation</topic><topic>Mutation - genetics</topic><topic>Neoplasm Staging</topic><topic>Phosphatidylinositol 3-Kinases - genetics</topic><topic>Prognosis</topic><topic>Proto-Oncogene Proteins - genetics</topic><topic>Proto-Oncogene Proteins B-raf - genetics</topic><topic>Proto-Oncogene Proteins p21(ras)</topic><topic>ras Proteins - genetics</topic><topic>Stomach Neoplasms - genetics</topic><topic>Stomach Neoplasms - pathology</topic><topic>Studies</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Takahashi, Naoki</creatorcontrib><creatorcontrib>Yamada, Yasuhide</creatorcontrib><creatorcontrib>Taniguchi, Hirokazu</creatorcontrib><creatorcontrib>Fukahori, Masaru</creatorcontrib><creatorcontrib>Sasaki, Yusuke</creatorcontrib><creatorcontrib>Shoji, Hirokazu</creatorcontrib><creatorcontrib>Honma, Yoshitaka</creatorcontrib><creatorcontrib>Iwasa, Satoru</creatorcontrib><creatorcontrib>Takashima, Atsuo</creatorcontrib><creatorcontrib>Kato, Ken</creatorcontrib><creatorcontrib>Hamaguchi, Tetsuya</creatorcontrib><creatorcontrib>Shimada, Yasuhiro</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Opposing Viewpoints</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>BMC research notes</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Takahashi, Naoki</au><au>Yamada, Yasuhide</au><au>Taniguchi, Hirokazu</au><au>Fukahori, Masaru</au><au>Sasaki, Yusuke</au><au>Shoji, Hirokazu</au><au>Honma, Yoshitaka</au><au>Iwasa, Satoru</au><au>Takashima, Atsuo</au><au>Kato, Ken</au><au>Hamaguchi, Tetsuya</au><au>Shimada, Yasuhiro</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Clinicopathological features and prognostic roles of KRAS, BRAF, PIK3CA and NRAS mutations in advanced gastric cancer</atitle><jtitle>BMC research notes</jtitle><addtitle>BMC Res Notes</addtitle><date>2014-04-29</date><risdate>2014</risdate><volume>7</volume><issue>1</issue><spage>271</spage><epage>271</epage><pages>271-271</pages><artnum>271</artnum><issn>1756-0500</issn><eissn>1756-0500</eissn><abstract>RAS-RAF-MEK-ERK and PI3K-AKT pathways form a significant cascade for potential molecular target therapy in advanced cancer. The clinical significance of mutations in these genes in advanced gastric cancer (AGC) is uncertain.
We collected formalin-fixed, paraffin-embedded and fresh frozen tumor samples from AGC patients and analyzed the KRAS, NRAS, BRAF and PIK3CA mutations by direct-sequencing. We retrospectively investigated the clinicopathological features of these mutations in AGC patients, and selected patients with metastatic gastric cancer.
Among 167 AGC patients, mutations of KRAS codons 12/13 (N = 8/164, 4.9%), PIK3CA (N = 9/163, 5.5%), and NRAS codon 12/13(N = 3/159, 1.9%) were detected. Comparison of the clinicopathological features of the mutated KRAS, PIK3CA, NRAS genes with an all-wild type of these genes showed that the frequency of the intestinal type was significantly higher in patients whose tumor tissue contained KRAS mutations (P = 0.014). Among 125 patients with metastatic gastric cancer, patients with NRAS codon 12/13 mutations in their tumors had shorter overall survival compared with NRAS wild-type patients (MST: 14.7 vs 8.8 months, P = 0.011). By multivariate analyses, NRAS codon 12/13 mutation was an indicator for poor prognosis in patients with metastatic gastric cancer (adjusted HR 5.607, 95% CI: 1.637-19.203).
Our study indicated that mutations of KRAS, PIK3CA and NRAS were rare in AGC. NRAS mutations were likely to associate with poor prognosis in metastatic state of AGC patients, but further validation of other research is required.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>24774510</pmid><doi>10.1186/1756-0500-7-271</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Analysis Chemotherapy Class I Phosphatidylinositol 3-Kinases Codon Cohort Studies Comparative analysis Female Genes Genetic aspects GTP Phosphohydrolases - genetics Health aspects Humans Kinases Male Medical research Membrane Proteins - genetics Metastasis Middle Aged Mutation Mutation - genetics Neoplasm Staging Phosphatidylinositol 3-Kinases - genetics Prognosis Proto-Oncogene Proteins - genetics Proto-Oncogene Proteins B-raf - genetics Proto-Oncogene Proteins p21(ras) ras Proteins - genetics Stomach Neoplasms - genetics Stomach Neoplasms - pathology Studies |
| title | Clinicopathological features and prognostic roles of KRAS, BRAF, PIK3CA and NRAS mutations in advanced gastric cancer |
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