KRAS and TP53 mutations in bronchoscopy samples from former lung cancer patients
Mutations in the KRAS and TP53 genes have been found frequently in lung tumors and specimens from individuals at high risk for lung cancer and have been suggested as predictive markers for lung cancer. In order to assess the prognostic value of these two genes’ mutations in lung cancer recurrence, w...
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Veröffentlicht in: | Molecular carcinogenesis 2017-02, Vol.56 (2), p.381-388 |
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description | Mutations in the KRAS and TP53 genes have been found frequently in lung tumors and specimens from individuals at high risk for lung cancer and have been suggested as predictive markers for lung cancer. In order to assess the prognostic value of these two genes’ mutations in lung cancer recurrence, we analyzed mutations in codon 12 of the KRAS gene and in hotspot codons of the TP53 gene in 176 bronchial biopsies obtained from 77 former lung cancer patients. Forty‐seven patients (61.0%) showed mutations, including 35/77 (45.5%) in the KRAS gene and 25/77 (32.5%) in the TP53 gene, among them 13/77 (16.9%) had mutations in both genes. When grouped according to past or current smoking status, a higher proportion of current smokers showed mutations, in particular those in the TP53 gene (P = 0.07), compared with ex‐smokers. These mutations were found in both abnormal lesions (8/20 or 40%) and histologically normal tissues (70/156 or 44.9%) (P = 0.812). They consisted primarily of G to A transition and G to T transversion in both the KRAS (41/56 or 73.2%) and TP53 (24/34 or 70.6%) genes, consistent with mutations found in lung tumors of smoking lung cancer patients. Overall, recurrence‐free survival (RFS) among all subjects could be explained by age at diagnosis, tumor stage, tumor subtype, and smoking (P |
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In order to assess the prognostic value of these two genes’ mutations in lung cancer recurrence, we analyzed mutations in codon 12 of the KRAS gene and in hotspot codons of the TP53 gene in 176 bronchial biopsies obtained from 77 former lung cancer patients. Forty‐seven patients (61.0%) showed mutations, including 35/77 (45.5%) in the KRAS gene and 25/77 (32.5%) in the TP53 gene, among them 13/77 (16.9%) had mutations in both genes. When grouped according to past or current smoking status, a higher proportion of current smokers showed mutations, in particular those in the TP53 gene (P = 0.07), compared with ex‐smokers. These mutations were found in both abnormal lesions (8/20 or 40%) and histologically normal tissues (70/156 or 44.9%) (P = 0.812). They consisted primarily of G to A transition and G to T transversion in both the KRAS (41/56 or 73.2%) and TP53 (24/34 or 70.6%) genes, consistent with mutations found in lung tumors of smoking lung cancer patients. Overall, recurrence‐free survival (RFS) among all subjects could be explained by age at diagnosis, tumor stage, tumor subtype, and smoking (P < 0.05, Cox proportional hazard). Therefore, KRAS and TP53 mutations were frequently detected in bronchial tissues of former lung cancer patients. However, the presence of mutation of bronchial biopsies was not significantly associated with a shorter RFS time. © 2016 Wiley Periodicals, Inc.</description><identifier>ISSN: 0899-1987</identifier><identifier>EISSN: 1098-2744</identifier><identifier>DOI: 10.1002/mc.22501</identifier><identifier>PMID: 27182622</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>Aged ; Biomarkers ; Biopsy ; Bronchoscopy ; Codons ; Disease-Free Survival ; Female ; Genes ; Genetics ; Health risks ; Histology ; Humans ; K-Ras protein ; KRAS mutation ; Lung - pathology ; Lung cancer ; Lung Neoplasms - diagnosis ; Lung Neoplasms - genetics ; Lung Neoplasms - pathology ; Male ; Middle Aged ; Mutation ; Neoplasm Recurrence, Local - diagnosis ; Neoplasm Recurrence, Local - genetics ; Neoplasm Recurrence, Local - pathology ; p53 Protein ; Proto-Oncogene Proteins p21(ras) - genetics ; recurrence‐free survival ; Smoking ; Smoking - adverse effects ; Survival analysis ; TP53 mutation ; Transversion ; Tumor Suppressor Protein p53 - genetics ; Tumors</subject><ispartof>Molecular carcinogenesis, 2017-02, Vol.56 (2), p.381-388</ispartof><rights>2016 Wiley Periodicals, Inc.</rights><rights>2017 Wiley Periodicals, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4101-74191b13feab3153fbc060c5cb9fd8d1e9924b41309c6747c214ca1b2012e10a3</citedby><cites>FETCH-LOGICAL-c4101-74191b13feab3153fbc060c5cb9fd8d1e9924b41309c6747c214ca1b2012e10a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fmc.22501$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fmc.22501$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>315,781,785,1418,27929,27930,45579,45580</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27182622$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gao, Weimin</creatorcontrib><creatorcontrib>Jin, Jide</creatorcontrib><creatorcontrib>Yin, Jinling</creatorcontrib><creatorcontrib>Land, Stephanie</creatorcontrib><creatorcontrib>Gaither‐Davis, Autumn</creatorcontrib><creatorcontrib>Christie, Neil</creatorcontrib><creatorcontrib>Luketich, James D.</creatorcontrib><creatorcontrib>Siegfried, Jill M.</creatorcontrib><creatorcontrib>Keohavong, Phouthone</creatorcontrib><title>KRAS and TP53 mutations in bronchoscopy samples from former lung cancer patients</title><title>Molecular carcinogenesis</title><addtitle>Mol Carcinog</addtitle><description>Mutations in the KRAS and TP53 genes have been found frequently in lung tumors and specimens from individuals at high risk for lung cancer and have been suggested as predictive markers for lung cancer. In order to assess the prognostic value of these two genes’ mutations in lung cancer recurrence, we analyzed mutations in codon 12 of the KRAS gene and in hotspot codons of the TP53 gene in 176 bronchial biopsies obtained from 77 former lung cancer patients. Forty‐seven patients (61.0%) showed mutations, including 35/77 (45.5%) in the KRAS gene and 25/77 (32.5%) in the TP53 gene, among them 13/77 (16.9%) had mutations in both genes. When grouped according to past or current smoking status, a higher proportion of current smokers showed mutations, in particular those in the TP53 gene (P = 0.07), compared with ex‐smokers. These mutations were found in both abnormal lesions (8/20 or 40%) and histologically normal tissues (70/156 or 44.9%) (P = 0.812). They consisted primarily of G to A transition and G to T transversion in both the KRAS (41/56 or 73.2%) and TP53 (24/34 or 70.6%) genes, consistent with mutations found in lung tumors of smoking lung cancer patients. Overall, recurrence‐free survival (RFS) among all subjects could be explained by age at diagnosis, tumor stage, tumor subtype, and smoking (P < 0.05, Cox proportional hazard). Therefore, KRAS and TP53 mutations were frequently detected in bronchial tissues of former lung cancer patients. However, the presence of mutation of bronchial biopsies was not significantly associated with a shorter RFS time. © 2016 Wiley Periodicals, Inc.</description><subject>Aged</subject><subject>Biomarkers</subject><subject>Biopsy</subject><subject>Bronchoscopy</subject><subject>Codons</subject><subject>Disease-Free Survival</subject><subject>Female</subject><subject>Genes</subject><subject>Genetics</subject><subject>Health risks</subject><subject>Histology</subject><subject>Humans</subject><subject>K-Ras protein</subject><subject>KRAS mutation</subject><subject>Lung - pathology</subject><subject>Lung cancer</subject><subject>Lung Neoplasms - diagnosis</subject><subject>Lung Neoplasms - genetics</subject><subject>Lung Neoplasms - pathology</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Mutation</subject><subject>Neoplasm Recurrence, Local - diagnosis</subject><subject>Neoplasm Recurrence, Local - genetics</subject><subject>Neoplasm Recurrence, Local - pathology</subject><subject>p53 Protein</subject><subject>Proto-Oncogene Proteins p21(ras) - genetics</subject><subject>recurrence‐free survival</subject><subject>Smoking</subject><subject>Smoking - adverse effects</subject><subject>Survival analysis</subject><subject>TP53 mutation</subject><subject>Transversion</subject><subject>Tumor Suppressor Protein p53 - genetics</subject><subject>Tumors</subject><issn>0899-1987</issn><issn>1098-2744</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kU1rGzEQhkVJqZ200F9QBLn0ss6MpP3Q0ZikCXGIad2z0MraZsNK2kpegv99NrHTQCA9zRyeeWaYl5CvCDMEYGfOzBjLAT-QKYKsMlYKcUSmUEmZoazKCTlO6R4AsczhE5mwEitWMDYlq-uf819U-w1dr3JO3bDV2zb4RFtP6xi8uQvJhH5Hk3Z9ZxNtYnC0CdHZSLvB_6FGezP2_Thn_TZ9Jh8b3SX75VBPyO-L8_XiMlve_rhazJeZEQiYlQIl1sgbq2uOOW9qAwWY3NSy2VQbtFIyUQvkIE1RitIwFEZjzQCZRdD8hHzfe_sY_g42bZVrk7Fdp70NQ1JY5VLIimE1oqdv0PswRD9ep5jkJYdCgvwfNbpEwSUX-etaE0NK0Taqj63TcacQ1FMWyhn1nMWIfjsIh9rZzT_w5fkjkO2Bh7azu3dF6maxFz4CWu6OoQ</recordid><startdate>201702</startdate><enddate>201702</enddate><creator>Gao, Weimin</creator><creator>Jin, Jide</creator><creator>Yin, Jinling</creator><creator>Land, Stephanie</creator><creator>Gaither‐Davis, Autumn</creator><creator>Christie, Neil</creator><creator>Luketich, James D.</creator><creator>Siegfried, Jill M.</creator><creator>Keohavong, Phouthone</creator><general>Wiley Subscription Services, Inc</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>7TM</scope><scope>7TO</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>RC3</scope></search><sort><creationdate>201702</creationdate><title>KRAS and TP53 mutations in bronchoscopy samples from former lung cancer patients</title><author>Gao, Weimin ; Jin, Jide ; Yin, Jinling ; Land, Stephanie ; Gaither‐Davis, Autumn ; Christie, Neil ; Luketich, James D. ; Siegfried, Jill M. ; Keohavong, Phouthone</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4101-74191b13feab3153fbc060c5cb9fd8d1e9924b41309c6747c214ca1b2012e10a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Aged</topic><topic>Biomarkers</topic><topic>Biopsy</topic><topic>Bronchoscopy</topic><topic>Codons</topic><topic>Disease-Free Survival</topic><topic>Female</topic><topic>Genes</topic><topic>Genetics</topic><topic>Health risks</topic><topic>Histology</topic><topic>Humans</topic><topic>K-Ras protein</topic><topic>KRAS mutation</topic><topic>Lung - pathology</topic><topic>Lung cancer</topic><topic>Lung Neoplasms - diagnosis</topic><topic>Lung Neoplasms - genetics</topic><topic>Lung Neoplasms - pathology</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Mutation</topic><topic>Neoplasm Recurrence, Local - diagnosis</topic><topic>Neoplasm Recurrence, Local - genetics</topic><topic>Neoplasm Recurrence, Local - pathology</topic><topic>p53 Protein</topic><topic>Proto-Oncogene Proteins p21(ras) - genetics</topic><topic>recurrence‐free survival</topic><topic>Smoking</topic><topic>Smoking - adverse effects</topic><topic>Survival analysis</topic><topic>TP53 mutation</topic><topic>Transversion</topic><topic>Tumor Suppressor Protein p53 - genetics</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gao, Weimin</creatorcontrib><creatorcontrib>Jin, Jide</creatorcontrib><creatorcontrib>Yin, Jinling</creatorcontrib><creatorcontrib>Land, Stephanie</creatorcontrib><creatorcontrib>Gaither‐Davis, Autumn</creatorcontrib><creatorcontrib>Christie, Neil</creatorcontrib><creatorcontrib>Luketich, James D.</creatorcontrib><creatorcontrib>Siegfried, Jill M.</creatorcontrib><creatorcontrib>Keohavong, Phouthone</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><jtitle>Molecular carcinogenesis</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gao, Weimin</au><au>Jin, Jide</au><au>Yin, Jinling</au><au>Land, Stephanie</au><au>Gaither‐Davis, Autumn</au><au>Christie, Neil</au><au>Luketich, James D.</au><au>Siegfried, Jill M.</au><au>Keohavong, Phouthone</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>KRAS and TP53 mutations in bronchoscopy samples from former lung cancer patients</atitle><jtitle>Molecular carcinogenesis</jtitle><addtitle>Mol Carcinog</addtitle><date>2017-02</date><risdate>2017</risdate><volume>56</volume><issue>2</issue><spage>381</spage><epage>388</epage><pages>381-388</pages><issn>0899-1987</issn><eissn>1098-2744</eissn><abstract>Mutations in the KRAS and TP53 genes have been found frequently in lung tumors and specimens from individuals at high risk for lung cancer and have been suggested as predictive markers for lung cancer. In order to assess the prognostic value of these two genes’ mutations in lung cancer recurrence, we analyzed mutations in codon 12 of the KRAS gene and in hotspot codons of the TP53 gene in 176 bronchial biopsies obtained from 77 former lung cancer patients. Forty‐seven patients (61.0%) showed mutations, including 35/77 (45.5%) in the KRAS gene and 25/77 (32.5%) in the TP53 gene, among them 13/77 (16.9%) had mutations in both genes. When grouped according to past or current smoking status, a higher proportion of current smokers showed mutations, in particular those in the TP53 gene (P = 0.07), compared with ex‐smokers. These mutations were found in both abnormal lesions (8/20 or 40%) and histologically normal tissues (70/156 or 44.9%) (P = 0.812). They consisted primarily of G to A transition and G to T transversion in both the KRAS (41/56 or 73.2%) and TP53 (24/34 or 70.6%) genes, consistent with mutations found in lung tumors of smoking lung cancer patients. Overall, recurrence‐free survival (RFS) among all subjects could be explained by age at diagnosis, tumor stage, tumor subtype, and smoking (P < 0.05, Cox proportional hazard). Therefore, KRAS and TP53 mutations were frequently detected in bronchial tissues of former lung cancer patients. However, the presence of mutation of bronchial biopsies was not significantly associated with a shorter RFS time. © 2016 Wiley Periodicals, Inc.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>27182622</pmid><doi>10.1002/mc.22501</doi><tpages>8</tpages></addata></record> |
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subjects | Aged Biomarkers Biopsy Bronchoscopy Codons Disease-Free Survival Female Genes Genetics Health risks Histology Humans K-Ras protein KRAS mutation Lung - pathology Lung cancer Lung Neoplasms - diagnosis Lung Neoplasms - genetics Lung Neoplasms - pathology Male Middle Aged Mutation Neoplasm Recurrence, Local - diagnosis Neoplasm Recurrence, Local - genetics Neoplasm Recurrence, Local - pathology p53 Protein Proto-Oncogene Proteins p21(ras) - genetics recurrence‐free survival Smoking Smoking - adverse effects Survival analysis TP53 mutation Transversion Tumor Suppressor Protein p53 - genetics Tumors |
title | KRAS and TP53 mutations in bronchoscopy samples from former lung cancer patients |
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