Mutations in exon 7 and 8 of p53 as poor prognostic factors in patients with non-small cell lung cancer
This study was performed to clarify the different effects of each mutant exon of p53 as indicators of a poor prognosis in patients with non-small cell lung cancer (NSCLC). Tumor tissues of 204 patients with NSCLC were analysed; 96 tumors were stage I, 22 stage II, and 86 stage III. DNA was extracted...
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| Veröffentlicht in: | Oncogene 1998-05, Vol.16 (19), p.2469-2477 |
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| description | This study was performed to clarify the different effects of each mutant exon of p53 as indicators of a poor prognosis in patients with non-small cell lung cancer (NSCLC). Tumor tissues of 204 patients with NSCLC were analysed; 96 tumors were stage I, 22 stage II, and 86 stage III. DNA was extracted from frozen specimens and polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) and direct sequencing were performed to investigate mutations of p53 from exon 5 to exon 8. Seventy-five patients with NSCLC (36.8%) had mutations in p53 which included 72 cases of missense mutations and three cases of non-missense mutations. The overall survival rate of patients with mutant p53 adenocarcinomas was strikingly worse than that of patients whose tumors had wild-type p53 (35.7% vs 53.8%; P=0.041), but no significant difference in survival was found in the patients with NSCLC and squamous cell carcinoma. Mutations in exon 5 of p53 occurred in 33 cases (16.2%), mutation in exon 6 was detected in only one case (0.5%), mutations in exon 7 in 20 cases (9.8%), and mutations in exon 8 in 18 cases (8.8%). The overall survival rate of patients with mutations in exon 7 was worse than that of patients with wild-type p53 in NSCLCs and adenocarcinomas (42.9% vs 56.0%; P=0.025 and 33.3% vs 53.8%; P=0.048, respectively), whereas the overall survival of patients with mutations in exon 5 was almost the same as that of patients with wild-type p53. In addition, the overall survival rate of patients with mutations in exon 8 was strikingly worse than that of patients with wild-type p53 in NSCLCs, adenocarcinomas and squamous cell carcinomas (22.9% vs 56.0%; P |
| doi_str_mv | 10.1038/sj.onc.1201776 |
| format | Article |
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Tumor tissues of 204 patients with NSCLC were analysed; 96 tumors were stage I, 22 stage II, and 86 stage III. DNA was extracted from frozen specimens and polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) and direct sequencing were performed to investigate mutations of p53 from exon 5 to exon 8. Seventy-five patients with NSCLC (36.8%) had mutations in p53 which included 72 cases of missense mutations and three cases of non-missense mutations. The overall survival rate of patients with mutant p53 adenocarcinomas was strikingly worse than that of patients whose tumors had wild-type p53 (35.7% vs 53.8%; P=0.041), but no significant difference in survival was found in the patients with NSCLC and squamous cell carcinoma. Mutations in exon 5 of p53 occurred in 33 cases (16.2%), mutation in exon 6 was detected in only one case (0.5%), mutations in exon 7 in 20 cases (9.8%), and mutations in exon 8 in 18 cases (8.8%). The overall survival rate of patients with mutations in exon 7 was worse than that of patients with wild-type p53 in NSCLCs and adenocarcinomas (42.9% vs 56.0%; P=0.025 and 33.3% vs 53.8%; P=0.048, respectively), whereas the overall survival of patients with mutations in exon 5 was almost the same as that of patients with wild-type p53. In addition, the overall survival rate of patients with mutations in exon 8 was strikingly worse than that of patients with wild-type p53 in NSCLCs, adenocarcinomas and squamous cell carcinomas (22.9% vs 56.0%; P<0.001, 19.0% vs 53.8%; P=0.004 and 33.3% vs 62.5%; P=0.042, respectively). Multivariate analysis with the Cox regression model of patients with NSCLC, adenocarcinoma and squamous cell carcinoma indicated that mutations in exon 8 were best correlated with the overall survival rate, followed by lymph node status (P<0.001, P=0.015 and P=0.006, respectively), and mutations in exon 7 of NSCLC were also revealed to have good correlation, followed by lymph node status and mutations in exon 8 (P=0.031). Mutation of p53 was a poor prognostic factor for adenocarcinoma as described previously. Moreover, mutations in exon 8 were more useful indicators of prognosis not only for adenocarcinoma but also for NSCLC. Worse overall survival of the patients with mutations in exon 8 of p53 was suggested to be associated with codon 273 mutations as well as mutations between codon 280 and 285 included into the H2 alpha helix corresponding to residues 278-286. These results suggested that abnormal conformation of H2 alpha helix might play an important role not only in the loss of normal function but also in the acquisition of tumorigenesis. Investigation of mutations in exon 8, especially codon 273 mutation and mutant H2 alpha helix was considered to be a clinically useful approach for determining the prognosis of patients with NSCLC.</description><identifier>ISSN: 0950-9232</identifier><identifier>EISSN: 1476-5594</identifier><identifier>DOI: 10.1038/sj.onc.1201776</identifier><identifier>PMID: 9627113</identifier><language>eng</language><publisher>Basingstoke: Nature Publishing</publisher><subject>Adenocarcinoma ; Adenocarcinoma - mortality ; Adult ; Aged ; Aged, 80 and over ; Biological and medical sciences ; Carcinoma, Non-Small-Cell Lung - genetics ; Carcinoma, Non-Small-Cell Lung - mortality ; Carcinoma, Non-Small-Cell Lung - physiopathology ; Carcinoma, Squamous Cell - mortality ; Conformation ; Exons ; Female ; Genes, p53 ; Humans ; Lung cancer ; Lung Neoplasms - genetics ; Lung Neoplasms - mortality ; Lung Neoplasms - physiopathology ; Lymph nodes ; Lymphatic system ; Male ; Medical prognosis ; Medical sciences ; Middle Aged ; Missense mutation ; Multivariate analysis ; Mutants ; Mutation ; Nicotiana ; Non-small cell lung carcinoma ; p53 Protein ; Plants, Toxic ; Pneumology ; Polymerase Chain Reaction ; Polymorphism, Single-Stranded Conformational ; Prognosis ; Small cell lung carcinoma ; Smoking ; Squamous cell carcinoma ; Survivors ; Tumorigenesis ; Tumors ; Tumors of the respiratory system and mediastinum</subject><ispartof>Oncogene, 1998-05, Vol.16 (19), p.2469-2477</ispartof><rights>1998 INIST-CNRS</rights><rights>Macmillan Publishers Limited 1998.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c378t-51c42a5aa42f8c55dfea97e5624830b6fbad970279406ba1ebadfe796e60d1e23</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2255177$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9627113$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>HUANG, C.-L</creatorcontrib><creatorcontrib>TAKI, T</creatorcontrib><creatorcontrib>ADACHI, M</creatorcontrib><creatorcontrib>KONISHI, T</creatorcontrib><creatorcontrib>HIGASHIYAMA, M</creatorcontrib><creatorcontrib>MIYAKE, M</creatorcontrib><title>Mutations in exon 7 and 8 of p53 as poor prognostic factors in patients with non-small cell lung cancer</title><title>Oncogene</title><addtitle>Oncogene</addtitle><description>This study was performed to clarify the different effects of each mutant exon of p53 as indicators of a poor prognosis in patients with non-small cell lung cancer (NSCLC). Tumor tissues of 204 patients with NSCLC were analysed; 96 tumors were stage I, 22 stage II, and 86 stage III. DNA was extracted from frozen specimens and polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) and direct sequencing were performed to investigate mutations of p53 from exon 5 to exon 8. Seventy-five patients with NSCLC (36.8%) had mutations in p53 which included 72 cases of missense mutations and three cases of non-missense mutations. The overall survival rate of patients with mutant p53 adenocarcinomas was strikingly worse than that of patients whose tumors had wild-type p53 (35.7% vs 53.8%; P=0.041), but no significant difference in survival was found in the patients with NSCLC and squamous cell carcinoma. Mutations in exon 5 of p53 occurred in 33 cases (16.2%), mutation in exon 6 was detected in only one case (0.5%), mutations in exon 7 in 20 cases (9.8%), and mutations in exon 8 in 18 cases (8.8%). The overall survival rate of patients with mutations in exon 7 was worse than that of patients with wild-type p53 in NSCLCs and adenocarcinomas (42.9% vs 56.0%; P=0.025 and 33.3% vs 53.8%; P=0.048, respectively), whereas the overall survival of patients with mutations in exon 5 was almost the same as that of patients with wild-type p53. In addition, the overall survival rate of patients with mutations in exon 8 was strikingly worse than that of patients with wild-type p53 in NSCLCs, adenocarcinomas and squamous cell carcinomas (22.9% vs 56.0%; P<0.001, 19.0% vs 53.8%; P=0.004 and 33.3% vs 62.5%; P=0.042, respectively). Multivariate analysis with the Cox regression model of patients with NSCLC, adenocarcinoma and squamous cell carcinoma indicated that mutations in exon 8 were best correlated with the overall survival rate, followed by lymph node status (P<0.001, P=0.015 and P=0.006, respectively), and mutations in exon 7 of NSCLC were also revealed to have good correlation, followed by lymph node status and mutations in exon 8 (P=0.031). Mutation of p53 was a poor prognostic factor for adenocarcinoma as described previously. Moreover, mutations in exon 8 were more useful indicators of prognosis not only for adenocarcinoma but also for NSCLC. Worse overall survival of the patients with mutations in exon 8 of p53 was suggested to be associated with codon 273 mutations as well as mutations between codon 280 and 285 included into the H2 alpha helix corresponding to residues 278-286. These results suggested that abnormal conformation of H2 alpha helix might play an important role not only in the loss of normal function but also in the acquisition of tumorigenesis. Investigation of mutations in exon 8, especially codon 273 mutation and mutant H2 alpha helix was considered to be a clinically useful approach for determining the prognosis of patients with NSCLC.</description><subject>Adenocarcinoma</subject><subject>Adenocarcinoma - mortality</subject><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Biological and medical sciences</subject><subject>Carcinoma, Non-Small-Cell Lung - genetics</subject><subject>Carcinoma, Non-Small-Cell Lung - mortality</subject><subject>Carcinoma, Non-Small-Cell Lung - physiopathology</subject><subject>Carcinoma, Squamous Cell - mortality</subject><subject>Conformation</subject><subject>Exons</subject><subject>Female</subject><subject>Genes, p53</subject><subject>Humans</subject><subject>Lung cancer</subject><subject>Lung Neoplasms - genetics</subject><subject>Lung Neoplasms - mortality</subject><subject>Lung Neoplasms - physiopathology</subject><subject>Lymph nodes</subject><subject>Lymphatic system</subject><subject>Male</subject><subject>Medical prognosis</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Missense mutation</subject><subject>Multivariate analysis</subject><subject>Mutants</subject><subject>Mutation</subject><subject>Nicotiana</subject><subject>Non-small cell lung carcinoma</subject><subject>p53 Protein</subject><subject>Plants, Toxic</subject><subject>Pneumology</subject><subject>Polymerase Chain Reaction</subject><subject>Polymorphism, Single-Stranded Conformational</subject><subject>Prognosis</subject><subject>Small cell lung carcinoma</subject><subject>Smoking</subject><subject>Squamous cell carcinoma</subject><subject>Survivors</subject><subject>Tumorigenesis</subject><subject>Tumors</subject><subject>Tumors of the respiratory system and mediastinum</subject><issn>0950-9232</issn><issn>1476-5594</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkM1r3DAQxUVpSTdpr7kVBA25easPS7KOJaRNIKWX9ixmZWnjxSu5Gpuk_32VxuSQywzD_N7j8Qg552zLmey-4GGbk99ywbgx-g3Z8NboRinbviUbZhVrrJDiPTlFPDDGjGXihJxYLQznckP2P5YZ5iEnpEOi4TEnaiiknnY0RzopSQHplHOhU8n7lHEePI3g51z-K6YqDmlG-jDM9zTl1OARxpH6UMe4pD31kHwoH8i7CCOGj-s-I7-_Xf-6umnufn6_vfp613hpurlR3LcCFEArYueV6mMAa4LSou0k2-m4g94aJoxtmd4BD_WOwVgdNOt5EPKMXD771rh_loCzOw74FAZSyAs6rlsplGEV_PwKPOSlpJrNCd1yyaTuZKW2z5QvGbGE6KYyHKH8dZy5p_4dHlzt3639V8Gn1XbZHUP_gq-F1__F-gf0MMZS2xnwBRNCqeoj_wFxiY2e</recordid><startdate>19980514</startdate><enddate>19980514</enddate><creator>HUANG, C.-L</creator><creator>TAKI, T</creator><creator>ADACHI, M</creator><creator>KONISHI, T</creator><creator>HIGASHIYAMA, M</creator><creator>MIYAKE, M</creator><general>Nature Publishing</general><general>Nature Publishing Group</general><scope>IQODW</scope><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>7U9</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope></search><sort><creationdate>19980514</creationdate><title>Mutations in exon 7 and 8 of p53 as poor prognostic factors in patients with non-small cell lung cancer</title><author>HUANG, C.-L ; TAKI, T ; ADACHI, M ; KONISHI, T ; HIGASHIYAMA, M ; MIYAKE, M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c378t-51c42a5aa42f8c55dfea97e5624830b6fbad970279406ba1ebadfe796e60d1e23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Adenocarcinoma</topic><topic>Adenocarcinoma - mortality</topic><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Biological and medical sciences</topic><topic>Carcinoma, Non-Small-Cell Lung - genetics</topic><topic>Carcinoma, Non-Small-Cell Lung - mortality</topic><topic>Carcinoma, Non-Small-Cell Lung - physiopathology</topic><topic>Carcinoma, Squamous Cell - mortality</topic><topic>Conformation</topic><topic>Exons</topic><topic>Female</topic><topic>Genes, p53</topic><topic>Humans</topic><topic>Lung cancer</topic><topic>Lung Neoplasms - genetics</topic><topic>Lung Neoplasms - mortality</topic><topic>Lung Neoplasms - physiopathology</topic><topic>Lymph nodes</topic><topic>Lymphatic system</topic><topic>Male</topic><topic>Medical prognosis</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Missense mutation</topic><topic>Multivariate analysis</topic><topic>Mutants</topic><topic>Mutation</topic><topic>Nicotiana</topic><topic>Non-small cell lung carcinoma</topic><topic>p53 Protein</topic><topic>Plants, Toxic</topic><topic>Pneumology</topic><topic>Polymerase Chain Reaction</topic><topic>Polymorphism, Single-Stranded Conformational</topic><topic>Prognosis</topic><topic>Small cell lung carcinoma</topic><topic>Smoking</topic><topic>Squamous cell carcinoma</topic><topic>Survivors</topic><topic>Tumorigenesis</topic><topic>Tumors</topic><topic>Tumors of the respiratory system and mediastinum</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>HUANG, C.-L</creatorcontrib><creatorcontrib>TAKI, T</creatorcontrib><creatorcontrib>ADACHI, M</creatorcontrib><creatorcontrib>KONISHI, T</creatorcontrib><creatorcontrib>HIGASHIYAMA, M</creatorcontrib><creatorcontrib>MIYAKE, M</creatorcontrib><collection>Pascal-Francis</collection><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>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><jtitle>Oncogene</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>HUANG, C.-L</au><au>TAKI, T</au><au>ADACHI, M</au><au>KONISHI, T</au><au>HIGASHIYAMA, M</au><au>MIYAKE, M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mutations in exon 7 and 8 of p53 as poor prognostic factors in patients with non-small cell lung cancer</atitle><jtitle>Oncogene</jtitle><addtitle>Oncogene</addtitle><date>1998-05-14</date><risdate>1998</risdate><volume>16</volume><issue>19</issue><spage>2469</spage><epage>2477</epage><pages>2469-2477</pages><issn>0950-9232</issn><eissn>1476-5594</eissn><abstract>This study was performed to clarify the different effects of each mutant exon of p53 as indicators of a poor prognosis in patients with non-small cell lung cancer (NSCLC). Tumor tissues of 204 patients with NSCLC were analysed; 96 tumors were stage I, 22 stage II, and 86 stage III. DNA was extracted from frozen specimens and polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) and direct sequencing were performed to investigate mutations of p53 from exon 5 to exon 8. Seventy-five patients with NSCLC (36.8%) had mutations in p53 which included 72 cases of missense mutations and three cases of non-missense mutations. The overall survival rate of patients with mutant p53 adenocarcinomas was strikingly worse than that of patients whose tumors had wild-type p53 (35.7% vs 53.8%; P=0.041), but no significant difference in survival was found in the patients with NSCLC and squamous cell carcinoma. Mutations in exon 5 of p53 occurred in 33 cases (16.2%), mutation in exon 6 was detected in only one case (0.5%), mutations in exon 7 in 20 cases (9.8%), and mutations in exon 8 in 18 cases (8.8%). The overall survival rate of patients with mutations in exon 7 was worse than that of patients with wild-type p53 in NSCLCs and adenocarcinomas (42.9% vs 56.0%; P=0.025 and 33.3% vs 53.8%; P=0.048, respectively), whereas the overall survival of patients with mutations in exon 5 was almost the same as that of patients with wild-type p53. In addition, the overall survival rate of patients with mutations in exon 8 was strikingly worse than that of patients with wild-type p53 in NSCLCs, adenocarcinomas and squamous cell carcinomas (22.9% vs 56.0%; P<0.001, 19.0% vs 53.8%; P=0.004 and 33.3% vs 62.5%; P=0.042, respectively). Multivariate analysis with the Cox regression model of patients with NSCLC, adenocarcinoma and squamous cell carcinoma indicated that mutations in exon 8 were best correlated with the overall survival rate, followed by lymph node status (P<0.001, P=0.015 and P=0.006, respectively), and mutations in exon 7 of NSCLC were also revealed to have good correlation, followed by lymph node status and mutations in exon 8 (P=0.031). Mutation of p53 was a poor prognostic factor for adenocarcinoma as described previously. Moreover, mutations in exon 8 were more useful indicators of prognosis not only for adenocarcinoma but also for NSCLC. Worse overall survival of the patients with mutations in exon 8 of p53 was suggested to be associated with codon 273 mutations as well as mutations between codon 280 and 285 included into the H2 alpha helix corresponding to residues 278-286. These results suggested that abnormal conformation of H2 alpha helix might play an important role not only in the loss of normal function but also in the acquisition of tumorigenesis. Investigation of mutations in exon 8, especially codon 273 mutation and mutant H2 alpha helix was considered to be a clinically useful approach for determining the prognosis of patients with NSCLC.</abstract><cop>Basingstoke</cop><pub>Nature Publishing</pub><pmid>9627113</pmid><doi>10.1038/sj.onc.1201776</doi><tpages>9</tpages></addata></record> |
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| subjects | Adenocarcinoma Adenocarcinoma - mortality Adult Aged Aged, 80 and over Biological and medical sciences Carcinoma, Non-Small-Cell Lung - genetics Carcinoma, Non-Small-Cell Lung - mortality Carcinoma, Non-Small-Cell Lung - physiopathology Carcinoma, Squamous Cell - mortality Conformation Exons Female Genes, p53 Humans Lung cancer Lung Neoplasms - genetics Lung Neoplasms - mortality Lung Neoplasms - physiopathology Lymph nodes Lymphatic system Male Medical prognosis Medical sciences Middle Aged Missense mutation Multivariate analysis Mutants Mutation Nicotiana Non-small cell lung carcinoma p53 Protein Plants, Toxic Pneumology Polymerase Chain Reaction Polymorphism, Single-Stranded Conformational Prognosis Small cell lung carcinoma Smoking Squamous cell carcinoma Survivors Tumorigenesis Tumors Tumors of the respiratory system and mediastinum |
| title | Mutations in exon 7 and 8 of p53 as poor prognostic factors in patients with non-small cell lung cancer |
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