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dc.contributor.authorYamaguchi, Norihiro
dc.contributor.authorVanderlaan, Paul A
dc.contributor.authorFolch, Erik E
dc.contributor.authorBoucher, David H.
dc.contributor.authorCanepa, Hannah M.
dc.contributor.authorKent, Michael
dc.contributor.authorGangadharan, Sidhu
dc.contributor.authorMajid, Adnan
dc.contributor.authorKocher, Olivier Nicolas
dc.contributor.authorGoldstein, Michael A.
dc.contributor.authorHuberman, Mark S.
dc.contributor.authorCosta, Daniel Botelho
dc.date.accessioned2018-04-25T18:01:41Z
dc.date.issued2013
dc.identifierQuick submit: 2017-07-13T09:34:44-0400
dc.identifier.citationYamaguchi, Norihiro, Paul A. VanderLaan, Erik Folch, David H. Boucher, Hannah M. Canepa, Michael S. Kent, Sidharta P. Gangadharan, et al. 2013. “Smoking Status and Self-Reported Race Affect the Frequency of Clinically Relevant Oncogenic Alterations in Non-Small-Cell Lung Cancers at a United States-Based Academic Medical Practice.” Lung Cancer 82 (1) (October): 31–37. doi:10.1016/j.lungcan.2013.07.013.en_US
dc.identifier.issn0169-5002en_US
dc.identifier.urihttp://nrs.harvard.edu/urn-3:HUL.InstRepos:36304198
dc.description.abstractIntroduction The identification of somatic genomic aberrations in non-small-cell lung cancer (NSCLC) is part of evidence-based practice guidelines for care of patients with NSCLC. We sought to establish the frequency and correlates with these changes in routine patient–tumor sample pairs. Methods Clinicopathologic data and tumor genotype were retrospectively compiled and analyzed from an overall cohort of 381 patient–tumor samples. Results Of these patients, 75.9% self-reported White race, 13.1% Asian, 6.5% Black, 27.8% were never-smokers, 54.9% former-smokers and 17.3% current-smokers. The frequency of EGFR mutations was 23.9% (86/359), KRAS mutations 34.2% (71/207) and ALK FISH positivity 9.1% (23/252) in tumor samples, and almost all had mutually exclusive results for these oncogenes. In tumors from White, Black and Asian patients, the frequencies of EGFR mutations were 18.4%, 18.2% and 62%, respectively; of ALK FISH positivity 7.81%, 0% and 14.8%, respectively; and of KRAS mutations 41.6%, 20% and 0%. These patterns changed significant with increasing pack-year history of smoking. In White patients, the frequencies of EGFR mutations and ALK FISH positivity decreased with increasing pack-year cohorts; while the frequencies of KRAS mutations increased. Interestingly, in Asian patients the frequencies of EGFR mutations were similar in never smokers and in the cohorts with less than 45pack-year histories of smoking and only decreased in the 45pack-year plus cohort. Conclusions The frequencies of somatic EGFR, KRAS, and ALK gene abnormalities using routine lung cancer tissue samples from our United States-based academic medical practice reflect the diverse ethnicity (with a higher frequency of EGFR mutations in Asian patients) and smoking patterns (with an inverse correlation between EGFR mutation and ALK rearrangement) of our tested population. These results may help other medical practices appreciate the expected results from introduction of routine tumor genotyping techniques into their day-to-day care of NSCLC.en_US
dc.language.isoen_USen_US
dc.publisherElsevier BVen_US
dc.relation.isversionof10.1016/j.lungcan.2013.07.013en_US
dc.relation.hasversionhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3800098/en_US
dash.licenseLAA
dc.subjectlung canceren_US
dc.subjectnon-small-cell lung canceren_US
dc.subjectnever smokersen_US
dc.subjectepidermal growth factor receptoren_US
dc.subjectEGFRen_US
dc.subjectanaplastic lymphoma kinaseen_US
dc.subjectALKen_US
dc.subjectKRASen_US
dc.subjecttumor genotypeen_US
dc.subjectethniciptyen_US
dc.subjectAsianen_US
dc.subjectWhiteen_US
dc.subjectBlacken_US
dc.titleSmoking status and self-reported race affect the frequency of clinically relevant oncogenic alterations in non-small-cell lung cancers at a United States-based academic medical practiceen_US
dc.typeJournal Articleen_US
dc.date.updated2017-07-13T13:34:54Z
dc.description.versionAccepted Manuscripten_US
dc.relation.journalLung Canceren_US
dash.depositing.authorVanderlaan, Paul A
dc.date.available2013
dc.date.available2018-04-25T18:01:41Z
dc.identifier.doi10.1016/j.lungcan.2013.07.013*
workflow.legacycommentscat.completeen_US
dash.authorsorderedfalse
dash.contributor.affiliatedGangadharan, Sidhu
dash.contributor.affiliatedMajid, Adnan
dash.contributor.affiliatedKent, Michael
dash.contributor.affiliatedKocher, Olivier
dash.contributor.affiliatedFolch, Erik
dash.contributor.affiliatedCosta, Daniel
dash.contributor.affiliatedVanderlaan, Paul


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