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Please use this identifier to cite or link to this item: http://arks.princeton.edu/ark:/88435/dsp01s1784p18m
Title: Effect of race and smoking status on frequency of oncogenic driver alterations in non-small cell lung cancer patients at Abramson Cancer Center
Authors: Ephrem, Elshaddai
Advisors: Zakian, Virginia A.
Department: Molecular Biology
Class Year: 2016
Abstract: Non-small cell lung cancer (NSCLC) is an exemplar of “personalized medicine” in oncology, a term defined by development of genotype-directed targeted therapies against activation of oncogenic driver signaling. Treatment of advanced stage NSCLC involves tumor genotyping to identify oncogenic driver alterations (ALK rearrangement, EGFR mutations, and KRAS mutations) that predict clinical response to targeted therapies. The prevalence of driver alterations in minorities is understudied, but differences in tumor biology are hypothesized to underlie racial disparities in lung cancer outcomes. I sought to determine the association between race and mutational positivity in NSCLC. I conducted a retrospective study of the frequency of ALK rearrangement, EGFR mutation, and KRAS mutation among patients with NSCLC at the ACC, stratified by demographic and clinical variables. Among 611 patients whose tumor had at least ALK FISH testing, the overall frequency of ALK rearrangement was 4.6%; of EGFR mutation 11.4%; and of KRAS mutations 28.1%. The findings of this study indicate that race is not significantly associated with the frequency of driver alterations in NSCLC. Race should not be considered when deciding which patients to screen for driver alterations. Smoking status was an independent predictor of harboring an oncogenic driver alteration in tumor. ALK-positive NSCLC and EGFR-positive NSCLC were more common in non-smokers, and KRAS-positive NSCLC was more common in smokers. Differences in pattern of oncogenic driver alterations between smokers and non-smokers supports theory that lung cancer in non-smokers is a distinct disease from that in smokers and may lead to elucidation of the molecular pathways that lead to lung adenocarcinoma.
Extent: 151 pages
URI: http://arks.princeton.edu/ark:/88435/dsp01s1784p18m
Type of Material: Princeton University Senior Theses
Language: en_US
Appears in Collections:Molecular Biology, 1954-2016

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