التفاصيل البيبلوغرافية
| العنوان: |
Driver mutations determine survival in smokers and never-smokers with stage IIIB/IV lung adenocarcinomas. |
| المؤلفون: |
Paik, Paul K., Johnson, Melissa L., D'Angelo, Sandra P., Sima, Camelia S., Ang, Daphne, Dogan, Snjezana, Miller, Vincent A., Ladanyi, Marc, Kris, Mark G., Riely, Gregory J. |
| المصدر: |
Cancer (0008543X); Dec2012, Vol. 118 Issue 23, p5840-5847, 8p |
| مصطلحات موضوعية: |
HEALTH of cigarette smokers, ADENOCARCINOMA, LUNG cancer patients, EPIDERMAL growth factor receptors, ONCOGENES |
| مستخلص: |
BACKGROUND: The authors previously demonstrated that never-smokers with stage IIIB/IV nonsmall cell lung cancer (NSCLC) lived 50% longer than former/current smokers. This observation persisted after adjusting for age, performance status, and sex. In this study, the authors hypothesized that smoking-dependent differences in the distribution of driver mutations may explain differences in prognosis between these subgroups. METHODS: In total, 293 never-smokers and 382 former/current smokers with lung adenocarcinoma who underwent testing for epidermal growth factor receptor ( EGFR) mutations and v-Ki- ras2 Kirsten rat sarcoma viral oncogene homolog ( KRAS) mutations and rearrangements in anaplastic lymphoma kinase ( ALK) between 2009 and 2010 were investigated. Clinical outcomes and patient characteristics were collected. Survival probabilities were estimated using the Kaplan-Meier method. Group comparison was performed with log-rank tests and Cox proportional hazards methods. RESULTS: Although the overall incidence of these mutations was nearly identical (55% never-smokers vs 57% current/former smokers; P = .48), there were significant differences in the distribution of mutations between these groups for EGFR mutations (37% never-smokers vs 14% former/current smokers; P < .0001), KRAS mutations (4% never-smokers vs 43% former/current smokers; P < .0001), and ALK rearrangements (12% never-smokers vs 2% former/current smokers; P < .0001). Among never-smokers and former/current smokers, the prognosis differed significantly by genotype. Patients who had KRAS mutations had the poorest survival. Smoking status, however, had no influence on survival within each genotype. CONCLUSIONS: Never-smokers and former/current smokers with lung adenocarcinomas were not homogeneous subgroups. Each was made up of individuals whose tumors had a unique distribution of driver mutations, which were associated with different prognoses, irrespective of smoking history. Cancer 2012. © 2012 American Cancer Society. [ABSTRACT FROM AUTHOR] |
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