Smoking Adversely Affects Survival in Acute Myeloid Leukemia Patients.

Abstract 979

Poster Board I-1

Smoking is the leading preventable cause of death. Smokers are approximately 1.5 times more likely to develop acute myeloid leukemia (AML) than non-smokers, but little is known about the relationship between cigarette smoking and AML outcome. We studied the effect of smoking on outcome in 282 newly diagnosed AML patients treated with high-dose cytarabine and idarubicin-containing regimens at Roswell Park Cancer Institute between 9/92 and 12/08. There were 161 males and 121 females (median age 56 years, range 18-85 years). The median follow up was 12.9 (range, <1-195) months. A total of 161 patients were <60 years and 121 patients were ≥60 years old. AML was de novo in 201 patients and secondary (50 with antecedent hematologic disorder; 31 with therapy-related AML) in 81. Karyotypes were favorable in 24 patients, intermediate in 122, unfavorable in 101, unknown-risk in 23 and unavailable in 12. White blood cell (WBC) count was <100×10⁹/L in 251 patients and WBC ≥100×10⁹/L in 31 at the time of diagnosis. Age ≥60 and secondary AML were associated with worse outcome [37.7 vs. 21.8 months; 95% confidence interval (CI) 30.6 to 44.7 vs. 15.5 to 28.1 for age (p=0.002) and 35.7 vs. 18.7 months; 95% CI 29.6 to 41.9 vs. 11.7 to 25.7 for AML presentation (p=0.002)]. Similarly, patients with unfavorable karyotype had worse outcome compared with intermediate and favorable karyotypes [20.4 vs. 34.8 vs. 70.2 months; 95% CI 13.2 to 27.5 vs. 27.3 to 42.2 vs. 45.4 to 95 respectively for karyotype (p<0.001)]. Sixteen patients underwent allogeneic transplantation in first remission. One hundred and eighty patients (64%) were smokers (current smokers 22% and previous smokers 42%), while 102 patients (36%) were non-smokers. There were no significant differences in age, AML presentation, karyotype or WBC count at diagnosis based on smoking status. Never-smokers had a significantly longer overall survival (OS) [39.5 months (95% CI 29.9-49.1)] than smokers [24 months (95% CI 18-30.2) for former smokers and 29.6 months (95% CI 19-40.3) for current smokers] (p=0.02). Similarly, there was a significant difference in progression-free survival between smokers and non-smokers (25.4 vs. 38.4 months; 95% CI 18.4 to 32.3 vs. 27.1 to 49.8; p=.040). Subgroup analysis revealed no difference in OS for the different smoking categories among patients <60 years old. For older patients, previous and current smokers survived only about half as long as never smokers (31.5 vs. 16.7 months; 95% CI 16.1 to 46.9 vs. 11.4 to 21.9; p=0.026). Similarly, smoking among secondary AML patients affected OS [previous and current smokers 13.1 months (95% CI 7.6-18.6) vs. never-smokers 30.6 months (95% CI 12.1-49); p=0.01], while no effect was seen among de novo AML patients (previous and current smokers 31.7 months vs. never smokers 42.5 months; p=0.09). Furthermore, previous and current smokers with intermediate karyotype had a shorter OS when compared to never-smokers [12.2 vs. 34.9 months; 95% CI 8.4 to 13.2 vs. 16.7 to 53.0; p=0.002] but smoking status had no effect among favorable (65.5 vs. 78.2 months; p=0.62) or unfavorable (32.1 vs. 39.2 months; p=0.36) karyotype groups. Finally, previous and current smokers with WBC count <100×10⁹/L had shorter OS when compared to never-smokers (27 vs. 41 months; 95% CI 21.1 to 32.8 vs. 30.6 to 51.0 months; p=0.012), while smoking had no effect among patients with WBC count ≥100×10⁹/L (16.8 vs. 30.4 months; p=0.34). In multivariate analysis using age, AML presentation, karyotype, WBC count and smoking status as covariates, age, smoking status and karyotype remained of prognostic value for overall survival. In conclusion, cigarette smoking has a deleterious effect on OS and progression free survival in similarly treated AML patients.