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1 1 vs 2), and smoking status (never-smoker vs ever-smoker).
2 between ages 20 and 64 years (52% male; 63% ever-smoker).
3 t the time of disease onset or at diagnosis (ever-smokers).
4 These associations seem to be stronger in ever smokers.
5 ssociations separately for never smokers and ever smokers.
6 was inversely associated with lung cancer in ever smokers.
7 G, OR = 1.46, 95% CI: 1.12, 1.90) but not in ever smokers.
8 %), while 43% of patients were classified as ever smokers.
9 subsequently categorized as never smokers or ever smokers.
10 rs was 10.3% for never smokers and 21.3% for ever smokers.
11 ded association with hip fracture risk among ever smokers.
12 s with pancreatic cancers in this study were ever smokers.
13 and all-cause mortality were only present in ever-smokers.
14 nger CHD protection in never-smokers than in ever-smokers.
15 C, especially in the ipsilateral lung, among ever-smokers.
16 n's disease was 0.59 (95% CI, 0.54-0.63) for ever smokers, 0.80 (95% CI, 0.69-0.93) for past smokers,
17 Study in our study: 2199 never-smokers, 5435 ever-smokers, 158 with asthma, 320 with COPD, 68 with as
18 he Norwegian GenKOLS study of 2003-2005, 947 ever-smokers (49% with COPD) aged 40-85 years performed
19 ed selection screening of the same number of ever-smokers (9.0 million) at highest 5-year lung cancer
20 f those who developed pancreatic cancer were ever smokers (92% vs 69%, respectively), but this did no
22 ith newly diagnosed SCCHN were matched to 50 ever smokers according to sex, age, tumor site, overall
23 adjusted OR, 1.32; 95% CI, 1.02-1.70) and in ever smokers (adjusted OR, 1.75; 95% CI, 1.37-2.22) than
25 del calibrated and discriminated well for US ever-smokers aged 50 to 80 years (NHIS 1997-2001: estima
28 ed tomography (CT) lung cancer screening for ever-smokers aged 55 to 80 years who have smoked at leas
29 ble fundamental differences in SCCHN between ever smokers and never smokers may exist, and further mo
31 ng-concordant pairs (r = 0.483, p < 0.01 for ever-smokers, and r = 0.280, p < 0.05 for never-smokers)
32 ified models, there were FEV1 deficits among ever-smokers associated with infant lower respiratory in
33 iple sclerosis severity score was greater in ever-smokers, by 0.68 (95% confidence interval: 0.36-1.0
38 Status Scale score milestones of 4 and 6 in ever-smokers compared to never-smokers was 1.34 (95% con
39 increased ESCC risk, particularly for males, ever-smokers, ever-drinkers, and those with age > 60, or
43 ere stronger for squamous cell carcinoma and ever smokers for the "fruits and vegetables" pattern, an
46 in the absence of CT screening using data on ever-smokers from the Prostate, Lung, Colorectal, and Ov
49 ; 95% CI, 1.01 to 2.57; P trend = .002) than ever-smokers (HR, 1.36; 95% CI, 0.86 to 2.15; P trend =
50 mokers who had stopped by choice (only 3% of ever-smokers in 1991, but 9% in 2006) had little smoking
51 he association with NBN E185Q was limited to ever smokers (interaction P = 0.002) and was strongest f
52 us mutations in the carcinomas obtained from ever smokers (mean, 53.1 mutations per tumor; SD, 27.9)
53 activity index, smoking (never compared with ever smokers), multivitamin use, season of BMD measureme
54 on-based cohorts examining all participants, ever smokers, never smokers, asthma-free participants, a
55 nd UC combined), comparing data for never vs ever smokers, never vs current smokers, and never vs for
59 ge, and lifetime pack-years of smoking among ever smokers or lifetime intensity-years of passive smok
62 45 years (ORadj = 4.79; 95% CI = 1.87-12.3), ever-smokers (ORadj = 5.55; 95% CI = 1.85-16.6), alcohol
64 fruit intake for men was more evident among ever smokers (P(trend) = 0.001) than never smokers (P(tr
65 ers (P=1.3x10(-16)) in comparison with 5% in ever-smokers (P=2.5x10(-4)), translating to a 60% loss o
67 All genetic effects were evident only in "ever smokers" (persons who had smoked >or=100 cigarettes
68 atic changes after simultaneous exclusion of ever smokers, persons with a history of cancer or cardio
71 e reductions in risk were more pronounced in ever smokers, suggesting a gene-environment interaction.
72 vel on pulmonary function was stronger among ever smokers than never smokers, suggesting an interacti
73 15q25.1 meeting genome-wide significance in ever smokers that includes AGPHD1, IREB2, and CHRNA5/CHR
74 .24, 0.62; P < 0.0001); after restriction to ever smokers, the difference in slopes was much smaller
76 effect modification by smoking: among women ever smokers, there was a positive, progressive dose-res
77 was 54 years, 52% were female, and 38% were ever-smokers; these characteristics were not significant
78 had never smoked cigarettes, the risk among ever smokers was not increased (odds ratio (OR) = 1.05,
79 ema progression quantified by CT scans among ever-smokers was highly variable; clinical factors and b
80 ecline in FEV1 and FEV1%VC, especially among ever smokers, where we found an excess change in FEV1 of
81 are significantly associated with CHD among ever smokers, whereas Prevotella nigrescens (OR=1.7; 95%
82 with never-smoking Gly-16 homozygotes, those ever-smokers who are Arg-16 homozygotes had a significan
83 ds ratios were 5.9 (95% CI, 2.7 to 12.8) for ever-smokers who did not receive PMRT and 18.9 (95% CI,
85 of less than 25 kg/m (OR: 1.6, CI: 0.8-3.5), ever smokers with never smokers (OR: 1.4, 95% CI: 0.7-2.
87 screening from ages 55 through 80 years for ever-smokers with a smoking history of at least 30 pack-
90 y into six subgroups: healthy never-smokers, ever-smokers without asthma and COPD, those with asthma
93 dations, the models estimated 9.0 million US ever-smokers would qualify for lung cancer screening and
94 T lung screening, assuming screening for all ever-smokers, yield the percent changes in lung cancer d
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