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Sex differences were not included in the model as the primary analyses did not suggest any sex-specific genetic effects.
Our primary analyses did include one individual who, on 3 of 12 visits, reported smoking one to three cigarettes or cigarillos within the previous 48 hr.
Although our primary analyses did not reveal associations between PI3K-pathway activation and overall survival or survival after BCBM, several secondary analyses are worthy of discussion.
Finally, the Egger and Begg tests for the primary analyses did not indicate the presence of publication bias in the analysis of total physical activity (prepregnancy P = 0.30; early pregnancy P = 0.81).
Assessed against the trial defined MCID (equal to Cohen's d=0.3), population estimates showed that the small, non-significant differences between trial arms in the primary analyses did not reach clinically significant levels for any outcome, in any cohort, at any time point (figs 6 and 7).
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In our primary analyses, we did not restrict the intercept in the calculation of the exposure response curve.
Still, when depression was included as a covariate in our primary analyses, results did not change substantially (see below).
Overexpression of ERBB3 appears to result from increased levels of gene transcription since in none of the cell lines or primary cancers analysed did we find evidence of gene amplification.
Although we found a statistically significant association between acute myocardial infarction and exclusive bevacizumab use when compared with exclusive ranibizumab exposure in the subgroup with diabetes, our primary analysis and other secondary analyses did not detect any excess risk with either bevacizumab or ranibizumab.
Primary analyses were done with a fixed effects model; secondary confirmatory analyses were done with a random effects model if there was significant heterogeneity.
Primary analyses were done on ITT basis.
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