The hemostatic system as a modulator of atherosclerosis.

نویسنده

  • José A Páramo
چکیده

n engl j med 365;3 nejm.org july 21, 2011 278 do not observe, in an underpowered study, a pattern of mutual exclusivity between NFKBIA deletion and EGFR amplification when analyzing together grades II, III, and IV gliomas, nor do they find a relationship between survival and having a tumor that bears an NFKBIA deletion. Since the publication of our report, we have gone on to test these associations with the use of extended data from the Cancer Genome Atlas (TCGA) project. Using gene copy-number data generated by two independent TCGA Genome Characterization Centers on different genotyping platforms, we again observed a pattern of relative mutual exclusivity between deletion of NFKBIA and amplification of EGFR in glioblastomas (P = 2×10−3 by Pearson’s chisquare test; odds ratio for concomitant deletion and amplification, 0.46; 95% confidence interval [CI], 0.29 to 0.74) (Fig. 1A in the Supplementary Appendix, available with the full text of this letter at NEJM.org). We also again observed that patients with tumors with the NFKBIA deletion had poorer outcomes than did those who had glioblastomas with normal gene dosages of NFKBIA and EGFR (hazard ratio for death with the NFKBIA deletion, as compared with normal dosages of both NFKBIA and EGFR, 1.41; 95% CI, 1.02 to 1.94; P = 0.039 by the Cox model), and had outcomes similar to those with tumors harboring EGFR amplification (hazard ratio for death with isolated NFKBIA deletion, as compared with isolated EGFR amplification, 0.93; 95% CI, 0.68 to 1.29; P = 0.68 by the Cox model) (Fig. 1B in the Supplementary Appendix). The estimated median survival times were 47 weeks for patients whose tumors harbored an isolated NFKBIA deletion, 53 weeks for those whose tumors had isolated EGFR amplification, and 67 weeks for those whose tumors had normal dosages of both NFKBIA and EGFR.

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عنوان ژورنال:
  • The New England journal of medicine

دوره 365 3  شماره 

صفحات  -

تاریخ انتشار 2011