It appears you don't have support to open PDFs in this web browser. To view this file, Open with your PDF reader
Abstract
Multiple primary lung cancers (MPLCs) harbour various genetic profiles among the tumours, even from individuals with same non-intrinsic risk factors. Paired mutational analyses were performed to obtain a census of mutational events in MPLC and assess their relationship with non-intrinsic risk factors. Thirty-eight surgical specimens from 17 patients diagnosed as MPLC were used. Extracted DNAs were sequenced for somatic mutations in 409 cancer-associated genes from a comprehensive cancer panel. We statistically analysed the correlation between each driver mutation frequency and non-intrinsic risk factors using Fisher's exact test, and whether genetic mutations occurred concomitantly or randomly in MPLC using an exact test. Comprehensive genetic analyses suggested different mutation profiles in tumours within the same individuals, with some exceptions. EGFR, KRAS, TP53, or PARP1 mutations were concomitantly detected in some MPLC cases. EGFR mutations were significantly more frequent in never or light smokers and females. Concomitant EGFR or KRAS mutations in MPLCs were significantly more frequent than expected by chance (P = .0023 and .0049, respectively) suggesting a more prominent role of non-intrinsic risk factors in EGFR and KRAS mutations than other mutations, which occurred more randomly. Concomitant EGFR or KRAS mutations were particularly prominent in never or light smokers and males.
You have requested "on-the-fly" machine translation of selected content from our databases. This functionality is provided solely for your convenience and is in no way intended to replace human translation. Show full disclaimer
Neither ProQuest nor its licensors make any representations or warranties with respect to the translations. The translations are automatically generated "AS IS" and "AS AVAILABLE" and are not retained in our systems. PROQUEST AND ITS LICENSORS SPECIFICALLY DISCLAIM ANY AND ALL EXPRESS OR IMPLIED WARRANTIES, INCLUDING WITHOUT LIMITATION, ANY WARRANTIES FOR AVAILABILITY, ACCURACY, TIMELINESS, COMPLETENESS, NON-INFRINGMENT, MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE. Your use of the translations is subject to all use restrictions contained in your Electronic Products License Agreement and by using the translation functionality you agree to forgo any and all claims against ProQuest or its licensors for your use of the translation functionality and any output derived there from. Hide full disclaimer
Details
1 Osaka City University, Department of Respiratory Medicine, Graduate School of Medicine, Osaka, Japan (GRID:grid.261445.0) (ISNI:0000 0001 1009 6411); Wakayama Medical University, Internal Medicine III, Wakayama, Japan (GRID:grid.412857.d) (ISNI:0000 0004 1763 1087)
2 Wakayama Medical University, Internal Medicine III, Wakayama, Japan (GRID:grid.412857.d) (ISNI:0000 0004 1763 1087)
3 Osaka City University, Department of Respiratory Medicine, Graduate School of Medicine, Osaka, Japan (GRID:grid.261445.0) (ISNI:0000 0001 1009 6411)
4 Osaka City University, Laboratory of Statistics, Graduate School of Medicine, Osaka, Japan (GRID:grid.261445.0) (ISNI:0000 0001 1009 6411)
5 Osaka City University, Department of Clinical Oncology, Graduate School of Medicine, Osaka, Japan (GRID:grid.261445.0) (ISNI:0000 0001 1009 6411)
6 Osaka City University, Department of Pathology, Graduate School of Medicine, Osaka, Japan (GRID:grid.261445.0) (ISNI:0000 0001 1009 6411)
7 Osaka City University, Department of Respiratory Medicine, Graduate School of Medicine, Osaka, Japan (GRID:grid.261445.0) (ISNI:0000 0001 1009 6411); Osaka City University, Department of Clinical Oncology, Graduate School of Medicine, Osaka, Japan (GRID:grid.261445.0) (ISNI:0000 0001 1009 6411)