CDKN2A/p16 inactivation mechanisms and their relationship to smoke exposure and molecular features in non-small-cell lung cancer.

@article{Tam2013CDKN2Ap16IM,
  title={CDKN2A/p16 inactivation mechanisms and their relationship to smoke exposure and molecular features in non-small-cell lung cancer.},
  author={Kit W Tam and Wei Zhang and Junichi Soh and Victor A. Stastny and Min Chen and Han Sun and Kelsie Thu and Jonathan J. Rios and Chenchen Yang and Crystal N Marconett and Suhaida A. Selamat and Ite A. Laird-Offringa and Ayumu Taguchi and Samir M Hanash and David Shames and Xiaotu Ma and Michael Q Zhang and Wan L. Lam and Adi Gazdar},
  journal={Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer},
  year={2013},
  volume={8 11},
  pages={1378-88}
}
INTRODUCTION CDKN2A (p16) inactivation is common in lung cancer and occurs via homozygous deletions, methylation of promoter region, or point mutations. Although p16 promoter methylation has been linked to KRAS mutation and smoking, the associations between p16 inactivation mechanisms and other common genetic mutations and smoking status are still controversial or unknown. METHODS We determined all three p16 inactivation mechanisms with the use of multiple methodologies for genomic status… CONTINUE READING
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