CDKN2A/p16 inactivation mechanisms and their relationship to smoke exposure and molecular features in non-small-cell lung cancer.
*Hamon Center for Therapeutic Oncology Research and †Division of Biostatistics, University of Texas Southwestern Medical Center, Dallas, Texas; ‡Department of Integrative Oncology, British Columbia Cancer Agency Research Centre, Vancouver, B.C., Canada; §Texas Scottish Rite Hospital for Children, Dallas, Texas; ‖Department of Surgery, Biochemistry, and Molecular Biology, Keck School of Medicine, USC/Norris Comprehensive Cancer Center, Los Angeles, California; ¶Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, Washington; #Oncology Biomarker Development, Genentech Inc., South San Francisco, California; **Department of Molecular and Cell Biology, Center for Systems Biology, University of Texas at Dallas, Dallas, Texas; and ††Department of Pathology, University of Texas Southwestern Medical Center, Dallas, Texas.
- Published Article
Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer
- Publication Date
Nov 01, 2013
Our results confirm that all the inactivation mechanisms are truly associated with loss of gene product and identify specific associations between p16 inactivation mechanisms and other genetic changes and smoking status.
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This record was last updated on 04/18/2018 and may not reflect the most current and accurate biomedical/scientific data available from NLM.
The corresponding record at NLM can be accessed at https://www.ncbi.nlm.nih.gov/pubmed/24077454