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

Authors
  • 1
  • 1 *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. , (Canada)
Type
Published Article
Journal
Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer
1556-1380
Publication Date
Volume
8
Issue
11
Pages
1378–1388
Identifiers
DOI: 10.1097/JTO.0b013e3182a46c0c
PMID: 24077454
Source
Medline

Abstract

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