Affordable Access

deepdyve-link
Publisher Website

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

Authors
  • Tam, Kit W1
  • Zhang, Wei
  • Soh, Junichi
  • Stastny, Victor
  • Chen, Min
  • Sun, Han
  • Thu, Kelsie
  • Rios, Jonathan J
  • Yang, Chenchen
  • Marconett, Crystal N
  • Selamat, Suhaida A
  • Laird-Offringa, Ite A
  • Taguchi, Ayumu
  • Hanash, Samir
  • Shames, David
  • Ma, Xiaotu
  • Zhang, Michael Q
  • Lam, Wan L
  • Gazdar, Adi
  • 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
Publication Date
Nov 01, 2013
Volume
8
Issue
11
Pages
1378–1388
Identifiers
DOI: 10.1097/JTO.0b013e3182a46c0c
PMID: 24077454
Source
Medline
License
Unknown

Abstract

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.

Report this publication

Statistics

Seen <100 times