- About this Journal ·
- Abstracting and Indexing ·
- Aims and Scope ·
- Article Processing Charges ·
- Articles in Press ·
- Author Guidelines ·
- Bibliographic Information ·
- Citations to this Journal ·
- Contact Information ·
- Editorial Board ·
- Editorial Workflow ·
- Free eTOC Alerts ·
- Publication Ethics ·
- Reviewers Acknowledgment ·
- Submit a Manuscript ·
- Subscription Information ·
- Table of Contents
Journal of Cancer Epidemiology
Volume 2009 (2009), Article ID 242151, 12 pages
Chromosome 5p Region SNPs Are Associated with Risk of NSCLC among Women
1Cancer Biology Program, School of Medicine, Wayne State University, 4100 John R, Detroit, MI 48201, USA
2Population Studies and Prevention Program, Karmanos Cancer Institute, 4100 John R, Detroit, MI 48201, USA
3Department of Internal Medicine, School of Medicine, Wayne State University, 4100 John R, Detroit, MI 48201, USA
4Biostatistics Core, Karmanos Cancer Institute, 716 Harper Professional Building, 4160 John R, Detroit, MI 48201, USA
5Applied Genomics Technology Center and Department of Obstetrics & Gynecology, Wayne State University School of Medicine & Genomics Core, Karmanos Cancer Institute, Mott Center, 275 E Hancock, Detroit, MI 48201, USA
Received 1 September 2009; Accepted 14 December 2009
Academic Editor: Carmen J. Marsit
Copyright © 2009 Alison L. Van Dyke et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
- A. Jemal, R. Siegel, E. Ward, et al., “Cancer statistics, 2008,” CA: Cancer Journal for Clinicians, vol. 58, no. 2, pp. 71–96, 2008.
- Y. Wang, P. Broderick, E. Webb, et al., “Common 5p15.33 and 6p21.33 variants influence lung cancer risk,” Nature Genetics, vol. 40, no. 12, pp. 1407–1409, 2008.
- T. Rafnar, P. Sulem, S. N. Stacey, et al., “Sequence variants at the TERT-CLPTM1L locus associate with many cancer types,” Nature Genetics, vol. 41, no. 2, pp. 221–227, 2009.
- J. U. Kang, S. H. Koo, K. C. Kwon, et al., “High frequency of genetic alterations in non-small cell lung cancer detected by multi-target fluorescence in situ hybridization,” Journal of Korean Medical Science, vol. 22, supplement, pp. S47–S51, 2007.
- R. T. Calado and J. Chen, “Telomerase: not just for the elongation of telomeres,” BioEssays, vol. 28, no. 2, pp. 109–112, 2006.
- L. K. Wai, “Telomeres, telomerase, and tumorigenesis,” Medscape General Medicine, vol. 6, pp. 19–31, 2004.
- C.-P. Hsu, J. Miaw, J.-Y. Hsia, S.-E. Shai, and C.-Y. Chen, “Concordant expression of the telomerase-associated genes in non-small cell lung cancer,” European Journal of Surgical Oncology, vol. 29, no. 7, pp. 594–599, 2003.
- T.-C. Wu, P. Lin, C.-P. Hsu, et al., “Loss of telomerase activity may be a potential favorable prognostic marker in lung carcinomas,” Lung Cancer, vol. 41, no. 2, pp. 163–169, 2003.
- H. Hara, K. Yamashita, J. Shinada, H. Yoshimura, and T. Kameya, “Clinicopathologic significance of telomerase activity and hTERT mRNA expression in non-small cell lung cancer,” Lung Cancer, vol. 34, no. 2, pp. 219–226, 2001.
- C. M. Counter, M. Meyerson, E. N. Eaton, et al., “Telomerase activity is restored in human cells by ectopic expression of hTERT (hEST2), the catalytic subunit of telomerase,” Oncogene, vol. 16, no. 9, pp. 1217–1222, 1998.
- J. Erblich, C. Lerman, D. W. Self, G. A. Diaz, and D. H. Bovbjerg, “Effects of dopamine D2 receptor (DRD2) and transporter (SLC6A3) polymorphisms on smoking cue-induced cigarette craving among African-American Smokers,” Molecular Psychiatry, vol. 10, pp. 407–414, 2005.
- S. Z. Sabol, M. L. Nelson, C. Fisher, et al., “A genetic association for cigarette smoking behavior,” Health Psychology, vol. 18, no. 1, pp. 7–13, 1999.
- P. Sokoloff, J.-F. Riou, M.-P. Martres, and J.-C. Schwartz, “Presence of dopamine D-2 receptors in human tumoral cell lines,” Biochemical and Biophysical Research Communications, vol. 162, no. 2, pp. 575–582, 1989.
- D. Campa, S. Zienolddiny, H. Lind, et al., “Polymorphisms of dopamine receptor/transporter genes and risk of non-small cell lung cancer,” Lung Cancer, vol. 56, no. 1, pp. 17–23, 2007.
- T. Suzuki, K. Matsuo, A. Hiraki, et al., “Impact of one-carbon metabolism-related gene polymorphisms on risk of lung cancer in Japan: a case-control study,” Carcinogenesis, vol. 28, no. 8, pp. 1718–1725, 2007.
- Q. Shi, Z. Zhang, G. Li, et al., “Polymorphisms of methionine synthase and methionine synthase reductase and risk of lung cancer: a case-control analysis,” Pharmacogenetics and Genomics, vol. 15, no. 8, pp. 547–555, 2005.
- G. Cao, H. Lu, J. Feng, J. Shu, D. Zheng, and Y. Hou, “Lung cancer risk associated with Thr495Pro polymorphism of GHR in chines population,” Japanese Journal of Clinical Oncology, vol. 38, no. 4, pp. 308–316, 2008.
- M. F. Rudd, E. L. Webb, A. Matakidou, et al., “Variants in the GH-IGF axis confer susceptibility to lung cancer,” Genome Research, vol. 16, no. 6, pp. 693–701, 2006.
- P. Gresner, J. Gromadzinska, E. Jablonska, et al., “Expression of selenoprotein-coding genes SEPP1, SEP15, and hGPX1 in non-small cell lung cancer,” Lung Cancer. In press.
- A. L. Van Dyke, M. L. Cote, A. S. Wenzlaff, et al., “Cytokine and cytokine receptor single-nucleotide polymorphisms predict risk for non-small cell lung cancer among women,” Cancer Epidemiology Biomarkers and Prevention, vol. 18, no. 6, pp. 1829–1840, 2009.
- Y. Benjamini and Y. Hochberg, “Controlling the false discovery rate: a practical and powerful approach to multiple testing,” Journal of the Royal Statistical Society: Series B, vol. 57, pp. 289–300, 1995.
- F. E. Harrell Jr., K. L. Lee, and D. B. Mark, “Multivariable prognostic models: issues in developing models, evaluating assumptions and adequacy, and measuring and reducing errors,” Statistics in Medicine, vol. 15, no. 4, pp. 361–387, 1996.
- L. Breiman, “Random forests,” Machine Learning, vol. 45, no. 1, pp. 5–32, 2001.
- S. Purcell, B. Neale, K. Todd-Brown, et al., “PLINK: a tool set for whole-genome association and population-based linkage analyses,” American Journal of Human Genetics, vol. 81, no. 3, pp. 559–575, 2007.
- B. French, T. Lumley, S. A. Monks, et al., “Simple estimates of haplotype relative risks in case-control data,” Genetic Epidemiology, vol. 30, no. 6, pp. 485–494, 2006.
- P. C. Ng and S. Henikoff, “Predicting deleterious amino acid substitutions,” Genome Research, vol. 11, no. 5, pp. 863–874, 2001.
- S. A. Savage, S. J. Chanock, J. Lissowska, et al., “Genetic variation in five genes important in telomere biology and risk for breast cancer,” British Journal of Cancer, vol. 97, no. 6, pp. 832–836, 2007.
- T. Mushiroda, S. Wattanapokayakit, A. Takahashi, et al., “A genome-wide association study identifies an association of a common variant in TERT with susceptibility to idiopathic pulmonary fibrosis,” Journal of Medical Genetics, vol. 45, no. 10, pp. 654–656, 2008.
- K. Wagner, K. Hemminki, E. Grzybowska, et al., “Polymorphisms in the growth hormone receptor: a case-control study in breast cancer,” International Journal of Cancer, vol. 118, no. 11, pp. 2903–2906, 2006.
- M. E. Reid, A. J. Duffield-Lillico, L. Garland, B. W. Turnbull, L. C. Clark, and J. R. Marshall, “Selenium supplementation and lung cancer incidence: an update of the nutritional prevention of cancer trial,” Cancer Epidemiology Biomarkers and Prevention, vol. 11, no. 11, pp. 1285–1291, 2002.
- U. Peters, N. Chatterjee, R. B. Hayes, et al., “Variation in the selenoenzyme genes and risk of advanced distal colorectal adenoma,” Cancer Epidemiology Biomarkers and Prevention, vol. 17, no. 5, pp. 1144–1154, 2008.
- M. L. Cooper, H.-O. Adami, H. Gronberg, F. Wiklund, F. R. Green, and M. P. Rayman, “Interaction between single nucleotide polymorphisms in selenoprotein P and mitochondrial superoxide dismutase determines prostate cancer risk,” Cancer Research, vol. 68, no. 24, pp. 10171–10177, 2008.
- A. Nassar, M. B. Amin, D. G. Sexton, and C. Cohen, “Utility of -methylacyl coenzyme A racemase (P504S antibody) as a diagnostic immunohistochemical marker for cancer,” Applied Immunohistochemistry and Molecular Morphology, vol. 13, no. 3, pp. 252–255, 2005.
- M. Zhou, A. M. Chinnaiyan, C. G. Kleer, P. C. Lucas, and M. A. Rubin, “Alpha-methylacyl-CoA racemase: a novel tumor marker over-expressed in several human cancers and their precursor lesions,” American Journal of Surgical Pathology, vol. 26, no. 7, pp. 926–931, 2002.
- K. Shilo, T. Dracheva, H. Mani, et al., “-methylacyl CoA racemase in pulmonary adenocarcinoma, squamous cell carcinoma, and neuroendocrine tumors: expression and survival analysis,” Archives of Pathology and Laboratory Medicine, vol. 131, no. 10, pp. 1555–1560, 2007.
- A. M. Levin, K. A. Zuhlke, A. M. Ray, K. A. Cooney, and J. A. Douglas, “Sequence variation in alpha-methylacyl-CoA racemase and risk of early-onset and familial prostate cancer,” Prostate, vol. 67, pp. 1507–1513, 2007.
- S. E. Daugherty, Y. Y. Shugart, E. A. Platz, et al., “Polymorphic variants in -methylacyl-CoA-racemase and prostate cancer,” Prostate, vol. 67, pp. 1487–1497, 2007.
- L. M. FitzGerald, R. Thomson, A. Polanowski, et al., “Sequence variants of -methylacyl-CoA racemase are associated with prostate cancer risk: a replication study in an ethnically homogeneous population,” Prostate, vol. 68, no. 13, pp. 1373–1379, 2008.
- E. Zudaire, N. Cuesta, V. Murty, et al., “The aryl hydrocarbon receptor repressor is a putative tumor suppressor gene in multiple human cancers,” Journal of Clinical Investigation, vol. 118, no. 2, pp. 640–650, 2008.
- M. Yoshikawa, K. Arashidani, T. Kawamoto, and Y. Kodama, “Aryl hydrocarbon hydroxylase activity in human lung tissue: in relation to cigarette smoking and lung cancer,” Environmental Research, vol. 65, pp. 1–11, 1994.
- K. Kawajiri, J. Watanabe, H. Eguchi, K. Nakachi, C. Kiyohara, and S.-I. Hayashi, “Polymorphisms of human Ah receptor gene are not involved in lung cancer,” Pharmacogenetics, vol. 5, no. 3, pp. 151–158, 1995.
- S. Cauchi, I. Stucker, S. Cenee, P. Kremers, P. Beaune, and L. Massaad-Massade, “Structure and polymorphisms of human aryl hydrocarbon receptor repressor (AhRR) gene in a French population: relationship with CYP1A1 inducibility and lung cancer,” Pharmacogenetics, vol. 13, no. 6, pp. 339–347, 2003.