Carcinogenesis Advance Access originally published online on August 14, 2003
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Carcinogenesis, Vol. 24, No. 11, 1779-1783,
November 2003
© 2003 Oxford University Press
MOLECULAR EPIDEMIOLOGY AND CANCER PREVENTION |
Hypoxia-inducible factor-1
polymorphisms associated with enhanced transactivation capacity, implying clinical significance
1 Department of Translational Cancer Research, Research Institute for Radiation Biology and Medicine, Hiroshima University, Hiroshima 734-8553, Japan, 2 Division of Frontier Medical Science, Programs for Biomedical Research, 3 Department of Molecular Epidemiology and 4 Department of Molecular Pathology, Hiroshima University Graduate School of Biomedical Sciences, Hiroshima 734-8551, Japan, 5 Department of Radiobiology/Molecular Epidemiology, Radiation Effects Research Foundation, Hiroshima 732-0815, Japan and 6 Cell and Molecular Biology, Medical Nobel Institute, Karolinska Institutet, Stockholm 171-77, Sweden
Hypoxia-inducible factor-1 (HIF-1) is a pivotal factor that regulates cellular responses to hypoxia and is presumably linked to regulation of angiogenesis and tumor growth. We assessed the difference in transcription activity of two HIF-1
polymorphic variants (P582S and A588T), along with molecular epidemiological study among head and neck squamous cell carcinoma (HNSCC) patients. Both HIF-1 variants revealed significantly higher transcription activity than wild-type (WT) did, under normoxic and hypoxic conditions (P < 0.02). Furthermore, tumors from HNSCC patients with heterozygous alleles having P582S or A588T had significantly increased numbers of microvessels compared with those with homozygous WT (P = 0.02). In addition, all patients with tumors of T1 (below 2 cm diameter) were WT, while 14 of 47 patients with tumors of 
T2 were heterozygous. The elevated transactivation capacity of variant forms of HIF-1 implies a role of HIF-1 polymorphisms in generating individually different tumor progression.
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  E. Konac, I. Dogan, H. I. Onen, A. S. Yurdakul, C. Ozturk, A. Varol, and A. Ekmecki Genetic Variations in the Hypoxia-Inducible Factor-1{alpha}Gene and Lung Cancer Experimental Biology and Medicine, September 1, 2009; 234(9): 1109 - 1116. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. Nakai, M. S. Rogers, T. Baba, T. Funakoshi, A. E. Birsner, D. S. Luyindula, and R. J. D'Amato Genetic loci that control the size of laser-induced choroidal neovascularization FASEB J, July 1, 2009; 23(7): 2235 - 2243. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S.-H. Tan, S.-C. Lee, B.-C. Goh, and J. Wong Pharmacogenetics in Breast Cancer Therapy Clin. Cancer Res., December 15, 2008; 14(24): 8027 - 8041. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. M. Schultheis, G. Lurje, K. E. Rhodes, W. Zhang, D. Yang, A. A. Garcia, R. Morgan, D. Gandara, S. Scudder, A. Oza, et al. Polymorphisms and Clinical Outcome in Recurrent Ovarian Cancer Treated with Cyclophosphamide and Bevacizumab Clin. Cancer Res., November 15, 2008; 14(22): 7554 - 7563. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Savas, I. W. Taylor, J. L. Wrana, and H. Ozcelik Functional nonsynonymous single nucleotide polymorphisms from the TGF-{beta} protein interaction network Physiol Genomics, April 24, 2007; 29(2): 109 - 117. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. H Maxwell Hypoxia-inducible factor as a physiological regulator Exp Physiol, November 1, 2005; 90(6): 791 - 797. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 N. Yamada, Y. Horikawa, N. Oda, K. Iizuka, N. Shihara, S. Kishi, and J. Takeda Genetic Variation in the Hypoxia-Inducible Factor-1{alpha} Gene Is Associated with Type 2 Diabetes in Japanese J. Clin. Endocrinol. Metab., October 1, 2005; 90(10): 5841 - 5847. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. R. Resar, A. Roguin, J. Voner, K. Nasir, T. A. Hennebry, J. M. Miller, R. Ingersoll, L. M. Kasch, and G. L. Semenza Hypoxia-Inducible Factor 1{alpha} Polymorphism and Coronary Collaterals in Patients With Ischemic Heart Disease Chest, August 1, 2005; 128(2): 787 - 791. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. Ukon, K. Tanimoto, T. Shimokuni, T. Noguchi, K. Hiyama, H. Tsujimoto, M. Fukushima, T. Toge, and M. Nishiyama Activator Protein Accelerates Dihydropyrimidine Dehydrogenase Gene Transcription in Cancer Cells Cancer Res., February 1, 2005; 65(3): 1055 - 1062. [Abstract] [Full Text] [PDF]
|
|