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[1]C. E. DeSantis, R. L. Siegel, A. G. Sauer, K. D. Miller, S. A. Fedewa, K. I. Alcaraz and A. Jemal: Cancer statistics for African Americans, 2016: Progress and opportunities in reducing racial disparities. CA Cancer J Clin, 66(4), 290-308 (2016)
[2]O. Bratt, A. Borg, U. Kristoffersson, R. Lundgren, Q. X. Zhang and H. Olsson: CAG repeat length in the androgen receptor gene is related to age at diagnosis of prostate cancer and response to endocrine therapy, but not to prostate cancer risk. Br J Cancer, 81(4), 672-6 (1999)
[3]C. L. Bennett, D. K. Price, S. Kim, D. Liu, B. D. Jovanovic, D. Nathan, M. E. Johnson, J. S. Montgomery, K. Cude, J. C. Brockbank, O. Sartor and W. D. Figg: Racial variation in CAG repeat lengths within the androgen receptor gene among prostate cancer patients of lower socioeconomic status. J Clin Oncol, 20(17), 3599-604 (2002)
[4]K. A. Nelson and J. S. Witte: Androgen receptor CAG repeats and prostate cancer. Am J Epidemiol, 155(10), 883-90 (2002)
[5]D. Feldman: Androgen and vitamin D receptor gene polymorphisms: the long and short of prostate cancer risk. J Natl Cancer Inst, 89(2), 109-11 (1997)
[6]G. A. Coetzee and R. K. Ross: Re: Prostate cancer and the androgen receptor. J Natl Cancer Inst, 86(11), 872-3 (1994)
[7]D. O. Hardy, H. I. Scher, T. Bogenreider, P. Sabbatini, Z. F. Zhang, D. M. Nanus and J. F. Catterall: Androgen receptor CAG repeat lengths in prostate cancer: correlation with age of onset. J Clin Endocrinol Metab, 81(12), 4400-5 (1996)
[8]K. Mir, J. Edwards, P. J. Paterson, M. Hehir, M. A. Underwood and J. M. Bartlett: The CAG trinucleotide repeat length in the androgen receptor does not predict the early onset of prostate cancer. BJU Int, 90(6), 573-8 (2002)
[9]D. K. Price, C. H. Chau, C. Till, P. J. Goodman, C. E. Baum, S. B. Ockers, B. C. English, L. Minasian, H. L. Parnes, A. W. Hsing, J. K. V. Reichardt, A. Hoque, C. M. Tangen, A. R. Kristal, I. M. Thompson and W. D. Figg: Androgen Receptor CAG Repeat Length and Association With Prostate Cancer Risk: Results From the Prostate Cancer Prevention Trial. Journal of Urology, 184(6), 2297-2302 (2010)
[10]A. R. Kristal, D. K. Price, C. Till, J. M. Schenk, M. L. Neuhouser, S. Ockers, D. W. Lin, I. M. Thompson and W. D. Figg: Androgen Receptor CAG Repeat Length Is Not Associated With the Risk of Incident Symptomatic Benign Prostatic Hyperplasia: Results From the Prostate Cancer Prevention Trial. Prostate, 70(6), 584-590 (2010)
[11]C. Bisbal and R. H. Silverman: Diverse functions of RNase L and implications in pathology. Biochimie, 89(6-7), 789-98 (2007)
[12]R. H. Silverman: A scientific journey through the 2-5A/RNase L system. Cytokine Growth Factor Rev, 18(5-6), 381-8 (2007)
[13]J. R. Smith, D. Freije, J. D. Carpten, H. Gronberg, J. Xu, S. D. Isaacs, M. J. Brownstein, G. S. Bova, H. Guo, P. Bujnovszky, D. R. Nusskern, J. E. Damber, A. Bergh, M. Emanuelsson, O. P. Kallioniemi, J. Walker-Daniels, J. E. Bailey-Wilson, T. H. Beaty, D. A. Meyers, P. C. Walsh, F. S. Collins, J. M. Trent and W. B. Isaacs: Major susceptibility locus for prostate cancer on chromosome 1 suggested by a genome-wide search. Science, 274(5291), 1371-4 (1996)
[14]M. S. Meyer, K. L. Penney, J. R. Stark, F. R. Schumacher, H. D. Sesso, M. Loda, M. Fiorentino, S. Finn, R. J. Flavin, T. Kurth, A. L. Price, E. L. Giovannucci, K. Fall, M. J. Stampfer, J. Ma and L. A. Mucci: Genetic variation in RNASEL associated with prostate cancer risk and progression. Carcinogenesis, 31(9), 1597-603 (2010)
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[16]A. Matsumoto, M. Naito, H. Itakura, S. Ikemoto, H. Asaoka, I. Hayakawa, H. Kanamori, H. Aburatani, F. Takaku, H. Suzuki, Y. Kobari, T. Miyai, K. Takahashi, E. H. Cohen, R. Wydro, D. E. Housman and T. Kodama: Human Macrophage Scavenger Receptors - Primary Structure, Expression, and Localization in Atherosclerotic Lesions. Proc Natl Acad Sci U S A, 87(23), 9133-9137 (1990)
[17]H. Suzuki, Y. Kurihara, M. Takeya, N. Kamada, M. Kataoka, K. Jishage, O. Ueda, H. Sakaguchi, T. Higashi, T. Suzuki, Y. Takashima, Y. Kawabe, O. Cynshi, Y. Wada, M. Honda, H. Kurihara, H. Aburatani, T. Doi, A. Matsumoto, S. Azuma, T. Noda, Y. Toyoda, H. Itakura, Y. Yazaki, S. Horiuchi, K. Takahashi, J. K. Kruijt, T. J. C. vanBerkel, U. P. Steinbrecher, S. Ishibashi, N. Maeda, S. Gordon and T. Kodama: A role for macrophage scavenger receptors in atherosclerosis and susceptibility to infection. Nature, 386(6622), 292-296 (1997)
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[19]J. Xu, S. L. Zheng, A. Komiya, J. C. Mychaleckyj, S. D. Isaacs, J. J. Hu, D. Sterling, E. M. Lange, G. A. Hawkins, A. Turner, C. M. Ewing, D. A. Faith, J. R. Johnson, H. Suzuki, P. Bujnovszky, K. E. Wiley, A. M. DeMarzo, G. S. Bova, B. Chang, M. C. Hall, D. L. McCullough, A. W. Partin, V. S. Kassabian, J. D. Carpten, J. E. Bailey-Wilson, J. M. Trent, J. Ohar, E. R. Bleecker, P. C. Walsh, W. B. Isaacs and D. A. Meyers: Germline mutations and sequence variants of the macrophage scavenger receptor 1 gene are associated with prostate cancer risk. Nat Genet, 32(2), 321-5 (2002)
[20]D. C. Miller, S. L. Zheng, R. L. Dunn, A. V. Sarma, J. E. Montie, E. M. Lange, D. A. Meyers, J. Xu and K. A. Cooney: Germ-line mutations of the macrophage scavenger receptor 1 gene: association with prostate cancer risk in African-American men. Cancer Res, 63(13), 3486-9 (2003)
[21]I. Hanukoglu and Z. Hanukoglu: Stoichiometry of Mitochondrial Cytochromes-P-450, Adrenodoxin and Adrenodoxin Reductase in Adrenal-Cortex and Corpus-Luteum - Implications for Membrane Organization and Gene-Regulation. European Journal of Biochemistry, 157(1), 27-31 (1986)
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[26]C. M. Zeigler-Johnson, E. Spangler, M. Jalloh, S. M. Gueye, H. Rennert and T. R. Rebbeck: Genetic susceptibility to prostate cancer in men of African descent: implications for global disparities in incidence and outcomes. Can J Urol, 15(1), 3872-82 (2008)
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Frontiers in Bioscience-Scholar (FBS) is published by IMR Press from Volume 13 Issue 1 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.
Racial disparities: disruptive genes in prostate carcinogenesis
1 Department of Biological Sciences, Cleveland State University, Cleveland, Ohio, USA,
2 Center for Gene Regulation in Health and Disease, Cleveland State University, Cleveland, Ohio, USA
*Author to whom correspondence should be addressed.
Abstract
Population specific studies in prostate cancer (PCa) reveal a unique heterogeneous etiology. Various factors, such as genetics, environment and dietary regimen seems to determine disease progression, therapeutic resistance and rate of mortality. Enormous disparity documented in disease incidences, aggressiveness and mortality in PCa among AAs (African Americans) and CAs (Caucasian Americans) is attributed to the variations in genetics, epigenetics and their association with metabolism. Scientific and clinical evidences have revealed the influence of variations in Androgen Receptor (AR), RNAse L, macrophage scavenger receptor 1 (MRS1), androgen metabolism by cytochrome P450 3A4, differential regulation of microRNAs, epigenetic alterations and diet in racial disparity in PCa incidences and mortality. Concerted efforts are needed to identify race specific prognostic markers and treatment regimen for a better management of the disease.
Keywords
- Androgen Receptor
- RNase L
- Prostate Cancer
- Cancer Disparity
- miRNA
- Review
References
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- [3] C. L. Bennett, D. K. Price, S. Kim, D. Liu, B. D. Jovanovic, D. Nathan, M. E. Johnson, J. S. Montgomery, K. Cude, J. C. Brockbank, O. Sartor and W. D. Figg: Racial variation in CAG repeat lengths within the androgen receptor gene among prostate cancer patients of lower socioeconomic status. J Clin Oncol, 20(17), 3599-604 (2002)
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- [5] D. Feldman: Androgen and vitamin D receptor gene polymorphisms: the long and short of prostate cancer risk. J Natl Cancer Inst, 89(2), 109-11 (1997)
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