Share This Article:

RNase L Variants Do Not Appear to Impact on Clinical Features of Sporadic Prostate Cancer Patients

Full-Text HTML Download Download as PDF (Size:190KB) PP. 287-292
DOI: 10.4236/oju.2013.37054    2,514 Downloads   3,491 Views  


Introduction: Prostate cancer is the most common non-cutaneous male cancers, contributing to significant mortality rates globally. Mutations of RNase L, an enzyme involved in inflammatory and immunological pathways, have been speculated to predispose to cancer. This study assesses three different mutations of the RNase L gene in Irish prostate cancer patients, including one linked with general cancer susceptibility never investigated before in prostate cancer (rs3738579), and reports on links with aggressive cancer. Methods: 134 patients had their RNase L mutation status determined by polymerase chain reaction (PCR) of serum DNA. Complementary clinical details for each patient are statistically analysed. Results: No link to age of diagnosis, high grade disease or prostate specific antigen (PSA) level at diagnosis was demonstrated with any of the studied single nucleotide polymorphisms (SNP). The SNP variation was consistent with that of published international series. Conclusion: SNP genotypic frequencies in Ireland are consistent with international findings. The studied RNase L mutations including rs3738579 do not appear to have a significant impact on our patient population.

Conflicts of Interest

The authors declare no conflicts of interest.

Cite this paper

F. D’Arcy, R. Foley and T. Lynch, "RNase L Variants Do Not Appear to Impact on Clinical Features of Sporadic Prostate Cancer Patients," Open Journal of Urology, Vol. 3 No. 7, 2013, pp. 287-292. doi: 10.4236/oju.2013.37054.


[1] A. Rokman, T. Ikonen, E. H. Seppala, N. Nupponen, V. Autio, N. Mononen, J. Bailey-Wilson, J. Trent, J. Carpten, M. P. Matikainen, P. A. Koivisto, T. L. Tammela, O. P. Kallioniemi and J. Schleutker, “Germline Alterations of the RNASEL Gene, a Candidate HPC1 Gene at 1q25, in Patients and Families with Prostate Cancer,” The American Journal of Human Genetics, Vol. 70, No. 5, 2002, pp. 1299-1304.
[2] J. Carpten, N. Nupponen, S. Isaacs, R. Sood, C. Robbins, J. Xu, M. Faruque, T. Moses, C. Ewing, E. Gillanders, P. Hu, P. Bujnovszky, I. Makalowska, A. Baffoe-Bonnie, D. Faith, J. Smith, D. Stephan, K. Wiley, M. Brownstein, D. Gildea, B. Kelly, R. Jenkins, G. Hostetter, M. Matikainen, J. Schleutker, K. Klinger, T. Connors, Y. Xiang, Z. Wang, A. De Marzo, N. Papadopoulos, O. P. Kallioniemi, R. Burk, D. Meyers, H. Gronberg, P. Meltzer, R. Silverman, J. Bailey-Wilson, P. Walsh, W. Isaacs and J. Trent, “Germline Mutations in the Ribonuclease L Gene in Families Showing Linkage with HPC1,” Nature Genetics, Vol. 30, No. 2, 2002, pp. 181-184.
[3] A. Orr-Urtreger, A. Bar-Shira, D. Bercovich, N. Matarasso, U. Rozovsky, S. Rosner, S. Soloviov, G. Rennert, L. Kadouri, A. Hubert, H. Rennert and H. Matzkin, “RNASEL Mutation Screening and Association Study in Ashkenazi and Non-Ashkenazi Prostate Cancer Patients,” Cancer Epidemiology, Biomarkers & Prevention, Vol. 15, No. 3, 2006, pp. 474-479.
[4] Y. Xiang, Z. Wang, J. Murakami, S. Plummer, E. A. Klein, J. D. Carpten, J. M. Trent, W. B. Isaacs, G. Casey and R. H. Silverman, “Effects of RNase L Mutations Associated with Prostate Cancer on Apoptosis Induced by 2’,5’-Oligoadenylates,” Cancer Research, Vol. 63, No. 20, 2003, pp. 6795-6801.
[5] L. Wang, S. K. McDonnell, D. A. Elkins, S. L. Slager, E. Christensen, A. F. Marks, J. M. Cunningham, B. J. Peterson, S. J. Jacobsen, J. R. Cerhan, M. L. Blute, D. J. Schaid and S. N. Thibodeau, “No Association of Germline Alteration of MSR1 with Prostate Cancer Risk,” Nature Genetics, Vol. 35, 2003, pp. 128-129.
[6] G. Casey, P. J. Neville, S. J. Plummer, Y. Xiang, L. M. Krumroy, E. A. Klein, W. J. Catalona, N. Nupponen, J. D. Carpten, J. M. Trent, R. H. Silverman and J. S. Witte, “RNASEL Arg462Gln Variant Is Implicated in up to 13% of Prostate Cancer Cases,” Nature Genetics, Vol. 32, No. 4, 2002, pp. 581-583.
[7] F. Wiklund, B. A. Jonsson, A. J. Brookes, L. Stromqvist, J. Adolfsson, M. Emanuelsson, H. O. Adami, K. Augustsson-Balter and H. Gronberg, “Genetic Analysis of the RNASEL Gene in Hereditary, Familial, and Sporadic Prostate Cancer,” Clinical Cancer Research, Vol. 10, No. 21, 2004, pp. 7150-7156.
[8] H. Li and B. C. Tai, “RNASEL Gene Polymorphisms and the Risk of Prostate Cancer: A Meta-Analysis,” Clinical Cancer Research, Vol. 12, 2006, pp. 5713-5719.
[9] F. C. Noonan-Wheeler, W. Wu, K. A. Roehl, A. Klim, J. Haugen, B. K. Suarez and A. S. Kibel, “Association of Hereditary Prostate Cancer Gene Polymorphic Variants with Sporadic Aggressive Prostate Carcinoma,” Prostate, Vol. 66, No. 1, 2006, pp. 49-56. 20320
[10] H. Nakazato, K. Suzuki, H. Matsui, N. Ohtake, S. Nakata and H. Yamanaka, “Role of Genetic Polymorphisms of the RNASEL Gene on Familial Prostate Cancer Risk in a Japanese Population,” British Journal of Cancer, Vol. 89, No. 4, 2003, pp. 691-696.
[11] C. Maier, J. Haeusler, K. Herkommer, Z. Vesovic, J. Hoegel, W. Vogel and T. Paiss, “Mutation Screening and Association Study of RNASEL as a Prostate Cancer Susceptibility Gene,” British Journal of Cancer, Vol. 92, 2005, pp. 1159-1164.
[12] B. E. Madsen, E. M. Ramos, M. Boulard, K. Duda, J. Overgaard, M. Nordsmark, C. Wiuf and L. L. Hansen, “Germline Mutation in RNASEL Predicts Increased Risk of Head and Neck, Uterine Cervix and Breast Cancer,” PLoS One, Vol. 3, No. 6, 2008, Article ID: e2492. pone.0002492
[13] S. Nair and M. R. Pillai, “Human Papillomavirus and Disease Mechanisms: Relevance to Oral and Cervical Cancers,” Oral Diseases, Vol. 11, 2005, pp. 350-359.
[14] A. Leodolter, M. Naumann and P. Malfertheiner, “Prevention of Gastric Cancer by Helicobacter pylori Eradication,” Digestive Diseases, Vol. 22, 2004, pp. 313-319.
[15] M. A. Epstein, B. G. Achong and Y. M. Barr, “Virus Particles in Cultured Lymphoblasts from Burkitt’s Lymphoma,” Lancet, Vol. 15, 1964, pp. 702-703.
[16] J. E. McGrory, D. J. Pritchard, K. K. Unni, D. Ilstrup and C. M. Rowland, “Malignant Lesions Arising in Chronic Osteomyelitis,” Clinical Orthopaedics and Related Research, Vol. 362, 1999, pp. 181-189.
[17] L. K. Dennis and D. V. Dawson, “Meta-Analysis of Measures of Sexual Activity and Prostate Cancer,” Epidemiology, Vol. 13, 2002, pp. 72-79.
[18] R. B. Hayes, L. M. Pottern, H. Strickler, C. Rabkin, V. Pope, G. M. Swanson, R. S. Greenberg, J. B. Schoenberg, J. Liff, A. G. Schwartz, R. N. Hoover and J. F. Fraumeni Jr., “Sexual Behaviour, STDs and Risks for Prostate Cancer,” British Journal of Cancer, Vol. 82, 2000, pp. 718-725. 10.1054/bjoc.1999.0986
[19] M. L. Taylor, A. G. Mainous 3rd and B. J. Wells, “Prostate Cancer and Sexually Transmitted Diseases: A Meta-Analysis,” Family Medicine Journal, Vol. 37, 2005, pp. 506-512.
[20] A. V. Sarma, J. C. McLaughlin, L. P. Wallner, R. L. Dunn, K. A. Cooney, D. Schottenfeld, J. E. Montie and J. T. Wei, “Sexual Behavior, Sexually Transmitted Diseases and Prostatitis: The Risk of Prostate Cancer in Black Men,” Journal of Urology, Vol. 176, No. 3, 2006, pp. 1108-1113. 10.1016/j.juro.2006.04.075

comments powered by Disqus

Copyright © 2018 by authors and Scientific Research Publishing Inc.

Creative Commons License

This work and the related PDF file are licensed under a Creative Commons Attribution 4.0 International License.