Canine Prostate Carcinoma: Four Clinical Cases in Sexually Intact and Neutered Dogs


Prostate cancer is one of the most important malignancies in men. In old men the frequency of prostate cancer at necroscopy has been reported to exceed 40%. Dogs are the only large mammals other than humans with a significant incidence of spontaneous prostate cancer. Adenocarcinoma, transitional cell carcinoma and undifferentiated carcinoma are the most common histological type but the precise cell of origin in dog is not known. The incidence of prostatic carcinoma in dogs is low (0.2% - 0.6%). Prostatic carcinomas occur in sexually intact and neutered dogs and the risk increase in castrated dogs associated to pulmonary and bone metastases. The castration does not initiate the development of prostatic carcinoma in dog but does favour tumour progression. In men the early stage detection of prostate cancer can offer various therapies as radical prostatectomy, radial therapy, thermal ablation, anti-androgen therapy, chemotherapy. In dogs the diagnosis is often in advanced stage of the cancer and the survival time for dogs with prostate cancer is poor. The median time reported is 30 days after diagnosis. In this study we reported three cases of prostatic carcinoma in intact sexually dogs and one in a neutered dog. The sexually intact subjects were older (mean age = 10.5 years) and they had prostatic adenocarcinoma (PCA). The interval between castration and onset of prostatic problems was 3 years. All the dogs showed dysuria, macroscopic hematuria, dyschezia and ataxia. All dogs have been euthanized in order to relieve pain and suffering.

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E. Bigliardi, C. Bresciani, A. Maria Cantoni, F. Di Ianni, G. Morini, S. Voccia, A. Corradi and E. Parmigiani, "Canine Prostate Carcinoma: Four Clinical Cases in Sexually Intact and Neutered Dogs," Open Journal of Urology, Vol. 2 No. 4, 2012, pp. 232-236. doi: 10.4236/oju.2012.24042.

Conflicts of Interest

The authors declare no conflicts of interest.


[1] M. Stefanov, “Extraglandular and Intraglandular Vascularization of Canine Prostate,” Microscopy Research and Technique, Vol. 64, No. 3, 2004, pp. 188-197.
[2] E. Bigliardi and L. Ferrari, “Contrast-Enhanced Ultrasound of the Normal Canine Prostate Gland,” Veterinary Radiology Ultrasound, Vol. 52, No. 1, 2011, pp. 107-110.
[3] E. Teske, E. C. Naan, E. M. Van Dijk, E. Van Garderen and J. A. Schalken, “Canine Prostate Carcinoma: Epidemiological Evidence of an Increased risk in Castrated Dogs,” Molecular and Cellular Endocrinology, Vol. 197, No. 1-2, 2002, pp. 251-255. doi:10.1016/S0303-7207(02)00261-7
[4] B. E. LeRoy and N. Northrup, “Prostate Cancer in Dogs: Comparative and Clinical Aspects,” The Veterinary Journal, Vol. 180, No. 2, 2009, pp. 149-162. doi:10.1016/j.tvjl.2008.07.012
[5] K. K. Cornell, D. G. Bostwick, D. M. Cooley, G. Hall, H. J. Harvey, M. J. Hendrick, B. U. Pauli, J. A. Render, G. Stoica, D. C.Sweet and D. J. Waters, “Clinical and Pathologic Aspects of Spontaneous Canine Prostate Carcinoma: A Retrospective: An Aalysis of 76 Cases,” The Prostate, Vol. 45, No. 2, 2000, pp. 173-183. doi:10.1002/1097-0045(20001001)45:2<173::AID-PROS12>3.0.CO;2-R
[6] F. W. Bell, J. S. Klausner, D. W. Hayden, D. A. Feeney and S. D. Johnston, “Clinical and Pathological Features of Prostatic Adenocarcinoma in Sexually Intact and Castrated Dogs: 31 Cases (1970-1987),” Journal of the American Veterinary Medical Association, Vol. 199, No. 11, 1991, pp. 623-630.
[7] A. Maini, C. Archer, C. Y. Wang and G. P. Haas, “Comparative Pathology of Bening Prostatic Hyperplasia and Prostate Cancer,” In Vivo, Vol. 11, No. 4, 1997, pp. 293-300.
[8] W. Mahapokai, Y. Xue, E. van Garderen, F. J. van Sluijs, J. A. Mol and J. A. Schalken, “Cell Kinetics and Differentiation after Hormonal-Induced Prostatic Hyperplasia in the Dog,” Prostate, Vol. 44, No. 1, 2000, pp. 40-48. doi:10.1002/1097-0045(20000615)44:1<40::AID-PROS6>3.0.CO;2-J
[9] A. R. Gunzel-Apel, C. Moehrke and C. P. Nautrup, “Colour-Codex and Pulsed Doppler Sonography of Canine Testis, Epididymis and Prostate Gland: Physiological and Pathological Findings,” Reproduction in Domestic Animals, Vol. 36, No. 5, 2001, pp. 236-240. doi:10.1046/j.1439-0531.2001.00288.x
[10] K. U. Sorenmo, M. Goldschmidt, F. Shofer, C. Goldkamp and J. Ferracone, “Immunohistochemical Characterization of Canine Prostatic Carcinoma and Correlation with Castration Status and Castration time,” Veterinary and Comparative Oncology, Vol. 1, No. 1, 2003, pp. 48-56. doi:10.1046/j.1476-5829.2003.00007.x
[11] F. R. Shidaifat, M. Daradka and R. Al Omari, “Effect of Androgen Ablation on Prostatic Cell Differentiation in Dogs,” Endocrine Research, Vol. 30, No. 3, 2004, pp. 327-334. doi:10.1081/ERC-200033196
[12] K. U. Sorenmo, M. Goldschmidt, F. Shofer, C. Goldkamp and J. Ferracone, “Evaluation of Cyclooxigenase-1 and Cyclooxygenase-2 Expression and the Effect of Cycloxygenase Inhibitors in Canine Prostatic Carcinoma,” Veterinary and Comparative Oncology, Vol. 2, No. 1, 2004, pp. 13-23.
[13] J. J. Arthur, M. M. Kleiter, D. E. Thrall and A. F. Pruitt, “Characterization of Normal Tissue Complications in 51 Dogs Undergoing Definitive Pelvic Region Irradiation,” Veterinary Radiology and Ultrasound, Vol. 49, No. 1, 2008, pp. 85-89. doi:10.1111/j.1740-8261.2007.00322.x

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