Prostate carcinoma - Veterinary Practice
Your browser is out-of-date!

Update your browser to view this website correctly. Update my browser now



Prostate carcinoma

Dr HENRY L’EPLATTENIER reviews the signs, management and treatment

Epidemiology and biological
Tumours of the prostate are not
commonly seen in dogs. Usually older
dogs are affected with an average age
of occurrence of 10 years (Cooley and
Waters, 2001) and it
appears that castrated
males have a greater
risk of developing
prostatic carcinoma
than intact male dogs
(Teske et al., 2002).

There is no
particular breed
disposition; however,
a recent retrospective
study at Utrecht
University in the
Netherlands revealed
that the Bouvier des
Flandres had almost
8.5 times more risk of
developing the disease than other
breeds (Teske et al., 2002).

All prostatic tumours reported are
malignant and the majority are
adenocarcinomas. In some cases
transitional cell carcinomas from the
bladder or urethra can extend into the prostate.
Prostatic carcinomas (PCA) are very malignant tumours and metastases
are frequently already present at the
time of diagnosis.

The main sites of
metatstatic spread are
the sublumbar lymph
nodes, lungs and
skeletal system,
particularly the lumbar

Pathogenesis in
humans and dogs

Androgens are known
to stimulate growth of
prostate cells in both
humans and dogs. In
humans, not only
normal prostate cells
but also PCA cells are
highly dependent on androgen for growth
and it has been recognised since the early 1940s that castration is an
effective treatment for PCA.

Today, hormone ablation therapy is
still the mainstay of systemic treatment
for PCA in humans. In most cases,
however, androgen ablation fails after a period of time
and PCA
progresses to a

In dogs, the
aetiologic role of
androgens is less
clear since PCA
has a higher
prevalence in
castrated animals than in intact males
(Teske et al., 2002). There appears to
be no relationship between the age at
castration and the age at the
development of PCA, suggesting that
castration does not initiate the
development of PCA in dogs but
might be a promoting factor.

In addition, in intact male dogs
with PCA, androgen ablation does not
have any anti-tumour effect. As the
histomorphology of canine PCA is
often poorly differentiated, canine
PCA thus resembles the hormone-
independent state of human PCA.

One of the possible explanations
for the development of PCA in the
absence of androgens is the fact that
canine PCA appears to originate from
basal cells in the duct areas of the
prostate rather than from acinar cells.

Clinical signs and diagnosis

The most common signs are straining
to defaecate (dyschezia), problems with urination (stranguria, haematuria)
and systemic signs (weight loss,
anorexia). Occasionally, signs of hind
limb lameness or neurological deficits
may be seen in cases where metastasis
to the lumbar spine, pelvis or femur
has occurred.

Prostatamegaly is found on
physical examination. Prostate
enlargement is more often
asymmetrical than symmetrical. No
haematologic or serum chemistry
findings are specific for PCA in dogs.
The most frequently encountered
change is leucocytosis.

Canine prostate-specific arginine
esterase (CPSE) is a secretory product
of the canine prostate and a known
marker of prostate secretion in the
dog. However, unlike PSA (prostate-
specific antigen) in men, its potential
diagnostic use is limited to non-
neoplastic diseases of the prostate.
The most common radiographic and
ultrasonographic findings are enlargement of the prostate and the
presence of intraprostatic

The presence of prostatic disease
in a castrated male dog carries a high
suspicion of carcinoma. However, the
definitive diagnosis is usually made by
cytological examination of a fine
needle aspirate of the prostate
performed under ultrasound guidance
(Figure 1).


Due to the high metastatic rate of
prostate carcinoma, both local and
systemic treatment are necessary to
control the disease.

Radical prostatectomy in dogs with
prostatic disease is associated with a
high incidence of peri-operative
mortality and post-operative
incontinence and is therefore not an
acceptable treatment option for dogs
with prostatic carcinoma.

Various techniques for partial or subtotal prostatectomy
have been described
using either an
electroscalpel (Vlasin et
., 2006), a Cavitron
Ultrasonic Surgical
Aspirator (CUSA)
(Rawlings et al., 1997) or
a Nd:YAG laser (Hardie
et al., 1990).

In dogs with prostate
carcinoma, subcapsular
partial prostatectomy
using a Nd:YAG laser,
combined with local administration of
interleukin-2, has been shown to
improve clinical signs in most dogs
and lead to survival times of up to
eight months (L’Eplattenier et al.,
2006). Dogs presenting with serious
stranguria or urinary obstruction
responded less well to this surgical

Photodynamic therapy (PDT) has
also been used for the local control of
prostate carcinoma in dogs. PDT
combines the administration of a
photosensitiser and the subsequent
illumination of the target organ with light of a determined wave length. The
light is absorbed by the photosensitiser
causing photochemical mechanisms
leading to tissue necrosis.

Treatment of PCA with
transurethral photodynamic therapy
allowed the only dog reported to
survive nearly nine months after
treatment (Lucroy et al., 2003).

PDT was also used intra-
operatively to treat tissue remaining
after partial subcapsular prostatectomy
(L’Eplattenier et al., 2008); however,
results were disappointing.
Radiotherapy is not generally
recommended for prostate cancer due
to the proximity of the bladder and
colon and the high risk of unwanted
side-effects to these organs.

COX-2 inhibitors

No effective chemotherapeutic
protocol is available for the systemic
treatment of PCA in dogs. COX-2 is
expressed in various types of canine cancer including PCA,
and is thought to play a
role in carcinogenesis.
This is supported by
evidence that treatment
with COX-2 inhibitors
may be beneficial in the
management of certain
tumours in dogs.

The COX-inhibitor
piroxicam has been
shown to effectively
inhibit transitional cell
carcinoma (TCC) of the bladder in dogs (Henry et al., 2003;
Knapp et al., 1994). Although it has
been shown that COX-2 is expressed
in canine PCA (L’Eplattenier et al.,
2007), the effect of NSAIDs on the
clinical outcome of dogs with PCA
has not been extensively investigated.

Preliminary findings in dogs with
PCA (Sorenmo et al., 2003) and in a
mouse prostate carcinoma model
(Gupta et al., 2000) suggest that COX-
2 inhibitors may play a significant role
in the management of PCA in dogs.

For dogs with severe stranguria or
urethral obstruction caused by neoplasms of the prostate, palliative
treatment with intraluminal stents can
be effective in improving quality of life
for several months (Weisse et al., 2006).
Urinary incontinence is seen in about
20% of these dogs.


  • Cooley, D. M. and Waters, D. J. (2001)
    Small Animal Clinical Oncology.
  • Withrow S. J.
    and Macewen, E. G. (eds). Saunders:
    Philadelphia, pp478-489.
  • Gupta, S., Srivastava, M., Ahmad, N.,
    Bostwick, D. G. and Mukhtar, H. (2000)
    Prostate 42: 73-78.
  • Hardie, E. M., Stone, E. A., Spaulding, K.
    A. and Cullen, J. M. (1990) Vet Surg. 19:
  • Henry, C. J., McCaw, D. L., Turnquist, S.
    E., Tyler, J. W., Bravo, L., Sheafor, S.,
    Straw, R. C., Dernell,
  • W. S., Madewell, B.
    R., Jorgensen, L., Scott, M. A.,
  • M. L. and Chun, R. (2003)
    Clin Cancer Res. 9: 906-911.
  • Knapp, D. W., Richardson, R. C., Chan, T.
    C., Bottoms, G. D., Widmer, W. R.,
    DeNicola, D. B., Teclaw, R., Bonney,
  • P. L.
    and Kuczek, T. (1994) J Vet Intern Med. 8:
  • H. F., Klem, B., Teske, E.,
    van Sluijs, F. J., van Nimwegen, S. A. and
    Kirpensteijn, J. (2008) Vet J. 178: 202-207.
  • L’Eplattenier, H. F., Lai, C. L., van den
    Ham, R., Mol, J., van Sluijs, F. and Teske,
    E. (2007) J Vet Intern Med. 21: 776-82.
  • L’Eplattenier, H. F., van Nimwegen, S. A.,
    van Sluijs, F. J. and Kirpensteijn, J. (2006)
    Vet Surg. 35: 406-11.
    Lucroy, M. D., Bowles, M. H., Higbee, R.
    G., Blaik, M. A., Ritchey, J. W. and
    Ridgway, T. D. (2003) J Vet Intern Med. 17:
  • Rawlings, C. A., Mahaffey, M. B., Barsanti,
    J. A., Quandt, J. E., Oliver, J. E., Jr.,
    Crowell, W. A., Downs, M. O., Stampley,
    A. R. and Allen, S. W. (1997) J Am Vet Med
    . 211: 868-71.
  • Sorenmo, K. U., Goldschmidt, M.,
    Schofer, F., Goldkamp, C. and Ferracone,
    J. (2003) Vet Comp Oncology 1: 48-56.
  • Teske, E., Naan, E. C., van Dijk, E. M.,
    Van Garderen, E. and Schalken, J. A.
    (2002) Mol Cell Endocrinol. 197: 251-255.
  • Vlasin, M., Rauser, P., Fichtel, T. and
    Necas, A. (2006) J Small Anim Pract. 47:
    Weisse, C., Berent, A., Todd, K., Clifford,
    C. and Solomon, J. (2006) J Am Vet Med
    . 229: 226-34.

Have you heard about our
IVP Membership?

A wide range of veterinary CPD and resources by leading veterinary professionals.

Stress-free CPD tracking and certification, you’ll wonder how you coped without it.

Discover more