Haemangiosarcoma is a form of cancer in which the tumour is caused
by unregulated proliferation of cells related to those that normally
develop to make up blood vessels.
The cancer may commonly be located in the spleen, the liver, or
beneath the skin, and also the right atrium of the heart. The forms
in the internal organs are highly aggressive and usually metastatic
(they spread to additional sites) whilst dermal (skin) tumours are a
little less so (about 30% show metastasis).
When dogs contract the visceral (internal) form of this cancer
symptoms are often not visible until rather late in the course of
the disease, by which time the outlook for the dog may be very poor.
The cancer is often associated with “disseminated coagulopathy” in
which vessel wall damage causes clotting to occur within blood
vessels. Paradoxically, this uses up many of the blood clotting
components rapidly, and as a consequence can also give rise to a
loss of normal blood clotting, so that the dog develops bleeding
from the nose or elsewhere. At the same time, splenic tumours are
prone to rupture, which the leads to serious internal bleeding. If
these splenic tumours are found early enough, a splenectomy (removal
of the spleen) is usually performed. This protects from
life-threatening sudden bleeds, but splenic haemangiosarcoma is
still a rapidly spreading malignancy. 25% of dogs with splenic
haemangiosarcoma also have a heart-based haemangiosarcoma.
This particular form of cancer is rather common in German Shepherd
dogs when compared with most other dog breeds. In fact, calculations
based on insurance records or on registers of cases treated suggest
that it may be around 3 times more common in this breed than in the
general dog population.
With collaborators in Holland, Sweden, the US and at the Animal
Health Trust in Newmarket England, we are now researching the reasons for the
more common incidence of haemangiosarcomas in this breed. We
hypothesis that the origins of the predisposition may be genetic.
The study of complex genetic defects in dogs at the molecular level
has been made feasible by advances in genetic technology over the
last two to three years, so that now we are receiving samples from
affected animals with this particular type of cancer, in order to
perform this analysis.
We would hope that the minimum outcome of the research will be an
improved understanding of the tumour leading to more effective
treatment in cases when the tumour is recognized early in its
growth. We would also hope that we can recognise genetic markers
that are associated with higher risk of hemangiosarcoma in the
German Shepherd dog. Although it is unlikely that simply through the
use of DNA based testing we shall be able to provide breeding advice
leading to complete elimination of this tumour from the German
Shepherd dog breed, the recognition of DNA markers associated with
the disease could lead to a testing programme allowing marked
reduction in incidence of haemangiosarcoma in the breed over the
medium term.
In addition to the hope of improving the health of German Shepherd
dogs the work also holds out the prospect that we may be able to
gain a better understanding of the tumour in humans, in whom it
occurs as a rare paediatric disease (a handful of cases per year in
this country), and so is difficult to study. Both for this and for a
human adult form associated with certain occupational toxins the
prognosis for the patient is currently as grim as it is for dogs
with the tumour.
To help us perform the study, we need blood samples from German
Shepherd dogs. First and foremost we need blood samples from dogs
that are or have been haemangiosarcoma patients. Ideally these would
be 2-3 ml samples in EDTA tubes. We also need similar samples from
older healthy German Shepherd dogs. These should be nine years or
older because the tumour typically has onset in older dogs, and we
are trying to minimize the chances that we sample dogs for our
control group who subsequently go on to get the tumour.