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Tumour Predisposition in German Shepherd
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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.
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