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Hemangiosarcoma
1
Christine B. Oakley, DVM and John D. Chretin, DVM, DACVIM (Oncology) 2
1 VCA Specialists of the Valley, Los Angeles, CA, USA
2 TrueCare for Pets, Los Angeles, CA, USA

Etiology and Pathophysiology Pathophysiology

Location
Etiology
Hemangiosarcoma as a primary tumor has been reported
Hemangiosarcoma (HSA) is a malignant cancer of to arise in the liver, kidney, bladder, prostate, perito­
vascular endothelial cells. Although ionizing radiation neum, lung, right auricle, muscle, bone, oral cavity,
has been associated with cutaneous HSA, there is no central nervous system (CNS) and integument, but can
clear etiology for the visceral and subcutaneous forms. arise from any vascular site in the body. In the dog, the
Vascular endothelial growth factor (VEGF) and other spleen is the most commonly affected organ (28–50%),
growth factors such as basic fibroblast growth factor followed by the right atrium and auricle (3–50%) and
(bFGF) and angiopoietin‐1 are found in above normal skin/subcutaneous tissue (13–14%). Multiple unrelated
levels in hemangiosarcoma. It is therefore hypothesized primary tumors can occur as has been speculated in
that dysregulation of angiogenesis may play a key role. dogs with concurrent splenic and myocardial forms.
Experimentally, it has been shown that overexpression of Dermal hemangiosarcoma is a much less aggressive
VEGF can lead to malignant transformation of vascular disease than visceral hemangiosarcoma. It has been pro­
endothelial cells. posed that there are two dermal forms: the solar‐induced
In humans, this disease is known as angiosarcoma and form, affecting thin‐coat predisposed breeds with a good
has been related to arsenicals, vinyl chloride exposure, prognosis, and a nonsolar‐induced, more aggressive
and androgens as well as radiation exposure. These may form seen in nonventral locations in thicker coated, non­
induce a mutation in the von Hippel–Lindau tumor predisposed breeds. Dermal hemangiosarcoma (both
suppressor gene leading to an increased synthesis of solar and nonsolar) has a low metastatic rate. Common
hypoxia‐inducible factor‐1 (a transcription factor for sites of metastasis include lungs, oral or nasal tissue,
angiogenic proteins such as VEGF). Mutations in other bone, heart, and CNS. The solar‐induced form histori­
tumor suppressor genes such as p53 and PTEN have cally carries the best prognosis. Hypodermal (subcuta­
also been found but studies are limited. neous) HSA is characterized as being aggressive with
The etiology of dermal hemangiosarcoma differs from higher local tumor invasion and a higher metastatic rate
visceral, myocardial, and other less common primary than dermal forms.
forms. Dogs with repeated, prolonged exposure to direct Hemangiosarcoma is much less common in cats
ionizing ultraviolet (UV) radiation have been documented than in dogs. In contrast to dogs, integumentary HSA
to have an increased risk. The predisposition for dogs to (subcutaneous and dermal) is more common than the
develop dermal HSA regionally on the ventral abdomen visceral or myocardial form. Seventy‐seven percent of
supports solar induction, as well as field cancerization all reported feline cases arise from the integument.
(a term used to describe the increased risk for regional The most common locations in decreasing order are
tumor development after exposure to carcinogens). head/face, pinna, and ventral abdomen/inguinal region.

Clinical Small Animal Internal Medicine Volume II, First Edition. Edited by David S. Bruyette.
© 2020 John Wiley & Sons, Inc. Published 2020 by John Wiley & Sons, Inc.
Companion website: www.wiley.com/go/bruyette/clinical