Forty-eight dogs with histologically confirmed appendicular osteosarcoma (OSA) entered a prospective clinical trial evaluating treatment with amputation and up to 4 doses of carboplatin given every 21 days. The median disease-free interval (DFI) was 257 days, with 31.2% of the dogs disease-free at 1 year. The median survival time was 321 days, with 35.4% of the dogs alive at 1 year. Dogs with proximal humeral OSA had shorter DFI ( P = .016) and survival ( P = ,037) times than dogs with OSA at other locations. Dogs with lower body weights (<40 kg) had longer DFI (P = .0056) and survival (P anine appendicular osteosarcoma (OSA) is an aggres-C sive tumor that has a poor prognosis without treatment.1.2 This tumor has been estimated to affect 8,000 to 10,000 dogs annually in the United States, and accounts for 85% of all primary bone tumors in dogs.'.' Amputation, which rarely results in a cure but relieves local discomfort, has traditionally been the standard treatment modality. Because 80% to 90% of patients have microscopic occult metastatic disease at presentation, amputation is only a palliative pr~cedure.~.' The median survival of dogs with OSA treated by amputation alone is 126 to 134 days, and only 10% to 12% of the dogs are alive at 1 year.' Therefore, to improve survival, some form of systemic therapy is necessary.Recently, cis-diamminedichloroplatinum (cisplatin) has shown activity against OSA in dogs and people.',7-" The median survival of dogs receiving cisplatin after surgery improved to 262 to 325 days, and 33% to 45% of the dogs

Twenty-four dogs and 30 cats with histopathologically confirmed salivary gland neoplasia were retrospectively reviewed in a multi-institutional study. The predominant presenting complaint for animals with salivary gland neoplasia was that of a mass being noted by the owner; other common complaints included halitosis, dysphagia, and exophthalmia. Siamese cats were overrepresented, indicating a possible breed predisposition. The most common histopathological type was simple adenocarcinoma. Cats had more advanced disease at diagnosis than did dogs, and clinical staging was prognostic in dogs. The median survival times for dogs and cats were 550 days and 516 days, respectively.

Fifty-one dogs treated for mandibular osteosarcomas (OSs) were studied retrospectively. Treatments were partial mandibulectomy (n = 32); partial mandibulectomy and chemotherapy (n = 10); partial mandibulectomy and radiation therapy (n = 3); partial mandibulectomy, radiation therapy, and chemotherapy (n = 4); and radiation therapy alone (n = 2). The overall one-year survival rate was 59.3%. Dogs treated with surgery alone had a one-year survival rate of 71%, which is higher than the one-year survival rate for dogs with appendicular OSs treated with surgery alone (p of 0.001 or less; hazard ratio of 0.29). There was no apparent effect of various treatment modalities, nor institution where treatment was given, nor histological type. Histological score and, to a lesser extent, histological grade were predictive of survival outcome.

Serum and seminal plasma concentrations or activities of acid phosphatase (AP), prostate specific antigen (PSA), and canine prostate specific esterase (CPSE) were measured in normal dogs, dogs with benign prostatic hyperplasia (BPH), dogs with bacterial prostatitis, and dogs with prostatic carcinoma t o determine if these assays would be of value in differentiating dogs with prostatic carcinoma from normal dogs, and dogs with other prostatic disorders. In addition, tissue sections of prostatic adenocarcinomas were stained with antiprostatic AP, anti-CPSE, and anti-PSA antibodies t o determine if these would be suitable immunohistochemical markers of prostatic carcinoma. Prostate-specific antigen was not detected in canine serum or seminal plasma. Serum and seminal AP activities did not differ significantly between normal dogs and those with prostatic diseases, or among dogs with different prostatic disorders. Serum CPSE activities were significantly higher in dogs with BPH than in normal dogs. Mean serum enign prostatic hyperplasia (BPH), prostatic carci-B noma, and bacterial prostatitis can be difficult to differentiate in dogs because of similarities in clinical presentation, and laboratory and radiographic findings. A definitive diagnosis often requires prostatic biopsy, which is complicated by the relative inaccessibility of the prostate gland. In patients with prostatic carcinoma, inability to rapidly confirm the diagnosis may contribute to the poor prognosis typically associated with thisIn men with prostatic carcinoma, the use of serum markers such as acid phosphatase (AP) and prostate-specific antigen (PSA) has facilitated diagnosis, determination of the extent of disease, evaluation of therapeutic response, and detection of relapse after the rap^.^.^ Prostate-specific antigen is a proteolytic glycoprotein found in normal, hyperplastic, and malignant human prostatic tissue. Increases in serum PSA concentrations have been reported in human patients with BPH, prostatitis, and prostatic carcinomx8 In human patients with prostatic carcinoma, PSA concentrations correlate with the stage ofdisease, and serum activities of PSA are considered more sensitive than serum acid phosphatase activities for monitoring the disease.6 Acid phosphatase and PSA have been identified in normal, neoplastic, and hyperplastic canine prostatic epithelial cells. ' Canine prostate specific esterase (CPSE), the major secretory product of the canine prostate gland, is similar to human PSA and, like PSA, is a serine protease. Although the proteins are closely related, they are clearly distinct from one another." Both CPSE and PSA are under hormonal regulation, and decreases in serum testosterone activities result in reduction in the serum and seminal plasma concentrations or activities.' ' 3 ' ' Canine prostate specific esterase has been identified in normal canine prostatic cells, in canine seminal fluid,I2-I5 and in hyperplastic and neoplastic prostatic tissue.' The esterase is predominantly localized to the apical portions of canin...

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A retrospective study was undertaken to characterise the biological behaviour of splenic haemangiosarcoma (HSA) in dogs. Metastatic pattern data for 25 dogs with splenic HSA that were presented for clinical signs relating to splenic lesions (eg, abdominal mass and, or, haemoperitoneum) and had undergone necropsy were analysed. Six of 25 dogs with splenic HSA that were presented for abdominal mass/haemoperitoneum had right atrial HSA. Fifteen of 19 (79 per cent dogs) with splenic HSA associated with abdominal mass/hemoperitoneum without right atrial involvement had disease confined to the peritoneal cavity. The most common metastatic sites in these dogs were liver, omentum and mesentery. Extraperitoneal metastases were seen in four of 19 (21 per cent) dogs without right atrial involvement. Analysis of signalment data of dogs in this series and the literature revealed no differences between dogs with disease confined to the peritoneal cavity and dogs with extraperitoneal metastases. The subjectivity of primary site designation, importance of ante mortem identification of individuals with concurrent right atrial involvement, and need for more aggressive therapy directed at intraperitoneal metastases are discussed.

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Sixteen dogs with histologically confirmed appendicular osteosarcoma were treated by amputation followed by cisplatin and doxorubicin chemotherapy. All dogs began chemotherapy within 24 hours of surgery. Cisplatin was administered at 50 mg/m2 intravenously (IV) concurrent with saline-induced diuresis. Doxorubicin was administered 24 hours later at 15 mg/m2 as a slow IV bolus. This protocol was given on a 21-day cycle for 4 cycles. No dose delays were required, but dose reduction of doxorubicin was required in 2 dogs because of neutropenia. Thoracic radiography was performed every 2 months after completion of therapy to monitor for metastatic disease. Two dogs were still alive and free from disease at the time of last contact (24 and 75 months, respectively). Postmortem examinations were performed on 13 of the 14 dogs that died. Eight of these dogs were euthanized because of metastatic osteosarcoma. Of the remaining 5 dogs, euthanasia was performed because of complications of idiopathic megaesophagus (n = 1), arthritis (n = 2), and hemangiosarcoma (n = 2). The median disease-free interval and survival times were 15.7 and 18 months, respectively. When compared to a historical group of 36 dogs with appendicular osteosarcoma treated with surgery and 4 doses of cisplatin. both disease-free interval and overall survival were significantly longer in the study population (P < .015 and P < .007, respectively).