Abstract. Case information and histologic slides for 688 admissions of feline tissues from 12 veterinary institutions were assembled and reviewed to determine tissues obtained by biopsy or necropsy, age and sex of cat, tumor topography, feline leukemia viral antigen status, histologic frequency of mitoses, diagnosis, presence of necrosis, and presence and degree of sclerosis. Histologic sections were examined to place the lesions in one of the diagnostic categories of the National Cancer Institute working formulation (NCI WF) for lymphomas or lymphoid leukemia. Correlations between the various factors determined were tested using contingency tables and chi-square analysis to provide a statistical comparison between the levels of observations determined by case examination with the numbers expected from chance alone. Significant correlations (P Յ 0.05) were found between diagnosis and tumor topography, the frequency of mitoses, necrosis, sclerosis, and age, between mitoses and necrosis, topography, age, and feline leukemia viral infection status, between topography and necrosis and age, and between leukemia viral status and age. Significant correlations between diagnosis and tumor topography included a greater than expected number of cases of acute and chronic lymphoid leukemia and multicentric distribution of tumor. Small cell lymphomas were more frequent than expected in enteric and cutaneous areas and less frequent than expected in mediastinal, renal, and multicentric areas. In contrast, the high-grade small noncleaved type of lymphomas was found significantly more frequently than expected in the mediastinum and less frequently than expected in enteric tissues. In comparing diagnosis and frequency of mitoses, the lymphomas classified as low grade by the NCI WF were significantly more frequent than expected in the lower categories (0-2/100ϫ) of mitoses, and those classified as high-grade lymphomas were more frequent than expected in the higher categories (4-8/100ϫ) of mitoses. In comparing diagnosis and sclerosis, diffuse sclerosis was more frequent than expected for the intermediate grade lymphomas of mixed cell type and for the highgrade lymphomas of the immunoblastic polymorphous type. In comparing diagnosis and locally extensive necrosis, this feature was more frequently observed than expected for cases of intermediate grade lymphoma of the small-cleaved cell category and for the high-grade lymphoma of the immunoblastic cell type. In comparing mitoses and necrosis, the lower grade lymphomas were, in general, characterized by a lower frequency of mitoses and a lower incidence of necrosis then would be expected from chance alone. In contrast, the higher grade lymphomas were characterized by more frequent mitoses and a higher incidence of necrosis. In tests comparing mitoses and tumor topography, lymphomas of the alimentary tract were more frequently observed than expected in the category with the lowest level of mitoses (0-1/100ϫ), whereas lymphomas of the mediastinum and kidney were more frequently observed ...

Seventy-one dogs with histologically confirmed appendicular osteosarcoma were evaluated. Seventeen dogs were treated with amputation and two dogs received postoperative doses of IV cisplatin given 21 days apart (group 1). Nineteen dogs were treated with IV cisplatin 21 days before amputation, with a second dose given immediately after amputation (group 2). Thirty-five dogs were treated by amputation of the affected limb with no chemotherapy (group 3). The median disease-free interval for group 1 was 226 days, and 177 days for group 2. This was not significantly different. The median survival time was 262 days for group 1,282 days for group 2 and 119 days for group 3. Group 1 and 2 dogs had survival times that were significantly longer than for dogs in group 3. Two IV courses of cisplatin given before or after amputation appears to improve the survival of dogs with osteosarcoma. (Journal of Veterinary Internal Medicine 1991; 5205-210) OSTEOSARCOMA (0s) is the most common primary bone cancer in dogs.',2 It accounts for approximately 4% of all canine neoplasms and has been estimated to affect approximately 7.9/ 100,000 dogs annually.' Treatment has generally included amputation, which relieves local discomfort but rarely results in a cure, with reported mean or median survivals of 3.6 to 5.8 ~~~~~ ~

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.

Rudolph Virchow first speculated on a relationship between inflammation and cancer more than 150 years ago. Subsequently, chronic inflammation and associated reactive free radical overload and some types of bacterial, viral, and parasite infections that cause inflammation were recognized as important risk factors for cancer development and account for one in four of all human cancers worldwide. Even viruses that do not directly cause inflammation can cause cancer when they act in conjunction with proinflammatory cofactors or when they initiate or promote cancer via the same signaling pathways utilized in inflammation. Whatever its origin, inflammation in the tumor microenvironment has many cancer-promoting effects and aids in the proliferation and survival of malignant cells and promotes angiogenesis and metastasis. Mediators of inflammation such as cytokines, free radicals, prostaglandins, and growth factors can induce DNA damage in tumor suppressor genes and post-translational modifications of proteins involved in essential cellular processes including apoptosis, DNA repair, and cell cycle checkpoints that can lead to initiation and progression of cancer.