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[Hemangiosarcoma of the breast: a case report and review of the literature].

A case of angiosarcoma of the breast in a 55-year-old woman is reported. It is clear that no effective treatment has so far been devised. The time from treatment to death was 41 months in this patient, compared with 25 months in collected cases from the literature. The possible value of adjuvant chemotherapy is stressed.

Breast

Carcinogenicity of vinyl chloride and vinylidene chloride.

Exposure of mice to 50, 250, or 1000 ppmm of vinyl chloride (VC) in the air for 6 h/d, 5 d/wk, caused a high incidence of bronchioloalveolar adenoma, mammary gland tumors, and hemangiosarcoma. Mammary gland tumors occurred in the females and included ductular adenocarcinoma and squamous and anaplastic cell carcinomas with metastasis to the lung. Hemangiosarcoma occurred in the liver and, to a lesser extent, in various other organs. The incidence and severity of these tumors increased with the concentration of VC and the length of exposure. Malignant lymphoma involving various organs was observed in several mice. Rats were more resistant to the carcinogenic effects of VC. Exposure of rats to 250 or 1000 ppm of VC caused hemangiosarcoma in the liver. Many rats with hepatic hemangiosarcoma also developed hemangiosarcoma in the lung. Extrahepatic hemangiosarcoma also occasionally occurred in other organs. Exposure to 55 ppm of vinylidene chloride (VDC) caused hepatic hemangiosarcoma and probably bronchioloalveolar adenoma in mice. Hemangiosarcoma also occurred in the mesenteric lymph node or subcutaneous tissue in two rats exposed to 55 ppm of VDC.

Aerosols

Cutaneous vascular neoplasia in 15 cats: clinical, morphologic, and immunohistochemical studies.

Seven cases of cutaneous hemangioma and nine of cutaneous hemangiosarcoma were diagnosed from biopsy specimens of 15 Domestic Shorthairs of 5,091 cats that were examined by necropsy or biopsy during the 5-year period from 1 January 1986 through 31 December 1990. All but three cats were male. Tumor cells of both hemangiomas and hemangiosarcomas were immunoreactive for factor VIII-related antigen and for vimentin by the avidin biotin peroxidase complex method. In cats with a median age of 10 years, hemangiomas occurred in skin with pigmented hair in six of seven cases without apparent site predilection. These solitary tumors did not recur after excision although one cat (No. 3) subsequently developed cutaneous hemangiosarcoma at another site. Seven of nine hemangiosarcomas occurred in dermis and subcutis of the head, usually on the pinna. All five hemangiosarcomas of the head, for which cutaneous pigmentation could be determined, occurred in unpigmented skin. Cats with hemangiosarcoma had a median age of 12.5 years at the time of diagnosis. Metastasis has not been documented, but hemangiosarcoma has recurred, from 1 month to 2 years after excision, in 6/7 cats that were studied.

Animals

Inhalation toxicity of vinyl chloride and vinylidene chloride.

Exposure of mice to 1000 ppm of vinyl chloride (VC), 6 hr/day, 5 days/week, caused some acute deaths with toxic hepatitis and marked tubular necrosis of the renal cortex. Starting the sixth month, mice exposed to 1000, 250, or 50 ppm of VC became lethargic, lost weight quickly, and died. Only a few mice exposed to 50 ppm survived for 12 months. Pulmonary macrophage count was elevated in some mice. There was a high incidence of bronchiolo-alveolar adenoma, mammary gland tumors including ductular adenocarcinoma, squamous and anaplastic cell carcinomas with metastasis to the lung, and hemangiosarcoma in the liver, and, to a lesser extent, in some other organs. The incidence of these tumors quickly increased, and the severity was in direct proportion to the levels of VC and the length of exposure. Malignant lymphoma involving various organs was observed in a few mice. Rats were more resistant to the toxic effects of VC. Exposure to 1000 ppm slightly depressed the body weight of the females. Exposures of 250 or 1000 ppm caused a number of deaths and hemangiosarcoma in the liver starting the ninth month. Most rats with hepatic hemangiosarcoma also developed hemangiosarcoma in the lung. Hemangiosarcoma occasionally occurred in other tissues of one or two rats exposed to 50 ppm or higher level of VC. Exposure of mice to 55 ppm of vinylidene chloride (VDC) also caused a few acute deaths and a few hepatic hemangiosarcomas. Inflammatory, degenerative, and mitotic changes occurred in the liver. No mouse exposed to VDC developed any mammary gland tumors. Several mice had bronchioloalveolar adenoma. Exposure of rats to 55 ppm of VDC slightly depressed the body weight. Hemangiosarcoma occurred in the mesenteric lymph node or subcutaneous tissue in two rats.

Adenoma

Prevalence, type, and importance of splenic diseases in dogs: 1,480 cases (1985-1989).

The prevalence data of splenic diseases from 3 sources were studied. Group 1 consisted of a general diagnostic survey of accessions submitted from private veterinary hospitals in California during a period of approximately 4 years and included 1,372 submissions of canine splenic tissue. Group 2 consisted of surgical splenectomy specimens from 92 dogs; the specimens were submitted to the laboratory for gross and histologic evaluation prior to fixation, and a questionnaire was subsequently sent to determine the outcome of the disease. Group 3 was made up of specimens of 105 splenic lesions derived from a large colony of Beagles with complete medical records and records of pathologic findings. In this study, splenic hematoma and hyperplastic nodule, not hemangiosarcoma, made up the bulk of splenic lesions. Hemangiosarcoma was the most frequent neoplasm of the canine spleen, but the combined prevalence of all other splenic neoplasms was similar to that of hemangiosarcoma alone. Splenic hematoma and hemangiosarcoma were grossly indistinguishable in most cases. Hyperplastic lymphoid nodules and hematomas of the spleen appeared to represent a continuum. If that finding was correlated with microscopic splenic blood flow, specific causal relationship could be suggested. Prognostically, the live/dead ratio and mean survival of dogs with various splenic lesions differed significantly.

Age Factors

Comparative pathology of bone tumors in animals, with particular emphasis on the dog.

A review of bone tumors in animals, based on cases reported in the literature and on personal examination of cases from several universities in the U.S.A. and Europe, has shown that: 1. The following bone tumors occur in decreasing order of frequency in animals: osteosarcoma, chondrosarcoma, osteochondroma, hemangiosarcoma, fibrosarcoma, and liposarcoma; 2. The dog has by far the highest frequency of bone tumors; and osteosarcomas account for approximately 80 percent of bone tumors in dog, followed by chondrosarcomas and hemangiosarcomas; 3. Bone tumors occur less frequently in the cat than in the dog, and are of essentially the same types and incidence as in the dog; 4. Sheep has a unique propensity for chondrosarcoma and primary bone tumors are rare in other species; 5. Giant cell tumors, reticulum cell sarcomas, and Ewing's sarcomas are exceptional findings in animals.

Animals

An experimental study of intraoral carcinogenesis in rats.

A new method has been devised for preparing artificial cecal pouches lined with mucous epithelium in the lower lips of Wistar and Sprague-Dawley rats in order to make carcinogens act continuously for a long time in the oral mucosa. When a 0.5 per cent mineral oil solution of DMBA, a crystal of MC, and a crystal of NG were administered, squamous-cell carcinoma, carcinoma in situ, papilloma, adenoma sebaceum. neurofibroma, fibroma, hemangiosarcoma, hemangiosarcoma, hemangioma, and lymphangioma were successfully produced in the oral mucosa of rats. In addition, interesting findings were obtained concerning tissue changes in the process of carcinogensis in the mucous epithelium.

Animals

Primary liver tumors in the pediatric age group: an angiographic challenge.

Eleven children, ranging in age from three months to fifteen years, with primary liver tumors were examined by large volume direct magnification arteriography (2.5--3 ml of contrast material per 1 kg body weight for a single selective study). The following tumors were found: hepatoblastoma (1), hepatocellular carcinoma of the adult type, hepatoma (3), infantile hemangioendothelioma (4), hemangiosarcoma (1), focal nodular hyperplasia (1) and cystic mesenchymal hamartoma (1). Some of the tumors have a quite typical angiographic appearance as infantile hemangioendothelioma, hemangiosarcoma, cystic mesenchymal hamartoma. The other highly vascular neoplasms show unspecific signs of vascular malignant tumors; subtile angiographic signs may, however, be present and help in the differential diagnosis.

Adolescent

Effect of lifetime exposure to aflatoxin b1 in rats.

Aflatoxin B1 was fed at 2 ppm in the diet to a group of pregnant F344 rats from the time of conception; it was then fed to their offspring until death. This diet was also given to another group of rats 6-7 weeks old for comparison. The survival time of male rats was significantly shorter than that of the female rats of both groups. However, the survival times of rats of the same sex in both groups did not differ significantly. The major causes of death were hepatic neoplasms with matastases, although some early deaths occurred before neoplasms developed. Most deaths were from a malignant hemorrhagic liver tumor, histologically diagnosed as a hemangiosarcoma, which caused rupture and hemorrhage into the peritoneal cavity or metastases to the lungs. These hemangiosarcomas were readily transplantable and did not produce alpha-fetoprotein. Ultrastructurally, they were composed of poorly differentiated cells resembling endothelial cells. Nodules of hyperplasia induced by aflatoxin B1 sometimes grew large (greater than 1.5 cm), and 2 were transplanted. Approximately 20% of the rats had colon tumors; a few rats had tumors of the kidney, oral cavity, and hematopoietic system.

Aflatoxins