Florid pulmonary veno-occlusive disease.

A young woman presented with rapidly progressive dyspnea and clinical findings strongly suggestive of primary pulmonary hypertension or possible pulmonary embolism (or both). She died of acute right-sided heart failure. A diagnosis of pulmonary veno-occlusive disease was made at autopsy. Approximately 100 cases of this disease have been reported previously in the literature. We describe a patient with a particularly florid progression of this unusual disease. Death occurred within six weeks of the onset of symptoms.

Histiocytic sarcoma with a granuloma-like component occurring in a large colony of Sprague-Dawley rats.

Tumors from a large colony of over 2000 Sprague-Dawley rats were reviewed by a panel of pathologists under the auspices of Universities Associated for Research and Education in Pathology, In the course of this study, a distinct malignancy in 105 rats was segregated and given the name "histiocytic sarcoma." This report describes the histologic features and anatomic distribution of the tumor, along with its incidence by age and sex of the rat. The neoplasm is characterized by a spectrum of histologic patterns, one extreme resembling a sarcomatous process and the other a granulomatous process. The exact morphologic composition varied from animal to animal, as well as in tumors from the same animal. The sarcomatous pattern is composed of sheets of uniform cells, occasionally exhibiting phagocytosis. The granulomatous pattern contains epithelioid histiocytes, central areas of tumor necrosis surrounded by palisading cells, and multinucleate giant cells. The liver is the organ most commonly containing histiocytic sarcoma, both in animals with multiple tumors and in those with involvement of only one organ. Hepatic invasion is typified by expansion of the portal areas and infiltration of the sinusoids by tumor cells. The lung is the second most common site. The distribution of pulmonary tumors is bronchiolocentric and angiocentric. Other common sites included the lymph node and spleen, along with large soft tissue tumors of the mediastinum and retroperitoneum. Although occasional previous reports apparently have described a similar or identical neoplasm under varying names, no large group of tumors of this unique type in rats has been studied and characterized previously.

A pathologist looks at spontaneous regression of cancer.

We are all subjected to varying amounts of mutating, potential cancer-inducing events, which are cumulative. In most instances, the accumulations are repaired or are lethal. If a viable clone survives, it must proliferate in order to become manifest and eventually to overpower the host's normal regulatory and defense mechanisms. The proliferation may be incited and sustained by cocarcinogens, hormone excess, chronic infections such as schistosomiasis, and in the case of lymphoid cells, by immune incompetence. On the other side are the protective reparing enzymes, which serve to cut out the damaged segments of DNA and repair them as fast as they can. The normal homeostatic mechanisms tend to keep cell proliferation and activity within the beneficial bounds of need. The controlling forces that cause cells to stop reproducing themselves and differentiate to perform a useful function also tend to slow or even stop the useless proliferation if all the cells can undergo maturation to a postmitotic state. There are also the protective mechanisms of immunity: Sensitized B lymphocytes tag the antigenic sites of tumor cells and activate the T-cell macrophages to destroy the tagged cells.

Acute and chronic effects of intraperitoneal injection of two types of asbestos in rats with a study of the histopathogenesis and ultrastructure of resulting mesotheliomas.

Malignant mesotheliomas were induced in the rat peritoneum by a single injection of chrysotile or crocidolite asbestos fibers. The immediate toxicity of the fibers was noted in both groups of animals, producing approximately 40% mortality, within 8 days after the injection associated with acute peritonities. Tissue reactions to these two types of asbestos were significantly different. Crocidolite fibers were easily seen by light microscopy, in the tissue sections throughout the period of study, and they produced foreign-body giant cell granulomas. However, giant cells were not seen in chrysotile granulomas, and the asbestos fibers were only seen by electron microscopic study. They appeared to be coated by a protein-like substance. During earlier stages of tumorigenesis, the epithelioid and/or mixed cell type mesotheliomas seemed to have no specific relationship to granulomas, but pure spindle cell tumors were seen to develop in close relationship to granulomas, and they appear to be fibrosarcomas. Electron microscopic and histochemical methods were used to define the morphologic characteristics of the tumor cells. The formation of hyaluronic acid was found in cells of the epithelioid type, contrasted with extracellular accumulation in the spindle cell tumors.