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A clinical and pathologic analysis of 30 lipid cell tumors of the ovary shows that both adrenocortical-like and hilus-like cells are present in most instances and that attempts to separate them objectively into adrenal-like tumors, hilus cell tumors or stromal luteomas is often impossible. Inasmuch as there is no histogenetic basis for employing this terminology, such a separation is considered artificial and of no value in predicting either functional manifestations or clinical behavior. Therefore, lipid cell tumors are regarded as a specific entity and not a collection of different lesions. Lipid cell tumors are most often virilizing (77% of patients) and may be associated with Cushing's syndrome (10% of patients) or with evidence of estrogenic activity (23% of patients). Although these tumors usually are considered benign, six patients in this series died of recurrent or metastatic tumor. The clinically malignant lipid cell tumors tended to be larger than the benign ones, had involved contiguous pelvic structures at the time of operation in half of the cases, and occasionally exhibited sufficient cellular pleomorphism and mitotic activity to permit objective interpretation as malignant. On the basis of the authors' findings and the evidence available in the literature, the most likely origin of lipid cell tumors is from the specialized ovarian stromal cells within the medullary part of the ovaries.

1. An experimental study of the healing mechanism in circumscribed defects in femora of albino rats of the Wistar strain is described. 2. Only the outer one-fifth of the defect is repaired by subperiosteal bony callus, the rest of the defect being repaired by endosteal callus. 3. Subperiosteal callus does not bridge the defect until endosteal callus is developed fully. 4. As peripheral callus matures the greater part of the endosteal callus is resorbed, with the exception of trabeculae attached to the margin of the defect. 5. The resorbed area in the medullary part of the defect is gradually obliterated by deposition of inner circumferential lamellae. 6. There appear to be differences between the mechanism responsible for repair of fractures of a long bone and that which heals circumscribed bone defects.