The morphogenesis and hormonal relationships of a unique malignant basal-cell epithelioma in flank organs of the Syrian hamster are described. The life history of this androgen-estrogen-induced tumor involves three stages: 1. The migration of hair matrix cells into dermal sheaths and/or dermal papillae to form epithelial nodules which become surrounded by connective tissue lamellae; these lamellated corpuscles occur normally in males aged 185 or more days, but not in females; they require the presence of androgen and are inhibited by estrogen. 2. Under the influence of exogenous androgen they increase in size, up to approximately 1 mm. in diameter, and the central cores of epithelial cells migrate peripherally as radiating cords. Under the influence of exogenous androgen and estrogen together, the stage 2 nodules increase in size and fuse to form definitive stage 3 neoplasms, the mean latent period for induction of which is ca. 230 days, with a range of 110–500 days. Once formed neither the spontaneous nor the induced tumors ever undergo complete regression, even with estrogen treatment. With androgen treatment alone stage 1 nodules occur precociously, and induced nodules appear in females and in gonadectomized or hypophysectomized hamsters. The effects of surgical interference, and of other hormones, upon the induction and behavior of the tumor are described, as are its growth characteristics in both hormone-free and hormone-containing diffuse cell and organ cultures. The chaetepithelioma metastasizes and is transplantable as a hormone-dependent tumor. Specific hormone activity at the tissue level, rather than “hormonal imbalance,” is considered critical in the induction and growth of this tumor. During 21 serial passages the transplanted tumor has not become autonomous.

Some semantic problems in oncology and possible modes of hormone action in tumor induction and subsequent growth are discussed in relation to this tumor.

The value of the neoplasm in studies of carcinogenesis is emphasized.

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Aided by grant EDC-5 from the American Cancer Society, recommended by the Committee on Growth of the National Research Council, and Grants C-2596, C-2812, and C-4516 from the National Cancer Institute, National Institutes of Health.

The experimental work reported here was completed at Stanford University; the data were partly assembled and the manuscript partly prepared during the senior author's tenure of a Special U. S. Public Health Service Fellowship at the Chester Beatty Research Institute, London, England, 1958–1959; the study was completed and the manuscript finished in collaboration with the junior author, partly at Stanford University, and partly at the Strangeways Research Laboratory, Cambridge, England, during the junior author's tenure of a Senior U. S. Public Health Service Fellowship there in 1962–63.

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