A transparent chamber designed for insertion in the dorsal skin fold of athymic mice is described. The chamber is based on ingrowth of a layer of granulation tissue from the surrounding subcutis of the animals. The thickness of the tissue layer in the chamber is accurately given by an exchangeable chamber component and the construction allows repetitive access to the tissue inside the chamber. A freely movable skin flap is prepared surgically on the back of the animals, and the chamber is inserted in this flap in a second operation about 2 weeks later. In the absence of air bubbles, infectious foci and excessive adipose tissue in the chamber, ingrowth of granulation tissue is completed 2–4 weeks after the insertion. When infections of the skin enclosing the chamber and atrophy of the skin flap are prevented, the functioning time of the transparent chamber is determined by the life span of the animals. In the present study the athymic mice remained healthy for 4–5 months after insertion of the chamber although they were kept under conventional conditions, but were given antimicrobial covering. Since athymic mice accept some human xenografts, both normal tissues and neoplasms, vital microscopical studies of such xenografts implanted into the chamber can be performed. Preliminary results of such studies on a human malignant melanoma are presented.

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The formation of micronuclei in two human melanoma xenografts (E. E. and V. N.) following hyperthermic treatment (42.5 degrees C for 60 min) was studied and compared to that following single dose irradiation. The melanomas were grown in the hind leg of athymic mice and heated by immersing the tumour-bearing leg into a water-bath. Histological sections were prepared from tumours removed from the mice at predetermined times after treatment and the fraction of abnormal mitotic figures and the number of micronuclei per nucleus were scored. During the first 24 h after treatment, the fraction of abnormal mitotic figures increased abruptly to 90%-100% followed by a rapid decrease to 40%-50%. It then decreased slowly towards about twice the level in untreated tumours. The number of micronuclei started to increase at about the same time as the fraction of abnormal mitotic figures was highest, reached a maximum at about 2-3 days after treatment, and then decreased slowly. The number of micronuclei seen after the hyperthermic treatment was lower than that seen after radiation treatments causing similar tumour regrowth delays. The same hyperthermic treatment resulted in more micronuclei and larger regrowth delays for E. E. than for V. N. melanoma. The present results indicate that DNA damage is involved in heat-induced cell death in tumours treated in vivo.