The subject of this investigation was twenty one patients with oral cancer.
Nine patients were administered UFT 300mg daily. In these cases, the 5-FU levels were 0.027±0.022μg/ml in SCC; 0.034μg/ml in malignant fibrous histeocytoma; 0.005±0.0008μg/ml in normal oral tissue; and 0.042±0.008μg/ml in metastatic lymph-node. The ratios of the concentrations of 5-FU in tumor and the normal tissues was 5.4 in serum; Similarly the node and the normal tissue was 10.
Twelve patients, who were administered UFT 600mg daily, were operated after a mean of 15.4 hours following the administration of UFT 200mg. In these patients, tumor tissue, node and salivary gland were at a high level of 5-FU; on the other hand, serum, muscle and normal oral tissue were of low level. As to tumor tissue, SCC was 0.052±0.033μg/ml; carcinoma in pleomorphic adenoma was 0.046μg/ml; adenoidcystic carcinoma was 0.027μg/ml. The concentration of 5-FU was also discussed with respect to the degree of tumor cell differentiation. The level of 5-FU was highest in undifferentiated carcinoma and high in poorly differentiated SCC.
We decided the relationship of 5-FU level of tumor to clinical effect of chemotherapy in 11 cases. For the UFT 300mg group, the response rate was 25% (1/4) . The effected one was treated with UFT and Bleomycin. For the UFT 600mg group, the response rate was 75% (5/7) . Among the effected cases, two were treated with UFT alone, three with UFT and Bleomycin (or Peplomycin) . Tumor disappearance was recognized in one. All patients whose 5-FU level in tumor remained high responded to treatment with UFT alone, or to a combination with other drugs.

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We examined the sensitivities to cisplatin in 7 cell lines: head and neck carcinoma, VEDA, NAKATA, KANETSUKI, HSG, and HSY, cervical carcinoma, HeLa and vulval A431. This study assumed that adenocarcinoma cells, contained in salivary gland tumors, were shown to be more sensitive to cisplatin compared to squamous carcinoma cells, indicating that chemotherapy might be useful for salivary gland tumor. On the other hand, squamous carcinoma cells were shown to be inherently resistant to cisplatin. The cells which were sensitive to cisplatin demonstrated an increased level of cisplatin, indicating that the accumulation of cisplatin should reflect the cytotoxity. In order to study the mechanisms of cisplatin resistance, we isolated a cisplatin-resistant HeLa subline (HeLa_DDP) which showed about 4. 3 fold stablely resistance than the HeLa parent cell line, subcultured without cisplatin for 17 months. There were no differnces in glutathione level between HeLa and HeLa_DDPcells. But, HeLa_DDPcells demonstrated a higher survival fraction after exposure to X-rays, and a decreased accumulation of cisplatin, and did not have increased efflux. Therefore, this finding suggests that the mechanisms of cisplatin-resistance should be correlated with the capacity of repair of DNA damage and the inhibition of the accumulation of cisplatin. HeLa_DDPcells might be usefull as a model of cisplatin-resistance.

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Xeroderma Pigmentosum, a genetic disease, whose nature is a defect in DNA-repair, is frequently accompanied by carcinoma of skin.
We experienced a case of maxillo-facial squamous cell carcinoma in a 24-year-old-male with Xeroderma Pigmentosum.
He died about 8 years and 9 months after the first examination at our clinic.
According to the autopsy, there was carcinoma infiltration recognized from the skull directly into the brain.

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The case of a male patient of 40 was first diagnosed histologically as fibrous dysplasia of the left mandible at our clinic on July 8, 1988. However, because there were the swelling and the bone absorption in the mandible in progress 2 months later, a biopsy was taken and his case was diagnosed as osteosarcoma. After intra-arterial chemotherapy from the superficial temporal artery with adriamycin, he received hemimandiblectomy with suprahyoidal neck dissection, which was followed by intravenous administration of a highdose of methotrexate and cisplatin about one month later. Unfortunately, the patient died of multiple metastases in thoraxes, lungs, heart, diaphragma, pancreas, etc. 13 months after the operation.
Some possible causes for this unsuccessful treatment to be taken up here are:
1. Prophylactic procedures to prevent metastasis of tumor cells were not taken at the first biopsy.
2. Insufficient information and clinical findings were given to the pathologist, which led to the wrong diagnosis at first.
3. It was 2 months after the first biopsy that the final diagnossin was established.
4. Postoperative chemotherapy started too late, and his medications were insufficient.

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