FAM is not effective adjuvant therapy for TNM stage I, II, and III patients with resected gastric cancer. Future adjuvant studies must emphasize prospective surgical quality control to assure enrollment of appropriately staged and resected cases and wide participation to assure adequate case accrual over a reasonable period.

Background. The use of chemotherapy in patients with metastatic carcinoid tumors has been of limited value, and investigation of new agents is necessary. Previous reports have suggested that dimethyltriazenoimidazole carboxamide (DTIC) may have antitumor activity. Methods. A Phase II trial to investigate the clinical response rate to DTIC in patients with metastatic carcinoid tumors was performed. DTIC was administered at low (650 mg/m2) or high (850 mg/m2) doses every 28 days. Results. Sixty‐three patients were entered into the study, and 56 were evaluable for toxicity and response. Toxicity was moderate, with the most common side effect being nausea and vomiting (88%). Nine patients (16%; 95% confidence interval, 8–28%) had partial responses, 5 of 25 receiving 850 mg/m2 and 4 of 31 receiving 650 mg/m2 of DTIC. Median survival time of all patients was 20 months. Conclusions. DTIC has minimal activity in patients with metastatic carcinoid tumors. Cancer 1994; 73:1505–8.

In developing a chemotherapeutic program for children with disseminated neuroblastoma, we established three human neuroblastoma lines in cell culture to study the effects of dibutyryl cyclic AMP, papaverine, 5-trifluoromethyl-2'-deoxyuridine, and cyclophosphamide on cell growth, biochemical behavior, and morphology. Based upon our studies, a clinical treatment program was designed. We have treated 15 patients with disseminated neuroblastoma and have established the optimum dose range and sequence of these drugs. Early results were promising; plans for continuation of clinical and experimental studies were discussed.

We have performed cytogenetic studies on five renal oncocytic neoplasms (three grade 2 tumors and two grade 1 tumors) identified histologically by light microscopy. One grade 1 tumor failed to produce mitotic cells. The other four tumors exhibited both normal and abnormal cell lines. Numerical abnormalities were found in both the single grade 1 and two of the grade 2 tumors whereas structural abnormalities were limited to grade 2 tumors. Aneuploidy of chromosome 12 was observed in both grade 1 and 2 tumors. Grade 2 tumors showed more extensive numerical change than the grade 1 tumors. Abnormalities of chromosome 3 characteristic of renal cell carcinoma were not found in any tumor in this series. A combination of C-banding and HaeIII endonuclease banding was used to identify an ambiguous marker. In our four cases and in the cases previously reported, loss of a sex chromosome, abnormalities of chromosomes 1 and 22, and trisomy 12 are findings most often observed in renal oncocytoma.