Disturbed cell cycle-regulating checkpoints and impairment of genomic stability are key events during the genesis and progression of malignant tumors. We analyzed 80 epithelial ovarian tumors of benign (n = 10) and borderline type (n = 18) in addition to carcinomas of early (n = 26) and advanced (n = 26) stages for the expression of Ki67, cyclin A and cyclin E, p21WAF-1, p27KIP-1 and p53 and correlated the results with the clinical course. Genomic instability was assessed by DNA ploidy measurements and, in 35 cases, by comparative genomic hybridization. Overexpression of cyclin A and cyclin E was observed in the majority of invasive carcinomas, only rarely in borderline tumors and in none of the benign tumors. Similarly, high expression of p53 together with undetectable p21 or loss of chromosome arm 17p were frequent events only in adenocarcinomas. Both borderline tumors and adenocarcinomas revealed a high number of chromosomal gains and losses. However, regional chromosomal amplifications were found to occur 13 times more frequently in the adenocarcinomas than in the borderline tumors. The expression pattern of low p27 together with high Ki67 was found to be an independent predictor of poor outcome in invasive carcinomas. The results provide a link between disturbed cell cycle regulatory proteins, chromosomal aberrations and survival in ovarian carcinomas.

A series of 205 patients with inoperable, non-oat cell carcinoma of the lung were treated with thrdk different dose-fractionation schedules. Fifty-six patients received 5000 rads in 25 fractions over five weeks (continuous, A); 79 patients received 2000 rads in five fractions over five days, with two weeks' rest, followed by 2000 rads in five fractions over five days (split-course, B); 70 patients received 3000 rads in 10 fractions over two weeks, followed by three weeks' rest and another 3000 rads (split-course, C). The 24-month survival was 33% for A, 15% for B and 25% for C. The split course was better tolerated and radiation fibrosis was dose-related.

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A review of the literature reveals that Wilms tumor is rare in adolescence. At the time of diagnosis 78 per cent of children are less than 5 years old. Of 17 cases of Wilms tumor seen at the Ontario Cancer Foundation Clinic in Kingston from 1973 to 1975, 3 children were between 16 and 17 years old. Of 316 cases registered in Ontario with the Ontario Cancer Treatment and Research Foundation only 5 were in the 15 to 19-year age group. The possibility of Wilms tumor in patients beyond the usual age group is not considered as a differential diagnosis because of its relative rarity. Patients may present with features suggestive of neuroblastoma, renal cell carcinoma, hydronephrosis, cholecystitis, appendicitis and twisted ovarian cyst as seen in our 3 patients. In comparison, a review of 84 reported cases of renal cell carcinoma in children from 1934 to 1974 showed 5 cases in the 15 to 18-year age group.

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