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Background. Thrombocytosis (a platelet count >400 × 109/I) is found frequently in association with malignant disease and recently has been suggested to be a poor prognostic indicator in patients with cervical cancer. The authors decided to see if these findings could be verified. Methods. The pretreatment platelet counts of 643 women treated for cervical cancer between 1983 and 1992 were reviewed and correlated to each patient's age, stage of disease, histologic type, node status (when available), and outcome. Differences between groups were analyzed using the x2 test, and survival was compared using the log rank test on Kaplan‐Meier life tables. Results. The 5‐year survival rate for patients with thrombocytosis was 57.1%, which was significantly worse than the 76.5% for those with normal platelet counts (P < 0.01). When adjusted for stage of disease, however, thrombocytosis failed to have a significant effect on patient survival. There was also no relation between thrombocytosis and the incidence of positive lymph nodes. Conclusion. Thrombocytosis was not found to be an independent prognostic factor in patients with carcinoma of the cervix in this series of 643 patients.

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The CDKN2 gene encodes a cell cycle regulatory protein and is located on chromosome 9p21, a region deleted in a wide variety of primary tumours. While mutations in the CDKN2 gene itself are frequently observed in tumour cell lines, they are less common in primary tumours. We have investigated the role of the CDKN2 gene in ovarian cancer by analysis for allelic loss of 9p21 and single-strand conformational polymorphism analysis of exons 1 and 2 of CDKN2 in 67 primary ovarian tumours. Loss of heterozygosity on 9p21 was frequently observed (24/50 informative tumours) and was common in early-stage tumours, suggesting that it is an early event in ovarian tumorigenesis. Homozygous deletion of the CDKN2 gene was detected in only 1 tumour. No somatic or germline mutations were observed in CDKN2, though a codon 140 polymorphism was detected in 2 cases. This suggests that CDKN2 is not involved in ovarian tumorigenesis and that another gene(s) may be the target of the frequent 9p allelic losses observed.