CA125 is currently the most widely used tumor marker for ovarian epithelial cancer. The aim of this article is to provide guidelines for the routine clinical use of CA125 in patients with ovarian cancer. Due to lack of sensitivity for stage I disease and lack of specificity, CA125 is of little value in the detection of early ovarian cancer. At present, therefore, CA125, either alone or in combination with other modalities, cannot be recommended for screening for ovarian cancer in asymptomatic women outside the context of a randomized controlled trial. Preoperative levels in postmenopausal women, however, may aid the differentiation of benign and malignant pelvic masses. Serial levels during chemotherapy for ovarian cancer are useful for assessing response to treatment. Although serial monitoring following initial chemotherapy can lead to the early detection of recurrent disease, the clinical value of this lead-time is unclear. CA125 is the ovarian cancer marker against which new markers for this malignancy should be judged.

Summary The influence of tamoxifen on plasma lipids and lipoproteins was monitored in 46 postmenopausal and 8 premenopausal women treated for advanced breast cancer up till 6 months. Total cholesterol (total-C) did not significantly change. However, high density lipoprotein cholesterol (HDL-C) and the HDL-C/ total-C ratio rose significantly. Low density lipoprotein cholesterol was significantly decreased. Triglycerides and free fatty acids did not change markedly. The concomitant rise of sex hormone binding globulin and thyroxine binding globulin indicates that the increase of HDL-C with prolonged use of tamoxifen is compatible with an intrinsic oestrogenic effect of tamoxifen on the liver. The increased HDL-C/total-C ratio lends no support to the concern that long-term administration of this anti-oestrogenic drug might lead to an increased cardiovascular risk.

Background. The clinical value of pretreatment serum concentrations of cytokeratin 19 fragments, measured by Cyfra 21‐1, was compared with tissue polypeptide antigen (TPA) and squamous cell carcinoma antigen (SCC‐Ag) in 78 patients with squamous cell cervical cancer. Methods. Serum levels were compared with tumor stage, size, lymph node status, parametrial involvement, and prognostic data. The clinical performance of the different tests was evaluated by their receiver operating characteristic (ROC) curves. Results. Serum levels of all markers were related significantly to tumor stage and size. Elevated serum levels of these markers were not found to be predictive for the presence of lymph node metastases. In contrast, a positive relation was found between quantitative serum Cyfra 21‐1, TPA, and SCC‐Ag levels and the presence of either lymph node metastases or parametrial involvement (i.e., extracervical disease). An elevated, i.e. positive, serum Cyfra 21‐1 level was related significantly to the presence of extracervical disease (P = 0.020). The clinical performance of each serum marker in predicting lymph node metastases or parametrial involvement appeared to be similar as expressed by their ROC curves. In the univariate analysis, Cyfra 21‐1, TPA, and SCC‐Ag showed prognostic value with respect to disease free interval and survival. Elevated serum levels were associated with a poor prognosis. However, after adjusting for tumor stage and size, none of these markers remained statistically significant. Conclusions. Cyfra 21‐1 may be of additional value in assessing stage of disease, tumor size, and the presence of extracervical disease in patients with cervical cancer. Determining its value during follow‐up warrants further study.

Summary It has recently been found by various authors that despite a normal serum concentration of oestradiol (E2), the percentage of non-protein-bound or free E2 is abnormally high in breast cancer patients. Since it is the free E2 which is considered to be biologically active, confirmation of this finding would matched controls. Our findings do not support the hypothesis that the pathogenesis of breast cancer is related to an elevated free fraction of the total E2 concentration in blood. However, the free E2 concentration, as calculated from the total E2 concentration and the free E2 fraction is shown to be abnormally high in postmenopausal breast cancer patients as a consequence of their elevated total serum E2 concentration. Subjects and methods SubjectsSerum samples were obtained from 38 postmenopausal breast cancer patients and a control group of 67 women admitted for malignant lymphoma (n = 21), melanoma (n = 5), cancer of the lung (n = 21) or large bowel (n = 20). The two groups were matched for age, parity and Quietelet index (in Kg m 2) as shown in Table I. All women were clinically judged to have normal thyroid function.Heparinized plasma was collected by continuous venous sampling from 68 premenopausal women belonging to one of the following 4 groups: 18 women at a high familial risk for breast cancer, i.e. mother and at least one sister having breast cancer (group R), 17 women curatively treated for early (TINOMO) breast cancer at least 6 months ago (group C), 17 women with histologically defined

Recently, a new ‘specific tissue polypeptide antigen (TPA)’ test was introduced and designated tissue polypeptide-specific antigen (TPS); it is based on the monoclonal antibody (MAb) anti-TPS, M3. We have tested the specificity of this antibody by immunocyto- and immunohistochemistry, gel electrophoresis and immunoblotting. MAb M3 bound to intermediate filaments of epithelial cells and revealed a staining pattern identical to cytokeratin (CK) 18-specific MAb (DE-K18) on tissue sections of various human tissues. On immunoblots of proteins extracted from various epithelial cell lines, M3 reacted with a 45-kD protein corresponding to CK18, and on immunoblots of proteins isolated from MCF-7 culture fluid M3 stained three bands, 45, 33 and 29 kD. The same bands were stained with CK18-specific MAb, indicating that they represent CK18 and its degradation products. TPA, used as a tumor marker in clinical diagnoses and follow-up, was shown to be a degradation product of CK 8, 18 and 19. In contrast to TPA, MAb M3 did not stain CK8 and CK19 present on immunoblots.