Abstract
This study examines two associated tumor markers in malignant melanoma, sialic acid and sialyltransferase (EC 2.4.99.1). Both markers were measured in the same sera from 66 malignant melanoma patients, 20 rheumatoid arthritis patients, and age- and sex-matched normal controls. Bound sialic acid was measured by the thiobarbituric acid method, and sialyltransferase activity was measured by cytidine 5′-monophosphate-N-[4-14C]acetylneuraminic acid incorporation in desialated fetuin. Serum values for both markers were higher among rheumatoid arthritis patients than among controls (p = < 0.0001). Melanoma patients were divided into three groups: Group I, 34 patients with no evidence of disease at the time of sampling; Group II, 13 patients with minimal tumor burden; and Group III, 19 patients with advanced metastatic disease. For sialic acid, there were significant differences between all group comparisons except the normals versus Group I. By contrast, for sialyltransferase only sera from Group III patients showed significant increased activity. Using the calculated upper limit of normal of 2.37 µmol/ml for sialic acid and 18.1 nmol/ml/hr for sialyltransferase, 2 (6%) Group I, 4 (31%) Group II, and 18 (95%) Group III patients had sialic acid elevations, while corresponding results for sialyltransferase were 0, 0, and 4 (42%). There was a direct relationship between sialic acid and sialyltransferase, especially for melanoma patients with established disease (p = 0.00002). Of 24 patients with objective evidence of changing tumor burden 19 (79%) showed corresponding alterations in sialic acid concentration, while 14 (58%) showed such changes in sialyltransferase. Sialic acid was directly related to recurrence rate in Group I patients, while sialyltransferase was not. When used as monitors of tumor burden either to detect recurrent disease or to follow response to treatment, tumor markers need not be tumor specific. In our hands, sialic acid levels more closely reflect tumor burden than does sialyltransferase activity.
Supported by the British Columbia Health Care Research Foundation and the Cancer Control Agency of British Columbia. Preliminary results presented at the Fourteenth Annual Meeting of the American Society of Clinical Oncology, April 1978 (27).
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