Cancer associated serum galactosyltransferase activity. Demonstration in an animal model system

Two different lines of solid tumors were produced in outbred hamsters by subcutaneous injection of polyoma transformed BHK cells. Growth of the tumors correlated with the appearance in serum of an electrophoretically distinct peak of galactosyltransferase:NeuAc, Gal gree fetuin acceptor activity on polyacrylamide gels. This slow moving peak of enzyme activity (GT IIH) was detected before solid tumors could be grossly observed and the amount of activity in this peak was also found to be linearly related with growth of the tumor. GT IIH was not detectable in control animals and separated from a faster migrating major area of serum galactosyltransferase activity (GT IH) found in sera of both control and tumor bearing hamsters. These 2 activities were shown to maintain their respective mobilities on reelectrophoresis. Solubilized enzyme derived from excised tumors demonstrated an electrophoretic mobility on polyacrylamide gels identical to that for GT IIH present in serum from tumor bearing animals. In contrast, enzyme activity solubilized from livers of both control or tumor bearing hamsters showed a mobility similar to that of the faster moving serum galactosyltransferase enzyme activity, i.e. GT IH. In addition, medium derived from nonconfluent BHKpy cells in tissue culture contained galactosyltransferase activity which coelectrophoresed with the slower migrating GT IIH found in sera of tumor bearing animals. The kinetic characteristics of galactosyltransferase activities derived from serum (control and tumor bearing), solid tumors, liver and BHKpy cells in tissue culture were compared. All kinetic properties were similar with the exception that the Km UDP galactose of GT IIH (1.0 x 10^-5M) was half that of GT IH (2.0 x 10^-5M).