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Incidentally discovered prostatic cancer can pursue a benign clinical course or it can rapidly progress. Differentiating those tumors with low biological potential from more aggressive lesions has been the focus of many reports. To define more completely the variables that can be used to predict those patients with low biological potential requiring limited treatment from those needing more extensive therapy, a retrospective study of 232 patients with incidentally discovered cancer was undertaken. Progressive disease was used as an endpoint for statistical analysis with the Kaplan-Meier technique and Cox's multiple hazard regression mode. This extensive analysis of multiple parameters demonstrated a significant advantage of survival free of disease for patients presenting with tumors manifesting a lower Gleason score and volume extent. Probability tables were constructed to allow for prediction of the probability of progression for a given patient with incidentally discovered prostate cancer directly related to patient age at diagnosis, Gleason score, and initial volume extent of the tumor. With these tables a logical therapeutic approach can be derived for each patient in an attempt to maximize survival free of disease with minimal intervention.

Two routinely used antikeratin monoclonal antibodies, AE1:AE3 (Hybritech Inc., La Jolla, CA) and CAM-5.2 (Becton-Dickinson, Mountain View, CA), were compared with a new antikeratin monoclonal antibody mixture, MAK-6 (Triton Biosciences, Inc., Alameda, CA). Various poorly differentiated epithelial neoplasms, lymphomas, melanomas, and sarcomas were studied with the use of the avidin-biotin-peroxidase technic. All three antibodies had similar staining profiles, however, some differences were noted. The MAK-6 and CAM-5.2 antibodies illustrated stronger staining for some grade III transitional cell carcinomas, whereas the AE1:AE3 was variably positive to negative in all cases. Three renal cell carcinomas were positive with all three antibodies, two were negative with all three, and one had scattered positive cells with MAK-6 only. All lymphomas and plasmacytomas were negative with MAK-6 and CAM-5.2, however, AE1:AE3 faintly stained two of three plasmacytomas and two of the seven large cell lymphomas. Two out of three hepatomas evaluated were strongly positive with CAM-5.2 and MAK-6 and variably positive with AE1:AE3. The third case had both positive and negative cells with all three antibodies. In conclusion, MAK-6 antikeratin antibody is as useful as AE1:AE3 and CAM-5.2 for identification of poorly differentiated epithelial neoplasms.

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