Tumour-associated immunity in prostatic cancer

In an attempt to ultimately provide earlier and more effective means of diagnosis, prognosis and therapy of prostatic cancer, in vitro parameters of immunologic responsiveness have been applied toward identifying and evaluating the presence of tumor-associated immunity (TAI), an its clinical relevancy, in patients with prostatic cancer. Of the various humoral and cellular responses noted thus far, results of immunofluoresecent (IF) and antigen induced leukocyte adherence inhibition (LAI) studies, as a means to identify and evaluate these respective manifestations of immunity, appear to provide evidence of TAI to presumptively identified prostatic tumour-associated antigens. Specifically, at the humoral level, identification of prostatic antibodies by IF with an incidence of 54% (13 of 24) in prostatic cancer vs. 10% (11 of 106)in non-prostatic cancer patients, while not sufficiently specific for diagnosis, have been suggested in view of their high incidence, i.e., 92% (11 of 12) in metastatic disease (Stage D) vs. 20% (1 of 5) in essentially still localized disease (Stage B), to possibly be useful as a prognostic index of disease progression. At the cellular level, results of studies demonstrating the presence of significant levels of TAI by LAI in 79% (73 of 92) prostatic cancer patients vs. an absence of significant levels with tissues other than malignant prostate and in 52 non prostatic cancer patients, have been suggested to warrant a clinical trial of the diagnostic potential of cell-mediated TAI. It has further been suggested, from a technical point of view, that compared to other assays of cellular immunity reported in patients with prostatic cancer, including inhibitiion of leukocyte migration, that the LAI test has the advantages of brevity, simplicity, economy of materials and objectivity. The reported specific inhibition ('blocking') of TAI by an autologus serum factor may provide insight of one means by which the potential effects of sensitized immunocompetent cells are inhibited in situ. The relevancy of these observations, together with reports of the identification of cytophilic antibody ('arming' factor) suggested to permit distinction between localized (Stage A) and metastatic (Stage D) disease and the effect of therapy, i.e. non hormonal vs. hormonal, on TAI provide additional and confirmatory evidence clearly establishing an immunologic response to tumour, suggested to be of clinical relevance, in patients with prostatic cancer.