Tarle M
Nuclear Medicine and Oncology Clinic, University Hospital Sestre Milosrdnice, Zagreb, Croatia.
Anticancer Res. 1993 May-Jun;13(3):769-77.
Blood tissue polypeptide specific antigen (TPS) concentration was serially measured by IRMA radioimmunodetective procedure in hormonally treated prostate cancer patients with Stage Do-D1 tumor (20 subjects free of bone lesions) and Stage D2 disease (20 subjects with bone metastases). Monoclonal antibody against the principle M3-TPA epitope was used in this TPS assay. Serum TPS values were compared with respective blood prostate specific antigen (PSA), prostatic acid phosphatase (PAP), carcinoembryonic antigen (CEA) and testosterone levels in a retrospective manner. A control group included healthy men, patients with benign prostatic hypertrophy (BPH), subjects with inflammation of the prostate, and men with diabetes. PSA is reported to be a quantitative calibration for prostate cancer load in untreated patients, especially during early stages of the disease. In hormonally treated, advanced, and dedifferentiated prostatic carcinoma this serotest fails to reflect properly both tumor status and response to treatment. In Stage Do-D1 patients TPS concentrations remain normal or become slightly elevated even during local tumor progression. This finding is in accord with the slow proliferation of nonaggressive primary tumors. Circulating TPS concentrations are elevated in progressive metastatic patients, in the majority of Stage D2 subjects with stable disease and even in some of these patients during partial tumor remission. This latter result may be attributed not only to the heterogeneity of the advanced prostatic cancer but also to the actual tumor response to treatment, since serum PSA level fails to reflect properly the outcome of hormonal treatment. There is some evidence that an abrupt elevation in serum TPA level in such patients is a consequence of NK cell-mediated lysis of circulating tumor cells, thus giving rise to a simultaneous and rapid delivery of intracellular TPS into the bloodstream. Prostatic inflammation elevates TPS concentrations only slightly, while diabetes, even during a proper treatment, raises TPS concentration more intensely. In patients with BPH normal or slightly increased TPS values were measured. The results ot these preliminary investigations seem to open the way for further prospective studies.
采用免疫放射分析程序，对激素治疗的Do-D1期肿瘤（20例无骨转移患者）和D2期疾病（20例有骨转移患者）的前列腺癌患者，连续检测血液组织多肽特异性抗原（TPS）浓度。该TPS检测采用针对主要M3-TPA表位的单克隆抗体。以回顾性方式比较血清TPS值与相应血液中前列腺特异性抗原（PSA）、前列腺酸性磷酸酶（PAP）、癌胚抗原（CEA）和睾酮水平。对照组包括健康男性、良性前列腺增生（BPH）患者、前列腺炎症患者和糖尿病男性。据报道，PSA是未治疗患者前列腺癌负荷的定量校准指标，尤其是在疾病早期。在激素治疗的晚期和去分化前列腺癌中，这种血清检测无法正确反映肿瘤状态和治疗反应。在Do-D1期患者中，即使在局部肿瘤进展期间，TPS浓度仍保持正常或略有升高。这一发现与非侵袭性原发性肿瘤的缓慢增殖一致。在进展性转移患者中，大多数疾病稳定的D2期患者，甚至在部分肿瘤缓解期的一些患者中，循环TPS浓度都会升高。后一结果可能不仅归因于晚期前列腺癌的异质性，还归因于肿瘤对治疗的实际反应，因为血清PSA水平无法正确反映激素治疗的结果。有证据表明，此类患者血清TPA水平的突然升高是自然杀伤细胞介导的循环肿瘤细胞裂解的结果，从而导致细胞内TPS同时快速释放到血液中。前列腺炎症仅使TPS浓度略有升高，而糖尿病即使在适当治疗期间，也会更强烈地升高TPS浓度。在BPH患者中，测得TPS值正常或略有升高。这些初步研究结果似乎为进一步的前瞻性研究开辟了道路。
