PATIENTS AND METHODS: According to previous literature incomplete tumor resection, coccygeal or ovarian primary site and immaturity are known risk factors for relapse in teratoma. To establish a risk score points are allocated for resection, primary site and histology in the following manner and added: incomplete resection 4 points, primary site coccyx 3 points, ovary 2 points, other site 1 point, histological grading 0-3 points. This score system is evaluated on 270 extracranial non-testicular teratoma cases collected between 1982 and 1995 in the MAKEI cooperative treatment protocols of the German Society of Pediatric Oncology and Hematology. Treatment was resection alone (230 patients) or resection followed by postoperative adjuvant chemotherapy (40 patients). RESULTS: Patients treated with surgery alone: 28/230 (12%) patients relapsed, 14/230 (6%) patients showed highly malignant histology (mostly yolk sac tumor) in relapse. Mortality in case of relapse was 6/28 (21%). Patients scoring > or = 6 points (n = 45) had a relapse rate of 21/45 (47%) resulting in a 23%-mortality (5/21). Patients scoring < 6 points (n = 185) had a 4%-relapse risk (8/185) resulting in 13%-mortality (1/8) (p < 0.01). Patients treated with surgery and adjuvant chemotherapy: 7/40 patients (18%) suffered a relapse, none of them showing malignant histology. Mortality rate in case of relapse was 3/7 (43%). Patients scoring > or = 6 points initially treated with adjuvant chemotherapy (n = 18) had a relapse rate of 7/18 (39%), compared to patients scoring < 6 points (n = 22), in whom no relapses occurred (p < 0.01). There were no highly malignant relapses in the group treated with adjuvant chemotherapy. Regardless of the scored points the difference in highly malignant relapse histology comparing the group treated with surgery and adjuvant chemotherapy to the group treated with surgery was statistically significant (p = 0.02). CONCLUSION: The risk score system marks a high risk group including 63/270 (23%) of all evaluated extracranial non-testicular teratoma cases (scoring > or = 6 points). In this group 28/35 (80%) of relapses and 8/9 (89%) of tumor deaths occurred. For this high risk group a randomized trial will be suggested to evaluate the effect of adjuvant chemotherapy on the rate of malignant relapses. It should also be investigated, if adjuvant chemotherapy will influence relapse rate and mortality.

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Effect of hyperthermia 42.5 degrees C/120 min on 3H-thymidine incorporation in different tissue components of Wilms' tumors: an in vitro study.

BACKGROUND: Survival rates of Wilms' tumors are correlated to tumor histology. Clinical studies and histological investigations have shown that different histological tumor components of Wilms' tumors also reveal different sensitivities to cytostatic agents and ionizing radiation. The aim of this study is to examine the effect of hyperthermia to Wilms' tumors, generally, and to the different tumor tissues composing nephroblastomas. MATERIAL AND METHOD: The 3H-thymidine labelling indices (LI) of 23 Wilms' tumors and one renal rhabdomyosarcoma were studied by an autoradiographic in vitro method at temperatures of 37.5 degrees C/120 min and 42.5 degrees C/120 min. The LI of each tumor was measured and likewise the LI of all histological tumor components defining standard risk and high risk. The effect of hyperthermia was calculated as the percentage of inhibition of 3H-thymidine incorporation. RESULTS: Labelling indices between 22.4% and 46.3% (mean 33.2%) characterized Wilms' tumors as highly malignant and fast growing tumors. The LI of Wilms' tumors of standard risk and high risk did not differ significantly (33.8% vs. 30.4%). Also, epithelium and blastema of the same groups showed comparable high LI of 31.4% and 34.4%, respectively, and of 32.1% and 26.8%, respectively. The LI of stroma was significantly lower (11.9% and 10.9%). The mean LI of fetal-like rhabdomyoblastic cell elements of ten tumors was 24.5%. These tumor cells revealed a significantly higher LI than rhabdomyosarcomatous cells in one Wilms' tumor and one renal rhabdomyosarcoma (10.2% and 9.0%, respectively). The LI of anaplastic structures of one tumor was more than twice as high as the LI of surrounding tumor tissue. In vitro hyperthermia significantly inhibited 3H-thymidine incorporation into all nephroblastomas. Inhibition ranged between 13.7% and 84.6%, at an average of 47.3%. Four high risk tumors, as well as the single anaplastic and rhabdomyosarcomatous cells responded significantly stronger to heat than standard risk tumors (mean inhibition of 62.6% vs. 42.1%). Hyperthermia was more effective for blastema compared to epithelium and stroma. There was no correlation between the effect of hyperthermia and the amount of the 3H-thymidine LI at normothermia. CONCLUSION: The tremendous inhibition of DNA synthesis by hyperthermia particularly in high risk tumors and highly malignant tumor components is of clinical interest for children with Wilms' tumors resistant to conventional therapy.

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