CRITICAL OBSERVATIONS ON NEUROBLASTOMA TREATMENT WITH 131-I-METAIODOBENZYLGUANIDINE AT DIAGNOSIS

Results of treatment with 131-1-Metaiodobenzylguanidine (131-I-MIBG) i n patients with resistant neuroblastoma appear encouraging if one cons iders that most of the patients had far advanced, intensively pre-trea ted disease. To further explore the potential role of this new drug in untreated patients, we treated 3 children with stage III neuroblastom a. All three of our cases received 131-I-MIBG at relatively low dose w ith the complete disappearance of the tumor mass in case 1, whereas in cases 2 and 3 CT scan showed a significant reduction of the tumor mas s and, interestingly enough, no evidence of 131-I-MIBG uptake of a tra cer dose in the remaining tumor. Particularly, in case 2, the persiste nce and subsequent progression of part of the tumor mass without 131-I -MIBG uptake after a therapeutic dose of 131-I-MIBG, which apparently destroyed the 131-I-MIBG-positive cell population, clearly suggest het erogeneity at diagnosis, with a dual neuroblastoma cell population, on e with 131-I-MIBG uptake and the other without. Besides the biological implications of the 131-I-MIBG uptake heterogeneity in neuroblastoma at diagnosis, our findings suggest that in stage III neuroblastoma pat ients even a relatively small dose of 131-I-MIBG administered at diagn osis is sufficient to destroy either the primary tumor completely (cas e 1) or the part of the tumor (case 2 and 3) which shows 131-I-MIBG up take, without any significant hematologic toxicity. Furthermore, a sin gle course of 131-I-MIBG at the dosage employed does not appear to jeo pardize the subsequent use of chemotherapy. In conclusion, if our data are confirmed by further investigation, 131-I-MIBG may be included as a front line drug shortly followed by chemotherapy in future treatmen t strategies of advanced neuroblastoma without or with minimal bone ma rrow filtration. (C) 1993 Wiley-Liss, Inc.