Search PubMed⌕ Search

Biomedical subjects

R Mastrangelo

Publications and source records attributed to R Mastrangelo.

69 records · Page 4Linked to original sources
PubMedDate not supplied

A melanotic neuroectodermal tumor of infancy arising from the anterior fontanel.

A case of local recurrence of melanotic neuroectodermal tumor of infancy (MNT), arising from the anterior fontanel in a 6-month-old female, is presented. The follow-up of 48 months after surgery confirms the benign nature of this tumor despite its local recurrence. Clinical and histopathologic chracteristics of this rare tumor are discussed. A review of 12 cases of MNT involving the skull is given. It is emphasized that this entity should be kept in mind in the differential diagnosis of a mass in the craniofacial structures in infancy.

Female↗
PubMedDate not supplied

Biology of metaiodobenzylguanidine interactions with human neuroblastoma cells.

[131I]Metaiodobenzylguanidine (131I-MIBG) is selectively taken up and stored by tumors derived from the neural crest and is utilized in the diagnosis and treatment of neuroblastoma (NB). Variable MIBG uptake has been observed, although the underlying mechanisms are not known. We have studied the uptake kinetics of 125I-MIBG and uptake characteristics of NB cell clones with different phenotypes (SH-SY5Y and SH-EP1, the neuroblastic and the substrate-adherent sublines of SK-N-SH respectively, BE(2)-M17 and LA-N-1n with neuroblastic phenotype). We have been able to correlate the MIBG uptake with the neuroblastic phenotype: a specific uptake system satisfying all the characteristics of the neuronal uptake-1 (temperature dependency, sodium dependency, high affinity, saturability and imipramine sensitivity) was observed in all the neuroblastic sublines. In contrast, MIBG accumulation was a passive diffusion phenomenon in the substrate-adherent clone SH-EP1. In addition, terminal neuronal differentiation induced in SH-SY5Y by retinoic acid caused a marked increase of the uptake and retention of MIBG. Our findings may be pertinent to an understanding of the variability of the MIBG uptake in vivo.

3-Iodobenzylguanidine↗
PubMedDate not supplied

The use of [131I]metaiodobenzylguanidine in the treatment of neuroblastoma after conventional therapy.

Eleven cases of neuroblastoma (10 males and 1 female; 9 aged 1-13 years, and two aged 17 and 38 years, respectively) ten of which were refractory to chemotherapy, were submitted to treatment with [131I]metaiodobenzylguanidine (131I-MIBG). The therapeutic procedure consisted essentially of single doses (2.6-9.5 GBq) of 131I-MIBG mostly split into two parts, administered by slow i.v. infusion and given in several therapeutic courses, usually at 1-2 month intervals. The treatment resulted in: 1 complete response, 1 partial response, 1 minor response, 4 stabilized diseases and 2 progressive diseases (two patients were not evaluable due to rapid progression of the disease). Pain relief was observed in all cases and particularly in four patients who suffered severe tumor pain. The major side-effects recorded were: hypertensive crises over a 6-day period in one case, fever lasting a few days in another and bone marrow depression in two intensively pretreated patients. A slight hematologic toxicity was observed, however, in almost all cases.

3-Iodobenzylguanidine↗
PubMedDate not supplied

[131I]metaiodobenzylguanidine in neuroblastoma patients at diagnosis.

Treatment of resistant neuroblastoma with high dosage [131I]metaiodobenzylguanidine (131I-MIBG) appears effective since encouraging results have been obtained so far even in patients with very advanced, intensively pre-treated disease. We have already reported a stage III NB patient treated at diagnosis, who is at present in complete remission with a 4-year follow-up. To further explore the potential role of this new drug in untreated patients, we administered radionuclide to two children with stage III neuroblastoma. Both cases received 131I-MIBG at relatively low doses, and showed a significant reduction of the tumor mass and, interestingly enough, no evidence of 131I-MIBG uptake of a tracer dose in the remaining tumor. Particularly in case 1, the permanence and subsequent progression of the part of the tumor mass without 131I-MIBG uptake, after therapeutic doses of 131I-MIBG which apparently destroyed the 131I-MIBG-positive cell population, clearly suggest heterogeneity at diagnosis, with a dual neuroblastoma cell population, one with 131I-MIBG uptake and the other without. Aside from the biological implications of the heterogeneous MIBG uptake in neuroblastoma at diagnosis, our findings suggest that in stage III neuroblastoma patients even a relatively small dose of 131I-MIBG administered at diagnosis is sufficient to either completely destroy the primary tumor, as reported by our group, or to destroy that part of the tumor which shows 131I-MIBG uptake (as in the present cases), without any significant hematologic toxicity. Furthermore, a single course of 131I-MIBG at the dosage employed here does not appear to jeopardize the subsequent use of chemotherapy.(ABSTRACT TRUNCATED AT 250 WORDS)

3-Iodobenzylguanidine↗
PubMedDate not supplied

[Relapse modalities in medulloblastoma].

We evaluated the modality of relapse and progression of medulloblastoma in 45 patients observed between 1981-1991. Children aged over 2 years were treated with surgery and postoperative radio-chemotherapy; among 12 children younger than 2 years, 8 were treated with surgery and chemotherapy and 4 with postoperative irradiation of remaining tumor. Cerebrospinal fluid shunting system was placed in 32 patients (71.1%). Patients were organized into three groups: group I (25 cases) = total tumor removal; group II (11 cases) = subtotal tumor removal; group III (9 cases) = partial tumor removal. 22 children died (48.8%: 10 of group I; 7 of group II; 5 of group III) at variable time interval from the operation during the following period. Among 23 alive patients, 3 are surviving with recurrence and progression of disease (all of group I), 20 are disease-free (44.4%: 12 of group I; 4 of group II; 4 of group III). Average postoperative follow-up period: 6 years for group I/II and 2 years for group III. Even if disease-free children are those treated by total-subtotal surgical removal (while local relapse occurs principally in patients treated by partial surgical resection: 44.4% of local relapse vs 12% of group I and 27% of group II), extensive surgery does not exclude possibility of metastatic localization in cerebrospinal axis, that occurs in 1/5-1/6 of all the patients without differences in each group. CSF shunting system did not cause extraneural metastases in our patients. We obtained long term survival rates or apparent recovery in almost 50% of cases.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗