The effect of cisplatin pretreatment on the accumulation of MIBG by neuroblastoma cells in vitro

Armour, Alexis D.; Cunningham, S.; Gaze, M.; Wheldon, T. E.; Mairs, Robert J.

doi:10.1038/bjc.1997.82

Cited by 37 publications

(19 citation statements)

References 20 publications

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“…3 The only available study using this approach was that of Sisson et al 17 Only 1 of 6 patients completed the entire study protocol, making it difficult to draw any conclusion. Other attempts to increase the 131-MIBG uptake were limited to experimental model systems and included norepinephrine transporter gene transfer 18 and increasing expression of the norepinephrine transporter by pretreatment of tumor cells with cisplatin 19 and retinoic acid combined with interferon-␥ and tumor necrosis factor-␣. 20 In summary, our study demonstrated that the low dose 131-…”

Section: Discussionmentioning

confidence: 99%

Low-Dose Iodine-131 Metaiodobenzylguanidine Therapy for Patients With Malignant Pheochromocytoma and Paraganglioma

Shilkrut¹,

Bar-Deroma²,

Bar-Sela³

et al. 2010

American Journal of Clinical Oncology

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The following is a report on the clinical experience of an Israeli referral center for iodine-131 metaiodobenzylguanidine (131-MIBG) therapy for malignant pheochromocytoma (MPCC) and malignant paraganglioma (MPGG). The charts of 10 patients with MPCC (n = 7) and MPGG (n = 3) treated between 2000 and 2008 were reviewed. Response to 131-MIBG therapy was evaluated by tumor, hormone, and symptomatic relief criteria. The median follow-up was 18 months (2-48 months). The number of 131-MIBG treatments ranged from 1 to 4 (mean: 2.1). The average single dose of 131-MIBG was 5.4 +/- 0.2 GBq (145 +/- 5.0 mCi). The average cumulative dose was 11.6 +/- 1.6 GBq (310 +/- 44.0 mCi). There were no complete responses. Three patients (30%) had partial tumor response, 5 (50%) had stable disease, and 2 (20%) progressed after therapy. Five patients (50%) experienced symptomatic response. Hormone response was noted in 5 patients (50%). Progression-free survival was 17.5 months (2-47 months). One patient (10%) had thrombocytopenia and 2 patients (20%) developed subclinical hypothyroidism. Hormonal and symptomatic relief can be achieved with 131-MIBG therapy in patients with MPCC and MPGG with minor side effects.

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Section: Discussionmentioning

confidence: 99%

Low-Dose Iodine-131 Metaiodobenzylguanidine Therapy for Patients With Malignant Pheochromocytoma and Paraganglioma

Shilkrut¹,

Bar-Deroma²,

Bar-Sela³

et al. 2010

American Journal of Clinical Oncology

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“…However, observations both 'in vitro' and 'in vivo' in xenograft models (Meco et al, 1997;Riccardi, unpublished observations) and in 6 of our patients, showed no evident alteration in MIBG uptake (Table 4). In fact, it is worth noting that NB cells, pre-incubated with cisplatin, concentrate MIBG more efficiently than untreated NB cells (Armour et al, 1997). Our primary concern was haematological and non-haematological toxicity as a result of this new therapeutic regimen.…”

Section: Discussionmentioning

confidence: 99%

Treatment of advanced neuroblastoma: feasibility and therapeutic potential of a novel approach combining 131-I-MIBG and multiple drug chemotherapy

et al. 2001

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Biological and clinical observations suggest that initial marked reduction of resistant clones may be critical in any attempt to improve long-term results in advanced neuroblastoma (NB). The aim of this pilot study is to determine short-term toxicity and efficacy of a new therapeutic model based on the simultaneous use of multiple drug chemotherapy and specific irradiation using 131-I-MIBG. The study population consisted of 21 patients, from 1 to 8 years of age with good 131-I-MIBG uptake. 16 extensively pre-treated patients with refractory or relapsed disease were divided into 2 groups. In Group 1 (9 patients) the basic chemotherapy regimen consisted in cisplatin at the dose of 20 mg/m 2 i.v. per day infused over 2 h, for 4 consecutive days; on day 4 Cy 2 g/m 2 i.v. was administered over 2 h followed by Mesna. Group 2 (7 patients) was treated with basic chemotherapeutic regimen plus VP16 and Vincristine. VP16 at the dose of 50 mg/m 2 i.v. per day was administered as a 24 h infusion on days 1–3; Vincristine 1.5 mg/m 2 i.v. was administered on days 1 and 6. On day 10 a single dose of 131-I-MIBG (200 mCi) with a high specific activity (>1.1 GBq/mg) was administered to both Groups by i.v. infusion over 4–6 hours. A further 5 patients were treated at diagnosis: 2 with the same regimen as Group 1 and 3 with the same as Group 2. The severity of toxicity was graded according to World Health Organization (WHO) criteria. Assessment of tumour response was monitored 4–6 weeks after the beginning of combined therapy (CO-TH). Response was defined according to INSS (International Neuroblastoma Staging System) criteria. No extra-medullary toxicity was observed in any patient. Haematological toxicity was the only toxicity observed and seemed mainly related to chemotherapy. Myelosuppression was mild in the 5 patients treated at diagnosis. No serious infections or significant bleeding problems were observed. In the 16 resistant patients, 12 PR, 1 mixed response and 3 SD were obtained. In the 5 patients treated at diagnosis 2 PR, 1 CR and 2 VGPR were observed. No alteration in 131-I-MIBG uptake was observed after the chemotherapy preceding radio-metabolic treatment. The therapeutic results of this pilot regimen of CO-TH resulted in a high percentage of major response after only a single course in both resistant patients and patients treated at diagnosis. Because of the minimal toxicity observed in patients studied at diagnosis so far, there is room for gradual intensification of the treatment. It is to be hoped that this suggested novel approach may represent an important route of investigation to improve final outcome in patients with advanced NB. © 2001 Cancer Research Campaign http://www.bjcancer.com

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“…Preclinical mechanistic justifications for such a combination include enhancement of NET expression or activity, for example, by vorinostat (143); synergistic effect on inhibition of radiation-induced DNA repair, for example, by topoisomerase inhibitors (144); and synergistic elicitation of autophagy and apoptosis, for example, by arsenic trioxide (145). Cisplatin pretreatment may also enhance expression of NET and MIBG uptake (146). Coadministration with poly (adenosine diphosphate) ribose polymerase induced increased DNA damage in xenografts (147).…”

Section: Combination Therapy With Net-targeting Agents With Radiosensmentioning

confidence: 99%

Norepinephrine Transporter as a Target for Imaging and Therapy

Pandit‐Taskar

Modak

2017

J Nucl Med

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The norepinephrine transporter (NET) is essential for norepinephrine uptake at the synaptic terminals and adrenal chromaffin cells. In neuroendocrine tumors, NET can be targeted for imaging as well as therapy. One of the most widely used theranostic agents targeting NET is metaiodobenzylguanidine (MIBG), a guanethidine analog of norepinephrine. 123 I/ 131 I-MIBG theranostics have been applied in the clinical evaluation and management of neuroendocrine tumors, especially in neuroblastoma, paraganglioma, and pheochromocytoma. 123 I-MIBG imaging is a mainstay in the evaluation of neuroblastoma, and 131 I-MIBG has been used for the treatment of relapsed high-risk neuroblastoma for several years, however, the outcome remains suboptimal. 131 I-MIBG has essentially been only palliative in paraganglioma/pheochromocytoma patients. Various techniques of improving therapeutic outcomes, such as dosimetric estimations, high-dose therapies, multiple fractionated administration and combination therapy with radiation sensitizers, chemotherapy, and other radionuclide therapies, are being evaluated. PET tracers targeting NET appear promising and may be more convenient options for the imaging and assessment after treatment. Here, we present an overview of NET as a target for theranostics; review its current role in some neuroendocrine tumors, such as neuroblastoma, paraganglioma/ pheochromocytoma, and carcinoids; and discuss approaches to improving targeting and theranostic outcomes.

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The effect of cisplatin pretreatment on the accumulation of MIBG by neuroblastoma cells in vitro

Cited by 37 publications

References 20 publications

Low-Dose Iodine-131 Metaiodobenzylguanidine Therapy for Patients With Malignant Pheochromocytoma and Paraganglioma

Low-Dose Iodine-131 Metaiodobenzylguanidine Therapy for Patients With Malignant Pheochromocytoma and Paraganglioma

Treatment of advanced neuroblastoma: feasibility and therapeutic potential of a novel approach combining 131-I-MIBG and multiple drug chemotherapy

Norepinephrine Transporter as a Target for Imaging and Therapy

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