The uptake and retention of metaiodobenzyl guanidine by the neuroblastoma cell line NB1-G

Mairs, Robert J.; Gaze, M.; Barrett, Ann

doi:10.1038/bjc.1991.294

Cited by 29 publications

(24 citation statements)

References 11 publications

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“…At concentrations of mIBG lower than 0.1 iLM, preferential accumulation of the drug by Uptake-l is apparent in those cells which possess the specific transport mechanism (Smets et al, 1989;Lashford et al, 1991;Mairs et al, 1991;Montaldo et al, 1991), whereas at higher concentrations of the radiopharmaceutical there is an increasng contribution to total drug uptake by non-specific transport processes. In the present study carrier-free '3'I-mIBG was used at extremely low concentrations (less than 100 pM) in the incubation medium in order to enhance the detectability of specific, desmethylimipramine-inhibitable transport.…”

Section: Cell Culturementioning

confidence: 99%

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Prediction of accumulation of 131I-labelled meta-iodobenzylguanidine in neuroblastoma cell lines by means of reverse transcription and polymerase chain reaction

Mairs

Livingstone²,

Gaze³

et al. 1994

Br J Cancer

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S_inaary Radiolabelled meta-iodobenzylguanidine (mIBG) currently provides one of the most promising options for targeted radiotherapy of neuroblastoma. No means currently exists for prediction of mIBG uptake in tumour cells of individual patients other than semiquantitative inferences from diagnostic scanning which depend on the continued existence of a macroscopic tumour mass. A biological rapid assay which could be applied at initial biopsy would be invaluable in selecting patients for therapeutic strategies which incorporate radiolabeled mIBG. We have assesed the expression of the noradrenahne transporter gene in six human neuroblastoma cell lines and in three non-neural crest-derived cell lines using reverse transcription followed by the polymerase chain reaction. Transcription of this gene was observed in five out of six neuroblastoma cell lines but in none of the control cells. A highly significant correlation was established (P<0.O1) between gene expression and active cellular accumulation of mIBG. It is suggested that semiquantitative evaluation of noradrenaline transporter gene transcripts may be predictive of mIBG uptake by tumours in vivo.

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Section: Cell Culturementioning

confidence: 99%

“…Dorset, UK). mIBG uptake The ability of cell lines to take up mIBG was assessed as previously described (Mairs et al, 1991). Briefly, the cell monolayers were incubated with 7 kBq of n.c.a.…”

Section: Cell Culturementioning

confidence: 99%

Prediction of accumulation of 131I-labelled meta-iodobenzylguanidine in neuroblastoma cell lines by means of reverse transcription and polymerase chain reaction

Mairs

Livingstone²,

Gaze³

et al. 1994

Br J Cancer

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“…After 2 d, when the cultures were 70% confluent, medium was removed and replaced with fresh medium containing the appropriate concentration of test drug. Cells were incubated with 131 I-MIBG for 2 h, after which uptake is maximal (26). Cells were incubated with topotecan or PJ34 for 24 h.…”

Section: Determination Of Cytotoxicity After Combination Therapymentioning

confidence: 99%

Inhibition of Poly(ADP-Ribose) Polymerase Enhances the Toxicity of ¹³¹I-Metaiodobenzylguanidine/Topotecan Combination Therapy to Cells and Xenografts That Express the Noradrenaline Transporter

McCluskey

Mairs²,

Tesson³

et al. 2012

J Nucl Med

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Targeted radiotherapy using 131 I-metaiodobenzylguanidine ( 131 I-MIBG) has produced remissions in some neuroblastoma patients. We previously reported that combining 131 I-MIBG with the topoisomerase I inhibitor topotecan induced long-term DNA damage and supraadditive toxicity to noradrenaline transporter (NAT)-expressing cells and xenografts. This combination treatment is undergoing clinical evaluation. This present study investigated the potential of poly(adenosine diphosphate [ADP]-ribose) polymerase (PARP-1) inhibition, in vitro and in vivo, to further enhance 131 I-MIBG/topotecan efficacy. Methods: Combinations of topotecan and the PARP-1 inhibitor PJ34 were assessed for synergism in vitro by combination-index analysis in SK-N-BE(2c) (neuroblastoma) and UVW/NAT (NAT-transfected glioma) cells. Three treatment schedules were evaluated: topotecan administered 24 h before, 24 h after, or simultaneously with PJ34. Combinations of PJ34 and 131 I-MIBG and of PJ34 and 131 I-MIBG/topotecan were also assessed using similar scheduling. In vivo efficacy was measured by growth delay of tumor xenografts. We also assessed DNA damage by gH2A.X assay, cell cycle progression by fluorescence-activated cell sorting analysis, and PARP-1 activity in treated cells. Results: In vitro, only simultaneous administration of topotecan and PJ34 or PJ34 and 131 I-MIBG induced supraadditive toxicity in both cell lines. All scheduled combinations of PJ34 and 131 I-MIBG/topotecan induced supraadditive toxicity and increased DNA damage in SK-N-BE(2c) cells, but only simultaneous administration induced enhanced efficacy in UVW/NAT cells. The PJ34 and 131 I-MIBG/ topotecan combination treatment induced G 2 arrest in all cell lines, regardless of the schedule of delivery. In vivo, simultaneous administration of PJ34 and 131 I-MIBG/topotecan significantly delayed the growth of SK-N-BE(2c) and UVW/NAT xenografts, compared with 131 I-MIBG/topotecan therapy. Conclusion: The antitumor efficacy of topotecan, 131 I-MIBG, and 131 I-MIBG/ topotecan combination treatment was increased by PARP-1 inhibition in vitro and in vivo.

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“…This mechanism is a characteristic of catecholamine-synthesising cells such as adrenergic nerves and chromaffin cells (Jacques et al, 1987). This specific uptake process has been well characterised in a number of neuroblastoma cell lines in culture (Buck et al, 1985;Lashford et al, 1991;Mairs et al, 1991). The use of mIBG for diagnostic imaging and targeted radiotherapy of neuroblastoma and phaeochromocytoma exploits this mechanism (Hoefnagel et al, 1987).…”

mentioning

confidence: 99%

“…To differentiate between active (type 1) uptake and passive (type 2) accumulation, experiments were performed in the presence or absence of a tricyclic antidepressant, desmethylimipramine. This prevents the reuptake of neurotransmitters by adrenergic neurones and has previously been shown to inhibit type 1 active uptake (Mairs et al, 1991).…”

mentioning

confidence: 99%

Modification of meta-iodobenzylguanidine uptake in neuroblastoma cells by elevated temperature

Armour

Mairs²,

Gaze³

et al. 1994

Br J Cancer

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SummarySuccessful imaging or treatment of neuroblastoma With '3'I-meta-iodobenzy1guanidine depends on the selectivity of active (type 1) uptake of mIBG in neuroblastoma cells relative to passive (type 2) uptake present in most normal tissues. This study investigates the effects of moderately elevated temperature (39-41'C) on the cellular uptake of '3'I-mIBG in two neuroblastoma cell lines [SK-N-BE(2c) and and in a non-neuronal (ovarian carcinoma) cell line (A2780). In SK-N-BE(2c), a cell line with high active uptake capacity. the specific (type 1) uptake was reduced by 75% (P<0.001) at 39"C. Both IMR-32 and A2780 have a low capacity for accumulation of mIBG by active uptake. These cell lines demonstrated a statistically significant increase in accumulation at 39C, mainly as a result of increased non-specific transport.At 41°C uptake of "3'I-mIBG was reduced in all cell lines. Thus, the active component of mIBG uptake is more vulnerable to increased temperature than the passive component. It seems probable that moderately increased temperature will have an unfavourable effect on the therapeutic differential for targeted radiotherapy of neuroblastoma using radiolabelled mIBG.

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The uptake and retention of metaiodobenzyl guanidine by the neuroblastoma cell line NB1-G

Cited by 29 publications

References 11 publications

Prediction of accumulation of 131I-labelled meta-iodobenzylguanidine in neuroblastoma cell lines by means of reverse transcription and polymerase chain reaction

Prediction of accumulation of 131I-labelled meta-iodobenzylguanidine in neuroblastoma cell lines by means of reverse transcription and polymerase chain reaction

Inhibition of Poly(ADP-Ribose) Polymerase Enhances the Toxicity of ¹³¹I-Metaiodobenzylguanidine/Topotecan Combination Therapy to Cells and Xenografts That Express the Noradrenaline Transporter

Modification of meta-iodobenzylguanidine uptake in neuroblastoma cells by elevated temperature

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The uptake and retention of metaiodobenzyl guanidine by the neuroblastoma cell line NB1-G

Cited by 29 publications

References 11 publications

Prediction of accumulation of 131I-labelled meta-iodobenzylguanidine in neuroblastoma cell lines by means of reverse transcription and polymerase chain reaction

Prediction of accumulation of 131I-labelled meta-iodobenzylguanidine in neuroblastoma cell lines by means of reverse transcription and polymerase chain reaction

Inhibition of Poly(ADP-Ribose) Polymerase Enhances the Toxicity of 131I-Metaiodobenzylguanidine/Topotecan Combination Therapy to Cells and Xenografts That Express the Noradrenaline Transporter

Modification of meta-iodobenzylguanidine uptake in neuroblastoma cells by elevated temperature

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Inhibition of Poly(ADP-Ribose) Polymerase Enhances the Toxicity of ¹³¹I-Metaiodobenzylguanidine/Topotecan Combination Therapy to Cells and Xenografts That Express the Noradrenaline Transporter