Treatment of metastatic carcinoid tumours, phaeochromocytoma, paraganglioma and medullary carcinoma of the thyroid with <sup>131</sup>I‐meta‐iodobenzylguanidine (<sup>131</sup>I‐mIBG)

Mukherjee, J. J.; Kaltsas, Gregory; Islam, Najmul; Plowman, P. N.; Foley, Rosemary; Hikmat, J.; Britton, K. E.; Jenkins, P; Chew, Shern L.; Monson, John P.; Besser, G. M.; Grossman, Ashley

doi:10.1046/j.1365-2265.2001.01309.x

Cited by 163 publications

(105 citation statements)

References 27 publications

(59 reference statements)

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“…In general, patients with limited disease had an increased change of tumour response, while those with soft tissue metastases responded better than osseous metastases (Loh et al 1997, Kaltsas et al 2003. Hormonal and symptomatic responses were more frequently seen after 131 I-MIBG therapy irrespective of the tumour response (Troncone & Rufini 1997, Mukherjee et al 2001. In those patients with a response or stable disease at 6 months after the last treatment, a prolonged progression-free survival was seen; however, in another series 72% of patients developed progression of the disease at 18 months after an initial response (Buscombe et al 2005).…”

Section: Surgery Of the Primary Tumour And Cytoreductive Techniquesmentioning

confidence: 99%

“…The impact of treatment depends on the extent of disease at the time of therapy, and therefore 131 I-MIBG could be a useful tool to eradicate residual disease shortly after surgery in an adjuvant setting (Mukherjee et al 2001, Kaltsas et al 2005. In addition, possible synergistic effects with other forms of therapy need to be addressed (Scholz et al 2007).…”

Section: Treatment Of Malignant Chromaffin-cell Tumours With Radiophamentioning

confidence: 99%

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The diagnosis and management of malignant phaeochromocytoma and paraganglioma

Chrisoulidou

Kaltsas²,

Ilias³

et al. 2007

Endocr Relat Cancer

292

219

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Malignant phaeochromocytomas are rare tumours accounting for w10% of all phaeochromocytomas; the prevalence of malignancy among paragangliomas is higher, especially those associated with succinate dehydrogenase subunit B gene mutations. Although a subset of these tumours has metastatic disease at initial presentation, a significant number develops metastases during follow-up after excision of an apparently benign tumour. Clinical, biochemical and histological features cannot reliably distinguish malignant from benign tumours. Although a number of recently introduced molecular markers have been explored, their clinical significance remains to be elucidated from further studies. Several imaging modalities have been utilised for the diagnosis and staging of these tumours. Functional imaging using radiolabelled metaiodobenzylguanidine (MIBG) and more recently, 18 F-fluorodopamine and 18 F-fluorodopa positron emission tomography offer substantial sensitivity and specificity to correctly detect metastatic phaeochromocytoma and paraganglioma and helps identify patients suitable for treatment with radiopharmaceuticals. The 5-year mortality rate of patients with malignant phaeochromocytomas and paragangliomas greater than 50% indicates that there is considerable room for the improvement of currently available therapies. The main therapeutic target is tumour reduction and control of symptoms of excessive catecholamine secretion. Currently, the best adjunctive therapy to surgery is treatment with radiopharmaceuticals using 131 I-MIBG; however, this is very rarely curative. Chemotherapy has been used for metastatic disease with only a partial and mainly palliative effect. The role of other forms of radionuclide treatment either alone or in combination with chemotherapy is currently evolving. Ongoing microarray studies may provide novel intracellular pathways of importance for proliferation/cell cycle control, and lead to the development of novel pharmacological agents.

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Section: Surgery Of the Primary Tumour And Cytoreductive Techniquesmentioning

confidence: 99%

Section: Treatment Of Malignant Chromaffin-cell Tumours With Radiophamentioning

confidence: 99%

The diagnosis and management of malignant phaeochromocytoma and paraganglioma

Chrisoulidou

Kaltsas²,

Ilias³

et al. 2007

Endocr Relat Cancer

292

219

View full text Add to dashboard Cite

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“…It is thought that emission of ionising radiation at this site results in tumour decay (Mukherjee et al, 2001;Rose et al, 2003;Pasieka et al, 2004). This therapy has been used to treat NETs of various types, including gastroenteropancreatic NETs (Pathirana et al, 2001;Pasieka et al, 2004;Safford et al, 2004;Sywak et al, 2004;Buscombe et al, 2005), paraglangliomas (Mukherjee et al, 2001;Safford et al, 2003;Fitzgerald et al, 2006), phaeochromocytomas (Castellani et al, 2000;Rose et al, 2003;Safford et al, 2004;Fitzgerald et al, 2006), medullary carcinoma of the thyroid (Castellani et al, 2000(Castellani et al, , 2003Mukherjee et al, 2001) and neuroblastomas (Howard et al, 2005;Matthay et al, 2007). A number of previous studies had demonstrated significant symptomatic benefit in 40 -60% of patients with metastatic NETs following 131 I-MIBG therapy (Safford et al, 2004;Sywak et al, 2004), in a safe and cost-effective manner (Pathirana et al, 2001).…”

mentioning

confidence: 99%

Assessment of the efficacy and toxicity of 131I-metaiodobenzylguanidine therapy for metastatic neuroendocrine tumours

et al. 2008

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131 I-metaiodobenzylguanidine ( 131 I-MIBG) is a licensed palliative treatment for patients with metastatic neuroendocrine tumours. We have retrospectively assessed the consequences of 131 I-MIBG therapy in 48 patients (30 gastroenteropancreatic, 6 pulmonary, 12 unknown primary site) with metastatic neuroendocrine tumours attending Royal Liverpool University Hospital between 1996 and 2006. Mean age at diagnosis was 57.6 years (range 34 -81). 131 I-MIBG was administered on 88 occasions (mean 1.8 treatments, range 1 -4). Twenty-nine patients had biochemical markers measured before and after 131 I-MIBG, of whom 11 (36.7%) showed 450% reduction in levels post-therapy. Forty patients had radiological investigations performed after 131 I-MIBG, of whom 11(27.5%) showed reduction in tumour size post-therapy. Twenty-seven (56.3%) patients reported improved symptoms after 131 I-MIBG therapy. Kaplan -Meier analysis showed significantly increased survival (P ¼ 0.01) from the date of first 131 I-MIBG in patients who reported symptomatic benefit from therapy. Patients with biochemical and radiological responses did not show any statistically significant alteration in survival compared to non-responders. Eleven (22.9%) patients required hospitalisation as a consequence of complications, mostly due to mild bone marrow suppression. 131 I-MIBG therefore improved symptoms in more than half of the patients with metastatic neuroendocrine tumours and survival was increased in those patients who reported a symptomatic response to therapy.

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“…This agent is used for the treatment of neural crest derived tumours. [5][6][7] These neuroendocrine tumours naturally express the membrane-bound noradrenaline transporter (NAT), enabling them to actively take up [ 131 I]MIBG, resulting in specific irradiation of the target tumour cells. Previously, we have demonstrated that plasmid-mediated transfection of the NAT gene into glioma cells, which do not endogenously possess NAT, leads to expression of a functional transporter, demonstrating the potential application of [ 131 I]MIBG therapy for malignancies other than neuroendocrine tumours.…”

Section: Introductionmentioning

confidence: 99%

Combining a targeted radiotherapy and gene therapy approach for adenocarcinoma of prostate

Fullerton

Boyd

Mairs

et al. 2004

Prostate Cancer Prostatic Dis

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A targeted radiotherapy/gene therapy approach for prostate cancer, using the radiopharmaceutical [ 131 I]meta-iodobenzylguanidine ([ 131 I]MIBG), would restrict the effects of radiotherapy to malignant cells, thereby increasing efficacy and decreasing morbidity of radiotherapy. Prostate cancer cells were transfected with a transgene encoding the noradrenaline transporter (NAT) under the control of tumour-specific telomerase promoters, enabling them to actively take up [ 131 I]MIBG. This led to tumour-specific cell kill. This strategy has the advantage of generating a radiological bystander effect, leading to the destruction of neighbouring tumour cells that have escaped transfection. This targeted approach could be a promising tumour-specific treatment option for prostate cancer.

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Treatment of metastatic carcinoid tumours, phaeochromocytoma, paraganglioma and medullary carcinoma of the thyroid with ¹³¹I‐meta‐iodobenzylguanidine (¹³¹I‐mIBG)

Cited by 163 publications

References 27 publications

The diagnosis and management of malignant phaeochromocytoma and paraganglioma

The diagnosis and management of malignant phaeochromocytoma and paraganglioma

Assessment of the efficacy and toxicity of 131I-metaiodobenzylguanidine therapy for metastatic neuroendocrine tumours

Combining a targeted radiotherapy and gene therapy approach for adenocarcinoma of prostate

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Treatment of metastatic carcinoid tumours, phaeochromocytoma, paraganglioma and medullary carcinoma of the thyroid with 131I‐meta‐iodobenzylguanidine (131I‐mIBG)

Cited by 163 publications

References 27 publications

The diagnosis and management of malignant phaeochromocytoma and paraganglioma

The diagnosis and management of malignant phaeochromocytoma and paraganglioma

Assessment of the efficacy and toxicity of 131I-metaiodobenzylguanidine therapy for metastatic neuroendocrine tumours

Combining a targeted radiotherapy and gene therapy approach for adenocarcinoma of prostate

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Treatment of metastatic carcinoid tumours, phaeochromocytoma, paraganglioma and medullary carcinoma of the thyroid with ¹³¹I‐meta‐iodobenzylguanidine (¹³¹I‐mIBG)