Cancer de la thyroïde après exposition aux rayonnements ionisants

Schlumberger, Martin; Chevillard, Sylvie; Ory, Katherine; Dupuy, Corinne; Guen, B. Le; Vathaire, F. de

doi:10.1016/j.canrad.2011.05.002

Cited by 16 publications

(10 citation statements)

References 35 publications

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“…En effet, après exposition aux radiations ionisantes, l'incidence du cancer de la thyroïde augmente à partir de cinq à dix ans, passe par un maximum à environ 15-25 ans, puis diminue au-delà de 30 ans mais reste plus élevée que l'incidence dans une population témoin non irradiée [55]. Chez notre patient, le carcinome thyroïdien est apparu huit ans après radiothérapie externe, période reconnue suffisante pour la genèse du cancer thyroïdien [56,57].…”

Section: Discussionunclassified

“…Cela a été vérifié pour des doses supérieures à 100 mGy ; la relation entre la dose et le risque est linéaire, mais pour des doses élevées (> 5-10 Gy) le risque n'augmente plus et diminue même pour des doses très élevées, ce qui est attribué à des phénomènes de mort cellulaire programmée ou apoptose [55,56].…”

Section: Discussionunclassified

“…Cette prédisposition pourrait être en rapport avec des anomalies dans la réparation de l'ADN et qui font encore l'objet de nombreuses analyses [55,59]. Toujours dans la même optique, le diagnostic de CBC radio-induits pourrait être retenu devant les antécédents de radiothérapie, le caractère agressif des lésions et la survenue des CBC dans l'aire d'irradiation.…”

Section: Discussionunclassified

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Carcinome papillaire de la thyroïde associé à deux autres carcinomes primitifs cutanés : approche épidémiologique et physiopathologique - À propos d’un cas

2012

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Section: Discussionunclassified

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Carcinome papillaire de la thyroïde associé à deux autres carcinomes primitifs cutanés : approche épidémiologique et physiopathologique - À propos d’un cas

2012

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“…In the last decades, TC incidence in the United States has increased [93]. The increasing diagnosis of TC is related to the use of neck ultrasonography for the diagnosis of thyroid nodules, but also to ionizing radiations [94], the exposure to fall-out of nuclear accidents [95], the exposure to iodine deficiency that increases frequency of FTC [96]. Furthermore, autoimmune thyroiditis has been shown to be a risk factor for papillary thyroid caner (PTC) [97,98], and new risk factors are emerging [99][100][101].…”

Section: Tzds In Differentiated Thyroid Carcinoma (Dtc)mentioning

confidence: 99%

Antineoplastic Effects of PPAR? Agonists, with a Special Focus on Thyroid Cancer

Ferrari¹,

Materazzi²,

Baldini³

et al. 2016

CMC

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Peroxisome Proliferator-Activated Receptor-γ (PPARγ) is a ligand-activated nuclear hormone receptor that functions as transcription factor and plays an important role in lipid metabolism and insulin sensitization. Recent studies have shown that PPARγ is overexpressed in many tumor types, including cancers of breast, lung, pancreas, colon, glioblastoma, prostate and thyroid differentiated/anaplastic cancers. These data suggest a role of PPARγ in tumor development and/or progression. PPARγ is emerging as a growth-limiting and differentiation-promoting factor, and it exerts a tumor suppressor role. Moreover, naturally-occurring and synthetic PPARγ agonists promote growth inhibition and apoptosis. Thiazolidinediones (TZDs) are synthetic agonists of PPARγ that were developed to treat type II diabetes. These compounds also display anticancer effects which appear mainly to be independent of their PPARγ agonist activity. Various preclinical and clinical studies strongly suggest a role for TZDs both alone and in combination with existing chemotherapeutic agents, for the treatment of cancer. Differentiation therapy involves the use of agents with the ability to induce differentiation in cells that have lost this ability, i.e. cancer cells, targeting pathways capable of re-activating blocked terminal differentiation programs. PPARγ agonists have been shown to induce differentiation in solid tumors such as thyroid differentiated/ anaplastic cancers and sarcomas. However, emerging data suggest that chronic use of TZDs is associated with increased risk of adverse cardiovascular events. The exploration of newer PPARγ agonists can help in unveiling the underlying mechanisms of these drugs, providing new molecules that are able to treat cancer, without increasing the cardiovascular risk of neoplastic patients.

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“…The increasing diagnosis of small thyroid cancers (TCs) is related to the use of neck ultrasonography and fine needle aspiration (FNA) of thyroid nodules, and also to ionizing radiations (2–4% of subjects exposed to radiation during childhood show TC) ( 2 ), the exposure to fall-out of nuclear explosions or accidents ( 3 ), low doses of radiation exposure ( 4 ), and the exposure to iodine deficient areas, where a higher frequency of follicular thyroid cancer (FTC) has been observed ( 5 ). Furthermore, autoimmune thyroiditis has been shown to be a risk factor for PTCs ( 6 , 7 ), and new risk factors are emerging ( 8 , 9 ).…”

Section: Introductionmentioning

confidence: 99%

Molecular Targeted Therapies of Aggressive Thyroid Cancer

et al. 2015

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Differentiated thyroid carcinomas (DTCs) that arise from follicular cells account >90% of thyroid cancer (TC) [papillary thyroid cancer (PTC) 90%, follicular thyroid cancer (FTC) 10%], while medullary thyroid cancer (MTC) accounts <5%. Complete total thyroidectomy is the treatment of choice for PTC, FTC, and MTC. Radioiodine is routinely recommended in high-risk patients and considered in intermediate risk DTC patients. DTC cancer cells, during tumor progression, may lose the iodide uptake ability, becoming resistant to radioiodine, with a significant worsening of the prognosis. The lack of specific and effective drugs for aggressive and metastatic DTC and MTC leads to additional efforts toward the development of new drugs. Several genetic alterations in different molecular pathways in TC have been shown in the past few decades, associated with TC development and progression. Rearranged during transfection (RET)/PTC gene rearrangements, RET mutations, BRAF mutations, RAS mutations, and vascular endothelial growth factor receptor 2 angiogenesis pathways are some of the known pathways determinant in the development of TC. Tyrosine kinase inhibitors (TKIs) are small organic compounds inhibiting tyrosine kinases auto-phosphorylation and activation, most of them are multikinase inhibitors. TKIs act on the aforementioned molecular pathways involved in growth, angiogenesis, local, and distant spread of TC. TKIs are emerging as new therapies of aggressive TC, including DTC, MTC, and anaplastic thyroid cancer, being capable of inducing clinical responses and stabilization of disease. Vandetanib and cabozantinib have been approved for the treatment of MTC, while sorafenib and lenvatinib for DTC refractory to radioiodine. These drugs prolong median progression-free survival, but until now no significant increase has been observed on overall survival; side effects are common. New efforts are made to find new more effective and safe compounds and to personalize the therapy in each TC patient.

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Cancer de la thyroïde après exposition aux rayonnements ionisants

Cited by 16 publications

References 35 publications

Carcinome papillaire de la thyroïde associé à deux autres carcinomes primitifs cutanés : approche épidémiologique et physiopathologique - À propos d’un cas

Carcinome papillaire de la thyroïde associé à deux autres carcinomes primitifs cutanés : approche épidémiologique et physiopathologique - À propos d’un cas

Antineoplastic Effects of PPAR? Agonists, with a Special Focus on Thyroid Cancer

Molecular Targeted Therapies of Aggressive Thyroid Cancer

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