Radiation-Associated Thyroid Cancer - Facts and Fiction

Hall, Per; Holm, Lars‐Erik

doi:10.1080/028418698430539

Cited by 32 publications

(18 citation statements)

References 32 publications

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“…Exposure to ionizing radiation is the only verified cause of thyroid carcinogenesis in humans, especially when exposure occurs at young age, although dietary iodine deficiency has also been linked to this pathology (4)(5)(6). Exposure to ionizing radiation could lead to the formation of radicalar DNA reactive species in target tissues that are related with acute and late radiation effects (7). However, individuals without previous exposure to ionizing radiation can also develop thyroid cancers, usually defined as sporadic tumors (8), suggesting that other risk factors could also be involved in the etiology of sporadic tumors.…”

Section: Introductionmentioning

confidence: 99%

Association of Polymorphisms in ERCC2 Gene with Non-Familial Thyroid Cancer Risk

Silva¹,

Gil

Oliveira³

et al. 2005

Cancer Epidemiology, Biomarkers &Amp; Prevention

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The ERCC2 protein is an evolutionary conserved ATPdependent helicase that is associated with a TFIIH transcription factor complex and plays an important role in nucleotide excision repair. Mutations in this gene are responsible for xeroderma pigmentosum and also for Cocayne syndrome and trichothiodystrophy. Several single nucleotide polymorphisms have been identified in the ERCC2 locus. Among them, a G23591A polymorphism in the codon 312 results in an Asp ! Asn substitution in a conserved region and a A35931C polymorphism in the codon 751 results in a Lys ! Gln substitution. Because these polymorphisms have been associated with an increased risk for several types of cancers, we carried out an hospital based case-control study in a Caucasian Portuguese population to evaluate the potential role of these polymorphisms on the individual susceptibility to thyroid cancer. The results obtained did not reveal a significant association between each individual polymorphism studied (G23591A and A35931C) and an increased thyroid cancer risk, but individuals homozygous for non-wild-type variants are overrepresented in patients group. The evaluation of the different haplotypes generated by these polymorphisms showed that individuals simultaneously homozygous for rare variants of both polymorphisms have an increased risk for thyroid cancer [adjusted odds ratio (OR) 3.084; 95% confidence interval (95% CI), 1.347-7.061; P = 0.008] and for papillary thyroid -type tumors (adjusted OR, 2.997; 95% CI, 1.235-7.272; P = 0.015) but not for follicular thyroid -type tumors. These results suggest that genetic polymorphisms in this gene might be associated with individual susceptibility towards thyroid cancer, mainly papillary-type tumors, but larger studies are required to confirm these results. (Cancer Epidemiol Biomarkers Prev 2005;14(10):2407 -12)

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Section: Introductionmentioning

confidence: 99%

Association of Polymorphisms in ERCC2 Gene with Non-Familial Thyroid Cancer Risk

Silva¹,

Gil

Oliveira³

et al. 2005

Cancer Epidemiology, Biomarkers &Amp; Prevention

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“…There is no doubt that exposure to radiation may induce thyroid cancer in children [4][5][6][7]. According to the review of Ron et al "The thyroid gland in children has one of the highest risk coefficients of any organ and is the only with convincing evidence for risk at about 0.1 Gy [6].…”

Section: Discussionmentioning

confidence: 99%

Benefit and side effects of radioiodine therapy in radiation-induced childhood thyroid carcinoma

Reiners

Biko

Demidchik³

et al. 2007

International Congress Series

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“…More is known about radiation as a carcinogen, and radiation-induced thyroid cancers in particular, than virtually any other human carcinogen (Hall and Holm 1998). There are over 20 well-designed epidemiologic studies with individual estimates of radiation dose to the thyroid gland (Ron et al 1995;Shore 1996;Hall and Holm 1998;Boice 1998Boice , 2005Boice , 2006bUNSCEAR 2000;Damber et al 2002;Dickman et al 2003).…”

Section: Studies Of Radiation-induced Thyroid Cancermentioning

confidence: 97%

Cancer Mortality Among Populations Residing in Counties Near the Hanford Site, 1950???2000

Boice

Mumma²,

Blot³

2006

Health Physics

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A descriptive epidemiologic study of cancer mortality among residents of counties near the Hanford nuclear facility site in Richland, Washington, was conducted. Between 1944 and 1957, radioactive 131I was released into the environment from the Hanford site. Cancer mortality from 1950 through 2000 was evaluated in four counties with the highest estimated exposure to 131I and compared with the cancer mortality experience in five demographically similar counties in Washington State with minimal 131I exposure. Overall, cancer rates in the study counties were slightly below those in the comparison counties [relative risk (RR) 0.95; 95% confidence interval (CI) 0.93-0.97], due mainly to a low risk for lung cancer (RR 0.89; 95% CI 0.85-0.93). Thyroid cancer (n=33; RR 0.84; 95% CI 0.56-1.26), female breast cancer (n=1,233; RR 0.99; 95% CI 0.92-1.06), leukemia other than chronic lymphocytic leukemia (n=492; RR 0.95; 95% CI 0.85-1.06), and childhood leukemia (n=71; RR=1.06; 95% CI 0.78-1.43) were not significantly increased in the exposed counties. Furthermore, there was no evidence that the cancer death rates over time differed between study and comparison counties. Patterns over time of thyroid cancer in particular were similar for exposure and comparison counties. Although based on a geographic correlation design, these data suggest that living near the Hanford site has not increased cancer rates.

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Radiation-Associated Thyroid Cancer - Facts and Fiction

Cited by 32 publications

References 32 publications

Association of Polymorphisms in ERCC2 Gene with Non-Familial Thyroid Cancer Risk

Association of Polymorphisms in ERCC2 Gene with Non-Familial Thyroid Cancer Risk

Benefit and side effects of radioiodine therapy in radiation-induced childhood thyroid carcinoma

Cancer Mortality Among Populations Residing in Counties Near the Hanford Site, 1950???2000

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