NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines

In most areas of the world, thyroid cancer incidence has been appreciably increasing over the last few decades, whereas mortality has steadily declined. We updated global trends in thyroid cancer mortality and incidence using official mortality data from the World Health Organization (1970-2012) and incidence data from the Cancer Incidence in Five Continents (1960-2007). Male mortality declined in all the major countries considered, with annual percent changes around -2/-3% over the last decades. Only in the United States mortality declined up to the mid 1980s and increased thereafter. Similarly, in women mortality declined in most countries considered, with APCs around -2/-5% over the last decades, with the exception of the UK, the United States and Australia, where mortality has been declining up to the late 1980s/late 1990s to level off (or increase) thereafter. In 2008-2012, most countries had mortality rates (age-standardized, world population) between 0.20 and 0.40/100,000 men and 0.20 and 0.60/100,000 women, the highest rates being in Latvia, Hungary, the Republic of Moldova and Israel (over 0.40/100,000) for men and in Ecuador, Colombia and Israel (over 0.60/100,000) for women. In most countries, a steady increase in the incidence of thyroid cancer (mainly papillary carcinomas) was observed in both sexes. The declines in thyroid cancer mortality reflect both variations in risk factor exposure and changes in the diagnosis and treatment of the disease, while the increases in the incidence are likely due to the increase in the detection of this neoplasm over the last few decades.

https://onlinelibrary.wiley.com/doi/pdf/10.1002/ijc.29251

Thyroid cancer mortality and incidence: A global overview

The carcinogenic risk induced by low doses of ionizing radiation is controversial. It cannot be assessed with epidemiologic methods alone because at low doses the data are imprecise and often conflicting. Since the 1970s, the radiation protection community has estimated the risk of low doses by means of extrapolation from the risk assessed at high doses, generally by using the linear no-threshold (LNT) model.

The LNT relationship implies proportionality between dose and cancer risk. This approach is based on one set of data and two hypotheses: (a) The relationship between dose and DNA damage in vivo seems linear from 1 mGy to 100 Gy with use of H2AX foci as a marker for DNA double-strand breaks (DSBs)—however, this marker is not specific (1); (b) each DSB is hypothesized to have the same probability of inducing cell transformation, irrespective of the quantity of DSBs present simultaneously in the cell; and (c) each transformed cell is hypothesized to have the same probability of developing into an invasive cancer, irrespective of the dose delivered to the tissue. The advances during the past 2 decades in radiation biology, the understanding of carcinogenesis, and the discovery of defenses against carcinogenesis challenge the LNT model, which appears obsolete (2–6).

Life developed in a bath of ionizing radiation and solar ultraviolet radiation and created aerobic organisms requiring (a) defenses against the metabolically induced reactive oxygen species, (b) DNA repair, and (c) elimination of damaged cells. Several sets of data show the efficacy of these defenses to be much higher at low than at high doses and for fractionated or protracted irradiation than for acute irradiation.

The LNT model was introduced as a concept to facilitate radiation protection (7). But the use of this model led to the claim that even the smallest dose (one electron traversing a cell) may initiate carcinogenesis—for instance, from diagnostic x-ray sources (8,9). This claim is highly hypothetical and has resulted in medical, economic, and other societal harm.

The French Academies report (10) concluded that the LNT model and its use for assessing the risks associated with low doses are not based on scientific evidence. In contrast, the Biological Effects of Ionizing Radiation (BEIR) VII report (11) and that of the International Commission on Radiological Protection (ICRP) (12) recommended the use of the LNT model. We wish to update this debate by using recent radiation biologic and epidemiologic data.

/pdf/the-linear-no-threshold-relationship-is-inconsistent-with-2qoq9lg8nq.pdf

The linear no-threshold relationship is inconsistent with radiation biologic and experimental data.

BACKGROUND

The American Cancer Society, Centers for Disease Control and Prevention, National Cancer Institute, and North American Association of Central Cancer Registries collaborate annually to provide U.S. cancer information, this year featuring the first comprehensive compilation of cancer information for U.S. Latinos.



METHODS

Cancer incidence was obtained from 90% of the Hispanic/Latino and 82% of the U.S. populations. Cancer deaths were obtained for the entire U.S. population. Cancer screening, risk factor, incidence, and mortality data were compiled for Latino and non-Latino adults and children (incidence only). Long-term (1975–2003) and fixed-interval (1995–2003) trends and comparative analyses by disease stage, urbanicity, and area poverty were evaluated.



RESULTS

The long-term trend in overall cancer death rates, declining since the early 1990s, continued through 2003 for all races and both sexes combined. However, female lung cancer incidence rates increased from 1975 to 2003, decelerating since 1991 and breast cancer incidence rates stabilized from 2001 to 2003. Latinos had lower incidence rates in 1999–2003 for most cancers, but higher rates for stomach, liver, cervix, and myeloma (females) than did non-Latino white populations. Latino children have higher incidence of leukemia, retinoblastoma, osteosarcoma, and germ-cell tumors than do non-Latino white children. For several common cancers, Latinos were less likely than non-Latinos to be diagnosed at localized stages.



CONCLUSIONS

The lower cancer rates observed in Latino immigrants could be sustained by maintenance of healthy behaviors. Some infection-related cancers in Latinos could be controlled by evidence-based interventions. Affordable, culturally sensitive, linguistically appropriate, and timely access to cancer information, prevention, screening, and treatment are important in Latino outreach and community networks. Cancer 2006. Published 2006 by the American Cancer Society.

/pdf/annual-report-to-the-nation-on-the-status-of-cancer-1975-5ft8ss8c3u.pdf

Annual report to the nation on the status of cancer, 1975-2003, featuring cancer among U.S. Hispanic/Latino populations.

Cancer gender disparity in incidence, disease aggressiveness and prognosis has been observed in a variety of cancers. Thyroid cancer is one of the fastest growing cancer diagnoses worldwide. It is 2.9-times more common in women than men. The less aggressive histologic subtypes of thyroid cancer are more common in women, whereas the more aggressive histologic subtypes have similar gender distribution. The gender disparity in incidence, aggressiveness and prognosis is well established for thyroid cancer but the cause of the disparity is poorly understood. The aim of this article is to evaluate the current evidence on the cause of thyroid cancer gender disparity. Dietary and environmental factors do not appear to have a significant role in thyroid cancer gender disparity. Common somatic mutations in BRAF, rearranged in transformation/papillary thyroid carcinomas (RET/PTC) and neurotrophin receptor-tyrosine kinase (NTRK) also do not account for the gender disparity in thyroid cancer. While reproductive factors would seem a logical hypothesis to account for the gender disparity, there appears to be no conclusive effect on the risk of developing thyroid cancer. Recent studies on estrogen receptor status in thyroid cancer show a difference in the receptor subtypes expressed based on the histology of thyroid cancer. Moreover, the response to estrogen is dependent on the specific estrogen receptor expressed in thyroid cancer cells. However, what determines the tumor-specific sex hormone receptor expression is unclear. No established molecular factors appear to explain gender differences in thyroid cancer. Therefore, the application of high-throughput genomic and proteomic approaches to the study of thyroid cancer gender disparity could be helpful for better understanding the molecular basis for gender differences in thyroid and other cancers.

Thyroid cancer gender disparity.

relationship was observed up to 1.5 – 2 Gy. The risk of radiation-related thyroid cancer was three times higher in iodine-defi cient areas (relative risk [RR]= 3.2, 95% CI = 1.9 to 5.5) than elsewhere. Administration of potassium iodide as a dietary supplement reduced this risk of radiation-related thyroid cancer by a factor of 3 (RR = 0.34, 95% CI = 0.1 to 0.9, for consumption of potassium iodide versus no consumption). Conclusion: Exposure to 131 I in childhood is associated with an increased risk of thyroid cancer. Both iodine defi ciency and iodine supplementation appear to modify this risk. These results have important public health implications: stable iodine supplementation in iodine-defi cient populations may substantially reduce the risk of thyroid cancer related to radioactive iodines in case of exposure to radioactive iodines in childhood that may occur after radiation accidents or during medical diagnostic and therapeutic procedures. [J Natl Cancer Inst 2005;97:724 – 32]

Risk of Thyroid Cancer After Exposure to 131I in Childhood

A population-based case-control study of thyroid cancer was carried out in contaminated regions of Belarus and Russia among persons who were exposed during childhood and adolescence to fallout from the Chernobyl accident. For each study subject, individual thyroid doses were reconstructed for the following pathways of exposure: (1) intake of 131I via inhalation and ingestion; (2) intake of short-lived radioiodines (132I, 133I, and 135I) and radiotelluriums (131mTe, 132Te) via inhalation and ingestion; (3) external dose from radionuclides deposited on the ground; and (4) ingestion of 134Cs and 137Cs. A series of intercomparison exercises validated the models used for reconstruction of average doses to populations of specific age groups as well as of individual doses. Median thyroid doses from all factors for study subjects were estimated to be 0.37 and 0.034 Gy in Belarus and Russia, respectively. The highest individual thyroid doses among the subjects were 10.2 Gy in Belarus and 5.3 Gy in Russia. Iodine-131 intake was the main pathway for thyroid exposure. Estimated doses from short-lived radioiodines and radiotelluriums ranged up to 0.53 Gy. Reconstructed individual thyroid doses from external exposure ranged up to 0.1 Gy, while those from internal exposure due to ingested cesium did not exceed 0.05 Gy. The uncertainty of the reconstructed individual thyroid doses, characterized by the geometric standard deviation, varies from 1.7 to 4.0 with a median of 2.2.

Reconstruction of radiation doses in a case-control study of thyroid cancer following the chernobyl accident

/pdf/response-re-risk-of-thyroid-cancer-after-exposure-to-131i-in-52e7xxovl5.pdf

Guennadi Goulko

Papers

Risk of Thyroid Cancer After Exposure to 131I in Childhood

Reconstruction of radiation doses in a case-control study of thyroid cancer following the chernobyl accident

RESPONSE: Re: Risk of Thyroid Cancer After Exposure to 131I in Childhood

Clinical Aspects of Radiation Accident Medical Management

Comment on: Risk of thyroid cancer after exposure to 131I in childhood. Authors' reply