Abstract
Aims: The main goal of this review-article was to shed light on the impact of senescence on thyroid carcinogenesis, a promising but still neglected field. Source of data: PubMed database and Google Scholar search was performed for English language articles with terms: ionizing radiation exposure, thyroid cancer, radiation signature, RET/PTC, senescence and radiation-induced senescence. We have no date restrictions. Summary of findings: Ionizing radiation (IR) is undoubtedly the most well characterized risk factor for thyroid cancer of the papillary histotype and its pivotal role as senescence inducer has been proposed. A paradoxical role of senescence on carcinogenesis – a barrier to cancer cell proliferation in early steps and a driving force to cancer progression by secreting proinflamatory cytokines and matrix degrading enzymes – is the heart of the matter of age- related cancer and bring to life new insights to thyroid cancer research field. This review-article briefly points out the major findings that link ionizing radiation to thyroid carcinogenesis, highlighting the molecular alterations mediated by acute and chronic radiation exposure in thyroid cells. Conclusions: Evidences provided by our group and other few reports suggest that, like other oncogenic stimuli in different cell types, IR induces a senescent phenotype in thyroid cells, what could represent an initial barrier to transformation. However, how senescence could contribute to tumor progression still remains elusive. The comprehension of these mechanisms could not only help elucidating thyroid cancer initiation and progression, but could also indicate new therapeutical targets.
Highlights
Its incidence rates have been continuously growing among developed countries, and in developing countries, which includes Brazil, where 9,200 new cases are estimated in 2014,2 mainly due to the increase in papillary thyroid carcinoma (PTC) (Cramer et al 2010) and the availability of diagnostic tools
One of our research interests is to investigate the parallel between thyroid carcinogenesis and premature senescence related to ionizing radiation, focusing on the turning point in which radiation might lead a normal thyroid cell to gain proliferative advantages among surrounding cells in early thyroid carcinogenesis or senescence
Once the senescence model was established, the future steps consist of full molecular characterization of each time point in order to identify molecular alterations that might guide us to a better understanding of thyroid carcinogenesis
Summary
Thyroid cancer is one of the most common endocrine-related neoplasia.[1]. Its incidence rates have been continuously growing among developed countries, and in developing countries, which includes Brazil, where 9,200 new cases are estimated in 2014,2 mainly due to the increase in papillary thyroid carcinoma (PTC) (Cramer et al 2010) and the availability of diagnostic tools. Nuclear test detonations in Marshall islands (1946-1958) significantly contributed to higher thyroid cancer rates in populations living around the archipelago (cumulative 0.1-10 Gy thyroid mean radiation dose).[7] Above all, these data highlighted that thyroid is more susceptible to the carcinogenic action of IR during childhood, especially in infants up to 5 years old, observed after Chernobyl accident (1987).[8,9] Currently, the main sources of radiation exposure are medical procedures (20%, 0.62 mSv) and environmental (80%, 2.4 mSv).[10]. Radiation-related PTC expressed higher protein levels of matrix metalloproteinases (MMP-1, MMP-9, MMP13), often correlated to tumor aggressiveness.[21]
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