ArticleEJNMMI research2015
Gene expression signature in mouse thyroid tissue after (131)I and (211)At exposure.
Article in EJNMMI research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 16 citations in OpenAlex.
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- Profiling proteomic responses in small intestinal neuroendocrine tumor GOT1 after [BMC cancer · 2026Article
- Short and long-term effects on the thyroid proteome after 131I exposure.Radiation protection dosimetry · 2025Article
- Early proteomic response in thyroid gland after 131I administration in female Balb/c mice.Radiation protection dosimetry · 2025Article
- Elevated MS4A12 expression is indicative of resistance to concurrent chemoradiotherapy and inferior survival in patients with rectal cancer.Radiation oncology (London, England) · 2025Article
- Development of a machine learning framework for radiation biomarker discovery and absorbed dose prediction.Frontiers in oncology · 2023Article
- Age-related long-term response in rat thyroid tissue and plasma after internal low dose exposure toScientific reports · 2022Article
- The IRI-DICE hypothesis: ionizing radiation-induced DSBs may have a functional role for non-deterministic responses at low doses.Radiation and environmental biophysics · 2020Article
- Long-term transcriptomic and proteomic effects in Sprague Dawley rat thyroid and plasma after internal low dose 131I exposure.PloS one · 2020Article
- Transcriptional effects ofEJNMMI research · 2019Article
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- Global Gene Expression Response in Mouse Models of DNA Repair Deficiency after Gamma Irradiation.Radiation research · 2018Article
- Deconvolution of expression microarray data reveals 131I-induced responses otherwise undetected in thyroid tissue.PloS one · 2018Article
- Priming increases the anti-tumor effect and therapeutic window ofEJNMMI research · 2017Article
- Article
- Circadian rhythm influences genome-wide transcriptional responses to (131)I in a tissue-specific manner in mice.EJNMMI research · 2015Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background(131)I and (211)At are used in nuclear medicine and accumulate in the thyroid gland and may impact normal thyroid function. The aim of this study was to determine transcriptional profile variations, assess the impact on cellular activity, and identify genes with biomarker properties in thyroid tissue after (131)I and (211)At administration in mice.
methodsTo further investigate thyroid tissue transcriptional responses to (131)I and (211)At administration, we generated a new transcriptional dataset that includes re-evaluated raw intensity values from our previous (131)I and (211)At studies. Differential transcriptional profiles were identified by comparing treated and mock-treated samples using Nexus Expression 3.0 software. Further data analysis was performed using R/Bioconductor and IPA.
resultsA total of 1144 genes were regulated. Hierarchical clustering subdivided the groups into two clusters containing the lowest and highest absorbed dose levels, respectively, and revealed similar transcriptional regulation patterns for many kallikrein-related genes. Twenty-seven of the 1144 genes were recurrently regulated after (131)I and (211)At exposure and divided into six clusters. Several signalling pathways were affected, including calcium, integrin-linked kinase, and thyroid cancer signalling, and the peroxisomal proliferator-activated receptor network.
conclusionsSubstantial changes in transcriptional regulation were shown in (131)I and (211)At-treated samples, and 27 genes were identified as potential biomarkers for (131)I and (211)At exposure. Clustering revealed distinct differences between transcriptional profiles of both similar and different exposures, demonstrating the necessity for better understanding of radiation-induced effects on cellular activity. Additionally, ionizing radiation-induced changes in kallikrein gene expression and identified canonical pathways should be further assessed.
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