ArticleOncogene2010
DNA breaks at fragile sites generate oncogenic RET/PTC rearrangements in human thyroid cells.
Article in Oncogene, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
What it found
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Who cites it
51 citing papers in PubMed, 88 citations in OpenAlex.
- Article
- A post-irradiation-induced replication stress promotes RET proto-oncogene breakage.European thyroid journal · 2024Article
- CCDC6-RET fusion protein regulates Ras/MAPK signaling through the fusion- GRB2-SHC1 signal niche.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Targeted treatments after chemoradiotherapy failure in a patient with relapsed, advanced non‑small cell lung cancer with on‑therapy circulating tumor biomarker monitoring: A case report.Oncology letters · 2023Article
- Article
- Assessing acute myeloid leukemia susceptibility in rearrangement-driven patients by DNA breakage at topoisomerase II and CCCTC-binding factor/cohesin binding sites.Genes, chromosomes & cancer · 2021Article
- Targeting Rearranged during Transfection in Cancer: A Perspective on Small-Molecule Inhibitors and Their Clinical Development.Journal of medicinal chemistry · 2021Review
- Communicating with residents about 10 years of scientific progress in understanding thyroid cancer risk in children after the Fukushima Dai-ichi Nuclear Power Station accident.Journal of radiation research · 2021Article
- Identifying Thyroid Carcinoma-Related Genes by Integrating GWAS and eQTL Data.Frontiers in cell and developmental biology · 2021Article
- The relationship between chimeric RNAs and gene fusions: Potential implications of reciprocity in cancer.Journal of genetics and genomics = Yi chuan xue bao · 2020Article
- Review
- State-of-the-Art Strategies for TargetingJournal of clinical oncology : official journal of the American Society of Clinical Oncology · 2020Review
- RET/PTC Gene Rearrangements in Thyroid Carcinogenesis: Assessment and Clinico-Pathological Correlations.Pathology oncology research : POR · 2020Article
- Review
- Coding Molecular Determinants of Thyroid Cancer Development and Progression.Endocrinology and metabolism clinics of North America · 2019Review
- Targeting RET-driven cancers: lessons from evolving preclinical and clinical landscapes.Nature reviews. Clinical oncology · 2018Review
- DNA fragile site breakage as a measure of chemical exposure and predictor of individual susceptibility to form oncogenic rearrangements.Carcinogenesis · 2017Article
- Fragility Extraordinaire: Unsolved Mysteries of Chromosome Fragile Sites.Advances in experimental medicine and biology · 2017Review
- A comprehensive overview of the role of the RET proto-oncogene in thyroid carcinoma.Nature reviews. Endocrinology · 2016Review
- Environmental and chemotherapeutic agents induce breakage at genes involved in leukemia-causing gene rearrangements in human hematopoietic stem/progenitor cells.Mutation research · 2015Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Human chromosomal fragile sites are regions of the genome that are prone to DNA breakage, and are classified as common or rare, depending on their frequency in the population. Common fragile sites frequently coincide with the location of genes involved in carcinogenic chromosomal translocations, suggesting their role in cancer formation. However, there has been no direct evidence linking breakage at fragile sites to the formation of a cancer-specific translocation. Here, we studied the involvement of fragile sites in the formation of RET/PTC rearrangements, which are frequently found in papillary thyroid carcinoma (PTC). These rearrangements are commonly associated with radiation exposure; however, most of the tumors found in adults are not linked to radiation. In this study, we provide structural and biochemical evidence that the RET, CCDC6 and NCOA4 genes participating in two major types of RET/PTC rearrangements, are located in common fragile sites FRA10C and FRA10G, and undergo DNA breakage after exposure to fragile site-inducing chemicals. Moreover, exposure of human thyroid cells to these chemicals results in the formation of cancer-specific RET/PTC rearrangements. These results provide the direct evidence for the involvement of chromosomal fragile sites in the generation of cancer-specific rearrangements in human cells.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.