Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

[Radiation-induced thyroid cancers].

A Bounacer1, M Schlumberger, B Caillou

  • 1IFR 1221 CNRS, UPR 42 du CNRS 94801 Villejuif, France.

Annales D'Endocrinologie
|July 13, 2000
PubMed
Summary

Radiation exposure can cause thyroid cancer in humans. Specific gene rearrangements, particularly RET/PTC, are key in radiation-induced thyroid tumors, suggesting a DNA repair defect contributes to genomic instability.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

The Iberian legacy into a young genetic xeroderma pigmentosum cluster in central Brazil.

Mutation research. Genetic toxicology and environmental mutagenesis·2020
Same author

Xeroderma pigmentosum in South Africa: Evidence for a prevalent founder effect.

The British journal of dermatology·2019
Same author

A genetic cluster of patients with variant xeroderma pigmentosum with two different founder mutations.

The British journal of dermatology·2016
Same author

Unexpected extradermatological findings in 31 patients with xeroderma pigmentosum type C.

The British journal of dermatology·2013
Same author

ROS-generating NADPH oxidase NOX4 is a critical mediator in oncogenic H-Ras-induced DNA damage and subsequent senescence.

Oncogene·2011
Same author

Do histological, immunohistochemical, and metabolic (radioiodine and fluorodeoxyglucose uptakes) patterns of metastatic thyroid cancer correlate with patient outcome?

Endocrine-related cancer·2010

Area of Science:

  • Oncology
  • Radiation Biology
  • Molecular Genetics

Background:

  • Human epithelial thyroid radiation-induced tumorigenesis is a significant health concern.
  • Understanding the molecular mechanisms is crucial for prevention and treatment.

Purpose of the Study:

  • To investigate the molecular mechanisms of radiation-induced thyroid tumorigenesis.
  • To compare genetic alterations in radiation-associated versus spontaneous thyroid tumors.
  • To identify key genetic factors in thyroid tumor development post-irradiation.

Main Methods:

  • Analysis of proto-oncogene activation (ras, gsp, trk) in thyroid tumors.
  • Investigation of RET/PTC rearrangements in radiation-associated thyroid tumors.
  • Assessment of genomic instability and DNA repair defects in patients with a history of irradiation.

Related Experiment Videos

Main Results:

  • No significant difference in ras, gsp, and trk proto-oncogene activation between radiation-associated and spontaneous thyroid tumors.
  • RET/PTC rearrangements play a crucial role in radiation-associated thyroid tumors, with specific types linked to therapeutic radiation and the Chernobyl accident.
  • Patients with radiation-induced thyroid tumors exhibit genomic instability, indicative of a DNA repair defect.

Conclusions:

  • RET/PTC rearrangements are critical drivers of radiation-induced thyroid tumorigenesis.
  • Genomic instability and DNA repair defects are implicated in the development of thyroid tumors following irradiation.
  • Further research into these mechanisms can inform strategies for managing radiation exposure risks.