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

Alternative genetic pathways in parathyroid tumorigenesis.

F Farnebo1, S Kytölä, B T Teh

  • 1Department of Molecular Medicine Endocrine Tumor Unit, Karolinska Hospital, Stockholm, Sweden.

The Journal of Clinical Endocrinology and Metabolism
|October 16, 1999
PubMed
Summary

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

Mutational Signatures in Mandibular Ameloblastoma Correlate with Smoking.

Journal of dental research·2019
Same author

Oncogenic activation of JAK3-STAT signaling confers clinical sensitivity to PRN371, a novel selective and potent JAK3 inhibitor, in natural killer/T-cell lymphoma.

Leukemia·2018
Same author

Towards a global cancer knowledge network: dissecting the current international cancer genomic sequencing landscape.

Annals of oncology : official journal of the European Society for Medical Oncology·2017
Same author

Mice deleted for cell division cycle 73 gene develop parathyroid and uterine tumours: model for the hyperparathyroidism-jaw tumour syndrome.

Oncogene·2017
Same author

JAK-STAT and G-protein-coupled receptor signaling pathways are frequently altered in epitheliotropic intestinal T-cell lymphoma.

Leukemia·2016
Same author

Haem oxygenase 1 expression is associated with prognosis in cholangiocarcinoma patients and with drug sensitivity in xenografted mice.

Cell proliferation·2016

Genomic alterations are common in sporadic and post-irradiation parathyroid tumors, often involving the MEN1 gene. This suggests MEN1 gene inactivation plays a key role in parathyroid tumor development, particularly after radiation exposure.

Area of Science:

  • Endocrinology
  • Cancer Genetics
  • Molecular Biology

Background:

  • Parathyroid adenomas are typically benign tumors.
  • Genetic alterations are implicated in parathyroid tumor development.
  • The role of the MEN1 gene in sporadic, familial, and irradiation-associated parathyroid tumors requires further investigation.

Purpose of the Study:

  • To investigate sequence copy number alterations in parathyroid tumors from sporadic, familial, and irradiation-associated cases.
  • To identify specific chromosomal regions and genes involved in parathyroid tumorigenesis.
  • To explore the association between MEN1 gene alterations and parathyroid tumor development, especially after neck irradiation.

Main Methods:

  • Comparative genomic hybridization (CGH) was used to screen for copy number alterations in 44 parathyroid tumors.

Related Experiment Videos

  • Tumors were categorized into sporadic (26 cases), irradiation-associated (10 cases), and familial (8 cases).
  • Analysis included assessment of loss of heterozygosity and mutations in the MEN1 gene.

    • Main Results:

    • Sporadic adenomas frequently showed losses on chromosomes 11, 15q, and 1p, and gains on 19p and 7p.
    • Irradiation-associated tumors exhibited multiple CGH alterations, including frequent losses of 11q (50%), with 50% harboring MEN1 gene mutations.
    • Familial adenomas displayed fewer alterations, with some showing a gain of 19p13.2-pter.

    Conclusions:

    • Numerical copy number alterations are frequent in sporadic and irradiation-associated parathyroid adenomas.
    • The MEN1 gene locus is frequently involved, supporting its role in genomic stability.
    • MEN1 gene inactivation is a significant factor in parathyroid tumor development in post-irradiation patients.