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 Concept Videos

The Ras Gene02:38

The Ras Gene

5.7K
The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
Ras is a...
5.7K
Cancer-Critical Genes I: Proto-oncogenes01:33

Cancer-Critical Genes I: Proto-oncogenes

9.1K
Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
9.1K
Abnormal Proliferation02:23

Abnormal Proliferation

4.0K
Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
4.0K
Small GTPases - Ras and Rho01:24

Small GTPases - Ras and Rho

4.4K
Ras and Rho are small monomeric GTPases that act downstream of receptor tyrosine kinase (RTK) and regulate various cellular processes. These GTPases switch between active and inactive states by binding to guanine nucleotides.
Three regulatory proteins control their activity:
4.4K
Activation and Inactivation of G Proteins01:22

Activation and Inactivation of G Proteins

8.9K
Heterotrimeric G proteins are guanine nucleotide-binding proteins. As the name suggests, heterotrimeric G proteins are composed of three subunits: alpha, beta, and gamma. They remain GDP-bound or GTP-bound inside the cells and switch between inactive/active states. The Gα subunit possesses the nucleotide-binding pocket that binds guanine nucleotides and switches between GDP or GTP-bound states. In contrast, the Gꞵ and Gγ subunits are always bound together with high...
8.9K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

3.6K
The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
3.6K

You might also read

Related Articles

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

Sort by
Same author

ATR senses stiff extracellular matrix to promote epithelial-to-mesenchymal transition and immune suppression.

The Journal of clinical investigation·2026
Same author

Lumbar extradural extraosseous notochordal lesion resulting in radiculopathy: ecchordosis physaliphora versus chordoma. Illustrative case.

Journal of neurosurgery. Case lessons·2026
Same author

Spatially resolved single-cell landscape of tumor immunotypes reveals the central role of interferon signaling and plasmacytoid dendritic cells in triple-negative breast cancer.

Journal for immunotherapy of cancer·2026
Same author

Xanthogranulomatous Epithelial Tumor/Keratin-Positive Giant Cell-Rich Soft Tissue Tumor.

Mayo Clinic proceedings·2026
Same author

Perineurioma-like EMA-positive calvarial neoplasms: clinicopathological study of eight cases.

Histopathology·2026
Same author

Updates in keratin-positive mesenchymal neoplasia.

Seminars in diagnostic pathology·2026

Related Experiment Video

Updated: May 3, 2026

A Syngeneic Orthotopic Osteosarcoma Sprague Dawley Rat Model with Amputation to Control Metastasis Rate
07:31

A Syngeneic Orthotopic Osteosarcoma Sprague Dawley Rat Model with Amputation to Control Metastasis Rate

Published on: May 3, 2021

3.3K

Activating GNAS mutations in parosteal osteosarcoma.

Jodi M Carter1, Carrie Y Inwards, Long Jin

  • 1Departments of *Laboratory Medicine and Pathology †Radiology, Mayo Clinic, Rochester, MN.

The American Journal of Surgical Pathology
|February 15, 2014
PubMed
Summary
This summary is machine-generated.

Parosteal osteosarcoma diagnosis can be challenging. Activating GNAS mutations were found in 55% of parosteal osteosarcomas, suggesting limited utility in differentiating bone lesions.

More Related Videos

Defining Gene Functions in Tumorigenesis by Ex vivo Ablation of Floxed Alleles in Malignant Peripheral Nerve Sheath Tumor Cells
09:37

Defining Gene Functions in Tumorigenesis by Ex vivo Ablation of Floxed Alleles in Malignant Peripheral Nerve Sheath Tumor Cells

Published on: August 25, 2021

1.5K
Author Spotlight: Genetically Engineered Mouse Models and Pathological Characterization of Neurofibromatosis Type 1 Associated Tumors
08:57

Author Spotlight: Genetically Engineered Mouse Models and Pathological Characterization of Neurofibromatosis Type 1 Associated Tumors

Published on: May 17, 2024

3.1K

Related Experiment Videos

Last Updated: May 3, 2026

A Syngeneic Orthotopic Osteosarcoma Sprague Dawley Rat Model with Amputation to Control Metastasis Rate
07:31

A Syngeneic Orthotopic Osteosarcoma Sprague Dawley Rat Model with Amputation to Control Metastasis Rate

Published on: May 3, 2021

3.3K
Defining Gene Functions in Tumorigenesis by Ex vivo Ablation of Floxed Alleles in Malignant Peripheral Nerve Sheath Tumor Cells
09:37

Defining Gene Functions in Tumorigenesis by Ex vivo Ablation of Floxed Alleles in Malignant Peripheral Nerve Sheath Tumor Cells

Published on: August 25, 2021

1.5K
Author Spotlight: Genetically Engineered Mouse Models and Pathological Characterization of Neurofibromatosis Type 1 Associated Tumors
08:57

Author Spotlight: Genetically Engineered Mouse Models and Pathological Characterization of Neurofibromatosis Type 1 Associated Tumors

Published on: May 17, 2024

3.1K

Area of Science:

  • Oncology
  • Genetics
  • Pathology

Background:

  • Parosteal osteosarcoma presents diagnostic challenges due to bland cytologic features, especially in small biopsies.
  • Distinguishing parosteal osteosarcoma from benign fibro-osseous lesions like fibrous dysplasia (FD) is critical.
  • GNAS mutations are known in FD but uncharacterized in parosteal osteosarcoma.

Purpose of the Study:

  • To investigate the presence and utility of GNAS mutations in parosteal osteosarcoma and its mimics.
  • To differentiate parosteal osteosarcoma from benign fibro-osseous lesions using GNAS mutational analysis.

Main Methods:

  • Genomic DNA extraction from tumor samples.
  • Direct sequencing of GNAS gene codons 201 and 227.
  • Analysis of GNAS mutational status in parosteal osteosarcoma, FD, adamantinoma, and osteofibrous dysplasia.

Main Results:

  • GNAS mutations (R201C/H) were identified in 11 of 14 (79%) FD cases.
  • Activating GNAS mutations were detected in 5 of 9 (55%) parosteal osteosarcoma cases.
  • No GNAS mutations were found in adamantinoma or osteofibrous dysplasia.

Conclusions:

  • This study reports activating GNAS mutations in parosteal osteosarcoma for the first time.
  • GNAS mutational status shows limited utility in differentiating parosteal osteosarcoma from benign fibro-osseous lesions.
  • Further research is needed to establish definitive diagnostic markers for parosteal osteosarcoma.