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

Microtubule Instability02:17

Microtubule Instability

Microtubules are hollow cylindrical filaments having a diameter of approximately 25 nm and a length that varies from 200 nm to 25 μm. GTP-bound tubulin subunits form αβ-heterodimers for microtubule assembly. These core building blocks interact longitudinally, polymerizing into protofilaments. The protofilaments then interact with one another through lateral bonding forces to form stable cylindrical microtubules. These cylindrical filaments are dynamic as they undergo repeated assembly and...
Cancers Originate from Somatic Mutations in a Single Cell02:21

Cancers Originate from Somatic Mutations in a Single Cell

Cancer arises from mutations in the critical genes that allow healthy cells to escape cell cycle regulation and acquire the ability to proliferate indefinitely. Though originating from a single mutation event in one of the originator cells, cancer progresses when the mutant cell lines continue to gain more and more mutations, and finally, become malignant. For example, chronic myelogenous leukemia (CML) develops initially as a non-lethal increase in white blood cells, which progressively...
Destabilization of Microtubules01:45

Destabilization of Microtubules

The destabilization of microtubules can occur during different stages of the microtubule lifecycle, such as nucleation or elongation. It can take place at either end of the microtubule or in the microtubule lattices as a whole. The lifespan of individual microtubules within a cell varies according to the cell type and stage of the cell cycle. During interphase, the lifespan of the microtubule is about 30 minutes, while during cell division, it is about 15 minutes. In axonal microtubules of...
Drugs that Destabilize Microtubules01:10

Drugs that Destabilize Microtubules

Microtubules are dynamic structures and can be regulated by microtubule targeting agents (MTAs). Microtubule destabilizing drugs are a class of MTAs that destabilize and prevent microtubules' polymerization. Both natural and synthetic chemicals can be found under this class of drugs. Vincristine and vinblastine, two vinca alkaloids, and colchicine were among the first to be discovered. These drugs can affect cells in various ways, either by inducing a change in cell morphology, preventing...
Drugs that Stabilize Microtubules01:15

Drugs that Stabilize Microtubules

Microtubules are dynamic structures that undergo cycles of catastrophe and rescue. The microtubules play a central role in cell division by forming the spindle apparatus for segregating the chromosomes. This makes them ideal targets for regulating dividing cells in tumors and malignant cancer cells. Microtubule stabilizing drugs help stabilize the microtubule formation and promote its polymerization. Paclitaxel was the first microtubule stabilizing agent used as anticancer drug in chemotherapy...
Non-LTR Retrotransposons03:18

Non-LTR Retrotransposons

As the name suggests, non-LTR retrotransposons lack the long terminal repeats characteristic of the LTR retrotransposons. Additionally, both LTR and non-LTR retrotransposons use distinct mechanisms of mobilization. Non-LTR retrotransposons are further divided into two classes - Long interspersed nuclear elements (LINEs) and short interspersed nuclear elements (SINEs), both of which occur abundantly in most mammals, including humans. Some of the active non-LTR retrotransposons in humans are L1...

You might also read

Related Articles

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

Sort by
Same author

Correction: The KrasG12D;Trp53fl/fl murine model of undifferentiated pleomorphic sarcoma is macrophage dense, lymphocyte poor, and resistant to immune checkpoint blockade.

PloS one·2026
Same author

The DBD-α4 helix of EWSR1::FLI1 is required for GGAA microsatellite binding that underlies genome regulation in Ewing sarcoma.

eLife·2026
Same author

Neutrophil extracellular traps offer a new therapeutic target for elephant endotheliotropic herpes virus-hemorrhagic disease (EEHV-HD).

Communications biology·2026
Same author

Impact of Surgical Margins in Chest Wall Chondrosarcomas: A CanSaRCC Study.

Journal of surgical oncology·2026
Same author

Elective Surgical Care Pathways Are Associated With Lower Fracture Rates at Presentation and Contribute to Superior Clinical Outcomes in Metastatic Bone Disease.

Journal of surgical oncology·2026
Same author

Genome-wide association study meta-analysis identifies susceptibility loci informing Ewing sarcoma etiology and potential mechanisms of risk.

medRxiv : the preprint server for health sciences·2026

Related Experiment Video

Updated: May 14, 2026

Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells
11:42

Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells

Published on: April 7, 2017

Microsatellite instability in sarcoma: fact or fiction?

Michael J Monument1, Stephen L Lessnick, Joshua D Schiffman

  • 1Sarcoma Services, Department of Orthopaedics, Huntsman Cancer Institute, University of Utah School of Medicine, 2000 Circle of Hope, Salt Lake City, UT 84112, USA.

ISRN Oncology
|February 13, 2013
PubMed
Summary

Microsatellite instability (MSI), a DNA repair deficiency, is being investigated in sarcomas. While its frequency mirrors colorectal cancer, distinct biological attributes are unclear, though it may impact gene activation in Ewing sarcoma.

More Related Videos

Tumorsphere Derivation and Treatment from Primary Tumor Cells Isolated from Mouse Rhabdomyosarcomas
09:21

Tumorsphere Derivation and Treatment from Primary Tumor Cells Isolated from Mouse Rhabdomyosarcomas

Published on: September 13, 2019

Implementation of In Vitro Drug Resistance Assays: Maximizing the Potential for Uncovering Clinically Relevant Resistance Mechanisms
08:46

Implementation of In Vitro Drug Resistance Assays: Maximizing the Potential for Uncovering Clinically Relevant Resistance Mechanisms

Published on: December 9, 2015

Related Experiment Videos

Last Updated: May 14, 2026

Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells
11:42

Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells

Published on: April 7, 2017

Tumorsphere Derivation and Treatment from Primary Tumor Cells Isolated from Mouse Rhabdomyosarcomas
09:21

Tumorsphere Derivation and Treatment from Primary Tumor Cells Isolated from Mouse Rhabdomyosarcomas

Published on: September 13, 2019

Implementation of In Vitro Drug Resistance Assays: Maximizing the Potential for Uncovering Clinically Relevant Resistance Mechanisms
08:46

Implementation of In Vitro Drug Resistance Assays: Maximizing the Potential for Uncovering Clinically Relevant Resistance Mechanisms

Published on: December 9, 2015

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Microsatellite instability (MSI) signifies deficient DNA mismatch repair (MMR).
  • MSI is well-characterized in colorectal cancer, predicting susceptibility, pathogenesis, and prognosis.
  • MSI investigation in sarcoma yields heterogeneous results due to detection methods, undefined loci, and small sample sizes.

Purpose of the Study:

  • To review the current understanding of MSI in sarcoma.
  • To explore the potential biological implications of MSI in sarcomas, particularly Ewing sarcoma.
  • To highlight challenges and suggest future research directions for MSI in sarcoma.

Main Methods:

  • Literature review of studies investigating MSI in sarcoma.
  • Analysis of existing data on MSI frequency and biological characteristics in sarcoma.
  • Examination of emerging evidence on the mechanistic role of microsatellites in sarcoma gene activation.

Main Results:

  • MSI occurs in sarcomas at a frequency similar to sporadic colorectal cancers.
  • Limited evidence suggests MSI-positive sarcoma tumors do not share distinct biological attributes.
  • Emerging findings in Ewing sarcoma indicate microsatellite DNA's role in activating EWS/FLI-target genes.

Conclusions:

  • MSI in sarcoma requires further investigation with advanced techniques and larger studies.
  • The biological significance of MSI in sarcoma may differ from colorectal cancer.
  • Microsatellite DNA's role in gene activation presents a novel perspective for sarcoma research.