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

[Aspirin suppresses microsatellite instability].

S Wallinger1, W Dietmaier, K Beyser

  • 1Institut für Pathologie, Universität Regensburg.

Verhandlungen Der Deutschen Gesellschaft Fur Pathologie
|March 14, 2000
PubMed
Summary
This summary is machine-generated.

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

Gene expression signatures for tailoring adjuvant chemotherapy of luminal breast cancer: the pathologists' perspective.

Annals of oncology : official journal of the European Society for Medical Oncology·2021
Same author

Correction to: The natural course of pT2 prostate cancer with positive surgical margin: predicting biochemical recurrence.

World journal of urology·2020
Same author

[Microsatellite instability : Review of methods and applications].

Der Pathologe·2019
Same author

[Autopsy in oncology : Treatment validation in cancer centers and clinical cancer registries].

Der Pathologe·2017
Same author

Quality assurance trials for Ki67 assessment in pathology.

Virchows Archiv : an international journal of pathology·2017
Same author

[Hereditary colorectal cancer : An update on genetics and entities in terms of differential diagnosis].

Der Pathologe·2017

Nonsteroidal anti-inflammatory drugs (NSAIDs) reduce microsatellite instability in mismatch repair-deficient cells. This suggests NSAIDs like aspirin and sulindac may offer a prophylactic therapy for hereditary nonpolyposis colorectal cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Context:

  • Nonsteroidal anti-inflammatory drugs (NSAIDs) show promise in cancer prevention, including regression of adenomas in Familial Adenomatous Polyposis (FAP) patients.
  • The underlying mechanisms of NSAID-mediated cancer prevention, particularly their effect on DNA repair pathways, require further elucidation.

Purpose:

  • To investigate the impact of NSAIDs (Aspirin and Sulindac) on microsatellite instability (MSI) in colorectal cancer cell lines with varying mismatch repair (MMR) gene deficiencies.
  • To explore the relationship between NSAID treatment, cell cycle, apoptosis, and MSI.
  • To develop a rapid in vitro assay for MSI analysis.

Summary:

  • Six colorectal cancer cell lines, mostly deficient in MMR genes (hMSH2, hMLH1, hMSH6), were treated with Aspirin or Sulindac. A microcloning assay combining laser microdissection and PCR was used to analyze MSI.

Related Experiment Videos

  • Long-term NSAID treatment significantly reduced MSI frequency in MMR-deficient cells, an effect that was reversible, time-dependent, and concentration-dependent.
  • The MSI phenotype remained unchanged in a human PMS2-deficient cell line (HEC-1-A), and cell sorting indicated non-apoptotic cells were stable while apoptotic cells were unstable.
  • Impact:

    • These findings suggest that NSAIDs like aspirin and sulindac can induce genetic selection for microsatellite stability in a subset of MMR-deficient cells.
    • This selective pressure may position NSAIDs as a potential prophylactic therapy for hereditary nonpolyposis colorectal cancer (HNPCC) and related carcinomas.