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

Ascitic complement system in ovarian cancer.

L Bjørge1, J Hakulinen, O K Vintermyr

  • 1Department of Bacteriology and Immunology, Haartman Institute, University of Helsinki, FIN-00014 Helsinki, Finland. Line.Bjorge@gades.uib.no

British Journal of Cancer
|February 24, 2005
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

NSGO-OV-UMB1/ENGOT-OV30: A phase II study of durvalumab in combination with the anti-CD73 monoclonal antibody Oleclumab in patients with relapsed ovarian cancer.

Gynecologic oncology·2024
Same author

Overall survival in patients with endometrial cancer treated with dostarlimab plus carboplatin-paclitaxel in the randomized ENGOT-EN6/GOG-3031/RUBY trial.

Annals of oncology : official journal of the European Society for Medical Oncology·2024
Same author

Low incidence of severe bacterial infections in hospitalised patients with COVID-19: A population-based registry study.

Infectious diseases (London, England)·2022
Same author

Lipopolysaccharides and outer membrane proteins as main structures involved in complement evasion strategies of non-typhoidal Salmonella strains.

Molecular immunology·2022
Same author

Detection of SARS-CoV-2 nucleocapsid antigen from serum can aid in timing of COVID-19 infection.

Journal of virological methods·2022
Same author

Enhanced influenza A H1N1 T cell epitope recognition and cross-reactivity to protein-O-mannosyltransferase 1 in Pandemrix-associated narcolepsy type 1.

Nature communications·2021

The complement system in ovarian cancer ascites shows activation but is inhibited, hindering immune surveillance. However, it can be harnessed for antibody-based therapies by neutralizing inhibitors.

Area of Science:

  • Immunology
  • Oncology
  • Biochemistry

Background:

  • Ovarian cancer frequently spreads intraperitoneally, leading to ascites, which can delay diagnosis and treatment.
  • The complement system is crucial for immune surveillance and antibody-based therapies, potentially offering a cytotoxic effector mechanism.

Purpose of the Study:

  • To characterize the complement system within the ascitic fluid (AF) of ovarian cancer patients.
  • To evaluate the potential of the ascitic complement system as an effector mechanism for intraperitoneal antibody-based therapies.

Main Methods:

  • Assessed hemolytic activity of classical and alternative complement pathways in AF samples.
  • Quantified complement component levels (C3, C4) and activation products (C3a, soluble C5b-9) in AF.
  • Detected complement deposits (C1q, C3, C5b-9) on isolated malignant cells and analyzed complement regulators.

Related Experiment Videos

Main Results:

  • Most AF samples exhibited classical and alternative pathway hemolytic activity, with elevated C3a and soluble C5b-9 indicating in vivo complement activation.
  • Malignant cells showed surface C1q and C3 deposits but lacked the membrane attack complex (MAC), likely due to complement regulator expression (CD46, CD55, CD59).
  • AF contained higher concentrations of soluble complement inhibitors (C1 inhibitor, CD59, CD46, Factor H, FHL-1) than serum.

Conclusions:

  • The complement system in ovarian cancer ascites is activated but its effector functions are suppressed by intrinsic regulators, failing as an effective immune surveillance mechanism.
  • Despite regulatory inhibition, the ascitic complement system can be utilized as an effector mechanism for intraperitoneal antibody-based therapies, particularly if complement regulators are neutralized.