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

Tumor interaction with vascular endothelium.

H Al-Mondhiry1, V McGarvey

  • 1Department of Medicine, Pennsylvania State University, College of Medicine, Hershey.

Haemostasis
|January 1, 1987
PubMed
Summary

Certain tumors can damage endothelial cells (EC), leading to increased platelet adhesion. This interaction may initiate tumor invasion and metastasis by forming platelet-tumor thrombi on the vessel wall.

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

Fibrinogen interaction with human platelets: effect of other coagulation factors, prostaglandins and platelet inhibitors.

Thrombosis research·2010
Same author

Sweet's syndrome without granulocytosis.

International journal of dermatology·1998
Same author

Splenic rupture in afibrinogenemia: conservative versus surgical management.

The American journal of medicine·1995
Same author

Evaluation of the fibrinolytic system in calves implanted with an artificial heart and ventricular assist device.

ASAIO journal (American Society for Artificial Internal Organs : 1992)·1995
Same author

Congenital afibrinogenemia.

American journal of hematology·1994
Same author

Congenital afibrinogenemia and splenic rupture.

The American journal of medicine·1994

Area of Science:

  • Oncology
  • Vascular Biology
  • Cell Biology

Background:

  • Tumor-induced endothelial cell (EC) injury is a potential early event in metastasis.
  • The interaction between damaged EC and platelets in this process requires further investigation.

Purpose of the Study:

  • To investigate tumor-induced EC injury.
  • To examine the interaction between tumor-damaged EC and platelets.

Main Methods:

  • Cultured bovine EC and extracts from four human malignancies (melanoma, breast carcinoma, lung carcinoma, colon cancer) were used.
  • Endothelial cell injury was quantified by measuring the release of 51Cr and lactic dehydrogenase (LDH).
  • Platelet adhesion to EC was observed.

Main Results:

  • Melanoma, breast carcinoma, and lung carcinoma extracts induced significant EC injury, evidenced by LDH and 51Cr release.
  • Colon cancer extract did not appear to cause significant EC injury.
  • Increased adhesion of platelets to tumor-damaged EC was observed.

Conclusions:

  • Specific tumor types can inflict injury upon endothelial cells.
  • Platelet adhesion to tumor-injured EC promotes the formation of platelet-tumor thrombi.
  • This thrombus formation may be a critical initial step in tumor invasion of the vessel wall and subsequent metastasis.

Related Experiment Videos