Cancer Research CTRC-AACR San Antonio Breast Cancer Symposium  09 AM Call for Abstracts
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online

[Cancer Research 43, 1066-1073, March 1, 1983]
© 1983 American Association for Cancer Research

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Thomson, D. M. P.
Right arrow Articles by Scanzano, R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Thomson, D. M. P.
Right arrow Articles by Scanzano, R.

Oxidative Metabolism, Cytoskeletal System, and Calcium Entry of Leukocytes in the Phenomenon of Sensitizing Cancer Extract-induced Leukocyte Adherence Inhibition1

D. M. P. Thomson2, Kerry Phelan and Rosemarie Scanzano

Department of Clinical Immunology, Montreal General Hospital, Montreal, Quebec H3G 1A4, Canada

We examined some of the metabolic events that regulate sensitizing cancer extract-induced leukocyte adherence inhibition and found that human leukocytes adhere in a comparatively passive manner to glass in serum-free medium. Adherence of leukocytes to glass did not require oxidative metabolism, microtubules, microfilaments, or calcium entry, whereas leukocyte mobility excited by sensitizing cancer extract did. Calcium antagonists, lanthanum chloride, cromolyn sodium, nifedipine, trifluoperazine, and lidocaine, prevented sensitizing cancer extract-induced leukocyte mobility. Calcium agonist, ionophore A23187, excited leukocyte mobility. Ouabain, which inhibits Na+-K+-adenosine triphosphatase and may increase intracellular Ca2+ as a result, also excited leukocyte mobility. Monocytes, armed with serum from patients with early cancer and challenged with the same sensitizing tumor antigen, generated a leukotriene mediator that excited leukocyte mobility; cromolyn sodium, nifedipine, and trifluoperazine antagonized the synthesis of the mediator. The calcium antagonists inhibited the leukotriene mediator and authentic leukotrienes B4, C4, and D4 from exciting leukocyte mobility. The results showed that leukocyte mobility, excited by sensitizing cancer extract, is an active process depending upon immunologically triggered release of a leukotriene mediator from armed monocytes. Leukocyte adherence inhibition requires many of the same physiological events that chemokinesis and chemotaxis do and is thus an assay to study either immunologically released chemoattractants or chemoattractants themselves on leukocyte locomotion.

1 Supported by grants from the Medical Research Council of Canada and the National Cancer Institute.

2 To whom requests for reprints should be addressed, at the Montreal General Hospital, 1650 Cedar Avenue, Montreal, Quebec H3G 1A4, Canada.

Received 8/23/82. Accepted 12/ 8/82.







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online
Copyright © 1983 by the American Association for Cancer Research.