help button home button Am J Pathol Angiogenesis Meeting
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Order Full text via Infotrieve
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 HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Rouan, S. K.
Right arrow Articles by Rhodes, C. T.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Rouan, S. K.
Right arrow Articles by Rhodes, C. T.

American Journal of Pathology, Vol 137, 779-787, Copyright © 1990 by American Society for Investigative Pathology


REGULAR ARTICLES

Reversal of colchicine-induced mitotic arrest in Chinese hamster cells with a colchicine-specific monoclonal antibody

SK Rouan, IG Otterness, AC Cunningham, HE Holden and CT Rhodes
Department of Pharmaceutics, University of Rhode Island, Kingston.

The ability of a high-affinity colchicine-binding monoclonal antibody to reverse the effects of colchicine on Chinese hamster ovary cells was investigated. Using flow cytometry, a complete mitotic blockade was demonstrated after 16 hours with 2.5 x 10(-7) mol/l (molar) colchicine. Colchicine-induced changes were reversible when equimolar antibody was added simultaneously with or up to 6 hours after colchicine. With further delay in addition of antibody, a progressive irreversible increase in mitotic blockade and increase in mean cell size was observed. Prolonged colchicine exposure, without antibody reversal, led to polyploidy and structural chromosome breakage. Early antibody reversal restored cells to the diploid state, whereas delayed reversal resulted in a time-dependent increase in polyploidy. Colchicine-induced polyploidy and chromosomal aberrations may be the basis for both colchicine toxicity and the time-dependent increase in irreversibility of colchicine effects.


This article has been cited by other articles:


Home page
Clin. Cancer Res.Home page
G. Korpanty, J. G. Carbon, P. A. Grayburn, J. B. Fleming, and R. A. Brekken
Monitoring Response to Anticancer Therapy by Targeting Microbubbles to Tumor Vasculature
Clin. Cancer Res., January 1, 2007; 13(1): 323 - 330.
[Abstract] [Full Text] [PDF]


Home page
Endocr Relat CancerHome page
Y. Liang, R. A Brekken, and S. M Hyder
Vascular endothelial growth factor induces proliferation of breast cancer cells and inhibits the anti-proliferative activity of anti-hormones.
Endocr. Relat. Cancer, September 1, 2006; 13(3): 905 - 919.
[Abstract] [Full Text] [PDF]


Home page
Cancer Res.Home page
R. A. Brekken, J. P. Overholser, V. A. Stastny, J. Waltenberger, J. D. Minna, and P. E. Thorpe
Selective Inhibition of Vascular Endothelial Growth Factor (VEGF) Receptor 2 (KDR/Flk-1) Activity by a Monoclonal Anti-VEGF Antibody Blocks Tumor Growth in Mice
Cancer Res., September 1, 2000; 60(18): 5117 - 5124.
[Abstract] [Full Text]


Home page
NEJMHome page
F. J. Baud, A. Sabouraud, E. Vicaut, P. Taboulet, J. Lang, C. Bismuth, J. M. Rouzioux, and J.-M. Scherrmann
Treatment of Severe Colchicine Overdose with Colchicine-Specific Fab Fragments
N. Engl. J. Med., March 9, 1995; 332(10): 642 - 645.
[Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1990 by the American Society for Investigative Pathology.