JCP

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS REGISTER


[Advanced]
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this link to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Add article to my folders
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Dey, P
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Dey, P
Journal of Clinical Pathology 2004;57:1245-1249
© 2004 BMJ Publishing Group Ltd & Association of Clinical Pathologists

REVIEW

Aneuploidy and malignancy: an unsolved equation

P Dey

Correspondence to:
Dr P Dey
Pathology Department, Kuwait Cancer Control Centre, PO Box 42262, 70653 Shuwaikh, Kuwait; deypranab{at}hotmail.com
ABSTRACT
Aneuploidy is frequently noted in malignant tumours. There is much controversy about its cause and effect in relation to malignant tumours. Failure of the spindle checkpoint caused by mutation of the responsible genes may be one of the important factors for the development of aneuploidy. Telomere dysfunction may also be a possible source of failure of cytokinesis resulting in aneuploidy. Evidence such as tumour specific aneuploidy, presence of aneuploidy in various preneoplastic conditions, increased frequency of genetic instability in aneuploid cell lines compared with diploid cells, and mutation of mitotic checkpoint genes suggests that aneuploidy possibly plays an active role in carcinogenesis. In this brief review, the various aspects of aneuploidy with special emphasis on its mechanism of development and impact on progression of cancer are discussed.

Abbreviations: APC, anaphase promoting complex; CGH, comparative genomic hybridisation; FCM, flow cytometry; FISH, fluorescence in situ hybridisation; ICM, image cytometry

Keywords: aneuploidy; cancer; mitosis; mitotic checkpoint; genomic instability




This article has been cited by other articles:


Home page
 Cancer Res.Home page
A. Castillo, H. C. Morse III, V. L. Godfrey, R. Naeem, and M. J. Justice
Overexpression of Eg5 Causes Genomic Instability and Tumor Formation in Mice
Cancer Res., November 1, 2007; 67(21): 10138 - 10147.
[Abstract] [Full Text] [PDF]

Home page
 Mol. Biol. CellHome page
E. Octtaviani, J. C. Effler, and D. N. Robinson
Enlazin, a Natural Fusion of Two Classes of Canonical Cytoskeletal Proteins, Contributes to Cytokinesis Dynamics
Mol. Biol. Cell, December 1, 2006; 17(12): 5275 - 5286.
[Abstract] [Full Text] [PDF]

Home page
 EndocrinologyHome page
I. Donangelo, S. Gutman, E. Horvath, K. Kovacs, K. Wawrowsky, M. Mount, and S. Melmed
Pituitary Tumor Transforming Gene Overexpression Facilitates Pituitary Tumor Development
Endocrinology, October 1, 2006; 147(10): 4781 - 4791.
[Abstract] [Full Text] [PDF]

Home page
 J. Clin. Pathol.Home page
E Cristi, G Perrone, G Toscano, A Verzi, S Nori, D Santini, G Tonini, A Vetrani, A Fabiano, and C Rabitti
Tumour proliferation, angiogenesis, and ploidy status in human colon cancer
J. Clin. Pathol., November 1, 2005; 58(11): 1170 - 1174.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS REGISTER
Journal of Clinical Pathology Molecular Pathology
Terms and conditions relating to subscriptions purchased online  ¦  Website terms and conditions  ¦  Privacy policy
Copyright © 2004 by the BMJ Publishing Group Ltd & Association of Clinical Pathologists.