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Vol. 118, No. 2-4, 2007
Issue release date: November 2007
Section title: Paper
Cytogenet Genome Res 118:252–259 (2007)
(DOI:10.1159/000108308)

MicroRNAs in carcinogenesis

Hagan J.P. · Croce C.M.
Comprehensive Cancer Center, The Ohio State University Medical Center, Columbus, OH (USA)

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Article / Publication Details

First-Page Preview
Abstract of Paper

Published online: 11/22/2007

Number of Print Pages: 8
Number of Figures: 2
Number of Tables: 0

ISSN: 1424-8581 (Print)
eISSN: 1424-859X (Online)

For additional information: http://www.karger.com/CGR

Abstract

MicroRNAs are an abundant class of noncoding RNAs, typically 20–23 nucleotides in length that are often evolutionarily conserved in metazoans and expressed in a cell and tissue specific manner. MicroRNAs exert their gene regulatory activity primarily by imperfectly base pairing to the 3′ UTR of their target mRNAs, leading to mRNA degradation or translational inhibition. In cancer, microRNAs are often dysregulated with their expression patterns being correlated with clinically relevant tumor characteristics. Recently, microRNAs were shown to be directly involved in cancer initiation and progression. This review focuses primarily on emerging developments in the microRNA field that impact our understanding of how these molecules contribute to carcinogenesis.



 

Note added in proof


Since the acceptance of this review, many important papers have been published in relation to mammalian microRNA biology. For brevity’s sake, a few noteworthy studies in the context of this review will be mentioned. MicroRNA-125a/b whose expression is frequently lost or reduced in breast cancer has been reported to regulate the important oncogenes ERBB2 and ERBB3 (Scott et al., 2007). Two research groups have published a mouse knockout of miR-155, demonstrating that this microRNA is required for normal immune function (Rodriguez et al., 2007; Thai et al., 2007). Similarly, a mouse knockout of miR-1-2 is characterized by cardiac defects, leading to 50% lethality by weaning age (Zhao et al., 2007). Lastly, mouse screens that involve mapping of retroviral integration sites that lead to T-cell lymphoma development have identified the activation of two separate microRNA clusters, miR-17/18/19a/ 20a/19b-1/92-1 or miR-106a/20b/19b-2/92-2/ 363, as the causative event (Wang et al., 2006; Lum et al., 2007). These results confirm the significance of microRNAs in normal mammalian development and in cancer.

  

Author Contacts

Request reprints from John P. Hagan
Comprehensive Cancer Center
The Ohio State University Medical Center
400 West 12th Ave., Columbus, OH 43210 (USA)
telephone: +1 614 292 4134; fax: +1 614 292 3312
e-mail: john.hagan@osumc.edu

  

Article Information

Manuscript received: 31 July 2006
Accepted in revised form for publication by L. Cannizzaro,: 6 September 2006.
Number of Print Pages : 8
Number of Figures : 2, Number of Tables : 0, Number of References : 91

  

Publication Details

Cytogenetic and Genome Research

Vol. 118, No. 2-4, Year 2007 (Cover Date: November 2007)

Journal Editor: Schmid, M. (Würzburg)
ISSN: 1424–8581 (print), 1424–859X (Online)

For additional information: http://www.karger.com/CGR


Article / Publication Details

First-Page Preview
Abstract of Paper

Published online: 11/22/2007

Number of Print Pages: 8
Number of Figures: 2
Number of Tables: 0

ISSN: 1424-8581 (Print)
eISSN: 1424-859X (Online)

For additional information: http://www.karger.com/CGR


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Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in goverment regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.
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