Balkan Journal of Medical Genetics

CAG REPEAT NUMBER IN THE ANDROGEN RECEPTOR GENE AND PROSTATE CANCER
Madjunkova S, Eftimov A, Georgiev V, Petrovski D, Dimovski AJ, Plaseska- Karanfi lska D,
*Corresponding Author: Professor Dr. Dijana Plaseska-Karanfi lska, Macedonian Academy of Sciences and Arts, Research Center for Genetic Engineering and Biotechnology “Georgi D. Efremov”, Av. Krste Misirkov 2, POB 428, 1000 Skopje, Republic of Macedonia; Tel.: +389-2-3235-410; Fax: +389-2-3115- 434; E-mail: dijana@manu.edu.mk
page: 31

INTRODUCTION

Prostate cancer (PC) is the second leading cause of cancer deaths in men and is the most common male-specifi c cancer in most Western countries [1-5]. An expanding body of epidemiological data suggests several risk factors that predispose to PC development (for example, advanced age, positive family history, African ancestry and potentially ethnicity) [6], but the etiology of PC remains poorly understood. However, involvement of genetic and environmental factors, may also contribute to the ethnic differences in incidence rates [7-9]. The development and progression of prostate tumors are infl uenced by androgens [10]. The effects of androgens on prostatic tissue are mediated by the androgen receptor (AR) through the AR-androgen complex, stimulating transcription and expression of a cascade of androgen-responsive genes and genes involved in the cell cycle control [11]. The AR is a ligand-activated nuclear transcription factor encoded by the AR gene, which spans more than 90 kb of the genomic DNA on the X chromosome (Xq11-12). The gene consists of eight exons that encode four functional domains of AR for DNA binding, ligand binding and transcriptional regulation [12]. Exon 1 encodes the N-terminal (transactivation) domain that controls its transcriptional activity. The 5’ end of this exon 1 includes a CAG polymorphic trinucleotide repeat that codes for a polyglutamine tract in the N-terminal domain [13]. The triplet repeat numbers between 8 and 36 in the normal population [14]. The length of the CAG repeats is inversely related to the transactivation function of the AR gene so that shorter CAG repeats increase the transactivation activity [15]. Many studies have focused on establishing an association of CAG repeat with increased risk of developing PC. In these, shorter repeat lengths have been associated with increased risk of PC [14,16-18], but this fi nding has not been consistent [19-21]. The ethnic variation in the CAG repeat variation in the AR gene suggests that this may have a role in the substantial racial difference in PC risk [22-25]. In this study, we have examined the possible effect of short CAG repeats in the AR gene on PC risk in Macedonian males.

Number 27 VOL. 27 (2), 2024	Number 27 VOL. 27 (1), 2024
Number 26 Number 26 VOL. 26(2), 2023 All in one	Number 26 VOL. 26(2), 2023
Number 26 VOL. 26, 2023 Supplement	Number 26 VOL. 26(1), 2023
Number 25 VOL. 25(2), 2022	Number 25 VOL. 25 (1), 2022
Number 24 VOL. 24(2), 2021	Number 24 VOL. 24(1), 2021
Number 23 VOL. 23(2), 2020	Number 22 VOL. 22(2), 2019
Number 22 VOL. 22(1), 2019	Number 22 VOL. 22, 2019 Supplement
Number 21 VOL. 21(2), 2018	Number 21 VOL. 21 (1), 2018
Number 21 VOL. 21, 2018 Supplement	Number 20 VOL. 20 (2), 2017
Number 20 VOL. 20 (1), 2017	Number 19 VOL. 19 (2), 2016
Number 19 VOL. 19 (1), 2016	Number 18 VOL. 18 (2), 2015
Number 18 VOL. 18 (1), 2015	Number 17 VOL. 17 (2), 2014
Number 17 VOL. 17 (1), 2014	Number 16 VOL. 16 (2), 2013
Number 16 VOL. 16 (1), 2013	Number 15 VOL. 15 (2), 2012
Number 15 VOL. 15, 2012 Supplement	Number 15 Vol. 15 (1), 2012
Number 14 14 - Vol. 14 (2), 2011	Number 14 The 9th Balkan Congress of Medical Genetics
Number 14 14 - Vol. 14 (1), 2011	Number 13 Vol. 13 (2), 2010
Number 13 Vol.13 (1), 2010	Number 12 Vol.12 (2), 2009
Number 12 Vol.12 (1), 2009	Number 11 Vol.11 (2),2008
Number 11 Vol.11 (1),2008	Number 10 Vol.10 (2), 2007
Number 10 10 (1),2007	Number 9 1&2, 2006
Number 9 3&4, 2006	Number 8 1&2, 2005
Number 8 3&4, 2004	Number 7 1&2, 2004
Number 6 3&4, 2003	Number 6 1&2, 2003
Number 5 3&4, 2002	Number 5 1&2, 2002
Number 4 Vol.3 (4), 2000	Number 4 Vol.2 (4), 1999
Number 4 Vol.1 (4), 1998	Number 4 3&4, 2001
Number 4 1&2, 2001	Number 3 Vol.3 (3), 2000
Number 3 Vol.2 (3), 1999	Number 3 Vol.1 (3), 1998
Number 2 Vol.3(2), 2000	Number 2 Vol.1 (2), 1998
Number 2 Vol.2 (2), 1999	Number 1 Vol.3 (1), 2000
Number 1 Vol.2 (1), 1999	Number 1 Vol.1 (1), 1998

About the journal ::: Editorial ::: Subscription ::: Information for authors ::: Contact