Balkan Journal of Medical Genetics

ASSOCIATION OF RELATIVE TELOMERE LENGTH AND RISK OF HIGH HUMAN PAPILLOMAVIRUS LOAD IN CERVICAL EPITHELIAL CELLS
Albosale A H, Mashkina E V
*Corresponding Author: Dr. Abbas Hadi Albosale, Genetics Department, Southern Federal University, 344090, Stachki, 194/1, Rostov-on-Don Province, Russia. E-mail: abbashammadi4@gmail.com
page: 65

INTRODUCTION

Telomeres are comprised of complexes of nucleoprotein that enclose chromosome ends and not only offer protection against fusion and other injuries but also contribute to the preservation of genomic stability [1]. Each subsequent division of the cell reduces the length of the 5’-TTAGGG-3’ sequence of DNA telomere repetitions, the outcome being either apoptosis or senescence [2]. When atypical conditions cause the telomeres to reduce in length, the possibility of telomere end fusions arises, which could result in an increased level of chromosome instability. This is a primary triggering event in many cancers, including colon, prostate, and cervical cancers [3–5]. Research in this field has postulated that a potential correlation exists between different cancer stages and telomere length. Specifically, telomeres that are shorter in length are linked to the onset of cancer. However, they gradually lengthen as cancer progresses as a consequence of telomerase activation or alternative telomere lengthening (ALT) [6,7]. Telomerase acts to safeguard the telomere against shortening. The telomere is comprised of two subunits, namely: TERC (telomerase RNA component) and hTERT (human telomerase reverse transcriptase). TERC functions as a blueprint for telomere sequence amplification, whereas hTERT serves as a reverse transcriptase subunit [8]. In 85-90% of human cancers, telomerase activation causes telomeres to expand in length [9]. Thus, it is reasonable to assume that the stabilization of telomere length occurs at a later point in the tumorigenesis process. Specifically, it takes place following a period of active proliferation cycles and reduced telomere length [10]. Sexual contact is the most common vehicle for the transmission of the human papillomavirus (HPV). HPV infection has affected a considerable number worldwide, although both men and women are infected with HPV, adolescent girls and women under the age of 25 are the most infected [11,12]. HPV is a diminutive virus. It penetrates cells with its capsid proteins, with the infection commencing at the basal cell layer, after which it disseminates to elevated tiers of the cervical epithelium [13]. Dysplasia resulting from the relentless HR-HPV infection can ultimately develop into cancer [14]. The principal causative agents for different cancer types are HR-HPV genotypes (16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, and 59) [15]. HR-HPV has been implicated in cancers of the cervix, vulva, vaginal, penis, anus, and oropharyngeal cancers [16]. However, cervical cancer is the fourth most common malignant tumor in women globally, and it is associated with a significant mortality rate in women [17,18]. The cellular telomerase complex can be triggered by the hTERT transcription, which is stimulated by the HPV E6 protein [19]. Moreover, the cell immortalization that occurs during long-term high-risk human papillomavirus infection is dependent upon telomerase activation, which leads to cervical malignant neoplasm development [20]. The development of cancer passes through multiple stages, and one of the most common features is modifications to telomere length [21]. There is practically no data in the literature on the relationship between telomeric DNA length and the risk of the development of elevated viral load in cells infected with HPV. Therefore, the primary objective of the current study is to ascertain the existence of any disparities between comparative telomeric DNA lengths in the cervical epithelial cells of women with high HPV load and telomeric DNA lengths in the control group.

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