Balkan Journal of Medical Genetics

MITOCHONDRIAL DNA 4977 bp DELETION IN CHRONIC CERVICITIS AND CERVIX CANCERS
Kara M, Tatar A, Borekci B, Dagli F, Oztas S
*Corresponding Author: Murat Kara M.D., Department of Genetics, School of Medicine, Firat University, Universite cad. No. 2, 23119 Elazig, Turkey; Tel: +90-424-233-35-55/1938; Fax: +90-424-238-80-96; E-mail: drmuratkara@hotmail.com
page: 25

INTRODUCTION

Cervical cancer is still a frequent cancer found in women in all over the world and is a prominent cause of cancer-related deaths [1,2]. However, it is a preventable cancer [3]. Chronic cervicitis is the most common gynecological disease and occurs during the reproductive period of life in 50.0% of women. Although it is often seen, there are important problems in diagnosis, detection of etiologic agents and in treatment [4]. Although multiple genetic events have been identifi ed in the nuclear genome of cervical cancer cells, little is known about genetic changes occurring in the mitochondrial genome during cervical carcinogenesis. Human mitochondrial DNA (mtDNA) is a double-stranded, closed circular structured DNA molecule which is 16,569 bp long [5,6]. Mitochondrial DNA contains 37 genes that play a fundamental role in protein synthesis of mitochondrion. Of these, 22 are transfer RNA (tRNA) genes, two are ribosomal RNA (rRNA) genes (12S and 16S) and 13 are mRNA genes that are used in oxidative phosphorylation and respiratory chain [7,8]. Besides the gene-coding region, there is a 1124 bp region that is named displacement-loop (D-loop) [9]. This region contains basic sequences required for initiation of mtDNA replication and transcription [10,1]. Gene organization and structure of mtDNA are mostly conserved [11]. The mtDNA gene mutations are found in solid tumors such as bladder, breast, colon, stomach, liver, kidney, lung, pancreas, prostate, esophagus, thyroid, brain, head and neck cancers, and hematological cancers such as acute and chronic leukemia, myelodysplastic syndrome and lymphomas [10,12]. In general, gene point mutations, gene deletions and mitochondrial microsatellite instability leading to mitochondrial diseases are expressed in human neoplasms. However, the frequency of these events in different tissues may vary [13-16]. The relationship of mtDNA mutations and cancer is very striking. For instance, in 1998, Polyak et al. [15] reported that 70.0% of colorectal cancers have somatic mtDNA mutations. The mtDNA 4977 bp deletion is the single most common deletion of mtDNA that is demonstrated in many different types of human tumors including thyroid tumors, hepatocellular carcinoma, esophagus carcinoma and stomach cancer [14,17].

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