Uterine leiomyoma (ULM) ,which affects around 20–50 % of women over the age of 30, is the most frequent  gynecological benign tumor[1]. It is one of the most important causes of pregnancy complications, abnormal uterine bleeding, and infertility [2].While the molecular pathogenesis is still unknown, ULM has a multifactorial etiology which depends on both environmental factors and genetics as displayed by monozygotic female twins which are nearly twice as likely to be concordant for hysterectomy or for hospitalization as a result of a ULM as dizygotic twins [3].  A couple of candidate gene polymorphisms including ER-alpha, CYP, COMT, androgen receptor, IL-1, GSTM, and VEGF have been suggested to be susceptible factors for the development of ULM[4,10]. The COMT gene codes for the catechol-o-methyltransferase enzyme which catalyzes methyl conjugation of the hydroxyl groups of catechol estrogens [11] .

Controlling COMT activity may indirectly influence the biologic effects of estrogen and may have an etiological role in estrogeninduced tumorigenesis like leiomyoma formation .COMT Val158Met polymorphism leads to a valine (val)-to-methionine (met) substitution at position 158, which affects the thermostability and enzymatic activity of the COMT protein[11]. The Met/Met genotypes have been connected with a decreased enzymatic activity, while the Val/Val and Val/Met genotypes have been associated with high and intermediate enzymatic activities, respectively [12]. The associations of ULM with Val158Met polymorphism in COMT gene have been researched in different ethnic groups with discrepant results. The relationship between COMT gene polymorphism and leiomyoma is not yet clearly discovered.

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The genotypes’ frequency of COMT polymorphism, in different ethnic populations was varied. Furthermore, there was no data on the frequency of this polymorphism in Turkish ULM patients [6,13-16]. Therefore we researched COMT polymorphism in Turkish patients with ULM. Uterine leiomyomas or fibroids are the most frequent pelvic tumors in women which affect at least 25% of women of reproductive age [30]. Furthermore, the pervasiveness of uterine leiomyomas may be .77% overall i.e. presence of symptomatic and asymptomatic fibroids affecting women of reproductive age [31].

In the USA , Uterine leiomyomas are the most frequent signal for hysterectomy [32], and they frequently lead to serious irregular prolonged menstrual bleeding, infertility and abortion [33,34]. The present treatments for leiomyomas are not adequate, and surgical removal through either hysterectomy or myomectomy is sill the standard treatment.  At the present time there is no optimal medication approved by the Federal Drug Agency for uterine leiomyomas.

Non-surgical treatment of leiomyomas includes the use of GnRH agonists that functions through restraining circulating levels of estradiol (E2) and progesterone [35,36].  Sadly the present treatments have severe disadvantages such as the severe—adverse side effects related to GnRH agonist (GnRHa), such as osteoporosis and menopausal symptoms [37,38], and loss of procreative potential and finally the cost and post-operative complications of surgical approaches [39,40,41] Ovarian hormones have the main role in the pathogenesis of uterine leiomyoma [42,43]. E2 and its metabolites play a crucial role in initiating and promoting leiomyoma growth [44,45].  In addition, there is convincing evidence that endogenous levels of catechol estrogen (CE) metabolites are noticeably different between the uterine leiomyoma and adjacent normal myometrium [46]. As a result, using  estrogen-metabolizing enzymes could be potential therapeutic target for the non-surgical treatment of uterine fibroids.

Catechol-O-methyl transferase (COMT) metabolizes many endobiotics such as CE [47]. The cellular origin of uterine fibroids is still unknown. Several observations suggest that each fibroid comes from the trans- formation of a single somatic stem cell of the myometrium influenced by ovarian hormones. What early genetic studies propose is that fibroids are monoclonal tumors[48].  There are myometrial tissues in human and mouse multipotent somatic stem cells.

Through asymmetric division, this subset of tissue cells, under the influence of reproductive, hormones go through self-renewal and produces daughter cells (possibly ovarian hormones); this process is accountable for regeneration[49,50]. There are fewer stem cells in human uterine fibroid tissue than normal myometrium [51,52].