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      Association of XRCC3 18067 C>T (Thr241Met) polymorphism with risk of cervical and ovarian cancers: A systematic review and meta-analysis

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          Abstract

          The 18067 C>T polymorphism of XRCC3 gene has been considered to be implicated in the development of cervical and ovarian cancers, but the results are inconsistent. Thus, we conducted a meta-analysis to assess the association of XRCC3 18067 C>T polymorphism with risk of cervical and ovarian cancers. All studies on the association of XRCC3 18067 C>T polymorphism with cervical and ovarian cancers risk were retrieved. Finally, a total of 17 studies including 10 studies with 5,637 cases and 10,057 controls on ovarian cancer and 7 studies with 1,112 cases and 1,233 controls on cervical cancer were selected. Overall, pooled results showed that the XRCC3 18067 C>T polymorphism was significantly associated with increased risk of ovarian cancer (TC vs. CC: OR = 0.904, 95% CI = 0.841–0.972, p = 0.006; TT + TC vs. CC: OR = 0.914, 95% CI = 0.853–0.979, p = 0.010) and cervical cancer (TC vs. CC: OR = 1.00, 95% CI = 1.066–1.585, p = 0.009). Further subgroup analysis by ethnicity revealed an increased risk of cervical and ovarian cancer in Asians and Caucasians, respectively. The present meta-analysis inconsistent with the previous meta-analysis suggests that the XRCC3 18067 C>T polymorphism might be implicated in the pathogenesis of cervical and ovarian cancers.

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          Human papillomavirus and cervical cancer.

          Eileen M. Burd (2003)
          Of the many types of human papillomavirus (HPV), more than 30 infect the genital tract. The association between certain oncogenic (high-risk) strains of HPV and cervical cancer is well established. Although HPV is essential to the transformation of cervical epithelial cells, it is not sufficient, and a variety of cofactors and molecular events influence whether cervical cancer will develop. Early detection and treatment of precancerous lesions can prevent progression to cervical cancer. Identification of precancerous lesions has been primarily by cytologic screening of cervical cells. Cellular abnormalities, however, may be missed or may not be sufficiently distinct, and a portion of patients with borderline or mildly dyskaryotic cytomorphology will have higher-grade disease identified by subsequent colposcopy and biopsy. Sensitive and specific molecular techniques that detect HPV DNA and distinguish high-risk HPV types from low-risk HPV types have been introduced as an adjunct to cytology. Earlier detection of high-risk HPV types may improve triage, treatment, and follow-up in infected patients. Currently, the clearest role for HPV DNA testing is to improve diagnostic accuracy and limit unnecessary colposcopy in patients with borderline or mildly abnormal cytologic test results.
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            Genomic instability in human cancer: Molecular insights and opportunities for therapeutic attack and prevention through diet and nutrition

            Lynnette Ferguson, Helen Chen, Andrew Collins … (2015)
            Genomic instability can initiate cancer, augment progression, and influence the overall prognosis of the affected patient. Genomic instability arises from many different pathways, such as telomere damage, centrosome amplification, epigenetic modifications, and DNA damage from endogenous and exogenous sources, and can be perpetuating, or limiting, through the induction of mutations or aneuploidy, both enabling and catastrophic. Many cancer treatments induce DNA damage to impair cell division on a global scale but it is accepted that personalized treatments, those that are tailored to the particular patient and type of cancer, must also be developed. In this review, we detail the mechanisms from which genomic instability arises and can lead to cancer, as well as treatments and measures that prevent genomic instability or take advantage of the cellular defects caused by genomic instability. In particular, we identify and discuss five priority targets against genomic instability: (1) prevention of DNA damage; (2) enhancement of DNA repair; (3) targeting deficient DNA repair; (4) impairing centrosome clustering; and, (5) inhibition of telomerase activity. Moreover, we highlight vitamin D and B, selenium, carotenoids, PARP inhibitors, resveratrol, and isothiocyanates as priority approaches against genomic instability. The prioritized target sites and approaches were cross validated to identify potential synergistic effects on a number of important areas of cancer biology.
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              Cervical cancer in Central and South America: Burden of disease and status of disease control.

              Raúl Murillo, Rolando Herrero, Mónica S Sierra … (2016)
              More than 20 years after cytology-based screening was introduced in Central and South America (CSA), cervical cancer remains a leading cause of cancer incidence and mortality in the region. Although several population-based registries exist in the region, few comprehensive analyses have been conducted to describe the status of cervical cancer control.
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                Author and article information

                Journal
                Journal ID (pmc): imas
                Journal ID (publisher-id): 1646
                Title: Interventional Medicine and Applied Science
                Abbreviated Title: IMAS
                Publisher: Akadémiai Kiadó (Budapest )
                ISSN (Print): 2061-1617
                ISSN (Electronic): 2061-5094
                Publication date (Electronic, epub): 07 October 2019
                Volume:
                Issue:
                Pages: 1-10
                Affiliations
                [ 1 ]Department of Gynecology and Obstetrics, Iran University of Medical Sciences , Tehran, Iran
                [ 2 ]Department of Pathology, Shahid Sadoughi University of Medical Sciences , Yazd, Iran
                [ 3 ]Department of Gynecology and Obstetrics, Shahid Beheshti University of Medical Sciences , Tehran, Iran
                [ 4 ]Department of Gynecology and Obstetrics, Shahid Sadoughi University of Medical Sciences , Yazd, Iran
                [ 5 ]Department of Medical Genetics, Shahid Sadoughi University of Medical Sciences , Yazd, Iran
                [ 6 ]Mother and Newborn Health Research Center, Shahid Sadoughi University of Medical Sciences , Yazd, Iran
                Author notes
                [* ]Corresponding author: Dr. Mansour Moghimi; Department of Pathology, Shahid Sadoughi University of Medical Sciences, Bou Ali Ave, P.O. Box: 734, Yazd, Iran; Phone: +98 93727 26153; E-mail: moghimim1350@ 123456gmail.com
                Article
                DOI: 10.1556/1646.11.2019.21
                SO-VID: c9e97983-ca72-49c3-888e-b9b5af9f7ba2
                Copyright © © 2019 The Author(s)
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 International License, which permits unrestricted use, distribution, and reproduction in any medium for non-commercial purposes, provided the original author and source are credited, a link to the CC License is provided, and changes – if any – are indicated.

                History
                Date received : 10 March 2019
                Date revision received : 19 May 2019
                Date: 02 June 2019
                Date: 27 June 2019
                Date accepted : 30 June 2019
                Page count
                Figures: 3, Tables: 2, Equations: 0, References: 31, Pages: 10
                Funding
                Funding sources: None.
                Categories
                Subject: REVIEW

                ScienceOpen disciplines: Medicine,Immunology,Health & Social care,Microbiology & Virology,Infectious disease & Microbiology
                Keywords: ovarian cancer,polymorphism, XRCC3 gene,cervical cancer,meta-analysis
                Data availability:
                ScienceOpen disciplines: Medicine, Immunology, Health & Social care, Microbiology & Virology, Infectious disease & Microbiology
                Keywords: ovarian cancer, polymorphism, XRCC3 gene, cervical cancer, meta-analysis

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