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Original Research

Open Access

Association of myeloperoxidase -463G>A polymorphism with cervical cancer in Chinese Han women

  • D. Wu1
  • K-Y. Wang2
  • C-N. He1
  • H-J. Huang1,*,

1Department of Obstetrics and Gynecology, Fuzhou General Hospital of Nanjing Military Command/Dongfang Hospital, Xiamen University, Fuzhou, China

2Institute of Laboratory Medicine, Fuzhou General Hospital of Nanjing Military Command/Dongfang Hospital, Xiamen University, Fuzhou, China

DOI: 10.12892/ejgo3662.2017 Vol.38,Issue 5,October 2017 pp.756-759

Published: 10 October 2017

*Corresponding Author(s): H-J. Huang E-mail: dongbao1115@aliyun.com

Abstract

Objective: Myeloperoxidase (MPO) is an endogenous oxidant in neutrophilic and monocytic cytoplasmic granules. Several epidemiological studies indicate that MPO genetic polymorphisms are associated with cancer risk. Thus the present assessed an association between the MPO -463G>A polymorphism and cervical cancer risk in Chinese Han women. Materials and Methods: A hospital-based case-control study included 276 Chinese Han patients with cervical cancer and 284 age-, and ethnic-matched controls. The MPO -463G>A polymorphism was analyzed with PCR-restriction fragment length polymorphism (RFLP). Associations between the MPO polymorphism and cervical cancer risk were confirmed with χ2 tests. Results: No significant differences occurred among genotype distributions of the MPO -463G>A polymorphism between patients and controls. In a subgroup analysis of cervical cancer patients, there was no association between the MPO polymorphism and cervical cancer histological types or grades or tumor stage. Conclusions: The MPO -463G>A polymorphism is not associated with a risk of cervical cancer in Chinese Han women.

Keywords

Myeloperoxidase; Polymorphism; Cervical cancer; Chinese.

Cite and Share

D. Wu,K-Y. Wang,C-N. He,H-J. Huang. Association of myeloperoxidase -463G>A polymorphism with cervical cancer in Chinese Han women. European Journal of Gynaecological Oncology. 2017. 38(5);756-759.

References

[1] Global Burden of Disease Cancer Collaboration, Fitzmaurice C., Dicker D., Pain A., Hamavid H., Moradi-Lakeh M., et al.: “The Global Burden of Cancer 2013. JAMA Oncol., 2015, 1, 505.

[2] Chen W., Zheng R., Zeng H., Zhang S.: “The updated incidences and mortalities of major cancers in China, 2011”. Chin. J. Cancer, 2015, 34, 53.

[3] Gravitt P.E.: “The known unknowns of HPV natural history”. J. Clin. Invest., 2011, 121, 4593.

[4] Zhang X., Zhang L., Tian C., Yang L., Wang Z.: “Genetic variants and risk of cervical cancer: epidemiological evidence, meta-analysis and research review”. BJOG, 2014, 121, 664.

[5] Cao S., Yang C., Gan Y., Lu Z.: “The health effects of passive smoking: an overview of systematic reviews based on observational epidemiological evidence”. PLoS One, 2015, 10, e0139907.

[6] La Vecchia C., Boccia S.: “Oral contraceptives, human papillomavirus and cervical cancer”. Eur. J. Cancer Prev., 2014, 23, 110.

[7] Dugue P.A., Rebolj M., Garred P., Lynge E.: “Immunosuppression and risk of cervical cancer”. Expert Rev. Anticancer Ther., 2013, 13, 29.

[8] Economos K., Perez-Veridiano N., Mann M., Delke I., Tancer M.L.: “Abnormal cervical cytology in adolescents. A 15-year experience”. J. Reprod. Med., 1994, 39, 973.

[9] Zhang X., He R., Ren F., Tang R., Chen G.: “Association of miR-146a rs2910164 polymorphism with squamous cell carcinoma risk: a meta-analysis”. J. BUON., 2015, 20, 829.

[10] Zidi S., Gazouani E., Stayoussef M., Mezlini A., Ahmed S.K., Yacoubi-Loueslati B., et al.: “IL-10 gene promoter and intron polymorphisms as genetic biomarkers of cervical cancer susceptibility among Tunisians”. Cytokine, 2015, 76, 343.

[11] Castaldo S.A., da Silva A.P., Matos A., Inacio A., Bicho M., Medeiros R., et al.: “The role of CYBA (p22phox) and catalase genetic polymorphisms and their possible epistatic interaction in cervical cancer”. Tumour Biol., 2015, 36, 909.

[12] Zhang Y., Tong S., Guan L., Na F., Zhao W., Wei L.: “CD95 rs1800682 polymorphism and cervical cancer risk: evidence from a meta-analysis”. Tumour Biol., 2014, 35, 1785.

[13] Klebanoff S.J.: “Myeloperoxidase: friend and foe”. J. Leukoc. Biol., 2005, 77, 598.

[14] Yuzhalin A.E., Kutikhin A.G.: “Common genetic variants in the myeloperoxidase and paraoxonase genes and the related cancer risk: a review”. J. Environ. Sci. Health C. Environ. Carcinog. Ecotoxicol. Rev., 2012, 30, 287.

[15] Lai D., Tan C.L., Gunaratne J., Quek L.S., Nei W., Thierry F., et al.: “Localization of HPV-18 E2 at mitochondrial membranes induces ROS release and modulates host cell metabolism”. PLoS One, 2013, 8, e75625.

[16] Akong-Moore K., Chow O.A., von Kockritz-Blickwede M., Nizet V.: “Influences of chloride and hypochlorite on neutrophil extracellular trap formation”. PLoS One, 2012, 7, e42984.

[17] Pattison D.I., Davies M.J.: “Reactions of myeloperoxidase-derived oxidants with biological substrates: gaining chemical insight into human inflammatory diseases”. Curr. Med. Chem., 2006, 13, 3271.

[18] Gustafson H.L., Yao S., Goldman B.H., Lee K., Spier C.M., LeBlanc M.L., et al.: “Genetic polymorphisms in oxidative stress-related genes are associated with outcomes following treatment for aggressive B-cell non-Hodgkin lymphoma”. Am. J. Hematol., 2014, 89, 639.

[19] Zhou C., Luo Q., Qing Y., Lin X., Zhan Y., Ouyang M.: “Association between MPO 463G>A polymorphism and risk of lung cancer: a metaanalysi”:. Tumour Biol., 2013, 34, 3449.

[20] Pabalan N., Jarjanazi H., Sung L., Li H., Ozcelik H.: “Menopausal status modifies breast cancer risk associated with the myeloperoxidase (MPO) G463A polymorphism in Caucasian women: a metaanalysis”. PLoS One, 2012, 7, e32389.

[21] Nishino K., Sekine M., Kodama S., Sudo N., Aoki Y., Seki N., et al.: “Cigarette smoking and glutathione S-transferase M1 polymorphism associated with risk for uterine cervical cancer”. J. Obstet. Gynaecol.Res., 2008, 34, 994.

[22] Mustea A., Heinze G., Sehouli J., Koensgen D., Wolf A., Gutu L., et al.: “The -463G/A polymorphism in myeloperoxidase gene and cervical cancer”. Anticancer Res., 2007, 27, 1531.

[23] Castelao C., da Silva A.P., Matos A., Inacio A., Bicho M., Medeiros R., et al.: “Association of myeloperoxidase polymorphism (G463A) with cervix cancer”. Mol. Cell. Biochem., 2015, 404, 1.

[24] Czygier M., Lawicki S., Gacuta-Szumarska E., Bedkowska E., Szmitkowski M.: “The plasma level of sL-selectin, myeloperoxidase (MPO) and granulocyte-colony stimulating factor (G-CSF) in gynecological cancer patients”. Przegl Lek., 2010, 67, 184. [Article in Polish]

[25] Song M., Santanam N.: “Increased myeloperoxidase and lipid peroxide- modified protein in gynecological malignancies”. Antioxid. Redox. Signal., 2001, 3, 1139.

[26] Lages E.L., Belo A.V., Andrade S.P., Rocha M.A., de Freitas G.F., Lamaita R.M., et al.: “Analysis of systemic inflammatory response in the carcinogenic process of uterine cervical neoplasia”. Biomed. Pharmacother., 2011, 65, 496.

[27] Natter C., Polterauer S., Pils S., Castillo-Tong D.C., Zeilinger R., Heinze G., et al.: “Association of -463G/A MPO gene polymorphism and risk of cervical intraepithelial neoplasia”. Arch. Gynecol. Obstet., 2016, 293, 865

[28] de Castro-Sobrinho J.M., Rabelo-Santos S.H., Fugueiredo-Alves R.R., Derchain S., Sarian L.O., Pitta D.R., et al.: “Bacterial vaginosis and inflammatory response showed association with severity of cervical neoplasia in HPV-positive women”. Diagn. Cytopathol., 2016, 44, 80.

[29] Chu H., Wang M., Wang M., Gu D., Wu D., Zhang Z., et al.: “The MPO -463G>A polymorphism and cancer risk: a meta-analysis based on 43 case-control studies”. Mutagenesis, 2010, 25, 389.

[30] Klebanoff S.J.: “Estrogen binding by leukocytes during phagocytosis”. J. Exp. Med., 1977, 145, 983.

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