Genetic polymorphisms of CYP3A4*1B of cervical cancer patients in Bangladeshi population, Bangladesh

Shamim Md. Abdullah, Hossain Md. Shafayat, Sazib Md. Saifuzzaman, Shahariar Md. Fahim, Hossain Md. Golam


Background: Cervical cancer incidence rate in Bangladesh is 15.9 and age-standardized incidence rate is 19.2 (rates per 1,00,000 women per year). Polymorphisms of different genes have been affirmed to be associated with cervical cancer. Our prime purpose is to observe whether CYP3A4*1B polymorphisms are related with increasing cervical cancer risk in Bangladeshi population. The compilation of precise clinical information allows the clarity of different clinical phenotypes, which play a vital role in genetic studies of cervical cancer.

Methods: The study was a case-control study carried out between patients and volunteers matched by age, sex, height, weight and smoking status. Daly’s chemical method was used to isolate genomic DNA from venous blood. The demographic variables of cases and controls were put side by side using chi-square tests and Student’s t tests.

Results: Odds ratio and 95 % confidence interval were assigned to estimate the risk of cervical cancer. CYP3A4*1B polymorphisms and cervical cancer risk do not show any considerable relationship. The polymorphic frequencies of CYP3A4*1B allele (normal homozygote, heterozygote and mutant homozygote) in cervical cancer were 60%, 40% and 0% respectively; frequencies in control were 66.67%, 33.33% and 0% respectively (p<0.05). Finally, we conclude that CYP3A4*1B polymorphisms is not associated in susceptibility to developing cervical cancer, at least in Bangladeshi population.

Conclusions: In brief, the consequences of our study demonstrated that CYP3A4*1B polymorphism is not allied in susceptibility to develop cervical cancer, at least in Bangladeshi women.


Genetic polymorphism, CYP3A4*1B, Cervical cancer, DNA, Restriction enzyme

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Pisani P, Bray F, Parkin DM. Estimates of the world-wide prevalence of cancer for 25 sites in the adult population. Int J Cancer. 2002;97:72-81.

Bruni L, Barrionuevo-Rosas L, Albero G, Aldea M, Serrano B, Valencia S, et al. Human papillomavirus and related diseases report. ICO Information Centre on HPV and Cancer (HPV Information Centre). 2015. Available at:

Nesrin REIS, Nezihe K. BEJI, Dilek KILIC. Risk Factors for Cervical Cancer: Results from a Hospital-Based Case-Control Study. Intern J Hematol Oncol. 2015;21:1539.

Zur Hausen H. Papillomaviruses and cancer: from basic studies to clinical application. Nat Rev Cancer 2002;2:342-50.

Walboomers JM, Jacobs MV, Manos MM, Bosch FX, Kummer JA, Shah KV, et al. Human papillomavirus is a necessary cause of invasive cervical cancer worldwide. J Pathol. 1999;189:12-9.

Castellsagué X, Pawlita M, Roura E, Margall N, Waterboer T, Bosch FX, et al. Prospective seroepidemiologic study on the role of Human Papillomavirus and other infections in cervical carcinogenesis: evidence from the EPIC cohort. Int J Cancer. 2014;135(2):440-52.

Gierisch JM, Coeytaux RR, Urrutia RP, Havrilesky LJ, Moorman PG, Lowery WJ, et al. Oral contraceptive use and risk of breast, cervical, colorectal, and endometrial cancers: a systematic review. Cancer Epidemiol Biomarkers Prev. 2013;22(11):1931-43.

Vaccarella S, Herrero R, Snijders PJ, Dai M, Thomas JO, Hieu NT, et al. Smoking and human papillomavirus infection: pooled analysis of the International Agency for Research on Cancer HPV Prevalence Surveys. Int J Epidemiol. 2008;37(3):536-46.

Jégu J, Colonna M, Daubisse-Marliac L, Trétarre B, Ganry O, Guizard AV, et al. The effect of patient characteristics on second primary cancer risk in France. BMC Cancer. 2014;15(14):94.

Nielsen SF, Nordestgaard BG. Associations between first and second primary cancers: a population-based study. CMAJ. 2012;184(1):57-69.

Hussain SK, Sundquist JJ, Hemminki K. Familial clustering of cancer at human papillomavirus-associated sites according to the Swedish Family-Cancer Database. Int J Cancer. 2008;122(8):1873-8.

Gakidou E, Nordhagen S, Obermeyer Z. Coverage of Cervical Cancer Screening in 57 Countries: Low Average Levels and Large Inequalities. PLoS Medicine. 2008;5(6):863-8.

Dally H, Edler L, Jäger B, Schmezer P, Spiegelhalder B, Dienemann H, et al. The CYP3A4*1B allele increases risk for small cell lung cancer: effect of gender and smoking dose. Pharmacogenetics. 2003;10:607-18.

Zhou LP, Yao F, Luan H, Wang YL, Dong XH, Zhou WW, et al. CYP3A4*1B polymorphism and cancer risk. Tumor Biology. 2013;34(2):649-60.

Spurdle AB, Goodwin B, Hodgson E, Hopper JL, Chen X, Purdie DM, et al. The CYP3A4*1B polymorphism has no functional significance and is not associated with risk of breast or ovarian cancer. Pharmacogenetics and Genomics. 2002;12(50):355-66.

Keshava C, McCanlies EC, Weston A. CYP3A4 Polymorphisms-Potential Risk Factors for Breast and Prostate Cancer. American Journal of Epidemiology. 2004;160 (9):825-41.

Maruf AA, Ahmed MU, Azad MAK, Ahmed M, Hasnat A. CYP3A Genotypes in Bangladeshi Tuberculosis Patients. Bangladesh Medical Research Council Bulletin. 2012;38:1-5.

Daly AK, Monkman SC, Smart J, Steward A, Cholerton S. Analysis of cytochrome P450 polymorphisms. Methods in Molecular Biology. 1998;107:405-22.