HPV Research Papers - Academia.edu (original) (raw)

Objective: CDKN1A encodes for cyclin-dependent kinase inhib-itor 1A, which plays an important role in cell cycle regulation and apoptosis. The c.93C>A polymorphism of CDKN1A causes a serine-to-arginine substitution in the protein product, which could potentially influence its functionality. In this study, we investigated the association between CDKN1A c.93C>A polymorphism and cervical cancer risk. Material and Methods: The polymorphism was genotyped on 95 histopathologically confirmed cervical cancer patients and 95 cancer-free female controls by using PCR-RFLP technique. The risk association was evaluated by using logistic regression analysis. The finding was further stratified by self-reported ethnicity and human papillomavirus (HPV) type present in cervical smear of the subjects, as determined by using a flow-through hybridization method. Results: By using the wild type genotype as reference, we found no significant association between the polymorphism and cervical cancer risk (heterozygous OR = 0.821, 95% CI = 0.418–1.612, P = 0.57; homozygous variant OR = 0.936, 95% CI = 0.406–2.156, P = 0.88). A similar absence of significant association was observed when the results were stratified by the ethnicity of the study subjects (Malay, heterozygous P = 0.93, homozygous variant P = 0.78; Chinese, heterozygous P = 0.09, homozygous variant P = 0.31). Likewise, lack of association was observed when the results were stratified by HPV types (HPV-16, heterozygous P = 0.16, homozy-gous variant P = 0.08; HPV-18, heterozygous P = 0.13, homozygous variant P = 0.79; other minor HPV types, heterozygous P = 0.41, homozygous variant P = 0.29; HPV negative, heterozygous P = 0.91, homozygous variant P = 0.47; multiple HPV types, heterozygous P = 0.24, homozygous variant P = 0.31). Conclusion: In conclusion, the present study suggests a lack of association between CDKN1A c.93C>A polymorphism and cervical cancer risk.