Title: Presence and Positivity of High Risk HPV with Increase in the Severity of Cytological Abnormalities Detected on Pap Smear: A Study of 40 Cases
Authors: Prof. Dr Meena Mittal, Prof. Dr C.V. Kulkarni, Dr Sachin Sharma, Prof. Dr Ashok Panchonia, Dr Ankesh Kumar Jain, Dr Priya Jain
DOI: https://dx.doi.org/10.18535/jmscr/v7i6.117
Abstract
Introduction
Cervical cancer ranked second among most commonly diagnosed cancer and in less developed countries it is third leading cause of cancer related death among females[1,2,3] It is estimated that each year, 527,000 new case occur and 275, 000 deaths. Globally, 15% of all cancer in females is cervical cancer.[2,4]. In India about 20% of all cancer related deaths is due to cervical cancer in women and is the number one cause of death in middle aged Indian women.[5]
Cancer cervix is a multifactorial disease. Human Papilloma virus (HPV) infection is the most important risk factor.[6] It has been shown recently that cervical cancer is strongly associated with the presence of high risk or oncogenic Human Papilloma virus (HPV) types (up to 100%). [7,8] The HPV virus is belongs to the family Papovaviridae, genus papillomavirus.[9,10] having double stranded, circular DNA. The HPV subtypes which specifically affect the anogenital tract are 16, 18, 31, 33, 35, 39, 45,51, 52, 56, 58, 66 and 69. [11]. It is important to understand genomic organization of the virus to understand the oncogenic process induced by HPV that leads to development of cervical dysplasia. Significant regions include the early (E), the late (L),[12] and the long control region (LCR).[13] E6 binds with p53 tumor suppressor gene, causes its degeneration while E7 binds retinoblastoma gene products.[14] thus, inactivation of p53 and pRB leads to cell cycle progression[15] and immortalization of normal cervical cells, so it is the expression of viral oncogenes E6 /E7 which is prerequisite for progression toward malignancy and maintenance of the cancerous phenotype [16,17].As the severity of the lesion increases levels of E6/E7 also rises.[18,19] E6 and E7 transcripts could be useful as markers of disease progression.[18]
Thus, the objective of the study is to evaluate the expression of E6/E7 mRNA of HPV types 16, 18, 31, 33, 35, 39 ,45 , 51, 52, 56 , 58 , 59 , 68 and 82 (which together accounts for 95% of cervical cancer)[4] in cervical samples using flow cytometry and its correlation with epithelial cell abnormalities detected by pap smear
