{"title":"Detection of transcriptionally active high-risk human papillomavirus in patients with oesophageal carcinoma by real-time PCR.","authors":"Shravya Kotian, Pushkal S Ramesh, Jayaprakash Shetty, Kishan Prasad Hosapatna Laxminarayana, Veena Shetty, Devanand Devegowda","doi":"10.4103/jcrt.jcrt_1226_22","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Oesophageal malignancies (OC) are the sixth most common cause of cancer-related mortality worldwide. Traditional risk factors for OC include smoking, alcohol consumption, and poorly controlled acid reflux; however, the trends in the last decade have pointed out the potential carcinogenic roles of infectious agents, especially Human Papillomavirus (HPV), in the development of OC. The prevalence of HPV infection in OC varies greatly worldwide, mainly due to the inconsistencies of the detection assays employed. This study attempted to establish the association between high-risk HPV and oesophageal malignancies by detecting the transcriptionally active HPV mRNA.</p><p><strong>Materials and methods: </strong>In this cross-sectional study, 30 malignant oesophageal samples were subjected to real-time PCR to detect high-risk HPV-16 and 18 by targeting transcriptionally active E6/E7 genes. The positive samples were further subjected to viral load assessment.</p><p><strong>Results: </strong>Histopathological analysis of the patients showed that a moderately differentiated squamous cell carcinoma was seen in 56.2% of the cases. Of the 30 samples, 4 (13.3%) showed positive for HPV-16 E6/E7, and none showed positive for HPV-18 E6/E7. The viral load of HPV-16 E6/E7 in the positive samples was lesser than the copies present in the well-established cell line, SiHa.</p><p><strong>Conclusion: </strong>The role of HPV in the etiopathogenesis of oesophageal malignancies is unclear. Based on this study and the supporting data presented, it can be said that the association of high-risk HPV infection in oesophageal cancers does exist, but whether it is clinically and etiologically significant is the question that needs to be answered. Multicenter studies from different geographical locations, employing multiple molecular methods with a larger sample size, could aid in a better understanding of the etiopathogenesis of HPV in OC.</p>","PeriodicalId":94070,"journal":{"name":"Journal of cancer research and therapeutics","volume":"20 5","pages":"1440-1445"},"PeriodicalIF":0.0000,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of cancer research and therapeutics","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.4103/jcrt.jcrt_1226_22","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/1/22 0:00:00","PubModel":"Epub","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Background: Oesophageal malignancies (OC) are the sixth most common cause of cancer-related mortality worldwide. Traditional risk factors for OC include smoking, alcohol consumption, and poorly controlled acid reflux; however, the trends in the last decade have pointed out the potential carcinogenic roles of infectious agents, especially Human Papillomavirus (HPV), in the development of OC. The prevalence of HPV infection in OC varies greatly worldwide, mainly due to the inconsistencies of the detection assays employed. This study attempted to establish the association between high-risk HPV and oesophageal malignancies by detecting the transcriptionally active HPV mRNA.
Materials and methods: In this cross-sectional study, 30 malignant oesophageal samples were subjected to real-time PCR to detect high-risk HPV-16 and 18 by targeting transcriptionally active E6/E7 genes. The positive samples were further subjected to viral load assessment.
Results: Histopathological analysis of the patients showed that a moderately differentiated squamous cell carcinoma was seen in 56.2% of the cases. Of the 30 samples, 4 (13.3%) showed positive for HPV-16 E6/E7, and none showed positive for HPV-18 E6/E7. The viral load of HPV-16 E6/E7 in the positive samples was lesser than the copies present in the well-established cell line, SiHa.
Conclusion: The role of HPV in the etiopathogenesis of oesophageal malignancies is unclear. Based on this study and the supporting data presented, it can be said that the association of high-risk HPV infection in oesophageal cancers does exist, but whether it is clinically and etiologically significant is the question that needs to be answered. Multicenter studies from different geographical locations, employing multiple molecular methods with a larger sample size, could aid in a better understanding of the etiopathogenesis of HPV in OC.