Authors :
Nidhish P. Hari
Volume/Issue :
Volume 10 - 2025, Issue 11 - November
Google Scholar :
https://tinyurl.com/5n8x9r6n
Scribd :
https://tinyurl.com/yc7dmwd3
DOI :
https://doi.org/10.38124/ijisrt/25nov799
Note : A published paper may take 4-5 working days from the publication date to appear in PlumX Metrics, Semantic Scholar, and ResearchGate.
Note : Google Scholar may take 30 to 40 days to display the article.
Abstract :
Cervical cancer is a significant public health concern, ranking as the second most common cancer among women.
The incidence rate is particularly high in rural areas, with higher mortality rates compared to the global average. Although
screening is common for these cases, the time taken for screening can vary depending on age of patient and the frequencies
produced through each screening can interrupt actual results. Even though the most common cases are found in the age
group between 35 and 44, recent cases show that around 21% are diagnosed in women aged between 20-29. Since the last
decade, around 78% cases were found in women aged 30-39. This lets us pave an opportunity to discover on how the HPV
virus affects different age groups of women and how phytochemicals can reduce the risk of spreading by marking the
proteins with biomarkers that can be easily found by upcoming technologies that target specific cell lines or proteins in a
case.
References :
- Doorbar, J. (2006). Molecular biology of human papillomavirus infection and cervical cancer. Journal of Pathology, 208(2), 152–164. https://doi.org/10.1002/path.1866
- Hopman, A. H., Smedts, F., Dignef, W., Ummelen, M., Sonke, G., Mravunac, M., & Speel, E. J. (2004). Transition from episomal to integrated HPV 16 DNA during the development of cervical carcinoma is a non-random process. Journal of Pathology, 202(1), 23–33. https://doi.org/10.1002/path.1495
- Chung, S. H., Franceschi, S., & Lambert, P. F. (2010). Estrogen and ERα: culprits in cervical cancer? Cancer Research, 70(13), 5389–5397. https://doi.org/10.1158/0008-5472.CAN-09-4149
- Gravitt, P. E. (2012). The known unknowns of HPV natural history. The Lancet Oncology, 13(4), 333–334. https://doi.org/10.1016/S1470-2045(12)70043-0
- Wentzensen, N., Vinokurova, S., & von Knebel Doeberitz, M. (2009). Systematic review of genomic integration sites of human papillomavirus genomes in epithelial dysplasia and invasive cancer of the female lower genital tract. International Journal of Cancer, 124(7), 1575–1584. https://doi.org/10.1002/ijc.24162
- Scheffner M, et al. (1993). The HPV-16 E6 and E6-AP complex functions as a ubiquitin-protein ligase. Cell.
- Münger K, et al. (2004). Mechanisms of human papillomavirus-induced oncogenesis. Oncogene.
- Dyson N, et al. (1989). The human papilloma virus-16 E7 oncoprotein is able to bind to the retinoblastoma gene product. Science.
- McLaughlin-Drubin ME, Münger K. (2009). Oncogenic activities of human papillomaviruses. Journal of Virology.
- Moody CA, Laimins LA. (2010). Human papillomavirus oncoproteins: pathways to transformation. Annual Review of Microbiology.
- Yim EK, Park JS. (2006). The role of HPV E6 and E7 oncoproteins in HPV-associated cervical carcinogenesis. Cancer Letters.
- Saslow D, et al. (2012). American Cancer Society, ASCCP, and ASCP screening guidelines. CA: A Cancer Journal for Clinicians.
- The American College of Obstetricians and Gynecologists (ACOG). (2016). Practice Bulletin No. 157: Cervical Cancer Screening. Obstetrics & Gynecology.
- US Preventive Services Task Force (USPSTF). (2018). Screening for Cervical Cancer. JAMA.
- Perkins RB, et al. (2020). 2020 ASCCP Risk-Based Management Guidelines. Journal of Lower Genital Tract Disease.
- Gravitt PE. (2012). The known unknowns of HPV natural history. The Lancet Oncology.
- Wright TC Jr., et al. (2015). HPV-based cervical cancer screening: Rationale and clinical evidence. Gynecologic Oncology.
- Sankaranarayanan R, et al. (2013). HPV screening for cervical cancer in rural India. New England Journal of Medicine.
- Dyson, N., Guida, P., Munger, K., & Harlow, E. (1989). The human papilloma virus-16 E7 oncoprotein is able to bind to the retinoblastoma gene product. Science, 243(4893),934–937. https://doi.org/10.1126/science.2537532
- Filippova, M., Johnson, M. M., Bautista, M., Filippov, V., Fodor, N., & Tungteakkhun, S. S.(2002).8052–8064. https://doi.org/10.1038/sj.onc.1205942
- Martinez, I., Gardiner, A. S., Board, K. F., Monzon, F. A., Edwards, R. P., & Khan, S. A. (2008). Human papillomavirus type 16 reduces the expression of microRNA-218 in cervical carcinoma cells. Oncogene, 27(18), 2575–2582. https://doi.org/10.1038/sj.onc.1210919
- Scheffner, M., Werness, B. A., Huibregtse, J. M., Levine, A. J., & Howley, P. M. (1990). The E6 oncoprotein encoded by human papillomavirus types 16 and 18 promotes the degradation of p53. Cell, 63(6), 1129–1136. https://doi.org/10.1016/0092-8674(90)90409-8
- Spangle, J. M., & Münger, K. (2010). The human papillomavirus type 16 E6 oncoprotein activates mTORC1 signalling and increases protein synthesis. Journal of Virology, 84(18), 9398–9407. https://doi.org/10.1128/JVI.00844-10
- Thomas, M., & Banks, L. (1998). Inhibition of Bak-induced apoptosis by HPV-18 E6. Oncogene, 17(23), 2943–2954. https://doi.org/10.1038/sj.onc.1202199
- Wang, X., Wang, H. K., McCoy, J. P., Banerjee, N. S., Rader, J. S., Broker, T. R., & Chow, L. T. (2009). Oncogenic HPV infection interrupts the miR-34 regulatory network. The EMBO Journal, 28(22), 3256–3266. https://doi.org/10.1038/emboj.2009.244
- Zheng, Z. M., Wang, X., & Wang, X. (2013). Regulation of apoptosis and autophagy in cervical cancer by HPV. International Journal of Molecular Sciences, 14(2),2435–2456. https://doi.org/10.3390/ijms14022435
- Dyson, N., Guida, P., Munger, K., & Harlow, E. (1989). The human papilloma virus-16 E7 oncoprotein is able to bind to the retinoblastoma gene product. Science, 243(4893), 934–937. https://doi.org/10.1126/science.2537532
- 28.Scheffner, M., Werness, B. A., Huibregtse, J. M., Levine, A. J., & Howley, P. M. (1990). The E6 oncoprotein encoded by human papillomavirus types 16 and 18 promotes the degradation of p53. Cell, 63(6), 1129–1136. https://doi.org/10.1016/0092-8674(90)90409-8
- Spangle, J. M., & Münger, K. (2010). The human papillomavirus type 16 E6 oncoprotein activates mTORC1 signalling and increases protein synthesis. Journal of Virology, 84(18), 9398–9407. https://doi.org/10.1128/JVI.00844-10
- Straight, S. W., Herman, B., & McCance, D. J. (1995). The E5 oncoprotein of human papillomavirus type 16 enhances epidermal growth factor receptor recycling and signalling: Evidence for a role in activation of the ras-MAPK pathway. Proceedings of the National Academy of Sciences, 92(15), 7082–7086. https://doi.org/10.1073/pnas.92.15.7082
- Dyson, N., Guida, P., Munger, K., & Harlow, E. (1989). The human papilloma virus-16 E7 oncoprotein is able to bind to the retinoblastoma gene product. Science, 243(4893), 934–937. https://doi.org/10.1126/science.2537532
- Scheffner, M., Werness, B. A., Huibregtse, J. M., Levine, A. J., & Howley, P. M. (1990). The E6 oncoprotein encoded by human papillomavirus types 16 and 18 promotes the degradation of p53. Cell, 63(6), 1129–1136. https://doi.org/10.1016/0092-8674(90)90409-8
- Spangle, J. M., & Münger, K. (2010). The human papillomavirus type 16 E6 oncoprotein activates mTORC1 signaling and increases protein synthesis. Journal of Virology, 84(18), 9398–9407. https://doi.org/10.1128/JVI.00844-10
- Straight, S. W., Herman, B., & McCance, D. J. (1995). The E5 oncoprotein of human papillomavirus type 16 enhances epidermal growth factor receptor recycling and signaling: Evidence for a role in activation of the ras-MAPK pathway. Proceedings of the National Academy of Sciences, 92(15), 7082–7086. https://doi.org/10.1073/pnas.92.15.7082
- Doorbar, J. (2006). Molecular biology of human papillomavirus infection and cervical cancer. Journal of Pathology, 208(2), 152–164. https://doi.org/10.1002/path.1866
- Hopman, A. H., Smedts, F., Dignef, W., Ummelen, M., Sonke, G., Mravunac, M., & Speel, E. J. (2004). Transition of high-grade cervical intraepithelial neoplasia to micro-invasive carcinoma is characterized by integration of HPV 16/18 DNA and gain of telomerase (hTERT) gene expression. Journal of Pathology, 202(1), 23–33. https://doi.org/10.1002/path.1492
- Chung, S. H., Franceschi, S., & Lambert, P. F. (2010). Estrogen and ERα: Culprits in cervical cancer? Cancer Research, 70(2), 403–408. https://doi.org/10.1158/0008-5472.CAN-09-2264
- Gravitt, P. E. (2012). Evidence and impact of human papillomavirus latency. The Lancet Oncology, 13(3), 199–200. https://doi.org/10.1016/S1470-2045(12)70041-2
- Wentzensen, N., Vinokurova, S., & von Knebel Doeberitz, M. (2009). Systematic review of genomic integration sites of human papillomavirus genomes in epithelial dysplasia and invasive cancer of the female lower genital tract. International Journal of Cancer, 124(6), 1216–1224. https://doi.org/10.1002/ijc.24055
- Stanley, M. (2012). Epithelial cell responses to infection with human papillomavirus. Clinical Microbiology Reviews, 25(2), 215–222. https://doi.org/10.1128/CMR.05028-11
Cervical cancer is a significant public health concern, ranking as the second most common cancer among women.
The incidence rate is particularly high in rural areas, with higher mortality rates compared to the global average. Although
screening is common for these cases, the time taken for screening can vary depending on age of patient and the frequencies
produced through each screening can interrupt actual results. Even though the most common cases are found in the age
group between 35 and 44, recent cases show that around 21% are diagnosed in women aged between 20-29. Since the last
decade, around 78% cases were found in women aged 30-39. This lets us pave an opportunity to discover on how the HPV
virus affects different age groups of women and how phytochemicals can reduce the risk of spreading by marking the
proteins with biomarkers that can be easily found by upcoming technologies that target specific cell lines or proteins in a
case.