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 Table of Contents  
ORIGINAL ARTICLE
Year : 2021  |  Volume : 13  |  Issue : 6  |  Page : 1300-1302  

Determination of role of type 16 human papillomavirus and risk factors in assessing oropharyngeal cancer survival


1 Reader, Department of Oral Medicine Radiology, Hitkarini Dental College and Hospital, Jabalpur, Madhya Pradesh, India
2 Department of Oral Pathology and Microbiology, Dasmesh Institute of Research and Dental Sciences, Faridkot, Punjab, India
3 Department of Periodontics, Desh bhagat Dental College, Mandigobindghar, Punjab, India
4 Assistant professor, Department of ENT, GGS Medical college and Hospital, Faridkot, Punjab, India
5 Department of Oral Medicine Radiology, Hitkarni Dental College and Hospital, Jabalpur, Madhya Pradesh, India
6 Department of Oral Surgery, Bhabha College of Dental Sciences, Bhopal, Madhya Pradesh, India

Date of Submission02-Mar-2021
Date of Decision23-Mar-2021
Date of Acceptance25-Mar-2021
Date of Web Publication10-Nov-2021

Correspondence Address:
Rachna Dhingra
Assistant professor, Department of ENT, GGS Medical College and Hospital, Faridkot, Punjab
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jpbs.jpbs_132_21

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   Abstract 


Background: It is ascertained that the survival rate of patients infected with type 16 human papillomavirus (HPV16) positive is better as compared to those infected with HPV16 negative. The present study was conducted to determine rgw role of HPV16 and risk factors in assessing oropharyngeal cancer (OPC) death. Methodology: A total of 102 clinically and histologically proven cases of oral pharyngeal cancer were included. Seropositivity for HPV16 E6 as a marker of HPV16-positive cancer was estimated. Results: Out of 102 patients, there were 70 males and 32 females. Significant risk factors associated with OPC survival overall in the univariate analysis was female sex (hazard ratio [HR] 0.54, 95% confidence level [CL]: 0.36–80), alcohol use >2 drinks/day (HR 1.54, 95% CL: 1.12–2.08), smoking >10 pack-years (HR 2.20, 95% CL: 1.42–3.58), moderate dental (HR 1.54, 95% CL: 1.02–2.32), underweight (HR 2.24, 95% CL: 1.34–3.60), and Stage IV cancer (HR 2.82, 95% CL: 1.76–4.40). There was significant low risk for death among HPV16 positive (HR 0.48, 95% CL: 0.32–0.70). Conclusion: HPV16 status is an independent prognostic factor for OPC deaths. The common risk factors were female gender, moderate oral care, underweight body mass index, excessive alcohol, and smoking tobacco.

Keywords: Oropharyngeal cancer, smoking tobacco, type 16 human papillomavirus


How to cite this article:
Bhasin M, Singh HP, Singh P, Dhingra R, Kohli SA, Azad A. Determination of role of type 16 human papillomavirus and risk factors in assessing oropharyngeal cancer survival. J Pharm Bioall Sci 2021;13, Suppl S2:1300-2

How to cite this URL:
Bhasin M, Singh HP, Singh P, Dhingra R, Kohli SA, Azad A. Determination of role of type 16 human papillomavirus and risk factors in assessing oropharyngeal cancer survival. J Pharm Bioall Sci [serial online] 2021 [cited 2022 Aug 13];13, Suppl S2:1300-2. Available from: https://www.jpbsonline.org/text.asp?2021/13/6/1300/329941




   Introduction Top


The number of oral pharyngeal cancer is on rise since the last couple of years. It has high mortality and morbidity.[1] It is evident that the main etiological factor in these cases is tobacco and alcohol. Tobacco is consumed in both smoking and smokeless form. Smoking tobacco is the main reason for causing oral cancer.[2] Bidi, cigarette, hookah, hooki, etc., are smoking form of tobacco, whereas gutka, mawa, mishri, pan supari, etc., are smokeless forms. The role of alcohol is synergistic with its ability to cause dryness of oral mucosa, which increases the chances of carcinogen penetration.[3] Apart from these agents, type 16 human papillomavirus (HPV16) in causing oropharyngeal cancers (OPCs) cannot be underestimated. Few cases of cancer involving soft palate, tonsils, tongue, and oropharynx have been found associated with HPV16. Cancer of buccal mucosa is mostly associated with smokeless form of tobacco.[4]

Two different forms of HPV16 occur such as HPV16+ and HPV16−.[5] It is further ascertained that the survival rate of patients infected with HPV+ is better as compared to those infected with HPV−. It is found that HPV DNA and p16 expression determine the HPV status. History of smoking and disease stage help in differentiating patients into prognostic groups.[6] The present study determined role of HPV16 and risk factors in assessing OPC death.


   Methodology Top


The present study comprised 102 clinically and histologically proven cases of oral cancer found in both genders. Cases were enrolled after all agreed to participate in the study.

Demographic data consisted of information such as name, age, and gender. A thorough oral examination was performed. Cancer staging was done and patients were classified into smokers or nonsmokers. Frequency and amount of alcohol consumption (ml) were recorded. Body mass index (BMI) was also determined on the basis of formula (weight [kg] × height [m2]). Patients were classified into normal, underweight, overweight, and obese based on BMI.

Venous blood sample was obtained for the estimation of antibodies to HPV16 E6. HPV genotyping was executed with type-specific E7 polymerase chain reaction bead-based multiplex assay. Results were clubbed together and subjected to statistics for assessing significance of the data based on hazard ratios (HRs) and confidence intervals (CIs).


   Results Top


[Table 1] shows that out of 102 patients, there were 70 males and 32 females.
Table 1: Distribution of patients

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[Table 2] shows that the significant risk factors associated with OPC survival overall in the univariate analysis were female sex (HR 0.54, 95% CL: 0.36–80), alcohol use >2 drinks/day (HR 1.54, 95% CL: 1.12–2.08), smoking >10 pack-years (HR 2.20, 95% CL: 1.42–3.58), moderate dental (HR 1.54, 95% CL: 1.02–2.32), underweight (HR 2.24, 95% CL: 1.34–3.60), and Stage IV cancer (HR 2.82, 95% CL: 1.76–4.40). There was significant low risk for death among HPV16 positive (HR 0.48, 95% CL: 0.32–0.70).
Table 2: Analysis of risk factors in patients

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   Discussion Top


OPC contributes to significant death among various cancers of body.[7] The high use of tobacco among males and females is the leading cause of cancers.[8] It is observed that smoking form of tobacco such as bidi and cigarette increases the risk of cancer.[9] The present study was conducted to determine role of HPV16 and risk factors in assessing OPC death.

In the present study, we found that out of 102 patients, there were 70 (68.6%) males and 32 (31.4%) females. A study by Anantharaman et al.[10] determined factors linked with the outcome of OPC in 321 patients and attempted to consider seropositivity for HPV16 E6 for HPV16-positive cancer marker. The results of the present study demonstrated that there was 50% overall 5-year survival rate in patients. Results revealed that patients diagnosed with HPV16 positive had relatively and significantly low chances of mortality as compared to those diagnosed with HPV16 negative having HR of 0.51 and 95% confidence interval (CI) range of 0.32–0.80. Female gender exhibited a considerable effect on OPC survival with 0.50 HR and 0.29–0.85 95% CI. Similarly, underweight at diagnosis (adjusted HR [aHR]: 2.41, 95% CI: 1.38–4.21) showed effect on OPC survival. Results further showed that a 10-pack–year smoking history was not linked with overall survival (OS). It was observed that Stage III and IV look as the predominant factors significantly related with OPC recurrence (aHR: 4.88, 95% CI: 2.12–11.21).

In the present study, we found that significant risk factors associated with OPC survival overall in the univariate analysis were female sex (HR 0.54, 95% CL: 0.36–80), alcohol use >2 drinks/day (HR 1.54, 95% CL: 1.12–2.08), smoking >10 pack years (HR 2.20, 95% CL: 1.42–3.58), moderate dental (HR 1.54, 95% CL: 1.02–2.32), underweight (HR 2.24, 95% CL: 1.34–3.60), and Stage IV cancer (HR 2.82, 95% CL: 1.76–4.40). We found that there was significant low risk for death among HPV16 positive (HR 0.48, 95% CL: 0.32–0.70). Meng et al.[11] evaluated the association of p16 with OPC in 1470 patients. Results of the study showed that the expression of p16 was present in 5.51% (81) and HPV positive was present in 5.31% (78) of cases. Authors found a positive association between HPV-positive patients and p16 overexpression. It was found that smokers constituted approximately 89% of patients and approximately 70% of patients with p16 expression had the habit of alcoholism. Authors found that early-stage primary oropharyngeal squamous cell carcinomas (OPSCCs) is relatively linked with p16 expression, and similarly, patients with p16 expression showed good survival after being treated with surgery and radiotherapy.

Amini et al.[12] conducted a study by involving 3952 patients out of which 2454 (62%) were HPV positive. Study revealed overall survival rate of 93.1% in HPV positive patients and 77.8% in HPV negative patients. Multimodality treatment comprised chemoradiotherapy (CRT) and Surgery + Radiotherapy but not S-CRT as predictors for improved OS in HPV-positive Stage III–IVB disease. Results further demonstrated that Surgery + Chemotherapy + Radiotherapy was coupled with longer OS in HPV-negative OPSCC-positive patients during multimodality treatment. Similarly, a poor association was observed between lymph node stage with OS in HPV-positive cancers. It was found that the occurrence of positive margins and/or extracapsular extension was connected with worse OS in HPV negative with HR of 2.11 and with significant difference having P = 0.008 but not HPV-positive OPSCC patients (HR 1.61, P = 0.154).

The shortcoming of the study is small sample size.


   Conclusion Top


Authors found that HPV16 status is an independent prognostic factor for OPC deaths. Common risk factors were female gender, moderate oral care, underweight BMI, excessive alcohol, and smoking tobacco.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
   References Top

1.
Mork J, Møller B, Dahl T, Bray F. Time trends in pharyngeal cancer incidence in Norway 1981-2005: A subsite analysis based on a reabstraction and recoding of registered cases. Cancer Causes Control 2010;21:1397-405.  Back to cited text no. 1
    
2.
Mehanna H, Jones TM, Gregoire V, Ang KK. Oropharyngeal carcinoma related to human papillomavirus. BMJ 2010;340:c1439.  Back to cited text no. 2
    
3.
Huang SH, Xu W, Waldron J, Siu L, Shen X, Tong L, et al. Refining American Joint Committee on Cancer/Union for International Cancer Control TNM stage and prognostic groups for human papillomavirus-related oropharyngeal carcinomas. J Clin Oncol 2015;33:836-45.  Back to cited text no. 3
    
4.
Ang KK, Harris J, Wheeler R, Weber R, Rosenthal DI, Nguyen-Tân PF, et al. Human papillomavirus and survival of patients with oropharyngeal cancer. N Engl J Med 2010;363:24-35.  Back to cited text no. 4
    
5.
Lagiou P, Georgila C, Minaki P, Ahrens W, Pohlabeln H, Benhamou S, et al. Alcohol related cancers and genetic susceptibility in Europe: The ARCAGE project: Study samples and data collection. Eur J Cancer Prev 2009;18:76-84.  Back to cited text no. 5
    
6.
Lagiou P, Talamini R, Samoli E, Lagiou A, Ahrens W, Pohlabeln H, et al. Diet and upper-aerodigestive tract cancer in Europe: The ARCAGE study. Int J Cancer 2009;124:2671-6.  Back to cited text no. 6
    
7.
Ahrens W, Pohlabeln H, Foraita R, Nelis M, Lagiou P, Lagiou A, et al. Oral health, dental care and mouthwash associated with upper aerodigestive tract cancer risk in Europe: The ARCAGE study. Oral Oncol 2014;50:616-25.  Back to cited text no. 7
    
8.
Anantharaman D, Gheit T, Waterboer T, Abedi-Ardekani B, Carreira C, McKay-Chopin S, et al. Human papillomavirus infections and upper aero-digestive tract cancers: The ARCAGE study. J Natl Cancer Inst 2013;105:536-45.  Back to cited text no. 8
    
9.
Waterboer T, Sehr P, Michael KM, Franceschi S, Nieland JD, Joos TO, et al. Multiplex human papillomavirus serology based on in situ-purified glutathione stransferase fusion proteins. Clin Chem 2005;51:1845-53.  Back to cited text no. 9
    
10.
Anantharaman D, Billot A, Waterboer T, Gheit T, Abedi-Ardekani B, Lagiou P, et al. Predictors of oropharyngeal cancer survival in Europe. Oral Oncol 2018;81:89-94.  Back to cited text no. 10
    
11.
Meng HX, Miao SS, Chen K, Li HN, Yao G, Geng J, et al. Association of p16 as prognostic factors for oropharyngeal cancer: Evaluation of p16 in 1470 patients for a 16 year study in Northeast China. Biomed Res Int 2018;2018:9594568.  Back to cited text no. 11
    
12.
Amini A, Jasem J, Jones BL, Robin TP, McDermott JD, Bhatia S, et al. Predictors of overall survival in human papillomavirus-associated oropharyngeal cancer using the National Cancer Data Base. Oral Oncol 2016;56:1-7.  Back to cited text no. 12
    



 
 
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