Relationship among Tobacco Habits, Human Papilloma Virus (HPV) Infection, p53 Polymorphism/Mutation, and the Risk of Oral Squamous Cell Carcinoma
Background: Oral squamous cell carcinoma (OSCC) is a multifactorial malignancy influenced by various genetic and environmental factors. Tobacco habits, human papilloma virus (HPV) infection, and p53 polymorphisms or mutations have been implicated in its etiology. Understanding their interplay can pr...
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| Format: | Article |
| Language: | English |
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Wolters Kluwer Medknow Publications
2024-12-01
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| Series: | Journal of Pharmacy and Bioallied Sciences |
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| Online Access: | https://journals.lww.com/10.4103/jpbs.jpbs_903_24 |
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| author | Neha Gupta Gargi Yumnam Chetan Sharma Avani Patel Ripudaman Sharma Sachin Dev Mahesh Ghadage |
| author_facet | Neha Gupta Gargi Yumnam Chetan Sharma Avani Patel Ripudaman Sharma Sachin Dev Mahesh Ghadage |
| author_sort | Neha Gupta |
| collection | DOAJ |
| description | Background:
Oral squamous cell carcinoma (OSCC) is a multifactorial malignancy influenced by various genetic and environmental factors. Tobacco habits, human papilloma virus (HPV) infection, and p53 polymorphisms or mutations have been implicated in its etiology. Understanding their interplay can provide insights into OSCC risk assessment.
Materials and Methods:
A case–control study was conducted among 300 OSCC patients and 300 age- and sex-matched controls. Data on tobacco use (smoking and smokeless), HPV infection status (detected via PCR), and p53 polymorphism/mutation (analyzed by sequencing) were collected. Statistical analysis included logistic regression to assess the associations and interactions among these variables.
Results:
Among OSCC cases, 75% were tobacco users compared to 35% in controls. HPV prevalence was significantly higher in OSCC cases (30%) than controls (5%). P53 mutations were identified in 40% of OSCC cases compared to 10% in controls. Logistic regression revealed synergistic effects between tobacco use and HPV infection (OR 5.2, 95% CI 3.0–9.0) and additive effects with p53 mutations (OR 3.5, 95% CI 2.0–6.0).
Conclusion:
Tobacco habits, HPV infection, and p53 polymorphisms/mutations independently and synergistically contribute to the risk of OSCC. Strategies focusing on tobacco cessation, HPV vaccination, and genetic screening may help mitigate OSCC risk in susceptible populations. |
| format | Article |
| id | doaj-art-a9dd0c838a9a401fa5c3d8e38f5e22a4 |
| institution | Kabale University |
| issn | 0976-4879 0975-7406 |
| language | English |
| publishDate | 2024-12-01 |
| publisher | Wolters Kluwer Medknow Publications |
| record_format | Article |
| series | Journal of Pharmacy and Bioallied Sciences |
| spelling | doaj-art-a9dd0c838a9a401fa5c3d8e38f5e22a42025-01-13T09:50:06ZengWolters Kluwer Medknow PublicationsJournal of Pharmacy and Bioallied Sciences0976-48790975-74062024-12-0116Suppl 4S3424S342610.4103/jpbs.jpbs_903_24Relationship among Tobacco Habits, Human Papilloma Virus (HPV) Infection, p53 Polymorphism/Mutation, and the Risk of Oral Squamous Cell CarcinomaNeha GuptaGargi YumnamChetan SharmaAvani PatelRipudaman SharmaSachin DevMahesh GhadageBackground: Oral squamous cell carcinoma (OSCC) is a multifactorial malignancy influenced by various genetic and environmental factors. Tobacco habits, human papilloma virus (HPV) infection, and p53 polymorphisms or mutations have been implicated in its etiology. Understanding their interplay can provide insights into OSCC risk assessment. Materials and Methods: A case–control study was conducted among 300 OSCC patients and 300 age- and sex-matched controls. Data on tobacco use (smoking and smokeless), HPV infection status (detected via PCR), and p53 polymorphism/mutation (analyzed by sequencing) were collected. Statistical analysis included logistic regression to assess the associations and interactions among these variables. Results: Among OSCC cases, 75% were tobacco users compared to 35% in controls. HPV prevalence was significantly higher in OSCC cases (30%) than controls (5%). P53 mutations were identified in 40% of OSCC cases compared to 10% in controls. Logistic regression revealed synergistic effects between tobacco use and HPV infection (OR 5.2, 95% CI 3.0–9.0) and additive effects with p53 mutations (OR 3.5, 95% CI 2.0–6.0). Conclusion: Tobacco habits, HPV infection, and p53 polymorphisms/mutations independently and synergistically contribute to the risk of OSCC. Strategies focusing on tobacco cessation, HPV vaccination, and genetic screening may help mitigate OSCC risk in susceptible populations.https://journals.lww.com/10.4103/jpbs.jpbs_903_24human papilloma virusoral squamous cell carcinomatobacco habits |
| spellingShingle | Neha Gupta Gargi Yumnam Chetan Sharma Avani Patel Ripudaman Sharma Sachin Dev Mahesh Ghadage Relationship among Tobacco Habits, Human Papilloma Virus (HPV) Infection, p53 Polymorphism/Mutation, and the Risk of Oral Squamous Cell Carcinoma Journal of Pharmacy and Bioallied Sciences human papilloma virus oral squamous cell carcinoma tobacco habits |
| title | Relationship among Tobacco Habits, Human Papilloma Virus (HPV) Infection, p53 Polymorphism/Mutation, and the Risk of Oral Squamous Cell Carcinoma |
| title_full | Relationship among Tobacco Habits, Human Papilloma Virus (HPV) Infection, p53 Polymorphism/Mutation, and the Risk of Oral Squamous Cell Carcinoma |
| title_fullStr | Relationship among Tobacco Habits, Human Papilloma Virus (HPV) Infection, p53 Polymorphism/Mutation, and the Risk of Oral Squamous Cell Carcinoma |
| title_full_unstemmed | Relationship among Tobacco Habits, Human Papilloma Virus (HPV) Infection, p53 Polymorphism/Mutation, and the Risk of Oral Squamous Cell Carcinoma |
| title_short | Relationship among Tobacco Habits, Human Papilloma Virus (HPV) Infection, p53 Polymorphism/Mutation, and the Risk of Oral Squamous Cell Carcinoma |
| title_sort | relationship among tobacco habits human papilloma virus hpv infection p53 polymorphism mutation and the risk of oral squamous cell carcinoma |
| topic | human papilloma virus oral squamous cell carcinoma tobacco habits |
| url | https://journals.lww.com/10.4103/jpbs.jpbs_903_24 |
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