Dataset Information

Combined effects of smoking and HPV16 in oropharyngeal cancer.

ABSTRACT: Although smoking and HPV infection are recognized as important risk factors for oropharyngeal cancer, how their joint exposure impacts on oropharyngeal cancer risk is unclear. Specifically, whether smoking confers any additional risk to HPV-positive oropharyngeal cancer is not understood.Using HPV serology as a marker of HPV-related cancer, we examined the interaction between smoking and HPV16 in 459 oropharyngeal (and 1445 oral cavity and laryngeal) cancer patients and 3024 control participants from two large European multi-centre studies. Odds ratios and credible intervals [CrI], adjusted for potential confounders, were estimated using Bayesian logistic regression.Both smoking [odds ratio (OR [CrI]: 6.82 [4.52, 10.29]) and HPV seropositivity (OR [CrI]: 235.69 [99.95, 555.74]) were independently associated with oropharyngeal cancer. The joint association of smoking and HPV seropositivity was consistent with that expected on the additive scale (synergy index [CrI]: 1.32 [0.51, 3.45]), suggesting they act as independent risk factors for oropharyngeal cancer.Smoking was consistently associated with increase in oropharyngeal cancer risk in models stratified by HPV16 seropositivity. In addition, we report that the prevalence of oropharyngeal cancer increases with smoking for both HPV16-positive and HPV16-negative persons. The impact of smoking on HPV16-positive oropharyngeal cancer highlights the continued need for smoking cessation programmes for primary prevention of head and neck cancer.

SUBMITTER: Anantharaman D

PROVIDER: S-EPMC5841602 | biostudies-literature | 2016 Jun

REPOSITORIES: biostudies-literature

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Combined effects of smoking and HPV16 in oropharyngeal cancer.

Anantharaman Devasena D Muller David C DC Lagiou Pagona P Ahrens Wolfgang W Holcátová Ivana I Merletti Franco F Kjærheim Kristina K Polesel Jerry J Simonato Lorenzo L Canova Cristina C Castellsague Xavier X Macfarlane Tatiana V TV Znaor Ariana A Thomson Peter P Robinson Max M Conway David I DI Healy Claire M CM Tjønneland Anne A Westin Ulla U Ekström Johanna J Chang-Claude Jenny J Kaaks Rudolf R Overvad Kim K Drogan Dagmar D Hallmans Göran G Laurell Göran G Bueno-de-Mesquita H B HB Peeters Petra H PH Agudo Antonio A Larrañaga Nerea N Travis Ruth C RC Palli Domenico D Barricarte Aurelio A Trichopoulou Antonia A George Saitakis S Trichopoulos Dimitrios D Quirós J Ramón JR Grioni Sara S Sacerdote Carlotta C Navarro Carmen C Sánchez María-José MJ Tumino Rosario R Severi Gianluca G Boutron-Ruault Marie-Christine MC Clavel-Chapelon Francoise F Panico Salvatore S Weiderpass Elisabete E Lund Eiliv E Gram Inger T IT Riboli Elio E Pawlita Michael M Waterboer Tim T Kreimer Aimée R AR Johansson Mattias M Brennan Paul P

International journal of epidemiology 20160519 3

<h4>Background</h4>Although smoking and HPV infection are recognized as important risk factors for oropharyngeal cancer, how their joint exposure impacts on oropharyngeal cancer risk is unclear. Specifically, whether smoking confers any additional risk to HPV-positive oropharyngeal cancer is not understood.<h4>Methods</h4>Using HPV serology as a marker of HPV-related cancer, we examined the interaction between smoking and HPV16 in 459 oropharyngeal (and 1445 oral cavity and laryngeal) cancer pat ...[more]

PMID: 27197530

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Project description:Background: Anti-epidermal-growth-factor-receptor (EGFR) therapies in combination with radiotherapy are being studied on de-escalation clinical trials for HPV-related oropharyngeal cancer (OPC) patients. The HPV16-E5 oncoprotein increases recycling of activated EGFR to the cell surface, enhancing factor signal transduction. Our aim was to evaluate viral HPV16-E5 oncogene expression as well as EGFR and phosphorylated-EGFR (pEGFR), protein levels as biomarkers for clinical outcome in a retrospective cohort of OPC patients. Methods: Formalin-fixed-paraffin-embedded OPCs were collected from 1990 to 2013. OPC samples containing HPV-DNA were subject to viral E6 * I mRNA detection and p16INK4a immunohistochemistry (IHC). HPV16-positive cases were evaluated for HPV16-E5 (RT-PCR) and EGFR/pEGFR (IHC). A stratified and matched random sample of HPV-negative samples was used as control and evaluated for EGFR/pEGFR. Overall survival (OS) and disease free survival (DFS) estimates were assessed for locally advanced OPC patients (stage III, IVa,b 7th edition). Results: Among 788 OPC patient samples, 53 were double positive for HPV16-DNA/p16INK4a. HPV16-E5 expression was found in 41 of 53 samples (77.4%). EGFR expression was observed in 37.7 vs 70.8% of HPV16-positive vs HPV-negative samples, respectively; (adjusted OR = 0.15) 5% CI = 0.04-0.56]). Expression of pEGFR followed an inverse pattern with 39.6 and 24.9% detection in HPV16-positive and HPV-negative samples; (adjusted OR = 1.58 [95% CI = 0.48-5.17]). Within HPV16-positive cases, no association between HPV16-E5/EGFR nor pEGFR was observed. With a median follow-up of 39.36 months (min = 0.03 - max = 272.07), the combination of HPV status and EGFR or pEGFR expression were predictors of better OS (p < 0.001, for both) and DFS (p < 0.001 for EGFR and p = 0.003 for pEGFR). Conclusions: HPV16-E5 is highly expressed on HPV16-positive OPCs. Interestingly, HPV16-positive cases expressed significantly more pEGFR while HPV-negative cases expressed more EGFR. The combinations of HPV status and EGFR or pEGFR may be useful biomarkers for evaluating prognosis outcome in OPC patients.

Dataset Information

Combined effects of smoking and HPV16 in oropharyngeal cancer.

Publications

Combined effects of smoking and HPV16 in oropharyngeal cancer.

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