Smokeless tobacco increases aneuploidy in oral <scp>HPV</scp>16 E6/E7‐transformed keratinocytes <i>in vitro</i>

Merne, Marina; Rautava, Jaana; Ruutu, Merja; Syrjänen, Stina

doi:10.1111/jop.12185

Cited by 7 publications

(9 citation statements)

References 46 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Probably, there is a correlation between smoking and HPV 16 infection on the one hand and oropharyngeal squamous cell carcinoma, on the other [ 32 ]. Merne et al [ 33 ] suggest a possible synergy between tobacco components and viral oncogenes, especially HPV16 E6/E7 in transformation of oral epithelial cells. Studies by Haukioja et al [ 34 ] found out that smoking is a risk factor for a persistent oral HPV infection.…”

Section: Discussionmentioning

confidence: 99%

Prevalence of Human papillomavirus (HPV) and Epstein-Barr virus (EBV) in oral and oropharyngeal squamous cell carcinoma in south-eastern Poland

Polz-Gruszka

Morshed

Polz‐Dacewicz

2015

Infect Agents Cancer

View full text Add to dashboard Cite

ObjectiveThe aim of this study was to analyze the prevalence of HPV and EBV in oral and oropharyngeal squamous cell carcinoma in south-eastern Poland. The correlation between viral infection, OSCC, alcohol use, tobacco smoking, demographic data (gender, age, place of residence), anatomic location, pre-treatment staging, evidence of metastases to lymph nodes, and grading was also investigated.MethodsThe examination samples were collected from paraffin tissue blocks, from 154 patients. Viral DNA was amplified by the nested-PCR method.ResultsHPV DNA was detected in 29.2 % of the tested samples (in 27.4 % of oropharyngeal and in 30.4 % of oral cavity). The HPV type 16 was detected in 15.6 % of all samples, and in 53.3 % of HPV-positive group. In HPV-positive samples from oropharyngeal HPV 16 constitute 76.5 %, and in HPV-positive samples from oral cavity HPV 16 constitute 39.3 %. Mixed infection (more than one type of HPV) was observed in 23.5 and 60.7 %, respectively, and in 46.7 % of all HPV-positive samples, and in 12.3 % of the whole study group. EBV DNA was detected in 27.3 % of the cases and HPV-EBV co-infection in 7.8 % of samples.ConclusionsIn major patients from Southeastern region of Poland with oropharyngeal cancer HPV type 16 was detected but in oral cavity cancer other mixed infections were observed (i.e. 51, 52, 59, 66, 68, 71, 74). HPV 16 was detected more often among patients younger than 50 years of age, whereas the mixed HPV in the group aged 50–59. The pathogenesis of oral squamous cell carcinoma may be connected with EBV infection. Future studies on the mechanisms of HPV/EBV co-infection and/or superinfection and their role in oral squamous cell carcinoma are necessary.

show abstract

Section: Discussionmentioning

confidence: 99%

Prevalence of Human papillomavirus (HPV) and Epstein-Barr virus (EBV) in oral and oropharyngeal squamous cell carcinoma in south-eastern Poland

Polz-Gruszka

Morshed

Polz‐Dacewicz

2015

Infect Agents Cancer

View full text Add to dashboard Cite

show abstract

“…In a group of HPV-positive patients with oropharyngeal cancer, the risk of death increased significantly with pack-years of tobacco smoking [ 70 ]. The risk of neoplastic transformation is increased by tobacco products, which could potentiate the effects of HPV 16 [ 71 ], and smoking significantly increased the risk of persistent oral HPV infection, which, in turn, might increase the risk of cancer [ 72 ]. Head and neck epithelium is often exposed to tobacco carcinogens and might interact with HPV to stimulate neoplastic lesions [ 71 ].…”

Section: Discussionmentioning

confidence: 99%

“…HPV detection and identification of subtypes were performed by GenoFlow HPV (Human Papillomavirus) Array Test Kits (DiagCor Bioscience Inc., Hong Kong) which use biotin-labeled primers, specific probes, PCR and "flow-through" hybridization technology, which allows detection of 33 common HPV subtypes. The following are considered highrisk (16,18,31,33,35,39,45,51,52,53,56,58,59,66,68,73,82) and low-risk (6,11,26,40,42,43,44,54,55,57,61,70,71,72,81,84) subtypes based on their phylogenetic and epidemiological criteria and the biological niche. The extracted DNA was mixed with PCR reagent mix and DNA Taq Polymerase provided with the kit and amplified using a Mastercycler Personal Thermal Cycler (Eppendorf, Hamburg, Germany) according to the manufacturer's protocol.…”

Section: Hpv Detection and Type Determinationmentioning

confidence: 99%

The Prevalence of High- and Low-Risk Types of HPV in Patients with Squamous Cell Carcinoma of the Head and Neck, Patients with Chronic Tonsillitis, and Healthy Individuals Living in Poland

et al. 2021

View full text Add to dashboard Cite

Human papillomavirus (HPV) is a virus with the potential to infect human epithelial cells and an etiological agent of many types of cancer, including head and neck cancer. The aim of the study was to determine the prevalence of HPV infection in patients with head and neck squamous cell carcinoma (HNSCC), patients with chronic tonsillitis, and healthy individuals, and to establish high- and low-risk HPV genotypes in these groups. The objectives also comprised the delineation of the relationship between the infection with high- or low-risk HPV subtypes and clinicopathological and demographic characteristics of the study groups. This study was composed of 76 patients diagnosed with HNSCC, 71 patients with chronic tonsillitis, and 168 cases without either of these conditions (the control group). HPV detection and identification of subtypes were performed on isolated DNA using a test which allowed detection of 33 common high-risk and low-risk HPV subtypes. The prevalence of HPV infection was 42.1%, 25.4%, and 37.5% in HNSCC, chronic tonsillitis, and control groups, respectively. HPV 16 was the most prevalent genotype in all groups and the non-oncogenic HPV 43/44 was frequent in HNSCC patients. This analysis provides insight into the prevalence of oral oncogenic and non-oncogenic HPVs in patients with head and neck cancer, patients with chronic tonsillitis and healthy individuals, and leads to the conclusion that further investigations are warranted to examine a larger cohort of patients focusing on high- and low-risk HPV genotypes. Efforts should be focused on screening and prevention strategies, and therefore, it is important to introduce tools for effective detection of HPV genotypes. Furthermore, given the role of vaccines against oral HPV infection, our observations lead to the suggestion that HPV vaccination should be of considerable importance in public health strategies.

show abstract

“…There is increasing epidemiological evidence to suggest synergism between tobacco carcinogens and HPV infection in cancer induction [16][17][18][19][20]33,34]. Furthermore, synergism between tobacco carcinogens and hr-HPV was also observed in in vitro experiments using human cells derived from cervical, lung, and oral cancers [35][36][37][38][39][40][41]. AP, a typical flavonoid with low toxicity and multiple beneficial bioactivities, has been evaluated as a promising candidate for chemoprevention against a variety of cancers.…”

Section: Discussionmentioning

confidence: 99%

Chemopreventive Role of Apigenin against the Synergistic Carcinogenesis of Human Papillomavirus and 4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone

et al. 2020

View full text Add to dashboard Cite

Tobacco smoke and human papillomavirus (HPV) are both crucial causes of cancer, and their cooperative carcinogenesis has drawn more attention in recent years. Apigenin (AP), a typical flavonoid abundantly found in flowers of plants, vegetables, and fruits, has been demonstrated to exert an anti-carcinogenic effect on various types of cancer. In this study, we investigated the capability of AP against malignant transformation and DNA damage of immortalized human esophageal epithelial (SHEE) cells induced by the synergism of HPV18 and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK). The results indicated that the enhancement of migration, invasion, and proliferation ability of SHEE cells induced by HPV and NNK could be effectively inhibited by AP. Moreover, the levels of pyridyloxybutylated (POB)-DNA adducts induced by NNK via P450-catalyzed metabolic activation could also be significantly suppressed by AP. Further analyses on the molecular mechanism revealed that AP inhibited the synergistic carcinogenesis of NNK and HPV on SHEE cells by reducing the expression of mutp53, CDK4, Cyclin D1, and p-Rb (Ser 780), increasing caspase-3 activity, thereby arresting the cell cycle at G1 phase and promoting apoptosis of SHEE cells. We hypothesize that the decrease in NNK-induced POB-DNA adduct levels is related to the deactivation of P450 by AP, which needs to be confirmed in future studies. This study highlights that AP may be employed as a promising chemopreventive agent against cancers in smokers with an HPV infection.

show abstract

Smokeless tobacco increases aneuploidy in oral HPV16 E6/E7‐transformed keratinocytes in vitro

Cited by 7 publications

References 46 publications

Prevalence of Human papillomavirus (HPV) and Epstein-Barr virus (EBV) in oral and oropharyngeal squamous cell carcinoma in south-eastern Poland

Prevalence of Human papillomavirus (HPV) and Epstein-Barr virus (EBV) in oral and oropharyngeal squamous cell carcinoma in south-eastern Poland

The Prevalence of High- and Low-Risk Types of HPV in Patients with Squamous Cell Carcinoma of the Head and Neck, Patients with Chronic Tonsillitis, and Healthy Individuals Living in Poland

Chemopreventive Role of Apigenin against the Synergistic Carcinogenesis of Human Papillomavirus and 4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone

Contact Info

Product

Resources

About