Increasing rates of low-risk human papillomavirus infections in patients with oral cavity squamous cell carcinoma: Association with clinical outcomes

Lee, Li‐Ang; Huang, Chi‐Che; Tsao, Kuo‐Chien; Liao, Chun‐Ta; Kang, Chung‐Jan; Chang, Kuo‐Hsuan; Huang, Shiang‐Fu; Chen, I-How; Fang, Tuan‐Jen; Li, Hsueh‐Yu; Yang, Shu-Li; Hsueh, Chuen; Chen, Tse–Ching; Lin, Chien‐Tai; Fan, Kang‐Hsing; Wang, Hung‐Ming; Chang, Yu‐Cheng; Lai, Chyong‐Huey; Shih, Shin‐Ru; Yen, Tzu‐Chen

doi:10.1016/j.jcv.2013.04.010

Cited by 29 publications

(35 citation statements)

References 32 publications

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“…Tobacco consumption is defined as current smoking of at least 1 cigarette per day during the latest 3 mo. HPV infection was not taken in consideration in the present study, due to a relatively low prevalence in our and others' samples (Lee et al 2013) in Taiwan, although HPV infections have been causally linked to OSCC.…”

Section: Demographic Informationmentioning

confidence: 90%

RAGE Gene Polymorphism and Environmental Factor in the Risk of Oral Cancer

Chien

Lin

et al. 2015

J Dent Res

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Oral squamous cell carcinoma is a common neoplasm that is known to be causally associated with genetic factors and environmental carcinogens. The receptor for advanced glycosylation endproducts (RAGE) is a transmembrane protein of the immunoglobulin superfamily with broad specificity for multiple ligands, and it has been shown to play vital roles in several pathophysiologic processes, including diabetes, Alzheimer disease, renal disease, cardiovascular disease, and cancer. The present study aimed to assess the influences of RAGE gene polymorphisms, combined with environmental carcinogens on the predisposition to oral tumorigenesis. Five polymorphisms of the RAGE gene—including −374T>A (rs1800624), −429T>C (rs1800625), 1704G>T (rs184003), Gly82Ser (rs2070600), and a 63-bp deletion allele (−407 to −345)—were examined from 592 controls and 618 patients with oral cancer. We found that individuals carrying the polymorphic allele of rs1800625 are more susceptible to oral cancer (odds ratio [OR], 1.899; 95% confidence interval [CI], 1.355 to 2.661; adjusted OR [AOR], 2.053; 95% CI, 1.269 to 3.345) after adjustment for age, sex, betel nut chewing, and tobacco consumption. Moreover, we observed a significant association of rs1800625 variants with late-stage tumors (stage III/IV, OR, 1.736; 95% CI, 1.126 to 2.677; AOR, 1.771; 95% CI, 1.101 to 2.851) and large-size tumors (>2 cm in the greatest dimension; OR, 1.644; 95% CI, 1.083 to 2.493; AOR, 1.728; 95% CI, 1.089 to 2.741). Based on behavioral exposure of environmental carcinogens, the presence of 4 RAGE single-nucleotide polymorphisms (SNPs), combined with betel quid chewing and/or tobacco use, greatly augmented the risk of oral cancer. In addition, carriers of particular haplotypes of the 4 RAGE SNPs examined are more prone to develop oral cancer. These results indicate an involvement of RAGE SNP rs1800625 in the development of oral squamous cell carcinoma and implicate the interaction between RAGE gene polymorphisms and environmental mutagens as a predisposing factor of oral carcinogenesis.

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Section: Demographic Informationmentioning

confidence: 90%

RAGE Gene Polymorphism and Environmental Factor in the Risk of Oral Cancer

Chien

Lin

et al. 2015

J Dent Res

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“…This is important because virtually everything known about the clinical behavior of HPV-related OPC comes from studies of HPV16 and very little comparative data exist describing the clinical behavior of noncanonical genotypes in HPV-related OPC. [14][15][16] Because HPV testing is rapidly becoming an "emerging standard of care" for patients with HPVrelated OPC, and the excellent prognosis of patients with HPV-related OPC has inspired clinical trials testing various approaches to reduce treatment intensity, it is vital to understand whether the favorable clinical characteristics of HPV16 apply equally to high-risk non-HPV16 OPC. One Canadian study suggests that high-risk non-HPV16 genotypes were associated with less cervical metastasis and a trend toward better disease-free survival compared with HPV16 types; however, these conclusions were based on only 5 patients with high-risk non-HPV16.…”

Section: Discussionmentioning

confidence: 99%

Clinical characteristics and outcomes of oropharyngeal carcinoma related to high‐risk non–human papillomavirus16 viral subtypes

et al. 2016

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“…The Taiwan study demonstrated an overall HPV prevalence of 21.2% among 410 patients; HPV16 was the most common subtype followed by HPV18. 47 This group reported that HR-HPV was associated with decreased disease-free and disease-specific survivals at 2 years. Racial differences may contribute to these unusual findings.…”

Section: Discussionmentioning

confidence: 99%

“…30 Three published studies report that HPV þ oral cavity squamous cell carcinoma are associated with poorer prognosis; two studies are from the same group in Taiwan and include an expanded cohort. [46][47][48] The strengths of the combined Taiwanese study are the large patient numbers and multivariate analysis; study weaknesses include the lack of p16 INK4a analysis and absence of validation for the HPV genotype data. The Taiwan study demonstrated an overall HPV prevalence of 21.2% among 410 patients; HPV16 was the most common subtype followed by HPV18.…”

Section: Discussionmentioning

confidence: 99%

“…As mentioned, HPV was genotyped using only a blot hybridization assay, and not validated. 47 Duray et al 48 reported on 147 patients with oral cavity squamous cell carcinoma; HPV was detected by PCR with consensus and type-specific primers. HR-HPV was associated with decreased disease-free survival on KaplanMeier analysis; no multivariate analysis was performed.…”

Section: Discussionmentioning

confidence: 99%

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The protective effect of p16INK4a in oral cavity carcinomas: p16Ink4A dampens tumor invasion—integrated analysis of expression and kinomics pathways

Isayeva

Ragin

et al. 2015

Modern Pathology

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A large body of evidence shows that p16 INK4a overexpression predicts improved survival and increased radiosensitivity in HPV-mediated oropharyngeal squamous cell carcinomas.(OPSCC). Here we demonstrate that the presence of transcriptionally active HPV16 in oral cavity squamous cell carcinomas does not correlate with p16 INK4a overexpression, enhanced local tumor immunity, or improved outcome. It is interesting that HPVmediated oropharyngeal squamous cell carcinomas can be categorized as having a 'nonaggressive' invasion phenotype, whereas aggressive invasion phenotypes are more common in HPV-negative squamous cell carcinomas. We have developed primary cancer cell lines from resections with known pattern of invasion as determined by our validated risk model. Given that cell lines derived from HPV-mediated oropharyngeal squamous cell carcinomas are less invasive than their HPV-negative counterparts, we tested the hypothesis that viral oncoproteins E6, E7, and p16 INK4a can affect tumor invasion. Here we demonstrate that p16 INK4a overexpression in two cancer cell lines (UAB-3 and UAB-4), derived from oral cavity squamous cell carcinomas with the most aggressive invasive phenotype (worst pattern of invasion type 5 (WPOI-5)), dramatically decreases tumor invasiveness by altering expression of extracellular matrix remodeling genes. Pathway analysis integrating changes in RNA expression and kinase activities reveals different potential p16 INK4a -sensitive pathways. Overexpressing p16 INK4a in UAB-3 increases EGFR activity and increases MMP1 and MMP3 expression, possibly through STAT3 activation. Overexpressing p16 INK4a in UAB-4 decreases PDGFR gene expression and reduces MMP1 and MMP3, possibly through STAT3 inactivation. Alternatively, ZAP70/Syk might increase MUC1 phosphorylation, leading to the observed decreased MMP1 expression.

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Increasing rates of low-risk human papillomavirus infections in patients with oral cavity squamous cell carcinoma: Association with clinical outcomes

Cited by 29 publications

References 32 publications

RAGE Gene Polymorphism and Environmental Factor in the Risk of Oral Cancer

RAGE Gene Polymorphism and Environmental Factor in the Risk of Oral Cancer

Clinical characteristics and outcomes of oropharyngeal carcinoma related to high‐risk non–human papillomavirus16 viral subtypes

The protective effect of p16INK4a in oral cavity carcinomas: p16Ink4A dampens tumor invasion—integrated analysis of expression and kinomics pathways

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