Human Papillomavirus in Head and Neck Squamous Cell Carcinomas in Nonsmokers

Fouret, Pierre; Monceaux, Guy; Temam, Stéphane; Lacourreye, Laurent; Guily, Jean Lacau St

doi:10.1001/archotol.1997.01900050063008

Cited by 116 publications

(66 citation statements)

References 11 publications

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“…11,[14][15][16]18,22,25,49 Because of these factors, we limited our analysis to sites such as the tonsil and base of tongue, in which HPV has been found to be associated with all spectrums of disease. [33][34][35] Viral copy numbers for some tumors at these sites have been comparable to those reported in other HPV-associated malignancies, such as cervical cancer. 50 However, despite limiting our analysis in this way, some of the cancer cases in our analyses may have been misclassified because of the complexity of determining primary cancer sites in this anatomic region.…”

Section: Discussionsupporting

confidence: 73%

“…Because the NPCR and the SEER Program do not collect information regarding the presence of HPV within tumors, we relied exclusively on anatomic sites' proclivity for HPV reported in previous studies. 7,11,12,[14][15][16][17][18][19]21,22,24,25,[33][34][35] We divided potentially HPV-associated sites into 3 major anatomic areas: the tonsil, including the Waldeyer ring; the base of the tongue and the lingual tonsil; and other potentially HPV-associated sites within the oropharynx. Detailed descriptions and specific ICD-O-3 topography codes used to define these unique anatomic groupings are shown in Table 1.…”

mentioning

confidence: 99%

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Burden of potentially human papillomavirus-associated cancers of the oropharynx and oral cavity in the US, 1998-2003

Ryerson

Peters

Coughlin

et al. 2008

Cancer

268

210

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Section: Discussionsupporting

confidence: 73%

mentioning

confidence: 99%

Burden of potentially human papillomavirus-associated cancers of the oropharynx and oral cavity in the US, 1998-2003

Ryerson

Peters

Coughlin

et al. 2008

Cancer

268

210

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“…As expected by the high prevalence of HPV in our patient group, no correlation was established between viral presence and other clinicopathologic characteristics (age, gender, and cancer differentiation). Such associations have been reported by some groups (13,15,38) but could not be confirmed by others (34,43,59). In addition, anatomic site seems to be an important factor that determines the susceptibility of squamous epithelium to HPV transformation, with the tonsillar region being more sensitive (13,15,22,35).…”

Section: Discussionmentioning

confidence: 92%

“High Risk” HPV Types Are Frequently Detected in Potentially Malignant and Malignant Oral Lesions, But Not in Normal Oral Mucosa

et al. 2000

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Studies on the involvement of the human papillomavirus (HPV) in initiation and progression of oral neoplasia have generated conflicting results. The observed discrepancy is attributable mainly to the varying sensitivity of the applied methodologies and to epidemiologic factors of the examined patient groups. To evaluate the role of HPV in oral carcinogenesis, we analyzed 53 potentially neoplastic and neoplastic oral lesions consisting of 29 cases of hyperplasia, 5 cases of dysplasia, and 19 cases of squamous cell carcinomas, as well as 16 oral specimens derived from healthy individuals. A highly sensitive nested polymerase chain reaction (PCR) assay was used, along with type-specific PCR, restriction fragment length polymorphism analysis, dot blotting, and nonisotopic in situ hybridization. Nested PCR revealed the presence of HPV DNA in 48 of the 53 (91%) pathologic samples analyzed, whereas none (0%) of the normal specimens was found to be infected. Positivity for HPV was independent of histology and the smoking habits of the analyzed group of patients. At least one "high risk" type, such as HPV 16, 18, and 33, was detected by type-specific PCR in 47 (98%) infected specimens, whereas only 1 (2%) squamous cell carcinoma was solely infected by a "low risk" type (HPV 6). HPV 16 was the prevailing viral type, being present in 71% of infected cases. Single HPV 16 and HPV 18 infections were confirmed by restriction fragment length polymorphism. HPV 58 was detected by dot blotting in three hyperplastic lesions. HPV positivity and genotyping were further confirmed, and the physical status of this virus was evaluated by nonisotopic in situ hybridization. Diffuse and punctate signals, indicative of the episomal and integrative pattern of HPV infection, were observed for low-and high-risk types, respectively. Our findings are suggestive of an early involvement of high-risk HPV types in oral carcinogenesis.

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“…[6][7][8]10,12,17,18,44 In this report we have applied a highly sensitive FISH procedure to 81 TSCC, enabling HPV DNA detection up to the level of a single copy per cell nucleus, and discrimination between replicative (episomal) and integrated virus on the basis of the nuclear staining pattern. Using this approach 41% of these tumors exhibited nuclear HPV signals indicative for viral integration into the cellular genome.…”

Section: Discussionmentioning

confidence: 99%

Marked differences in survival rate between smokers and nonsmokers with HPV 16‐associated tonsillar carcinomas

Hafkamp

Manni

Haesevoets

et al. 2008

Intl Journal of Cancer

307

292

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Oncogenic human papillomavirus (HPV) is a causative agent in a subgroup of head and neck carcinomas, particularly tonsillar squamous cell carcinomas (TSCC). This study was undertaken because controversial data exist on the physical status of HPV-DNA and the use of p16INK4A overexpression as surrogate HPV marker, and to examine the impact of HPV and tobacco consumption on the clinical course of TSCC. Tissue sections of 81 TSCC were analyzed by HPV 16-specific fluorescence in situ hybridization (FISH) Head and neck squamous cell carcinomas (HNSCC) account for 4% of all malignancies in the Western world, for up to 50% of all malignancies in Southeast Asian countries and for 6.5% of all annual cancer cases worldwide.1 HNSCC is associated with severe disease-and treatment-related morbidity and because treatment has not improved greatly in recent years, the 5-year survival rate remains 50%. HNSCC develop in various anatomical defined regions, including the oral cavity, larynx and pharynx. These organ-specific tumors each show specific clinical presentations and outcome, and are treated by different strategies. 2,3 The median age at presentation is 60 years and approximately two-third of patients are male. Well-known risk factors in the etiology of HNSCC are cigarette smoking combined with alcohol consumption in Western countries, or with betel quid chewing in Asia. A history of tobacco use is present in 90% of patients who develop oral cavity cancers. 2,3Despite these evident associations, the exact mechanisms by which these factors cause tumor initiation and progression are not fully understood. Furthermore, the fact that most tobacco and alcohol users do not develop HNSCC and that in recent years more often individuals without a history of these traditional risk factors have been witnessed, 4 underlines the complexity of HNSCC pathogenesis and a role for additional factors in the disease process.Increasing evidence suggests that human oncogenic papillomaviruses (HPVs), known to cause uterine cervical and other anogenital cancers, may also be of importance in the pathogenesis of HNSCC. 5 The strongest association has been found for oropharyngeal carcinomas, especially tonsillar carcinomas.6-11 Sero-positive patients for HPV 16 or with a history of HPV-related anogenital cancer also show increased risk rates of developing oropharyngeal cancer.12,13 The prevalence of HPV-exhibiting HNSCC, however, varies broadly amongst several studies (2-76%) due to differences in the population, combination of histological subsites, type and number of specimens analyzed, and detection methods used. 7,14 Thus, besides determining the presence of HPV DNA it has been suggested to better define the biological association of oncogenic HPV with these tumors, e.g., by means of assessing the viral copy number per cell, the viral oncoprotein E6/E7 expression levels, perturbation of pRb-dependent cell cycle control, or the physical status of the virus (episomal or integrated). 15 In this way, several reports have shown that HPV 16 is predomi...

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Human Papillomavirus in Head and Neck Squamous Cell Carcinomas in Nonsmokers

Cited by 116 publications

References 11 publications

Burden of potentially human papillomavirus-associated cancers of the oropharynx and oral cavity in the US, 1998-2003

Burden of potentially human papillomavirus-associated cancers of the oropharynx and oral cavity in the US, 1998-2003

“High Risk” HPV Types Are Frequently Detected in Potentially Malignant and Malignant Oral Lesions, But Not in Normal Oral Mucosa

Marked differences in survival rate between smokers and nonsmokers with HPV 16‐associated tonsillar carcinomas

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