Recurrent Respiratory Papillomatosis (RRP): Enriched HLA DQw3 Phenotype and Decreased Class I MHC Expression

Bonagura, V.R.; O'Reilly, Mary Ellen; Abramson, Allan L.; Steinberg, Bettie M.

doi:10.1007/978-1-4615-2449-6_31

Cited by 6 publications

(6 citation statements)

References 26 publications

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“…For example, class I major histocompatibility antigen expression is markedly reduced in cervical cancers caused by HPV-16 [77], apparently mediated by a decrease in the peptide transporter protein TAP-1 [78]. We have seen a similar suppression of class I expression in laryngeal papillomas caused by HPVs 6/11 [79], and our preliminary evidence suggests reduced TAP-1 as well. There may be a genetic restriction to the effectiveness of immune surveillance of HPV infection.…”

Section: Hpv and Respiratory Papulomatosissupporting

confidence: 61%

“…There may be a genetic restriction to the effectiveness of immune surveillance of HPV infection. Wank and Thomssen [80] reported a correlation between the class I allele HLA-DQ3 and cervical cancer, and we saw a similar correlation between this allele and laryngeal papillomas [79]. While the correlation for cervical cancer is somewhat controversial [81], and may differ from one population to another, this is an area that clearly needs more study.…”

Section: Hpv and Respiratory Papulomatosismentioning

confidence: 88%

“…If genetic susceptibility to HPV infection or expression varies, as suggested for cervical carcinomas and laryngeal papillomas [79,80], different study groups could have disparate prevalence of HPV DNA in head and neck cancers. Exposure to carcinogenic cofactors, interacting with pre-existing HPV to induce malignancy, could also vary from one population to another.…”

Section: Other Head and Neck Carcinomasmentioning

confidence: 99%

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A possible role for human papillomaviruses in head and neck cancer

Steinberg

DiLorenzo

1996

Cancer Metast Rev

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Human papillomaviruses (HPVs) cause benign tumors in the respiratory tract. Mounting evidence suggests that they also play a role in the etiology of a subset of head and neck cancers. Carcinomas in patients with a history of recurrent respiratory papillomatosis clearly are caused by persisting HPV interacting with one of more carcinogenic agents. Verrucous carcinomas of the oral cavity, tonsillar and tongue carcinomas are strongly linked with HPVs, based on molecular epidemiologic data. Tonsillar cancer have been shown to express HPV RNA, presumed necessary to induce and maintain a carcinoma, supporting a viral etiology. This paper reviews the molecular and cellular basis for considering HPVs as causative agents of cancer, and reviews the literature that considers the possible role of HPVs in head and neck cancer.

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Section: Hpv and Respiratory Papulomatosissupporting

confidence: 61%

Section: Hpv and Respiratory Papulomatosismentioning

confidence: 88%

Section: Other Head and Neck Carcinomasmentioning

confidence: 99%

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A possible role for human papillomaviruses in head and neck cancer

Steinberg

DiLorenzo

1996

Cancer Metast Rev

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“…Of women with CIN, 38% were negative, 37% were heterozygous, and 23% were homozygous for the DQB1 * 03 locus (X2 trend = 39.01, p < 0.001). Compared with controls, the odds 33, and 16% were positive for multiple types. All types correlated strongly with DQB 1 * 03, but there was insufficient data to find differences in the strength of association between the types.…”

Section: Resultsmentioning

confidence: 88%

Association Between HLA DQBl * 03 and Cervical Intra-epithelial Neoplasia

Odunsi

Terry

et al. 1995

Mol Med

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Background: Cervical intraepithelial neoplasia (CIN) and cervical cancer have been shown to be strongly associated with infection by human papillomavirus (HPV). However, other factors may be contributory in the progression from normal epithelium to CIN and cervical cancer, since not all women with HPV infection develop disease. Recently, it was demonstrated that there is a high risk for cervical cancer and CIN in women with HLA DQB1 * 03 (RR = 7.1, p < 0.0009) (1). Subsequent reports have been conflicting, due to sample size, genetic heterogeneity and differences in the techniques employed for the detection of HLA DQB1 * 03. Materials and Methods: DNA from cervical smears of 178 women with CIN and 420 controls with normal cervical cytology was analyzed by polymerase chain reaction (PCR) with type-specific primers for HPV 16, 18, 31, and 33. The DNA from test and control samples were also analyzed by a novel PCR technique, which mutates the first base of codon 40 (DQ alleles) from T to G to create an artificial restriction site for an enzyme Mlu I that distinguish DQB1 * 03 from other alleles and are confirmed by digestion of amplified DNA with Mlu I. Further analysis of individual DQB 1 * 03 alleles was performed using PCR and allele-specific primers. Results: One hundred forty-four (34%) out of 420 controls (all HPV 16, 18, 31, or 33 negative and normal cytology), 37/66 (56%) of CIN I and 72/112 (64%) of CIN III were positive for DQB1 * 03 (trend test, p < 0.001, X2 = 37.3). A significant association was observed between DQB1 * 03 and CIN (odds ratio 3.03; 95% CI 2.11-3.45). Of women with CIN, 131/ 178 (73.5%) had HPV (types 16, 18, 31, or 33) infection. There was a significant association between DQB1 * 03 and presence of HPV (odds ratio 3.43; 95% CI 2.25-5.10). Homozygosity for DQB1 * 03 was more strongly associated with CIN than heterozygosity (odds ratios 4.0 and 2.63, respectively); and for the presence of HPV (odds ratio 4.47; 95% CI 2.58-7.77). HLA DQB1 * 0301 was the most strongly associated allele with CIN and HPV (odds ratios 2.53 and 2.63, respectively). Conclusions: HLA DQB1 * 03 is associated significantly with CIN and may be permissive for HPV infection. Further analysis of class II HLA typing in CIN is necessary to evaluate this association.

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“…This is supported by findings that cervical cancer and recurrent respiratory papillomatosis are frequently associated with an HLA-DQw3 allele. [83][84][85][86] In contrast, in individuals with HLA-DR5 or DR13 alleles, the prevalence of cervical cancer was found to be statistically lower. It was also suggested that the development of HPV-associated skin cancer in immunosuppressed renal transplant recipients (RTRs) is linked to the HLA-DR7 allele.…”

Section: Mhc Molecule Polymorphism Determines the Susceptibility To Hmentioning

confidence: 89%