New evidence for geographic variation in the role of human papillomavirus in tonsillar carcinogenesis.
OBJECTIVE
Our previous studies of tonsillar cancers from New South Wales, Australia, and Jilin Province in the north-east of China, provided evidence that the proportion of these cancers attributable to human papillomavirus (HPV) varies geographically. This study provides the first data on HPV in tonsillar cancers from Hong Kong.


METHODS
A total of 49 Hong Kong tonsillar cancers were analysed for HPV DNA by PCR/sequencing and for p16(INK4A), retinoblastoma (pRb) protein, cyclin D1 and p53 expression by semiquantitative immunohistochemistry as evidence of virus causality. Results were compared with those from New South Wales and Jilin Province.


RESULTS
Of the 31 Hong Kong cancers with amplifiable DNA, nine (29%) were HPV positive by PCR compared with 46% from New South Wales and 0% from Jilin Province. HPV positivity correlated with female gender, young age, over-expression of p16(INK4A) and loss of pRb and cyclin D1. Five-year disease-specific survival for patients with HPV positive and HPV negative cancers was 82 and 42%, respectively. Relationships between HPV status and cell protein expression in Hong Kong cancers were consistent with those from New South Wales and Jilin Province. The proportion of HPV-associated cancers reflected the relative incidence of oropharyngeal cancer in these regions.


CONCLUSIONS
HPV is responsible for a small proportion of tonsillar cancers in Hong Kong patients. Differences in the proportions of tumours attributable to HPV in Hong Kong, New South Wales and Jilin Province may be due to environmental, cultural or genetic factors in the different populations.
Li
Wei
W
Sydney Head & Neck Cancer Institute, Sydney Cancer Centre, Royal Prince Alfred Hospital, Sydney, Australia.
Tran
Nham
N
Lee
Soon C
SC
O'Brien
Christopher J
CJ
Tse
Gary M
GM
Scolyer
Richard A
RA
Hong
Angela
A
Milross
Christopher
C
Yu
Kwok Hung
KH
Rose
Barbara R
BR
D000328:Adult; D000367:Age Factors; D000368:Aged; D000369:Aged, 80 and over; D002471:Cell Transformation, Neoplastic; D056741:Cyclin D; D019941:Cyclin-Dependent Kinase Inhibitor p16 / Q000096:biosynthesis; D016213:Cyclins / Q000096:biosynthesis; D004279:DNA, Viral / Q000032:analysis; D005260:Female; D006723:Hong Kong / Q000453:epidemiology; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D018307:Neoplasms, Squamous Cell / Q000453:epidemiology / Q000821:virology*; D027383:Papillomaviridae; D030361:Papillomavirus Infections / Q000453:epidemiology*; D016133:Polymerase Chain Reaction; D016160:Retinoblastoma Protein / Q000096:biosynthesis; D014067:Tonsillar Neoplasms / Q000453:epidemiology* / Q000821:virology*; D016159:Tumor Suppressor Protein p53 / Q000096:biosynthesis; D014412:Tumor Virus Infections / Q000453:epidemiology*
D056741:Cyclin D; D019941:Cyclin-Dependent Kinase Inhibitor p16; D016213:Cyclins; D004279:DNA, Viral; D016160:Retinoblastoma Protein; D016159:Tumor Suppressor Protein p53