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Int J Cancer. 2017 Oct 15;141(8):1576-1584. doi: 10.1002/ijc.30871. Epub 2017 Jul 14.

Looking beyond human papillomavirus (HPV) genotype 16 and 18: Defining HPV genotype distribution in cervical cancers in Australia prior to vaccination.

Author information

Victorian Cytology Service Registries, East Melbourne, VIC, Australia.
School of Population and Global Health, University of Melbourne, Parkville, VIC, Australia.
Department of Microbiology and Infectious Diseases, Regional HPV Reference Laboratory Network, The Royal Women's Hospital, Parkville, VIC, Australia.
Department of Obstetrics and Gynaecology, University of Melbourne, Parkville, VIC, Australia.
Murdoch Children's Research Institute, Parkville, VIC, Australia.
Department of Anatomical Pathology, The Royal Women's Hospital, Parkville, VIC, Australia.
Department of Anatomical Pathology, SEALS Pathology, Randwick, NSW, Australia.
Department of Tissue Pathology and Diagnostic Oncology, Royal Prince Alfred Hospital, Camperdown, NSW, Australia.
Sydney Medical School, The University of Sydney, NSW, Australia.
Pathology Queensland, Royal Brisbane and Women's Hospital, Herston, QLD, Australia.
Department of Anatomical Pathology, Pathology North-Hunter, New Lambton Heights, NSW, Australia.
Department of Anatomical Pathology, Austin Hospital, Heidelberg, VIC, Australia.
Department of Anatomical Pathology, ICPMR Pathology, Westmead, NSW, Australia.
VCS Pathology, Victorian Cytology Service, Carlton, VIC, Australia.


Australia has implemented a high-coverage HPV vaccination program but has not, to date, established the distribution of HPV types that occur in cervical cancers in Australia. This information is important for determining the potential for cervical cancer prevention with both current and broader spectrum HPV vaccines. We analysed 847 cervical cancers diagnosed 2005 to 2015 in tertiary centres in the three most populous Australian states with resolution of specimens containing multiple HPV types using laser-capture microdissection. Archived FFPE tissue was reviewed by specialist pathologists, sandwich sectioned, and initially whole-tissue sections genotyped for HPV. Samples were first genotyped using SPF10-LiPA25 (version 1). Negative samples were screened with DNA ELISA kit HPV SPF10, followed by genotyping with SPF+ LiPA if ELISA positive. If still negative, samples were tested on a qPCR assay targeting the E6 region of HPV16, 18, 45 and 33. Of the 847 cancers (65.1% squamous, 28.7% adenocarcinoma, 4.3% adenosquamous, 2.0% other), 92.9% had HPV detected. Of the HPV-positive cancers, 607 of 787 (77.1%) contained HPV16 or 18, 125 of 787 (15.9%) contained HPV31/33/45/52 or 58, and 55 (7.0%) another HPV type. There was a strong correlation between HPV type and age, with younger women most likely to have HPV16/18 detected and least likely HPV negative. Our findings indicate that cervical cancers diagnosed in Australia more frequently contain HPV16/18 than in international series. This could be due to cervical screening in Australia increasing the proportion of adenocarcinomas, in which types 18 and 16 more strongly predominate, due to prevention of squamous cancers.


cervical cancer; genotyping; human papillomavirus; laser capture microdissection; vaccine

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