Hibma Lab Research
Research Overview
Several viruses are known to cause cancer. Much of our current understanding of the cellular processes of cancer comes from the study of DNA tumour viruses. One such virus is the human papillomavirus (HPV). This virus is fascinating as some types cause benign proliferation of skin cells (for example skin warts) whereas other ‘high-risk’ types cause cancer. We are particularly interested in HPV type 16, which causes cervical cancer because of its health relevance for New Zealanders and especially Maori who have an extremely high incidence of this disease.
Invasiveness is a defining step in malignancy and any treatment that blocks invasion and spread of cancer cells would drastically reduce cancer mortality. Human papillomavirus provided us with an extraordinary opportunity to explore tumour cell invasion and to identify ways to treat it. We have shown that these viruses can disrupt a cellular protein that is critical in the suppression of invasion that occurs in normal healthy cells. We have also shown that this may impact on the immune cells in the skin that are important in initiating the immune response to the viral infection. Our current research focus is to identify how the virus affects the suppression of invasion and to develop treatments to block it. Our interests extend to understanding how the regulation of this cellular pathway influences the immune response to the virus. This research is designed to increase our understanding of the fundamental processes and treatment of tumour invasiveness and will impact not only on cervical cancer but also on other cancer types.
Health Significance
More than one quarter of the deaths in New Zealand are attributed to cancer. Cancer mortality is predicted to increase as mortality due to infectious disease continues to decline. It is imperative that the prevention and treatment of cancer is improved so that the country’s disease burden in the 21st century can be reduced.
Recent Publications
Jemon, K., Young, V., Wilson, M., McKee, S., Ward, V., Baird, M., Young, S. and Hibma, M. An enhanced heterologous virus-like particle for human papillomavirus type 16 tumour immunotherapy. PLoS One in press (2013).
D'Costa, Z., Jolly, C., Androphy, E., Mercer, A., Matthews, C., Hibma, M. Transcriptional repression of E-cadherin by human papillomavirus type 16 E6. PLoS One 7:e48954 (2012).
Hibma, M. The immune response to papillomavirus in persistence and regression. Virology Journal. 6:e241 (2012).
Dutton, S., Fleming, S., Ueda, N., Heath, D., Hibma, M. and Mercer, A. Delivery of Echinococcus granulosus antigen EG95 to mice and sheep using recombinant vaccinia virus. Parasite Immunol. 34:312-317 (2012).
D’Costa, Z., Leong, C-M., Shields, J., Matthews, C. and Hibma, M. Screening of drugs to counteract human papillomavirus 16 E6 repression of E-cadherin expression. Invest. New Drugs, 30: 2236-2251 (2012).
Burn, C. and Hibma, M. Human papillomavirus virus-like particles and their potential as gene delivery vectors in the skin. New Zealand Medical Journal. 124:1-1 (2011).
Rose, S., Baker, M., Hibma, M., and Lawton, B. Predictors of intent to vaccinate against HPV/cervical cancer: a survey of 769 Maori and non-Maori parents. New Zealand Medical Journal. 125: 1-12 (2011).
Cheng Mee Leong, John Doorbar, Ingo Nindl, Han-Seung Yoon and Merilyn Hibma. Deregulation of E-cadherin by human papillomavirus is not confined to high-risk, cancer-causing types. Brit. J. Dermatol. 163: 1253-1263 (2010)
Rose SB, Lawton BA, Lanumata T, Hibma M, Baker MG. HPV/cervical cancer vaccination: Parental preferences on age, place and information needs. J Prim Health Care, 2:190-198 (2010).
Cheng Mee Leong, John Doorbar, Ingo Nindl, Han-Seung Yoon and Merilyn H. Hibma. Loss of epidermal Langerhans cells occurs in human papillomavirus α, γ and μ but not β genus infections. J. Invest. Dermatol. 130:472-480 (2010).
Dana Westphal, Elizabeth C. Ledgerwood, Joel D.A. Tyndall, Merilyn H. Hibma, Norihito Ueda, Stephen B. Fleming, and Andrew A. Mercer. The orf virus inhibitor of apoptosis functions in a Bcl-2-like manner, binding and neutralizing a set of BH3-only proteins and active Bax. Apoptosis, 14, 1317-1330 (2009).
Merilyn H. Hibma, Nicola C. Real, Anna Wiles, Deirdre Dobson-Le, Brett R. Dix, David Wynford-Thomas, Antony W. Braithwaite and Janice A. Royds. Increased apoptosis and reduced replication efficiency of the E3 region-modified dl309 adenovirus in cancer cells. Virus Res. 145:112-120 (2009).