09-05-2010 21:48:19 Accueil Sitemap
You are here : Home > Partners' presentation > IARC-ICB
MAIN MENU
International Agency for Research on Cancer at a glance

The International Agency for Research on Cancer (IARC) is part of the World Health Organization. IARC's mission is to coordinate and conduct research on the causes of human cancer, the mechanisms of carcinogenesis and to develop scientific strategies for cancer control. The Agency is involved in both epidemiological and laboratory research and disseminates scientific information through publications, meetings, courses, and fellowships.

Our contribution to INCA

High-risk human papillomaviruses (HPVs) have been associated with cervical cancer. However, the majority of HPV infections do not lead to the development of cervical lesions. Studies by our group and other laboratories indicate that HPV16 polymorphisms can influence the clinical outcome of an HPV infection. In this programme, in collaboration with partners Krüger Kjaer and Iftner we will investigate whether different variants in the oncogenes E6 and E7 of HPV16 and HPV18 are associated with different probabilities of progression to malignancy. The study will make use of a unique resource available to INCA, a prospective cohort study of 11,088 women in Copenhagen.

Reference publications

  • Zehbe I, Voglino G, Delius H, Wilander E and Tommasino M. (1998) Human papillomavirus 16 E6 polymorphisms: geographically related risk of cervical cancer development. Lancet, 352, 1441-42.
  • Zehbe I, Voglino G, Wilander E, Genta F and Tommasino M. (1999) Codon 72 polymorphism of p53 and its association with cervical cancer. Lancet, 354, 218-19.
  • Zehbe I, Voglino V, Wilander E, Delius H, Marongiu A, Edler L, Klimek F, Andersson S and Tommasino M. (2001) p53 codon 72 polymorphism and various HPV 16 E6 genotypes are risk factors for cervical cancer development. Cancer Res, 61, 608-11.
  • Giarrč M, Caldeira S, Malanchi I, Ciccolini F, Lećo MJ and Tommasino M. (2001) Induction of pRb degradation by the human papillomavirus type 16 E7 protein is essential to efficiently overcome p16INK4a-imposed G1 cell cycle arrest. J Virol, 75, 4705-12.
  • Zehbe I, Tahezy R, Mytilineos J, Voglino G, Mikyskova I, Delius H, Marongiu A, Gissmann L, Wilander E and Tommasino M. (2001) Human papillomavirus 16 E6 polymorphisms in cervical lesions from different European populations and their correlation with human leukocyte antigen class II haplotypes. Int J Cancer, 95, 711-716.
  • Caldeira S, Zehbe I, Accardi R, Malanchi I, Dong W, Giarrč M, de Villiers EM, Filotico R, Boukamp P and Tommasino M. (2003) The E6 and E7 proteins of the cutaneous human papillomavirus type 38 display transforming properties. J Virol, 77, 2195-2206.
  • Malanchi I, Accardi R, Diehl F, Smet A, Androphy E, Hoheisel J and Tommasino M. (2004) Human papillomavirus type 16 E6 promotes retinoblastoma protein phosphorylation and cell cycle progression. J Virol, 24:13769-78.
  • Dong W, Klotz U, Accardi R, Caldeira S, Tong WM, Wang ZQ, Jansen L, Dürst M, Sylla BS, Gissmann L and Tommasino M. (2005) Skin hyperproliferation and susceptibility to chemical carcinogenesis in transgenic mice expressing E6 and E7 of human papillomavirus type 38. J Virol, 79, 14899-14908.
  • Accardi R, Dong W, Smet A, Cui R, Hautefeuille A, Gabet AS, Sylla BS, Gissmann L, Hainaut P and Tommasino M. (2006) Skin human papillomavirus type 38 alters p53 functions via accumulation of ΔNp73. EMBO Reports, 7, 334-340.
  • Grodzki M, Besson G, Clavel C, Arslan A, Franceschi S, Birembaut P, Tommasino M, and Zehbe I. (2006) Increased risk for cervical disease progression of French women infected with the human papillomavirus type 16 E6-350G variant. Cancer Epidemiol Biomarkers Prev, 15, 820-822.

Copyright