Human papillomavirus type 16 (HPV-16) E7 oncoprotein-induced abnormal centrosome synthesis is an early event in the evolving malignant phenotype. Abnormal centrosome numbers have been detected in many cancers in which they are involved in multipolar spindle formation, chromosome missegregation, and genomic instability. However, in order to drive genomic destabilization and aneuploidy, centrosome abnormalities should develop in cells prior to extensive genomic and nuclear abnormalities. In a study combining immunofluorescence for the centrosomal marker &ggr;-tubulin (red dots) and fluorescence in situ hybridization (FISH) for chromosome 8 (green dots), Duensing et al. show that abnormal centrosome numbers (i.e., more than two per cell, in the given example there are three) can be induced by the HPV-16 E7 oncoprotein in primary human keratinocytes prior to the occurrence of extensive chromosomal imbalances as shown by normal copy numbers of chromosome 8. In contrast, in cells with isolated expression of the cooperating HPV-16 E6 oncoprotein, abnormal centrosome numbers accumulate in parallel with nuclear abnormalities. This observation shows that HPV-16 E7-induced abnormal centrosome synthesis represents an early event during HPV-associated carcinogenic progression and can therefore potentially drive the development of genomic instability. For more information, please see the article be Duensing et al. on p. 2343 of this issue.