Morgan et al. BMC Cancer 2010, 10:89 http://www.biomedcentral.com/1471-2407/10/89 Page 7 of 9 Figure 7 (a) HXR9 retards SK-OV3 tumour growth in mice. Mice were treated twice weekly with HXR9 (10 mg/Kg)iv, after an initial dose of 100 mg/Kg iv when the mean tumour volume reached 100 mm3. Error bars represent the SEM for each data point. * indicates a significant difference between treatment groups, p < 0.05 (Mann-Whitney test). (b) HXR9 accumulation in SK-OV3 tumours. Tumours were removed from mice at 4 hours, 12 hours and 24 hours after an initial dose of HXR9 at 100 mg/Kg iv and the amount of HXR9 in the tumour tissue was assessed using dot blotting with an anti-HXR9 antibody. extracted from tumours at the end of 32 days in order to measure cFos expression by QPCR; cFos was found to be expressed at an 18-fold higher level in tumours from HXR9 treated mice than in tumours from untreated mice (Fig 6). The uptake of HXR9 by tumours after the initial dose was measured by excising tumours at 4, 12 and 24 hours and assessing the amount of HXR9 using an anti- HXR9 antibody. This indicated that there is a rapid accumulation of peptide in the first four hours and that the amount of peptide remains stable beyond 24 hours (Fig 7b). Discussion It is becoming increasingly apparent that HOX genes are frequently dysregulated in different malignancies [15-17] including renal [7], bladder [18], prostate [19,20], lung [21] and ovarian cancer [9-11] (this study). The exact pattern of HOX expression varies for different malignan- cies and the significance of this is worthy of further