Figure 4From: Mammary gland tumor promotion by chronic administration of IGF1 and the insulin analogue AspB10 in the p53R270H/+WAPCre mouse model Hierarchical clustering of insulin (analogue) tumors based on IR and IGF1R signaling components. Quantitative expression levels of IGF1R-β, IR-β, p-Akt and p-Erk in mammary gland EMT tumors of all treatment groups were clustered using Euclidean distance and average linkage (A). Distinct clusters appeared in which the treatment groups are not equally distributed. In protein clusters 1, 2, 5 and 6, the highly mitogenic treatment groups (IGF1 and X10) are overrepresented. In graphs B and C the distribution of several parameters of the clusters are shown. B) Treatment group distribution. C) Latency time per cluster, in which it became apparent that the cluster with the highest p-Erk levels has the shortest tumor latency time. In the last two graphs the correlation between latency time and p-Erk (D) or latency time and p-Akt (E) is presented. Interestingly, high p-Akt levels are positively correlated with latency time, but only in the compound treatment groups and not in the vehicle treated animals. EMT, epithelial to mesenchymal transition; IGF1R, insulin-like growth factor 1 receptor; IR, insulin receptor.Back to article page