Figure 1

Bitransgenic MMTV-myr-Akt1, MMTV-c-ErbB2 mice have decreased mammary tumour latency, more aggressive tumour histology and decreased apoptosis compared with MMTV-c-ErbB2 mice. (a) Mammary tumour latency in bitransgenic MMTV-myr-Akt1, MMTV-c-ErbB2 mice and MMTV-c-ErbB2 mice. Sixty days after birth, bitransgenic MMTV-myr-Akt1, MMTV-c-ErbB2 and MMTV-c-ErbB2 mice were palpated weekly to monitor for the presence of mammary tumours. The graph shows the rate at which tumours were first detected for both genotypes. A total of 22 bitransgenic mice and 30 MMTV-c-ErbB2 mice were monitored and the graph shows the number of days to tumour detection versus the percentage of tumour-free mice. (b-e) Haematoxylin and eosin stained tumour sections. (b) Tumour derived from a MMTV-c-ErbB2 mouse. (c-e) Tumors derived from bitransgenic MMTV-myr-Akt1, MMTV-c-ErbB2 mice. (c) A bitransgenic tumour with histology similar to that of c-ErbB2 tumours. (d-e) Two different bitransgenic tumours demonstrating necrotic tumour tissue distal to a blood vessel (blood vessel marked with * and necrosis marker with **). ×200 original magnification. (f) Tumours from bitransgenic MMTV-myr-Akt1, MMTV-c-ErbB2 mice have less apoptosis than tumours from MMTV-c-ErbB2 mice. Apoptosis was quantitated by activated caspase-3 immunohistochemistry. The number of cells staining positively for activated caspase-3 was divided by the total number of cells counted to generate the apoptotic rate. (g) Tumours from bitransgenic mice have a higher proliferation rate than tumours from MMTV-c-ErbB2 mice. Proliferation rate was determined by counting the number of mitotic figures in 10 500× magnification fields of view and the data is presented as the mean +/- standard deviation for three tumours of each genotype.