Lung tumour growth kinetics in SPC-c-Raf-1-BB transgenic mice assessed by longitudinal in-vivo micro-CT quantification

156 non contrast-enhanced respiratory gated micro-CT of the lungs were obtained in 12 SPC-raf transgenic (n = 9) and normal (n = 3) mice at different time points. Region-growing segmentation of the aerated lung areas was obtained as an inverse surrogate for tumour burden. Time course of segmentation volumes was assessed to demonstrate the potential of the method for follow-up studies.Micro-CT allowed assessment of tumour growth kinetics and semiautomated region growing enabled quantitative analysis. Significant changes of the segmented lung volumes over time could be shown (p = 0.009). Significant group differences could be detected between transgenic and normal animals for time points 8 to 13 months (p = 0.043), when marked tumour progression occurred.The presented region-growing segmentation algorithm allows in-vivo quantification of multifocal lung adenocarcinoma in SPC-raf transgenic mice. This enables the assessment of tumour load and progress for the study of carcinogenesis and the evaluation of novel treatment strategies.A number of genetic animal models of lung cancer has been developed to better understand the molecular causes of this disease. In-vivo imaging in these disease models can allow a better understanding of biological processes and a time-course assessment of therapeutic approaches. We here report on longitudinal in-vivo micro-CT measurements of lung tumour in a transgenic mouse model of lung cancer.The animal model examined has been reported in the literature already [1-5]. In the SPC-c-Raf-1-BB (referred to as SPC-raf) transgenic mouse model overexpression of the serine-threonine-kinase c-raf to alveolar epithelium is achieved by use of the surfactant protein C (SPC) promoter. Raf is an essential constituent of the mitogen activated protein kinase (MAPK) signalling pathway, that has been found to communicate a cell surface receptor signal to the DNA in the nucleus [4]. This MAPK pathway is often found to be dysregulated in human malignancies [3