Skip to main content
. Author manuscript; available in PMC: 2010 Feb 27.
Published in final edited form as: Oncogene. 2009 Jun 22;28(34):3022–3032. doi: 10.1038/onc.2009.165

Figure 6. BMI1 in combination with H-RAS induces extensive lung metastases.

Figure 6

(A) MCF10A+H-RAS+BMI1 tail vein xenografts show fulminant gross pulmonary metastases involving all lung lobes (right, arrowheads), while other MCF10A-derived tail vein xenografts did not (left). (B) Histologically, mice with MCF10A+H-RAS tail vein xenografts developed small adenomatous lesions late in the disease course (left), while MCF10A+H-RAS+BMI1 xenografts formed destructive lesions (right) that led to rapid clinical illness (Bar = 100 μm). (C) Ex-vivo fluorescent imaging (D) and graphic representation of MCF10A+H-RAS and MCF10A+H-RAS+BMI1 GFP expressing tail vein xenografts. BMI1 overexpression in combination with H-RAS prevents massive loss and induces exponential proliferation of MCF10A cells over time in comparison to H-RAS overexpression alone (*p < 6×10-6, 10 fields observed per time point minimum).