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. Author manuscript; available in PMC: 2013 Jul 24.
Published in final edited form as: Cancer Cell. 2012 Jun 12;21(6):836–847. doi: 10.1016/j.ccr.2012.04.024

Figure 2. GM-CSF is upregulated in KrasG12D-PDEC as well as PanIN-harboring mouse and human pancreata.

Figure 2

(A) Levels of GM-CSF mRNA (black bar) and protein (gray bar) in GFP-KrasG12D- PDEC were assessed by quantitative RT-PCR and ELISA respectively. Data is presented as an average fold induction over values from isogenic GFP-WT-PDEC. Error bars indicate SD, (n=3).

(B) Normalized expression of GM-CSF mRNA GFP-KrasG12D-PDEC (black bars) after24 hour treatment with DMSO, MAPK inhibitor U0126 (2μM) or PI3K inhibitor LY294002(10μM) was analyzed by quantitative RT-PCR. Error bars indicate SD, (n=3).

(C) Levels of GM-CSF protein in pancreata grafted with GFP-KrasG12D-PDEC or pancreata from p48;LSL-KrasG12D mice. Data is presented as an average fold induction over values from normal pancreatic tissue. Error bars indicate SD, (n=3).

(D) Immunohistochemical staining for GM-CSF protein in representative samples of human pancreatic cancer containing PanIN lesions. (a–normal duct from adjacent non-malignant tissue; b and c - PanIN lesions; d–invasive PDA). White arrowheads indicate pancreatic duct (a), PanIN (b and c) and PDA (d). Scale bar, 50μm.See also Figure S2.