Tumor growth, tumor gene expression, tumor proliferation and apoptosis <i>in vivo</i>.

<p>(A) BxPC-3 tumors were established subcutaneously in mice. When the tumors reached approximately 120 mm³ in volume, the mice were randomly assigned to control, DHA, Apo2L/TRAIL, or DHA+Apo2L/TRAIL groups and treated as described in the methods section. The sizes (measured in mm³) of the tumors were monitored and recorded. A significant difference in tumor volume from the control is denoted by “*” (<i>P</i><0.05), and a significant reduction compared to the DHA or Apo2L/TRAIL-treated tumors is denoted by “**” (<i>P</i><0.01). (B) Representative animals and tumors are shown for each group. (C) Tumors from control mice and from mice treated with DHA, Apo2L/TRAIL, and DHA+Apo2L/TRAIL were homogenized and subjected to western blot analysis to detect the expression of caspase-3 and caspase-8. β-actin served as an internal control. (D) Analysis of proliferation marker PCNA by immunohistochemistry and apoptotic status of tumor cells by in situ TUNEL assay. PCNA positive (E) and TUNEL-positive (F) cells were also counted under microscope to calculate the proliferation index and apoptotic index, respectively. “*”: <i>P</i><0.05, compared with control. “**”: <i>P</i><0.01, compared with single agent.