Enhanced venous thrombogenicity in an HT-29–induced cancer model is abrogated by AHR inhibition. (A) Experimental design. An equal number of male and female athymic mice (N = 10) were injected with HT-29 and after 3 weeks randomized to 2 subgroups (N = 5 per group). HT-29 group had 3 male and 2 female mice and HT-29 + CH223191 had 2 male mice and 3 female mice. Mice were given CH223191 IP for a total of 7 days until the harvest of IVC clots. The group treated with the vehicle (dimethyl sulfoxide) served as controls. (B) Tumor volumes at the end of 4 weeks after cell injection are presented as box plots, P = .878. (C) Kyn levels in plasma of mice at the time of harvest are shown in box plots, P = .235. (D) IVC clots from both the groups as in Figure 6A are shown in box plots. The Student t test was used to compare the groups. **P = .001. (E) IVCs harvested from mice, as in Figure 6A from a parallel experiment without the IVC ligation surgery, were lysed and probed separately for TF and PAI-1. Equal amounts of lysates were used in each blot, and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) served as a loading control. The numbers at the top correspond to 5 separate mice used for the study. (F) TF and PAI-1 normalized to GAPDH for both groups, N = 5 per group represented as box plots. A Student t test was used to compare TF and PAI-2 separately between the groups. *P = .001 for TF and **P = .001 for PAI-1 and compares the HT-29 vs the HT-29 + CH223191 group.