Triple negative breast cancer TNBC cells upregulate the kynurenine pathway KP in forced suspension culture. The rate limiting enzyme in this pathway, TDO2 is responsible for tryptophan catabolism and production of the metabolite kynurenine Kyn. Kyn was recently identified as an endogenous ligand for AhR, a transcription factor that was also upregulated in suspension. Kyn activation of AhR promotes motility of glioma cells. AhR is also in many immune cell types and its activation decreases T-cell activity leading to tumor immune escape. The goal of our proposal is to determine if we can target this pathway that may facilitate TNBC metastasis by enabling tumor cell invasiveness, anchorage independence and immune escape. Our hypothesis is that upregulation of kynerinine by TNBC facilitates survival in transit to metastatic sites and immune suppression and thereby mediates the highly metastatic nature of this subtype.