Cancer cells are surrounded by the Tumor microenvironment (TME) - a unique milieu generated by the interactions between the normal cells surrounding the tumor cells. The TME supports the survival and proliferation of tumors. Current models suggest that cancer cells induce inflammation, and the TME responds by activation of an anti-inflammatory response. The core inflammatory pathways like Jun N-terminal Kinase (JNK), Tumor Necrosis Factor (TNF), Toll-like Receptor (TLR) and Immune Deficiency pathway (IMD) are conserved in Drosophila and likely participate in an evolutionarily conserved interaction amongst the TME and cancer cells. However, little is known about the molecular mechanisms underlying this interaction, and it is unclear if the inflammatory response is required for maintenance and progression of the tumor. We co-activated oncogenic Yki activity in scribble mutant epithelial cells by “flp-out” or GAL4 mediated drivers to model aggressively growing tumors in Drosophila epithelia. Our preliminary data showed that the key inflammatory pathway like TNF is induced in the neighboring normal cells whereas TLR and JNK pathways are upregulated in tumor cells. Using genetic interaction and epistasis approaches we have analyzed the effect of modulating levels of TLR and inflammatory cytokines on tumor growth and progression. Our research will help understand the interactions between inflammatory pathways and tumor progression in an in vivo model, and if targeting cytokine production in the TME or cancer cells is a useful strategy to suppress the growth and spread of cancer.