Hegab AE, Ozaki M, Kameyama N, et al. - Researchers characterized the contribution of cancer-associated fibroblasts (CAFs) and the fibroblast growth factor (FGF)/FGF receptor (FGFR) signalling pathway in preserving the lung tumors started by Fgf9 overexpression. It was discovered that CAF-secreted Fgf2 adds to tumor cell growth. CAFs overexpressed Tgfb, Mmp7, Fgf9, and Fgf2, moreover, synthesized more collagen, and secreted inflammatory cell-recruiting cytokines. It also improved the conversion of tumor-associated macrophages (TAMs) to the tumor-supportive M2 phenotype although it did not affect angiogenesis. , During early lung tumor development, in vivo inhibition of Fgfrs, led to significantly smaller and fewer tumor nodules, whereas inhibition in established lung tumors resulted into a notable decrease in tumor size and number. Fgfr inhibition also impacted tumor stromal cells, as it significantly annihilated TAM enrollment and decreased tumor vascularity. Nonetheless, the withdrawal of the inhibitor resulted in an important recurrence/regrowth of Fgf/Fgfr-independent lung tumors. These recurrent tumors did not have a greater proliferative or propagative potential. In conclusion, it was evident that fibroblasts correlated with the Fgf9-induced lung adenocarcinoma give various means of support to the tumor. However, the Fgfr blocker significantly suppressed the tumor and its stromal cells, it was not adequate to fully remove the tumor, mainly because of the emergence of alternative (resistance/maintenance) mechanism(s). Moreover, this model represents a superior tool to additionally examine the complex interactions between CAFs, their associated chemokines, and the progression of lung adenocarcinomait, further, it also gives further evidence to support the requirement for a combinatorial approach to treat lung cancer.