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Aberrant kinase activation resulting from mutation, amplification, or translocation can drive growth and survival in a subset of human cancer.  FGFR2  is amplified in breast and gastric cancer, and we report here the first characterization of  FGFR2  gene amplification in colorectal cancer in the NCI-H716 colorectal cancer cell line.  FGFR2  is highly expressed and activated in NCI-H716 cells, and FGFR selective small molecule inhibitors or FGFR2 shRNA strongly inhibited cell viability  in vitro , indicating “addiction” of NCI-H716 cells to FGFR2. NCI-H716 growth in a xenograft model was also inhibited by an FGFR small molecule inhibitor. FGFR2 was required for activation of multiple downstream signaling proteins including AKT, ERK, S6RP and NFKB. Inhibition of downstream kinases such as AKT or ERK alone had modest effects on proliferation, whereas combined inhibition of AKT and ERK signaling resulted in a loss of viability similar to FGFR2 inhibition. We identified elevated  FGFR2  expression in a small subset of primary colorectal cancer, however  FGFR2  amplification was not observed. Although  FGFR2  amplification is not common in primary colon cancer or lymph node and liver metastases, other subsets of colorectal cancer such as ascites, from which the NCI-H716 cell line was derived, have yet to be tested. These results suggest that emerging FGFR inhibitor therapeutics may have efficacy in a subset of colon cancer driven by  FGFR2  amplification.

FGFR2 Is Amplified in the NCI-H716 Colorectal Cancer Cell Line and Is Required for Growth and Survival