Primary DMBA induced mouse OSCC were generated as described (26 (link)). Single cell suspensions of individual primary oral cavity tumors were made with Collagenase IA (Sigma-Aldrich) and cultured in IMDM/F12 (2:1) with 5% FCS, penicillin/streptomycin, 1% amphotericin, 5 ng/mL EGF (Millipore), 400 ng/mL hydrocortisone, and 5 μg/mL insulin. Sequential differential trypsinization was then used to clear fibroblast contamination. MOC1, 7, 10, 22 and 23 were derived from primary tumors in C57BL/6 WT mice and MOC2 was derived from a chemokine receptor CXCR3deficient mouse on a pure C57BL/6 background (27 (link)) (of note, no major differences in the incidence of tumor formation were noted between the different genotypes). CXCR3 is not detectable on oral keratinocytes and does not contribute to MOC2 growth (Figure S3). Immunofluorescence staining for cytokeratin was performed to confirm an epithelial phenotype (Figure 1C and Figure S1C). PCI-13 was obtained from Dr. Theresa Whiteside, UPCI:SCC029B and UPCI:SCC068 were obtained from Dr. Suzanne Gollin, and all were used with minimal passaging. The UM-SCC-1 cell line (from Dr. Tom Carey) was genotyped in May, 2011 and concordance with published data was established (27 (link)).