Figure 2.
Figure 2. Primary tumor growth and tumor-induced neovascularization not affected in Src-deficient mice. (A) Syngeneic lung carcinoma cells (D121) were implanted subcutaneously in src–/– or control src+/– hosts and incubated for 12 days. Primary tumors were resected and weighed (n = 8). The difference in tumor weights grown in these hosts was insignificant (P > .44). (B) Tumor-induced neovascularization was determined by indirect immunofluorescence with the blood vessel marker CD31 in cryosections of primary D121 tumors from src–/– or control src+/– hosts. (C) Bar = 50 μm. The extent of CD31-positive staining blood vessels was determined as an indication of tumor-induced angiogenesis by quantitation of multiple random high-power fields from primary D121 tumors from src–/– or control src+/– hosts (P > .5) (n = 8). Quantitation of CD31 immunostaining was performed as described in “Materials and methods.” For panels A and C, error bars indicate standard error.

Primary tumor growth and tumor-induced neovascularization not affected in Src-deficient mice. (A) Syngeneic lung carcinoma cells (D121) were implanted subcutaneously in src/ or control src+/ hosts and incubated for 12 days. Primary tumors were resected and weighed (n = 8). The difference in tumor weights grown in these hosts was insignificant (P > .44). (B) Tumor-induced neovascularization was determined by indirect immunofluorescence with the blood vessel marker CD31 in cryosections of primary D121 tumors from src/ or control src+/ hosts. (C) Bar = 50 μm. The extent of CD31-positive staining blood vessels was determined as an indication of tumor-induced angiogenesis by quantitation of multiple random high-power fields from primary D121 tumors from src/ or control src+/ hosts (P > .5) (n = 8). Quantitation of CD31 immunostaining was performed as described in “Materials and methods.” For panels A and C, error bars indicate standard error.

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