TRAIL-R deficiency in mice enhances lymph node metastasis without affecting primary tumor development
J. Clin. Invest. Anne Grosse-Wilde, et al. 118:100 doi:10.1172/JCI33061 [Go to this article.]

Figure 2
TRAIL-R does not influence primary skin tumorigenesis. (A) Papilloma incidence rates. (B) Tumor initiation rates, as reflected in the average number of papillomas over time. (C) Tumor growth rates, represented by combined average papilloma area over time. (D) Carcinoma incidence rates. Vertical bars indicate deaths of mice with carcinomas. (E) Papilloma-to-carcinoma conversion rate per week of papilloma exposure. The 95% confidence intervals are displayed. (F) Cell surface–expressed TRAIL-R was examined using a TRAIL-R–specific antibody (MD5-1) on WT immortalized keratinocytes (cell line C-50), papilloma cells (cell line 308), and carcinoma cells (cell lines DT02 and DT12). Histological analysis (G–J) of tumor sections did not reveal any differences between the different Trail-r genotypes. Representative tissue sections (H&E staining and brown keratin staining) from Trail-r^–/– mice are shown. (G) Keratin-positive papilloma. Among all genotypes, primary malignant tumors were (H) SCC, (I) spindle cell variant of SCC (SVSCC), or (J) fibrosarcomas, which is shown with keratin-positive hair follicles (HF). (K) Tissue sections of malignant carcinomas (fibrosarcoma or SCC) were stained with antibodies against active caspase-3 or Ki-67. Representative fields are shown (original magnification, ×400).