Microarray analysis identifies a death-from-cancer signature predicting therapy failure in patients with multiple types of cancer
J. Clin. Invest. Gennadi V. Glinsky, et al. 115:1503 doi:10.1172/JCI23412 [Go to this article.]

Figure 1
Microarray (A–D) and RT-PCR (E) analyses reveal increased expression of BMI-1 mRNA in multiple human prostate cancer cell lines established from metastatic tumors (PC-3, LNCap, DuCap, VCap, etc.) compared with normal human prostate epithelial cells (NPEC) (A and E); in xenograft-derived human prostate cancer cell line variants (PC-3M, PC-3MLN4, PC-3MPro4) compared with the plastic-maintained parental cells (PC-3) (B); in highly metastatic human prostate carcinoma xenografts (PC-3MLN4) compared with the less metastatic parental counterparts (PC-3) growing orthotopically in nude mice (C); in lymph node metastases of human prostate cancer growing in the prostate of nude mice (MET) (C); and in invasive primary prostate tumors and distant metastatic lesions in the TRAMP transgenic mouse model of prostate cancer (D). Prostate tissues from age-matched wild-type C57BL/6 mice served as control samples in Figure 1D. The numbers 4, 5, and 7 indicate the age of TRAMP mice (in months). Each sample represents a pool of tissues from 3–5 mice. P values were obtained using a 2-tailed t test. LN3, LNCapLN3; LN4, PC-3MLN4; PRO4, PC-3MPRO4; PRO5, LNCapPRO5; SV, seminal vesicles; X, human xenograft tumors in nude mice.