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Table 1 Treatment with Ang1 and Ang2 inhibitors modulates the phenotype of human tumor cells

From: Inhibition of the angiopoietin/Tie2 axis induces immunogenic modulation, which sensitizes human tumor cells to immune attack

A. OV 17-1
  HLA-A2 CEA MUC-1 CD54 Calreticulin CD95 Trail-R1 Trail-R2
  % (MFI) % (MFI) % (MFI) % (MFI) % (MFI) % (MFI) % (MFI) % (MFI)
 Control 99.4(34250) 40.7(731) 55.9(1170) 93.8(16581) 3.5(431) 57.2(691) 27.4(604) 10.1(93)
 mL4-3 + L1-7(N) 99.1(34180) 40.0(872) 59.0(1124) 97.0(23584) 3.7(429) 65.3(813) 33.7(750) 10.1(107)
B. MDA-MB-231
  HLA-A2 CEA MUC-1 CD54 Calreticulin CD95 Trail-R1 Trail-R2
  % (MFI) % (MFI) %(MFI) % (MFI) % (MFI) % (MFI) % (MFI) % (MFI)
 Control 98.7(62083) 40.2(671) 56.0(2268) 97.9(30985) 10.6(377) 35.1(438) 44.0(775) 35.1(367)
 mL4-3 + L1-7(N) 99.1(60495) 43.7(666) 59.4(2670) 99.1(35652) 15.9(428) 41.2(493) 48.7(797) 30.5(292)
  1. The human ovarian cancer cell line OV17-1 (A), and human breast cancer cell line MDA-MB-231 (B) were treated with the Cmax of mL4-3 and L1-7(N) (16 and 10 μg/mL, respectively) or control (human IgG1-Fc at 26 μg/mL) for 3 days
  2. Cells were then harvested and analyzed by flow cytometry for expression of surface markers reported to be involved in CTL lysis (HLA-A2, CEA, MUC-1, ICAM-1, calreticulin, Fas, Trail-R1 and Trail-R2). Data indicate percentage of positive cells; MFI is in parentheses. Gating was performed using isotype controls Bold values indicate marker upregulation of > 10 % in percentage or MFI compared to controls