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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