Table 1.

Effects of Human rMig Treatment on Burkitt's Tumor in Athymic Mice

TreatmentMiceDay ofTumor SizeTotal DaysTumor Size% Tumor Necrosis% Damaged Vessels
TreatedFirst Injectionat First Injectionof Treatmentat End of Treatment(±SD)(±SD)ρ
(±SD)*(±SD)(±SD)(±SD)
None  —   —   —  8.06 (3.1) 11.5 (6.2) 56.6 (9.8) 
LCL 22 0.33  33.0  5.93  44.75  66.0  
Buffer 13.2 (2.2) 0.24 (0.1) 35.0 (1.7) 10.6 (1.1) 25.3 (7) 48.6 (15) 
rMig 13.7 (1.6) 0.34 (0.02) 39.0 (5.3) 9.9 (0.5) 40.6 (10.7) 76.5 (4.1) 
rIP-10 13.7 (1.8) 0.23 (0.1) 38.2 (5.3) 8.3 (2.4) 39.8 (10.8) 78.3 (2) 
TreatmentMiceDay ofTumor SizeTotal DaysTumor Size% Tumor Necrosis% Damaged Vessels
TreatedFirst Injectionat First Injectionof Treatmentat End of Treatment(±SD)(±SD)ρ
(±SD)*(±SD)(±SD)(±SD)
None  —   —   —  8.06 (3.1) 11.5 (6.2) 56.6 (9.8) 
LCL 22 0.33  33.0  5.93  44.75  66.0  
Buffer 13.2 (2.2) 0.24 (0.1) 35.0 (1.7) 10.6 (1.1) 25.3 (7) 48.6 (15) 
rMig 13.7 (1.6) 0.34 (0.02) 39.0 (5.3) 9.9 (0.5) 40.6 (10.7) 76.5 (4.1) 
rIP-10 13.7 (1.8) 0.23 (0.1) 38.2 (5.3) 8.3 (2.4) 39.8 (10.8) 78.3 (2) 

Nude mice bearing a Burkitt's tumor (CA46 line) induced as described in the Materials and Methods were injected daily into the tumor with human rMig or human rIP-10 at the dose of 400 ng (in 0.2 mL of a formulation buffer containing 50 mg/mL human serum albumin) for 30 to 43 days. Tumor-bearing control animals were injected into the tumor either with LCL (107 VDS cells/week in 0.2 mL normal saline) or with formulation buffer (0.2 mL daily).

*

Calculated from day of Burkitt's cell line injection; expressed as arithmetic mean for the group (±SD).

Calculated as the product of two-dimensional caliper measurement (longest perpendicular length and width); expressed in square centimeter as arithmetic mean for the group (±SD).

The percentage of tumor tissue necrosis was estimated by digital analysis of tumor cross-sections corresponding to the largest portion of the tumor. The slides were scanned using a flat bed scanner (Scanjet II CX; Hewlett Packard) and necrotic/total tumor area was measured; expressed as arithmetic mean for the group (±SD).

ρ Tumor sections were stained with EVG reagent and vessels staining at least in part with EVG were evaluated for vascular damage consisting of elastin fiber fragmentation and disruption with or without associated tumor infiltration, fibrinoid necrosis, or fibrin thrombi. The results are expressed as mean (±SD) percentage of damaged vessels estimated after evaluation of all EVG staining vessels in the tumor sections.

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