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The irradiation time Tirr indicates the time until the radiation cell kill outnumbers the tumour growth.
Micron size aggregates caused rapid membrane damage, resulting in acute cell kill.
Therefore, in contrast to the clonogenic cell kill resulting from bortezomib treatment, MG132-induced kill was not mediated by ROS.
Supra-additive clonogenic cell kill was observed only when bortezomib was administered 24 h after {131I-MIBG + topotecan} (Table 3).
This therapeutic activity was supported by our observation of enhanced radiation cell kill in the presence of bortezomib or MG132.
These results are large enough to suggest the potential for a meaningful amount of additional tumor cell kill.
These indicated that supra-additive clonogenic cell kill (CI < 1) was dependent on both the dose and the schedule.
The mechanism of bortezomib-induced clonogenic cell kill was investigated by determining the protection afforded by treatment with antioxidants.
A quantitative comparison of tumor cell kill determined from serial MRI volume measurements and BLI photon counts following 1,3-bis 2-chloroethyl -1-nitrosourea 1,3-bis 2-chloroethyl -1-nitrosourea 1,3-bis 2-chloroethyl -1-nitrosourea 1,3-bis 2-chloroethyl -1-nitrosourea 1,3-bis 2-chloroethyl -1-nitrosourea
BE3 esophageal adenocarcinoma cells were infected with NV1066 in vitro to determine cell kill and viral replication.
Atrophy (tissue shrinkage) reflects cell kill.
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