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Oxford University Press (OUP), Bioinformatics, 3(29), p. 347-354

DOI: 10.1093/bioinformatics/bts702

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Computational modelling of LY303511 and TRAIL-induced apoptosis suggests dynamic regulation of cFLIP

This paper is available in a repository.
This paper is available in a repository.

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Abstract

Motivation: TRAIL has been widely studied for the ability to kill cancer cells selectively, but its clinical usefulness has been hindered by the development of resistance. Multiple compounds have been identified that sensitize cancer cells to TRAIL-induced apoptosis. The drug LY303511 (LY30), combined with TRAIL, caused synergistic (greater than additive) killing of multiple cancer cell lines. We used mathematical modelling and ordinary differential equations to represent how LY30 and TRAIL individually affect HeLa cells, and to predict how the combined treatment achieves synergy.