Sentence examples for potent trail from inspiring English sources

Thus, more potent TRAIL death receptor-targeting reagents, such as oligomerized TRAIL, TRAIL fusion proteins with the capability to anchor to the cell surface or engineered TRAIL death receptor antibodies with high affinity for Fc γRIIb may have the potential to elicit improved anti-tumor activity, but this may come along with a risk for so far not recognized side effects.

Cancer cell resistance to TRAIL-induced apoptosis is likely to be a significant factor in this outcome, indicating that a TRAIL-comprising therapy will only be effective when a potent TRAIL sensitizer is applied in combination with a TRAIL-R agonist.

The formation of heterotrimeric non-apoptotic TRAIL receptor complexes and the receptor binding promiscuity of TRAIL endorsed the concept that DR selectivity may allow the creation of more potent TRAIL apoptosis inducers.

In addition, CDK9 inhibition-induced suppression of another short-lived protein, cFlip, was required to achieve potent TRAIL sensitization.

Histone deacetylase inhibitors have been established as potent TRAIL sensitisers (Bots and Johnstone, 2009; Spiegel et al, 2012).

Noteworthy, the latter principle not only allows potent TRAIL death receptor activation but also makes this activation dependent on cell surface antigen binding.

These findings have encouraged extensive research into identifying potent TRAIL-sensitizing agents that do not sensitize non-transformed cells.

It will hence be interesting to test whether enhanced clinical activity can be achieved by combining potent TRAIL-sensitizing treatments with high-activity TRAs.

We recently discovered selective inhibition of CDK9 as the most powerful approach to overcome TRAIL resistance of cancer cells that we have come across in more than a decade of searching for potent TRAIL-sensitizing strategies.

Hence, the challenge now is to determine whether newly devised high-activity TRAs combined with the most potent TRAIL-sensitizing strategies exert a therapeutic effect in these sophisticated mouse models of cancer to ultimately get TRAIL back on track to the cancer clinic.

Although our results using an antagonistic anti-TRAIL-R2 Ab support a potent mechanism of TRAIL resistance of #63 cells because of the lack of TRAIL receptors, the possibility that genotoxic agents may modify the signal transducers downstream of the receptors has to be elucidated.