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Several mechanisms may render cells resistant to FasL-induced apoptosis.
If it suppresses Nrf2 activation it may render cells more susceptible to oxidative stress.
Furthermore, the severity of the telomerase mutation may render cells completely unable to re-elongate telomeres.
Integrin down-regulation may render cells less adhesive and therefore less invasive.
Thus, any aberrant regulation of MAPK cascades may render cells insensitive to regulatory signals and contribute to tumor genesis [ 24].
Thus, aUPD at 13q13.2-q13.3 and 13q14.11-q14.2 regions may render cells homozygous of novel genes for existing abnormalities.
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Also, overstimulation may render cell signal resistance due to feedback block of signaling pathways.
Recent evidence indicates that alternative mechanisms, such as cell-cell fusion, may also render cells with the ability to escape cell cycle control, tissue invasion, and metastasis [ 10].
Increasing the activity of PHDs after PDT with α-ketoglutarate may therefore render cells less susceptible to HIF-1-mediated survival.
The depletion of ERα in combination with the up-regulation of p53 following WA treatment in MCF-7 cells may render the cells more sensitive to apoptosis.
Therefore, the observed induction of ERK in trastuzumab-resistant molecular apocrine cells may render these cells dependent on MAPK/ERK signaling and sensitizes them to the synergy between AR and MEK inhibitors.
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