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Here, we provide an overview of the literature and discuss which downstream molecular effects are likely to be the drivers of the oncogenic and survival-prolonging properties of IDH1/2 mutations.
A hybrid solution that employs molecular dynamics close to the walls where molecular effects are important and continuum fluid mechanics in the remainder of the domain (far field region) is obtained.
However, the underlying molecular effects are not well known yet.
For both cytostatics multiple molecular effects are known.
These unique GC-mediated unique molecular effects are likely time, dose, cell-type, and cell-lineage dependent.
On the other hand, we will not be satisfied with mere association research on a variant apparently having a clinical impact as long as the molecular effects are obscure.
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However, while Lrig1 is known to inhibit ErbB signaling, whether or not Lrig3 has the same molecular effects is unclear.
Multiple molecular effects were observed during osajin treatment including a significant loss of mitochondrial transmembrane potential, release of cytochrome c into the cytosol, enhanced expression of Fas ligand (FasL), suppression of glucose-regulated protein 78 kDa (GRP78), and activation of caspases-9, -8, -4 and -3.
These molecular effects were associated with significant tumor regression on MRI.
In addition, the molecular effects were specific for cranial NC but not pharyngeal mesoderm markers.
The fundamental question now, having documented drug safety and molecular effects, is what to do next.
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