*Should we forget DNA effect, and plunge on epigenic dysruption of etoposide and slowing of processes at the Mitochondria as mechanisms of action of this anti-topoisomerase to define it better? This may open-up a new way for use of this target therapy. Now we learn that c-MYC recruitment of Histone acetylase is highly disturbed under this drug! Acting here, the drug can affect the Histone cover of DNA?
*Is the use of the GLI as intermediate by the Hedgehog circumstantial? Is it because the Gli is more available?
*Stop the Dicer or Exporting to really be in the Belly of the beast (in liquid cancers?)
*Can work at the C-MYC decrease Cytokine production by disabling this area of the cell? How this disruption affect the Wnt (and the Notch... What Ptch1 has to do anyway?
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