The rationale is that chemotherapy and immunotherapy can induce autophagy in tumor cells, which in turn is used by tumor
cells as a survival mechanism to resist pharmaceutical invention.
Similar to capsaicin, tumor necrosis factor is suspected to both induce and reduce cancer
cell growth, and was shown to commit
cells to
survival when stimulating EGFR transactivation
mechanisms, indicating that EGFR could act
as a molecular switch determining the antiapoptotic effect of tumor necrosis factor (50).
The study, recently published in the journal Molecular Cancer Therapeutics, showed that dinaciclib disrupted a
cell survival mechanism known
as the unfolded protein response (UPR).