The report titled Cell Engineering Strategy to Enhance the Safety of Stem Cell Therapies, may provide the answer to one of the more perplexing questions in the Secret World of Myc. Why does Myc blockade or the inhibition of Myc cause cancer cells to freeze and die but 'appears to have no effect if it gets into normal cells'?
The researchers from MSK state that Myc is required to maintain a cancer-specific kinase called PKM2. The aberrant metabolism of cancer cells directly leads to an increased reliance upon Myc.
The article PKM2, cancer metabolism , and the road ahead published 17/12/2016, discusses the change in glucose metabolism in cancer cells and the role of specific 'pyruvate kinase isoforms' in supporting 'divergent energetic and biosynthetic requirements of cells in tumors and normal tissues'. The PKM2 isoform expression is implicated in the metabolic phenotype of cancer cells.
The article Tumor glycolysis as a target for cancer therapy: progress and prospects, published 03/12/2013 provides additional insight into the altered energy metabolism of cancer. The authors state that a change in energy metabolism within cells which become cancerous is a biochemical fingerprint which points towards tumor glycolysis as a target for cancer therapy.
So, is all this research relevant to understanding the mechanism of action for a Myc inhibitor such as Omomyc or iMYC? I guess we will find out.
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