MST valuation of RAC, page-207

After finally obtaining access to the PDF, I have found more exciting news. The researchers tested CS1 (bisantrene) and found that it was more effective at altering mitchondrial respiration with a concentration of 200nM. By comparison, R-2HG was used at the concentrations 50 - 300 uM (250 - 1500 fold greater concentrations than bisantrene).



The current findings highlight the use of bisantrene to attenuate (reduce in force) glycolytic flux (energy production) in leukemia cells, adding a new layer of mechanism.




For those among us that are not as science minded or who may not be aware of cellular respiration and why it is important, I will provide some insight. Cellular respiration and namely glycolysis is a process where glucose is broken down to produce molecules called ATP. ATP are what cells use for energy. Cancer cells use primarily glucose for energy for growth, which is why they can grow and multiple so fast. What is fascinating for me is that this article explains the reasons why FTO inhibition leads to a reduction in cancer cell growth and why overexpression is commonly associated with cell proliferation and growth. Essentially, this article has potentially identified the mechanism by which cancer fuels it's growth, a mechanism related to FTO and also have found that bisantrene is effective at manipulating cancer cell metabolism in leukemia therapy. What is fundamental to understand here is that this study can only talk about the effects seen in leukemia cells. Ultimately, you need to come up with your own interpretation of these findings, but I will leave a couple of question with you;

1. Would FTO overexpression in other cells lead to the same upregulation of glycolysis (energy production)?
2. Would FTO inhibition in other cells lead to the same downregulation of glycolysis (energy production)?

Make up your own mind.

All IMO - DYOR