According to the article titled, “Keap1 loss promotes Kras-driven lung cancer and results in dependence on glutaminolysis,” “Approximately 20% of KRAS-mutant LUAD tumors carry loss-of-function mutations in the KEAP1 gene encoding Kelch-like ECH-associated protein 1, a negative regulator of nuclear factor erythroid 2-like 2 (NFE2L2; hereafter NRF2), which is the master transcriptional regulator of the endogenous antioxidant response.” This article essentially states that we should look at a glutaminase inhibition approach. After doing some research, I have learned that if we were to remove glutamine from the body then this would mean a reduction in cell growth or prompt cell death. But what if we remove it and it leads to increase in cell death where there shouldn’t be. I remember from lecture it being mention how in some patients they affected red blood cells and then led to high risk patients with anemia. I am having a hard time wrapping my mind in figuring ways where we won’t be affecting other functions and cells. In my research it also mentions how this indicates that these cells are dependent on, or “addicted” to, glutamine.
Recent comments