Reactive oxygen species produced by altered tumor metabolism impacts cancer stem cell maintenance.
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TLDR
The delicate, yet complex, relationship between ROS and its pleiotropic role in modulating the CSC is explored, which provides survival advantages that sustain malignant features, such as proliferation and self-renewal, while producing the necessary antioxidants that reduce damage from oxidative stress.Abstract:
Controlling reactive oxygen species (ROS) at sustainable levels can drive multiple facets of tumor biology, including within the cancer stem cell (CSC) population Tight regulation of ROS is one key component in CSCs that drives disease recurrence, cell signaling, and therapeutic resistance While ROS are well-appreciated to need oxygen and are a product of oxidative phosphorylation, there are also important roles for ROS under hypoxia As hypoxia promotes and sustains major stemness pathways, further consideration of ROS impacts on CSCs in the tumor microenvironment is important Furthermore, glycolytic shifts that occur in cancer and may be promoted by hypoxia are associated with multiple mechanisms to mitigate oxidative stress This altered metabolism provides survival advantages that sustain malignant features, such as proliferation and self-renewal, while producing the necessary antioxidants that reduce damage from oxidative stress Finally, disease recurrence is believed to be attributed to therapy resistant CSCs which can be quiescent and have changes in redox status Effective DNA damage response pathways and/or a slow-cycling state can protect CSCs from the genomic catastrophe induced by irradiation and genotoxic agents This review will explore the delicate, yet complex, relationship between ROS and its pleiotropic role in modulating the CSCread more
Citations
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Transaminase Inhibition by 2-Hydroxyglutarate Impairs Glutamate Biosynthesis and Redox Homeostasis in Glioma
Samuel K. McBrayer,Jared R. Mayers,Gabriel J. DiNatale,Diana D. Shi,Januka Khanal,Abhishek A. Chakraborty,Kristopher A. Sarosiek,Kimberly J. Briggs,Alissa Robbins,Tomasz Sewastianik,Sarah J. Shareef,Sarah J. Shareef,Benjamin A. Olenchock,Seth J. Parker,Kensuke Tateishi,Kensuke Tateishi,Jessica B. Spinelli,Jessica B. Spinelli,Mirazul Islam,Mirazul Islam,Marcia C. Haigis,Ryan E. Looper,Keith L. Ligon,Bradley E. Bernstein,Bradley E. Bernstein,Ruben D. Carrasco,Ruben D. Carrasco,Daniel P. Cahill,John M. Asara,Christian M. Metallo,Neela H. Yennawar,Matthew G. Vander Heiden,Matthew G. Vander Heiden,William G. Kaelin,William G. Kaelin +34 more
TL;DR: This paper showed that (R)-2HG potently inhibits the 2OG-dependent transaminases BCAT1 and BCAT2, likely as a bystander effect, thereby decreasing glutamate levels and increasing dependence on glutaminase for the biosynthesis of glutamate and its products.
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Relaxometry with Nitrogen Vacancy (NV) Centers in Diamond
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References
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TL;DR: Induction of pluripotent stem cells from mouse embryonic or adult fibroblasts by introducing four factors, Oct3/4, Sox2, c-Myc, and Klf4, under ES cell culture conditions is demonstrated and iPS cells, designated iPS, exhibit the morphology and growth properties of ES cells and express ES cell marker genes.
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Cell signaling by receptor-tyrosine kinases
TL;DR: Understanding of the complex signaling networks downstream from RTKs and how alterations in these networks are translated into cellular responses provides an important context for therapeutically countering the effects of pathogenic RTK mutations in cancer and other diseases.