Natalya N. Pavlova

TL;DR: This Perspective has organized known cancer-associated metabolic changes into six hallmarks: deregulated uptake of glucose and amino acids, use of opportunistic modes of nutrient acquisition, useof glycolysis/TCA cycle intermediates for biosynthesis and NADPH production, increased demand for nitrogen, alterations in metabolite-driven gene regulation, and metabolic interactions with the microenvironment.

TL;DR: The diversity of biosynthetic and regulatory uses of glutamine and their role in proliferation, stress resistance, and cellular identity are examined, as well as the mechanisms that cells utilize in order to adapt to glutamine limitation.

TL;DR: By preventing nutritional consumption of extracellular proteins, mTORC1 couples growth to availability of free amino acids and may have important implications for the use of mTOR inhibitors as therapeutics.

TL;DR: It is shown that REST is regulated by ubiquitin-mediated proteolysis, and that β-TRCP overexpression, which is common in human epithelial cancers, causes oncogenic transformation of human mammary epithelial cells and that this pathogenic function requires REST degradation.

TL;DR: PTPN12 is identified as a commonly inactivated tumor suppressor in triple-negative breast cancer and a rationale for combinatorially targeting proto-oncogenic tyrosine kinases in TNBC and other cancers based on their profile of tyosine-phosphatase activity is provided.